diff --git "a/raw/pharmacology.json" "b/raw/pharmacology.json" new file mode 100644--- /dev/null +++ "b/raw/pharmacology.json" @@ -0,0 +1,1321 @@ +[ + { + "Introduction": "hello and welcome to chapter 12 principles of pharmacology emergency care and transportation of the sick and injured 12th edition repeat this chapter and the related", + "National EMS Education Standard Competencies": "coursework you will understand the significance and characteristics of general pharmacology and will be able to identify describe and demonstrate the steps for assisting administering medications carried by an emt okay so as an introduction medications", + "Introduction Continued": "are an important intervention available to you as an emt and when used appropriately medications may alleviate pain and improve a patient's condition but failure to administer medication safely and competently can lead to serious consequences for a patient including death", + "How Medications Work": "so let's talk about how medications work first we'll talk about medical definitions okay so pharmacology that's the signs of drugs including their ingredients preparation uses and actions on the body okay medication that's a substance used to treat or prevent disease or relieve pain pharmacodynamics is the process by which the medication works on the body and a medication can either produce an effect or block the receptors to prevent other chemicals or medications from binding\nan agonist is a medication that causes stimulation of receptors and an antagonist is a medication that binds to the receptor or blocks other medications or chemicals from attaching okay so dose that's the amount of medication that is given within it depends on the patient's weight age or desired action of the medication then you have action and the definition of action is the therapeutic effect that a medication is expected to have on the body so we talked about pharmacodynamics\nlet's talk about pharmacokinetics and that's the actions of the body upon the medication so the onset of the action that's the time from the medication administration until clinical effects occur the duration that's the length of time that the clinical effects persist the elimination that's how medications and chemicals are removed from the body and then peak the point or period when the maximum clinical effect is achieved okay factors affecting how medication works depends on the route of the medication and shock states there are indications okay so indications are the reasons or conditions for which a particular medication is given then there's contra indications and those are situations in which a medication would either harm the patient or have no positive effect and so there's two different types of contraindications there's absolute contraindications and that's a situation in which the medication should never be given if um if there's a contra indication is present if this is okay and then there's a relative contraindication that's situations which the benefits of administering the drug may outweigh the risk okay so if somebody's completely allergic to medication it causes anaphylaxis well of course that's an absolute contraindication relative contraindication might be it causes nausea right okay so adverse effects and that's any action of the medication other than the desired ones you have a couple adverse effects so you have unintended effects and that's effects that are undesirable but pose little risk to the patient and then you have untowards effects and those are effects that can be harmful to the patient", + "Medication Names": "all right so we talked a little bit about different definitions now let's talk about names and the medication names so when we talk about names we talk about a generic name or trade name okay so the generic name is a simple clear non-proprietary name generic names are not capitalized and so you can see on the slide there's an example of ibuprofen ibuprofen is in lower case and then there's trade names and that is a brand name that the manufacturer gives the drugs okay so trade names begin with a capital letter and one drug may have more than one trade name okay so an example would be tylenol prescription drugs are distributed only by pharmacists and require a physician's order okay so but over-the-counter or otc drugs may be purchased directly without a prescription then there are other types of drugs and so um there are recreational drugs and those are drugs such as heroin or cocaine there are herbal remedies enhanced drugs vitamin supplements alternative medicines and any medicine that a patient takes can be pharmacologically active and can cause an effect so ask the patient about any and all medications or drugs they are taking", + "Routes of Administration": "all right so that we talked about drug names now let's talk about routes okay so routes of an administration okay so there are internal medications and then there are parallel internal medications okay so two different ways to think about it the internal medications are entered the bodies for the digestive system it's often a pillar liquid form such as a cough or a cold medicine okay and uh medications administered via this route tend to absorb slowly and are not commonly used in the emergency setting okay and then we have the para internal para internal medications and they enter the body by some other means often in liquid form administered through needles or syringes and absorbed more quickly and offer a offer a more predictable or measurable response then we have absorption and this is the process by which the medications travel through the body tissues into the bloodstream okay so here we have common routes of administration um you'll see pr and that is per rectum and that's basically means by rectum and it's easy to administer provides reliable absorption okay and then there's oral po and this is um by mouth and it takes as long as one hour for absorption to occur okay then you have intravenous and so that's into the vein iv and that's the fastest delivery but cannot be used for all medications okay and then you have io and that's into the bone and it reaches the bloodstream through the bone marrow it requires drilling a needle into the outer layer of the bone then you have sc which is subcutaneous injection and sub beneath and cutaneous skin okay so just what it sounds like it's an injection given into the fatty tissue between the skin and the muscle then you have intramuscular and just what it sounds like into the muscle that is usually absorbed quickly but not all medications can be administered by the im route okay you have inhalation that's breathed into the lungs it's absorbed into the bloodstream quickly it forms include aerosols or fine powders and sprays and then you have sublingual okay so a sub is under lingual tongue and it's just what it sounds like under the tongue it enters through the oral mucosa under the tongue and is absorbed into the bloodstream within minutes then you have transcutaneous trans is through and cutaneous we just talked about this skin so through the skin it'll also be called transdermal and these could be patch that you put on the skin it's a longer lasting effect than other routes okay and then you have intranasal that's i n and relatively new format for delivery of medication medication is pushed through a mucosal atomizer device so a mad device mucosal atomizer and it air slices a liquid for delivery into the nostril it's very quick absorption okay and on this table you could see the routes of administration and the routes of absorption rate okay so you have the internal and the para internal and um you could see that the internal is a very um by mouth is a slow route okay", + "Medication Forms": "all right okay so medication forms in the form of the medication usually dictates the route of administration so the manufacturer chooses the form to ensure and the proper route of the administration timing of the medications release into the bloodstream and the effects of the target organs or body systems", + "Tablets and Capsules": "all right so let's talk about tablets and capsules most medications given by mouth are in tablet or capsule form capsules are gelatin shells filled with water or powder or liquid medication and tablets often contain other materials that are mixed with the medication and compressed", + "Solutions and Suspensions": "then you have solutions and suspensions so a solution is a liquid mixture of one or more substances that cannot be separated simply solutions can be given by almost any route okay so when given by mouth solutions may be absorbed from the stomach fairly quickly because the medication is already dissolved so many solutions can be given by as an inim or sc subcutaneous injection okay a suspension is a mixture of fine grand particles that are distributed evenly throughout the liquid by shaking or stirring but do not absolve okay so suspensions separate if they are left alone and it's important to shake or swirl a suspension before it's administered all right then you have meter dose", + "Metered-Dose Inhalers": "inhalers so liquids or solids that are broken into small enough droplets or particles can be inhaled and so a spray canister directs some substances through the nose and into the lungs it delivers the same amount of medication with each time and it's used and often used for respiratory illnesses such as asthma or emphysema", + "Topical Medications": "then you have topical medications and these are lotions creams and ointments and they can be applied to the skin surface and affect only that area so some examples are hydrocortisone cream and neosporin ointments calamine lotion okay", + "Transcutaneous Medications": "then you have trans cutaneous medications also referred to as transdermal so through the skin many transdermal medications have a systemic or a whole body effect so if you touch the medication with your skin you will absorb it just like the patient then you have gels so these are semi liquids and they are administered in capsules or through plastic tubes and there's a good example of gel that we use and that's that oral glucose for diabetic emergencies", + "Gases for Inhalation": "and then gas okay so one of the most commonly used gases is oxygen and usually delivered through a non-rebreather or nasal cannula general steps and administering", + "General Steps in Administering Medication": "medications medications should be administered only under the influen or the authorization of online or offline medical direction and you need to follow the rights and there's nine of them okay so follow the right patient you have to make sure that you have the right patient and you're going to ensure that the patient who needs the medication is the person who receives the medication and then the right medication and indication so verify the proper medication is and prescription right dose you're going to verify the form and dose of the medication the right route and you're going to verify the route of the medication the right time you need to check the expiration date and condition of the medicine right education you need to inform the patient of the medication you intend to administer including any likely adverse effects or unusual sensations he or she may experience the right to refuse so a patient with a decision making capacity can decline or refuse proposed interventions or medication and the right response and evaluation so monitor the patient's vital signs mental status signs of perfusion and respiratory effort after medication administration you need to assess for anticipated response and observe for any adverse medication effects okay and then number nine you need the right documentation you need to document your actions and the patient's response okay so medication administration so cross-check and procedures so using a verbal cross-check procedure that verifies you are giving the right drug and the right patient at the right dose has been found to reduce medication errors so this table in chapter 12 dash 3 that's the rights of medication that i just talked about and there's nine of them and just what i just mentioned so it's right patient right medication education right dose right route right time right education right to refuse right to response and evaluation and the right documentation", + "Medication Administration and the EMT": "so over the years emts have been allowed increasing responsibility to work with medications many departments have strict guidelines on when an emt is allowed to administer a medication okay so there's three different types of medication administration or or ways that you would be allowed to now there's the peer-assisted medication and that's when you administer medication to yourself or to your partner so for example if you're exposed to toxic agent you would do this okay then there's patient-assisted medication and this is when you assist the patient with administering his or her own medication so examples are an epi autoinjector or nitro or a metered dose inhaler then there is emt administration of medication okay so the emt directly administers the medication to the patient the patient may be severely confused or unable to understand the need for the medication so examples include oxygen oral glucose and aspirin medical control state guidelines and local protocols determine what an emt in your system may administer and you need to refer to your local standards to obtain a listing of how and when emts can administer medications okay so oral medications", + "Oral Medications": "now we're going to talk about the steps okay so follow the following steps to perform oral medications we want to take standard precautions okay then we're going to confirm the medication has not expired we need to obtain medical direction per our local protocol so we need to confirm that the patient has a patent airway and is able to swallow or chew this medication okay we need to monitor the patient's condition and then document so oral glucose oral glucose is a sugar that cells use for energy it is necessary for brain cells to survive and hypoglycemia that is extremely low glucose so oral glucose can counter optic counteract the effects of hypoglycemia an emt can give glucose only by mouth in the form of gel so never administer oral medication to an unconscious patient or to one who is unable to swallow or protect his own airway all right so another oil medication that we could prescribe or that we could give is aspirin now aspirin reduces fever it's pain and inflammation however we're only going to give it in the pre-hospital field to inhibit platelet aggregation okay so um which is useful during a potential heart attack so contraindications are hypersensitivity to aspirin a pre-existing liver damage or some type of bleeding disorder or asthma and should not be given to children okay all right sublingual medications now the", + "Sublingual Medications": "considerations of these are there are advantages it's easy to talk with awake and alert patients and advise them to place the pill under their tongue absorption rates are relatively quick now the disadvantages of these are any medication placed in the mouth requires consent constant evaluation of their airway okay and it should not be used if the patient is uncooperative or unconscious now nitro is a sublingual medication that we're going to use and many cardiac patients carry fast-acting nitro in it to relieve angina pain so what it does is it increases blood flow by relieving the spasm and causes arteries to dilate by relaxing muscles of the coronary arteries and veins it also relaxes veins throughout the body so that less blood return is returned to the heart and it decreases the workload and it will decrease blood pressure so before administering nitro we have to check the blood pressure okay and then we need to obtain orders or follow your local protocols to administer nitro it can have a potentially fader interactions with erectile dysfunction medication taken within the last 24 hours and these medications include viagra cialis levitro or drugs for any drug for erectile dysfunction may be shown and it can be used by both men and women in case because erectile dysfunction medications are vasodilators as well and um so because nitro is a vasodilator if you add two vasodilators together you could have a potentially fatal interaction all right so nitro it can be administered by a metered dose spray or by a tablet okay so let's talk about the tablet first you place the tablet under the tongue and it dissolves so the patient should experience a slight tingling or burning sensation nitro should be stored in its original glass container with the cap screwed tightly okay and administered by a meter to spray so deposit we're going to deposit the medication under the tongue one spray equals one tablet administration can considerations for both the tabloid and spray we want to wait five minutes for a response before repeating the dose we need to closely monitor the patient's vital signs particularly the blood pressure and then give repeated doses per medical control or local protocol we want to always wear gloves the medication can be absorbed by your skin and reconfirm the medication is still indicated for the patient know and understand local protocols", + "Intramuscular Medications": "all right so now we've moved on from sublingual we're going to go to intramuscular medications and the considerations for these there are advantages and they provide quick and easy access to the circulatory system without the need for placing a needle into the vein and blood flow to the muscles is relatively stable even during circumstances of severe illness and injury but there are disadvantages and that is that you have to use a needle and there is some pain involved\nokay and so the intramuscular medication we're going to use is the epi and this is also known as adrenaline and it releases inside the body when there is sudden stress okay so the main hormone that controls the body's fight-or-flight response\nand so characteristics is secreted naturally by the adrenal glands it dilates passages in the lungs constricts blood vessels and causes increased blood pressure it also increases heart rate and the blood pressure okay it should be given only to patients who are experiencing a life-threatening allergic reaction so epi may be just dispensed through an auto-injector automatically delivers a pre-set amount of medication and that's usually 0.3 milligrams and some services do not permit emts to carry epi but they do allow them to assist patients in administering their own okay oh and then there it we are going to talk about an intramuscle medication on narcan or naloxone and so there are im injections but there are also intranasal or narcan so probably talk about that next but um first we'll talk about the im and so this is used to reverse the effects of an opiate overdose it can be administered by a family member caregiver so some considerations we need to follow the local protocol of course and find out if naloxone has been administered by a bystander prior to arrival the effects of naloxone may not last as long as the opiates so repeated doses may be needed administration of naloxone to opiate dependent patients can cause severe withdrawal symptoms including seizures and cardiac arrest so consider your personal safety", + "Intranasal Medications": "all right and then the next of course is that intranasal naloxone and also called narcan the most common technique for naloxone administration is via the intranasal route the same considerations described for administering the i n or i m naloxone apply here if naloxone is not available we're just going to bag valve mask may be required", + "Inhalation Medications": "okay all right inhaled medications the ones we're going to use most often of course are oxygen by far the most commonly administered medication in the pre-hospital setting all cells especially those in the heart and brain need oxygen to function properly and it's generally administered via a non-rebreather mask at 10 to 15 meters or a nasal cannula at six two to six liters most also must also provide artificial ventilations if the patient's not breathing so using a bvm at 15 liters we're going to ensure that there's no open flame lit cigarettes or sparks in the area when we're administering oxygen okay all right now meter dose inhalers and nebulizers so used to administer liquid medications that have been uh turned into a fine mist and by flow of air oxygen so medication is atomized it's breathed into the lungs and delivered to the alveoli and the advantages are its face it's fast and relatively easy to uh route to excess the disadvantages though is the patient needs to be cooperative and controlled breathing they cannot be used for unconscious patients okay so medications administered using a meter disinhaler or small volume nebulizer svn um you an mdi requires a great deal of coordination to administer so may be difficult to achieve when a person is having trouble breathing all right and then there's the spacer for the meter disc inhaler so a spacer fits over the inhaler like a sleeve a spacer has an opening for the inhaler at one end and the mouthpiece at the other the patient sprays the prescription dose into the chamber and then breathes in and out of the mouthpiece until the mist is completely inhaled so spacer devices are especially useful with young children with difficulty using a metered dose inhaler okay so sv ends are much easier to use than meter dose inhalers and that small volume nebulizer they take longer to deliver the medication they require an external air or oxygen source they can be effective then they can be more effective than a meteor disinhaler in patients with moderate to severe respiratory distress and they can be used while the patient is on cpap and during bag valve mask ventilation so they can be easily adapted to a non-root breather mask okay so let's talk about the patient's", + "Patient Medications": "medications so patients medication so patient assisted includes finding out what with which medication the patient is currently taking this information may provide vital clues to the patient's condition so they may help guide your treatment and may be extremely useful to the emergency department physician and it can help you determine a chronic or underlying condition when a patient is unable to relate his or her medical history so discover what the patient takes and transport the medications or list of them with the patient to the emergency department ask about the use of non-prescription drugs such as over-the-counters or herbal or illegal drugs implications for ems providers do not underestimate the importance of obtaining a thorough medical history medications are frequently not taken or prescribed so consider a patient's medication in the context of the clinical encounter patient medications may significantly alter the clinical presentation of many acute medical problems or injuries okay so you have beta adrenergic blocking agents and calcium channel blockers those can slow the heart rates down of course you have anti-platelet and anticoagulant medications so if a patient even bumps their head they can have significant bleeding in the brain all right so so never underestimate the medications that a patient is taking", + "Medication Errors": "medication errors is what we're going to talk about next so a medication area is inappropriate use of a medication that could lead to patient harm so ensure that the environment does not contribute to these areas or era sorry and ensure that the lighting is sufficient organize the equipment limit distractions as much as possible and consider using a cheat sheet to help yourself remember all the critical steps to medication administration if a medication error does take place rapidly provide any appropriate care\nthat is required okay so notify medical control as quickly as possible follow your local protocols and document the incident thoroughly accurately and honestly talk with your partner supervisor or medical director this is an opportunity to learn identify areas to target during quality improvement all right so that concludes chapter 12 uh pharm ecology chapter and next we're going to just go through the review slides okay so pharmacology is defined as the what is it it's the field of science that deals with the study of drugs and medications which of the following statements regarding medications is false okay so false and we know it's over-the-counter drugs must be prescribed by a physician nope over-the-counter does not need a prescription which of the following routes of medication administration is the fastest all right so we know that oral is going to be the slowest and that iv you should have said iv iv is the fastest okay it's directly into the vein right into the bloodstream okay when administered to a patient a metered dose inhaler will well it looks like a is the very first one deliver the same dose each time it's administered that's why it's called a meter dose okay you're managing a 62 year old woman who complains of crushing chest pain the blood pressure is 84 over 64. her heart rate is 110 medical control advises you to assist her in taking her nitro what after receiving this order what should you do what should we do all right we're going to repeat the patient's blood pressure to the physician and confirm the order that's what i would do yeah because hopefully the physician heard it in the first place if not he's definitely going to hear it again b all right activated charcoal is indicated for patients who have ingested certain drugs and toxins because well goodness we didn't even really talk about activated charcoal it seems like they left it out of the slide um presentation so activated charcoal is indicated for patients who have ingested certain drugs and toxins because it it's going to bind to chemicals in the stomach and delay the absorption so d okay and we take this for overdoses it's an oral medication and it's charcoal with regard to pharmacology the term action refers to what do we know what action is action is as it implies to pharmacology the term action refers to the effect that the drug is expected to have on the patient's body okay so it is d which of the following patients is best candidate for oral glucose all right so this is a good question it's one that they ask on the national registry questions and you have to be very careful okay so we know right away unconscious we're not going to be doing that one you cannot administer oral glucose for unconscious all right conscious patient who is showing signs of hypoglycemia well that seems very um good answer we're not giving it for hyper and we're not giving it to a semi-conscious so conscious patient who's showing signs of hypoglycemia and that's a all right epi is given to patients with anaphylactic shock because of its effects on so what does it do it bronchodilates and it vasoconstricts we want the bronchioles open and then we want the vessels constricted right to increase the blood pressure perfect two major um complications associated with anaphylaxis shock or bronchoconstriction and then a vasodilation so we want to do the exact opposite very good okay the process by which medications travel to the body until they reach the bloodstream is called and it is the uh ab absorption absorption of adsorption refers to the binding of one chemical to another so it's absorption okay so we'll see thank you for joining me for chapter 12 the pharmacology chapter and if you liked this lecture go ahead and subscribe and we will be doing the rest of the book have a great night" + }, + { + "Introduction to Principles of Pharmacology": "hello and welcome to emergency care in the streets chapter 13 principles of pharmacology lecture medication administration is a defining element of paramedic clinical practice pre-hospital providers will encounter patients who are experiencing adverse effects of medication taken at home so it's critical to obtain a medical history during patient assessment paramedics must also understand pharmacology when administering medicines to treat patients symptoms during an ems response or while a patient who has been exposed to a potentially toxic chemical drug or medication okay so let's get started with the chapter so medication can be correct or decrease the severity of an illness or injury manage life-threatening conditions or substantially reduce patient discomfort severe often life-threatening consequences if paramedics administer the wrong medication or administer medication via the wrong route or the incorrect dose or fail to follow the correct technique so pharmacology is the scientific study of how various substances interact or alter the function of living organisms and it's used in a variety of ways so for treating patients who already receive medication or treating patients who have been exposed or administering medications to treat patient symptoms", + "Historical Perspective on Medication Administration": "historically perspective on medication administration so chemicals derived from plants and animals have been used for centuries to cure disease or relieve symptoms natural remedies were directed towards symptoms rather than the disease process and certain medications discovered in ancient times are still in use formal scientific study of the effect of medications began in late 17th and early 18th centuries the science of pharmacology has evolved into a highly profitable and highly regulated industry evidence-based guidelines assist clinicians using pharmacologic interventions and medications undergo extensive testing and clinical trials adverse reactions though are common so medication and drug uregulation so let's talk a little bit about this comprehensive u.s system of medication and drug regulation in 1906 the pure food and drug act prohibited altering or mislabeling medications in 1909 the opium exclusion act prohibited importing opium and in 1914 the harrison narcotic act restricted the use of opiates and cocaine the food and drug and cosmetic act of 1938 gave the u.s food and drug administration or the fda enforcement authority for approving new medications and removing unsafe ones so let's talk about approval of new", + "Approval of New Medication": "medication and how it typically takes years only a small fraction of medications submitted to the fda are approved and some medications are used off label and that's a purpose not approved by the fda and at doses different than they recommend and by the route of administration not approved common practice in healthcare it increases liability for the healthcare provider so paramedics need to be familiar with the rules and regulations implemented", + "Controlled Substances Act of": "under the controlled substances act of 1970. this act is also known as the", + "The Comprehensive Drug Abuse Prevention and Control Act": "comprehensive drug abuse prevention and control act it classifies certain medications into the potential of abuse into five categories it's a different schedule so it's schedule one through schedule five meds schedule one has a high abuse potential with no recognized medicinal purposes schedule 2 is high abuse potential with legitimate medical purposes 3 is lower potential for abuse and 4 is lower even so and then 5 is lower potential for abuse than for so the u.s drug enforcement agency is responsible for enforcing the act schedule one medications may not be prescribed dispensed used or administered for medical use and for example marijuana and this remains controversial and depends on the state of course paramedics are likely to carry and administer schedule two medications all schedule two through five medications required lock storage significant record keeping and controlled wasting procedures so let's talk about sources of medications now medications may include plants animals minerals or organisms such as bacteria or fungi or mold and other medications could be in synthetic which in synthetic means made in a laboratory or semi-synthetic which is made from chemicals derived from plant animal or mineral sources that have been chemically modified in a laboratory during manufacturing pharmaceutical companies control the following they control the concentration the purity the preservatives and other ingredients the united states pharmacopoeia national formula so it's usp dash nf provides information regarding the manufacturing details of medications and every medication must have a manufacturing lot number and expiration date okay so there's some forms of", + "Forms of Medications": "medications and most medications are administered as sterile injectable solutions so that require careful handling and aseptic technique during administration they are supplied in iv bags vials ampoules and glass bottles", + "Medication Names": "so the medication names medications in the united states have three distinct name there is the chemical name the non-proprietary which is also called the generic name and then it there is a brand which is the proprietary name okay so let's talk about these the chemical name is used during development it's long and difficult to pronounce usually and rarely used in clinical practice so some examples are sodium bicarbonate or potassium chloride non-proprietary names are proposed by the manufacturer so and they're approved by the us and adopted names council and world health organizations and so um some examples are these are it includes the stem word so links them to other medications in the same class such as midazolam or diazepam or lorazepam they're not safe to rely entirely on the stem when attempting to determine the class of the medication okay so and then there's the brand and that's the proprietary name and that's chosen by the manufacturer and approved by the fda it's selected for marketing purposes so let's talk about some examples of these now the first one's the chemical name and i'm not going to try and pronounce that the second one is the generic name which is fluorosmide and usually the generic name if you look on here it's lowercase and then the brand name so lasix that's a uppercase right so that's the brand name now let's also talk about many reference sources use a thing called tall man lettering when printing names of certain medications capitalized letters and medications with similar names so for an example diphyhydramine or diphyhydranate so you could see that there are all capitalized letters", + "Medication Referencing Sources": "okay so medication referencing sources when selecting a medication reference source paramedics must consider the reliability whether source is printed electronic or both the depth of the info accessibility cost and the availability of updates and the size of the materials a medications monograph is a medication profile and components include medication names categories use mechanism pregnancy risk contras available forms dosage administration and monitoring considerations potential incompatibilities adverse effects and pharmacokinetics so the physician's death reference or pdr it provides information about thousands of medications it's the size of a printed version makes this impractical in the pre-hospital setting though so electronic versions may be helpful to ems educators and administrators manufacturers provide package inserts in every package of the medicine it's approved by the fda and includes information on dosing route contras adverse effects and other characteristics hospital pharmacies often compile medications information into specific to the needs of the specific hospitals so the ama drug evaluations is published by the american medical association it provides details about medication selection and administration but not every medication is um in the compodium has received fda com approval so many choices are available for commercially published medication information references and many medication references can be easily accessed electronically so the american heart association classification of recommendations and level of evidence in most ems settings you will follow guidelines established and distributed by the american heart association these guidelines may be referenced directly or incorporated into an extensive department or", + "Policy and Procedures": "agency policy and procedures the medications and interventions listed have varying degrees of support through reliable scientific evidence the aha uses the following system to describe the relative importance of certain medications and interventions they do it by class system and so class 1 evidence there's strong evidence of supporting class 2a indicates modern moderate evidence class 2b indicates weak evidence class 3 indicates that the evidence does not support that there is a benefit and may support that there is a harmful consequence class intermittent indicates either that the research is being beginning on a treatment or that the research is continuing on a treatment there's no recommendation until further research is performed medication storage is next", + "Medication Storage": "we're going to talk about and so it must be stored in a location that provides adequate protection but is convenient and quick enough for access so it must be stored in a way that prevents physical damage to the medication and the container and it should be placed in a protective bin or surrounded by padding okay so it should be organized to facilitate quick and accurate identification you want to avoid direct sunlight extreme temperatures and physical damage medication warmers or refrigerators for transport vehicles might be needed", + "Medication Security": "medication security so controlled substances require additional security recording record keeping and disposable precautions controlled substances must be in a lock storage or continuously held by an ems provider disposal of partially used or damaged medication containers requires a witness and the returned damage or unused portion to the department responsible for dispensing the medication regulations vary slightly from region the region every last millimeter and milligram needs to be documented from ordering to administration controlled substances are often the target of tampering or diversion okay so the administration to produce a desired effect on the body so", + "Pharmacodynamics": "pharmacodynamics is the alteration of a function or process of the body as a medication is administered any medication capable of beneficial clinical effects can cause toxic effects though when given in the incorrect dose or the incorrect route or delivery device malfunctions so factors related to patient patient condition and particular medication can cause toxicity or adverse effects the process of medication or chemical following administration is the following so absorption disruption biotransformation and elimination pharmacokinetics is the action of the body on a medication so the principles research has demonstrated the presence of receptor sites in proteins connected to cells throughout the body various receptors are activated by you have chemicals and chemicals that occur naturally within the body and then you have medications and chemicals which are absorbed into the body when a medication binds with a receptor site one of the four actions occurs so you have chemicals permitting the passage of ions so the ions are charged particles in cell walls may be opened or closed you have a biochemical messenger becomes activated and that initiates other chemical actions within the cell or you have a normal function is prevented so the normal cell function could be prevented or a normal or abnormal function of the cell begins okay so development to reach and bind with particular receptor sites of target cells so newer medications target only specific receptor sites in an attempt to minimize adverse effects many older medicines affect cells and tissues totally unrelated to the condition being treated and so this causes adverse effects there are two types of medications or chemicals directly affect cellular activity by binding with receptor sites so you have agonist and antagonist so agonist medications initiate or alter a cell activity by attaching to receptor sites prompting a cell response and then you have antagonist medications and they prevent they prevent these chemicals from reaching cell receptor sites and initiating or altering a particular cellular activity okay so the figure on this slide shows how chemicals bind to receptor sites to cause or block actions", + "Agonist Medications Factors": "okay so agonist medications factors that determine the concentration of medication present at target cell receptor sites so the dose the route and a large number of other factors and the affinity so that's the ability of the medication to bind with a particular receptor site there's a threshold level and that's the level at which initiation of alteration of cellular activity begins increasing concentrations of medications cause increased effects until all receptor sites become occupied and the maximum capacity of the cell is reached", + "Potency of Agonist Medications": "when it comes to potency of agonist medications the potency is the concentration of the medication required to initiate a cellular response as the potency increases the concentration or dose required decreases and efficiency that's the ability to initiate or alter cell activity in a therapeutic or desired manner", + "Limit of Change in Activity": "okay so limit of change in activity once all cellular receptor sites become bound with agonist medications no further change inactivity is possible dose response curve so this illustrates the relationship of the medication concentration and efficiency okay so now we're going to talk about", + "Antagonists": "antagonists they bind with receptor sites to prevent a cellular response it may be used to inhibit normal cellular activity by naturally occurring agonist chemicals within the body or treat the harmful agonist effects of the medications or chemicals so it may be competitive antagonist and these agonists temporarily bind to cellular receptor sites displacing agonist chemicals so the efficiency is directly related to the antagonist concentration near the receptor sites the efficiency is related to the antagonist efficiency compared with the efficiency of the antagonist chemicals present okay so non-competitive antagonists they permanently bind with receptor sites and prevent activation by the agonist chemicals they have effects that continue until new receptor sites or cells are created and they cannot be overcome by increased doses of agonist chemicals and then you have partial agonist", + "Partial Agonist Chemicals": "chemicals they bind to the receptor sites but do not initiate as much cellular activity or change as do other agonists they effectively lower the efficiency of other chemicals present in the cells", + "Alternate Mechanisms of Drug Action": "okay so alternate mechanisms of drug action they alter cells tissues organ and system function without directly interacting with receptors or on individual cells they're engineered to target other sites throughout the body such as microorganisms lipids water or toxic substances okay so you could they target specific substances present in cell walls of bacteria or fungi such as antibiotics or anti-fungi fungals um you could have the agents that bind with heavy metals like lead or mercury or arsenic they could create a compound that can be eliminated there's sodium bicarb and that breaks down after administration producing bicarbonate ions you could have diuretics they create osmotic changes alter the disruption of fluids and electrolytes and you can have electrolyte based medications and they change the concentration and disruption of ions in the cells and fluids throughout the bodies", + "Factors Affecting the Response of the Medication": "so there's going to be factors affecting the response of the medication and those include the choice of the medication the dose route timing the manner of administration and monitoring so when you talk about the factors and how a medication affects a patient it could be due to weight based dosing all right and so the age so medications are just re distributed into three primary types of body substances water lipids are fat and protein with water-based medications higher water weight dosages may be administered to infants than to adults and elderly people fat and lipo soluble medications require higher weight based dosage in elderly people when treating pga pediatric or elderly patients consider careful titration of medication rather than administering a weight-based dose alteration of metabolism and elimination in pediatric and elderly patients may prolong the effects of medication or result in higher concentrations in various tissues patients at extremes of age are disproportionately prone to paradoxical medication reactions and patients experience clinical effects opposite of the intended effects of the medications when it comes to weight so these are um factors that are affect the response of the medicine so weight weight basing dosing of medications advances or advantages of weight-based dosing so the amount of medication administered is proportional to the size of the patient manufacturers have already calculated of factors affecting the absorption distribution metabolism and the rates of elimination and it can be used to calculate the appropriate medication dose for patients ranging from pre-term neonates through large adults limitations though of weight-based dosaging so you need to have the patient's weight in kilograms and it does not consider alterations in distribution metabolism and elimination like we just talked about and it's basis on the patient's ideal body weight rather than the actual body weight and then there's the environment and that affects the response to medicines and so hyperthermia may increase the metabolism and hypothermia impairs effectiveness of medications used in traditional cardiac life support then genetic factors affect response to medications so be extremely careful when deciding whether to administer medications to patients with specific genetic disorders pulmonary hypertension may have acute decompensation when vasopressin medications are used sickle cell disease diuretics may cause potentially fatal complications and patients with family members are good sources of information", + "Pregnancy": "and then pregnancy so pregnancy will affect the response of medications and many changes take place in the body cardiac output and intravascular volume increase diaphragmatically hematocrit decreases respiratory tidal volume and minute volume increases gi motility decreases and the ability of the exocrine glands undergoes some some degree of change each of these changes can affect the absorption distribution or elimination of medications you also need to consider the effect of the medicine on the fetus okay this table shows", + "Fda Pregnancy Risk Categories": "five fda pregnancy risk categories and there are letters for those categories a b c d and x and then this table shows the five fda pregnancy categories and it's continued okay and then there's psychosocial factors that will affect the response and that's pain anxiety or overall discomfort can vary among individual patients with the same illness or injury so be alert for verbal and non-verbal clues medication administration is further complicated by the placebo effect so let's talk about the types of", + "Types of Medication Responses": "medication responses there's a potential for adverse or toxic effects at excessive doses so", + "Therapeutic Response": "therapeutic response is the desired response pharmacologic interventions are based on the patient's actual or anticipated illness injury presenting complaint signs and symptoms the patient's condition should match the use indication listed on the profile for the specific medicine medication is administered in a dose intended to produce a desired clinical response okay so some require repeated dosage and these are capable of demonstrating cumulative action so not every medication or situation allows for that", + "Adverse Medication Effects": "adverse medication effects okay so you could have side effects or adverse effects and they are often used interchangeably but adverse effect clearly indicates possibility of serious consequences adverse effects are clinical changes caused by the medication that are not desired and cause some degree of harm or discomfort to the patient", + "Adverse Effects": "some common adverse effects include nausea and vomiting sedation respiratory depression or dizziness consider possible adverse effects in relation to the patient's condition when selecting the medicines adverse effects may range in severity from very minor to life-threatening so an adverse effect can be desirable in certain situations and harmful in others and some adverse effects can be completely unexpected and not previously known to occur with a particular medicine", + "Therapeutic Index": "and the therapeutic index so that's animal testing establishes a median lethal dose a median toxin dose toxic dose and a median effective dose okay and that's the weight-based dosage of the medicine that causes death 50 so that's the lethal the weight-based dose or above which 50 of the animals tested had a toxic effect and that's the median toxic dose and then the medium effective dose the therapeutic index is the relationship between the median affected dose and the median lethal dose if there is a large difference the medication is considered safe if it's a small difference the patient needs to be carefully selected and monitored so", + "Immune Mediated Medication Response": "immune mediated medication response so medication and substances in the environment can cause an exaggerated response from the body's immune system patients who are genetically predisposed have an initial exposure and sensitization to a particular allergen and a medication sensitivity may occur following the first exposure to the medicine or substance medication tolerance and so certain medications have a decreased efficiency when taken repetitively and tolerance results from a down regulation repeated exposure to the medicine with a particular class has the potential to cause tolerance to the medicines in the same class and that's known as cross tolerance and repeated dosage of the medications within a short time rapidly causes tolerance", + "Medication Abuse and Dependence": "medication abuse and dependence so two distinct groups of medication with chemicals are prone to misuse and abuse stimulants and that is for example caffeine cocaine and amphetamines and depressants and those examples are benzodiazepines alcohol and opiate chemicals repeated exposure can cause habituation and so prolonged or significant exposure can cause a degree of dependence", + "Medication Interactions": "when it comes to medication interactions medication um interference is an undesirable medication interaction the major concern with incompatibility during administration so when given simultaneously through the same iv tubing certain medications will change chemical composition and some medications will deactivate others so medications require the proper iv solutions and it is possible for a medication to increase or decrease or alter the effect of any other medication within the body when we talk about principles of pharmacogenetics so as a medication is administered the body begins moving and ultimately removing the medication from the body duration of and effectiveness of the medication are determined by the dose the route of administered and the clinical status of the patient", + "Pharmacokinetics": "the pharmacokinetics section of the medication profile states the following the onset is related to absorption and distribution the peak is related to absorption and distribution and the duration of effect is related to medication metabolism and elimination when you talk about the routes of", + "Medication Administration": "medication administration and most are capable of delivering an appropriate amount of medication to the correct location of the patient's body and it's determined by the physical and chemical properties of the medication the routes of the medication available and how quickly the effects are needed", + "Bioavailability": "bioavailability is the percentage of unchanged medication that reaches systemic circulation and it's determined by the route of administration and it varies by medication except for iv route so iv route has 100 percent availability irrelevant for medications sequestered in the gi the gi tract so oral or a gastric tube and nasal gaster tube a large number of medications are administered into the gi tracts the patient must be responsive and be able to swallow and ha or and have an ng tube or or gastric tube once", + "Medication Absorption": "administered the medication absorption varies um so the metabolism occurs in the liver and the metabolism may also occur within the gi tract patients with liver dysfunction are at risk of toxicity of the medications when they are given orally when you give it down the endotracheal tube it's no longer considered a reliable method of administration if endotracheal medications are given administer at least two to two and a half times the iv dose and follow with a 5 to 10 cc flesh with sterile water or normal saline", + "Intranasal": "intranasal so liquid medications are converted into a mist that is sprayed in one or both nostrils it's absorbs rapid and bioavailability is close to 100 percent in certain studies administration can begin in immediately and there's no risk for needle stick injury to the paramedic", + "Intravenous": "and then there's intravenous so this is the preferred method in the pre-hospital setting a small diameter catheter is inserted into the peripheral or external jugular vein bioability is 100 and the onset is quicker than medications given orally or through the oral gastric or nasogastric tube", + "Limitations": "there are limitations and so access is difficult in several groups of patients and those are the ones who are iv drug users or profound shock patients who have cardiovascular collapse or chronic medical conditions the procedure may cause pain or infection and certain classes such as sympathomimetics can cause pain or tissue damage and then you have the i o route and the needle's inserted through the patient's skin into the bone vascular uptake from the bone provides a reliable route for medications and iv fluids any medication that can be administered iv can be administered through the io an iom needle can generally be kept in place for 24 hours and it is contraindicated in bones that are fractured and this route is discouraged when patients have bone disease or skin infections over the insertion site intramuscular a sterile medication is drawn into the syringe attached to a needle and injected into the patient's larger muscles im route is used when iv access cannot be established or when clinical situation requires immediate medication administration medications have the bioavailability of about 75 to 100 percent and there is a contamination risk of the needle stick if the patient moves suddenly", + "Subcutaneous Route": "the subcutaneous route or sc route is similar to the im it's a sterile medication is drawn up in the syringe attached to the needle the medication is injected in the various subcutaneous tissue sites throughout the body certain medications are injected for sub-q or in intended for sub-q use only if slower absorption may prevent adverse cardiovascular effects dermal and transdermal is the is the route we're going to talk about next and these are patches and they commonly contain nicotine in antibiotics or analgesics or a nitro they may alter the patient's clinical presentation or interview fear with other medications administered and often cannot or contain a large quality quantity of medication and then sublingual so nitroglycerin is frequently given using the sublingual route by ability though is low and large dosages are required patients must be conscious and alert a lack of saliva may delay the absorption then you also have inhaled or nebulized so inhaled pre-hospital medications are limited to oxygen and antidote so this method of administration may assist patients with medications via meter dose inhalers and medications may be nebulized and that's when it's converted into a fine spray so nebulized medications have the potential to cause bronchospasms though and then rectal so preferred over oral if the patient is unresponsive or having seizures or vomiting the medication is usually not subject to first-past metabolism and the viability is about 90 percent medication should be administered into the lower rectum so whenever possible ophthalmolic so in the pre-hospital setting use is generally limited to um anesthetic agents to facilitate irrigation of eyes following a chemical exposure um and uh yeah", + "Distribution of Medicine": "okay so distribution of medicine how medicine moves through the body is determined by the chemical properties physical properties and the patient factors the body has a system of barriers designed to prevent the introduced introduction of foreign substances into the body and so medication molecules must move through these barriers to be effective osmosis is used to enhance the distribution of certain medicines so free water and certain particular particles can pass through semi-permeable membranes to equalize the concentration of water and other particles on each side of the membrane this allows iv fluids to leave the intravascular space and enter various tissues and cells this is one of the medications the kidneys use to regulate fluid balance", + "Filtration": "and then there's filtration so filtration is a process within the body that it used to redistribute water and other particles epithelial cells that create a continuous barrier are contained in the skin gi tract eyes and urinary tract medication molecules must pass directly through the cells to enter the body and so uncharged small uncharged or attracted fats and lipid medication molecules pass easily through these cell membranes but larger hydrophilic which are attracted to water molecules and ion charge medications molecules must pass and they must find another route to enter the cells okay medications must also move through capillary walls to reach some tissues and so uh three barriers prevent molecules from reaching the tissues and that's the blood brain barrier a blood testes barrier molecules pass freely through capillaries in the kidney thyroid and pancreas and molecules pass through leaf through capillaries in the lungs and peritoneum", + "Plasma Protein Binding": "in plasma protein binding medication molecules temporarily attach to proteins in blood plasma plasma protein binding increases the amount of medication necessary for a desired clinical effect plasma protein binding releases medication as circulating levels of the particular medication begins to fall fat tissue can alter the amount of medication available for action within the body the medication is really slowly causing prolonged effects", + "Volume of Distribution Method": "so let's talk about the volume of distribution method of distribution decreases the extent to which the medication will spread through the body some medications do not readily uh leave the plasma and some spread into the water and some bind with bone teeth and other tissues medications with a larger volume of distribution have higher levels present in the plasma at a given dose than medications with a higher volume of the distribution", + "Biotransformation": "biotransformation is a chemical change that many medications undergo in the body biotransformation has four possible effects on the medication absorbed so an inactive substance can become active an active medication could be changed and active medication can be completely are partially inactivated and an active medication can be transformed into a substance that is easier for the body to eliminate most biotransformation occurs in the liver the kidneys skin lungs gi tract and other body tissues have some availability to cause biotransformation as well though and suspect altered metabolism in patients with chronic alcoholism liver disease and any condition known to affect the liver so when it comes to medication elimination medication is primarily removed from the body by the kidneys a variety of factors influence so how quickly it is eliminated and so medications follow two patterns of metabolism and elimination and so zero order elimination it's a fixed amount of substance is removed during a certain period and then there's first order elimination and that's the rate of the elimination is directly influenced by the plasma level of the substance when you talk about the half-life this is the time needed in an average person for metabolism or elimination of 50 percent of the substance in the plasma and it of course is altered by factors such as disease status or changes in perfusion or medication interactions medications are administered at a dose and frequency that equals the body's rate of elimination resulting in constant level okay so next we're going to", + "Reducing Medication Errors": "talk about reducing medication errors and medication decisions are often based on memory and frequently occur in the context of stressful life-threatening patient situations paramedics are constantly at risk for a cognitive error or technical error", + "10 Rights of the Medication Administration": "so the 10 rights of the medication administration and you really need to get to know these and remember them you have the right patient right medication right dose right route right time right documentation and reporting right assessment right to refuse right evaluation and write patient education perform a verbal read back of the orders received from online medical control and call out the medication name and dose prior to administering unlabeled syringes pose a significant hazard in health care patient safety experts recommend building an environment in which ems providers feel comfortable reporting errors and near misses bring along a patient's home medicines when transporting the patient to the health care facility use a reliable reference source when administering unfamiliar medications or when an unusual dose of or route of administration is being considered have a partner confirm the volume in the syringe or a weight-based medication calculation evaluate the patient for medication allergies or hypersensitivity before each administration the institute for safe medication practices has developed a list of", + "Error-Prone Medicines and Abbreviations": "error-prone medicines and abbreviations the table shows examples of possible errors and misinterpretations and reporting the drugs that act on the sympathetic nervous system so receptor sites exist in proteins connected to cells throughout the body receptors are activated by chemicals whether naturally occurring or in form of a medication in the sympathetic nervous system react receptors are labeled as alpha or beta any beta agent will increase the heart's rate force and automaticity arteries have receptors for alpha and beta an alpha drug will cause vasoconstriction and a beta will cause vasodilation the lungs have alpha and beta receptors alpha agents may cause minor bronchial constriction and beta adrenergic agonist triggers significant bronchodilation drugs that have alpha and beta sympathetic properties are called sympathy and pathomemetic drugs if you know whether a sympathomimetic drug is an alpha beta agent you can predict the response by the heart lungs and arteries many sympathemomatic drugs have varying degrees of alpha and beta activity beta sympathetic agents can be classified into two groups based on the differences between the beta receptors in the heart and lungs drugs that act primarily on cardiac beta receptors are called beta ones and drugs that act chiefly on pulmonary beta receptors are called beta2 blockers block the action of the sympathetic agents by beating them to the receptor sites or preventing these agents from turning on the ignition beta adrenergic blockers accompany beta receptors in the heart lungs and arteries and elsewhere in the body indications for the major autonomic", + "Major Autonomic Stimulating and Blocking Agents": "stimulating and blocking agents can be deduced once you know the properties of the drugs and the manner in which they interact with the autonomic nervous system so atropine is a parasympathetic blocker norepi is a sympathetic agent primarily alpha epi is a sympathetic agent predominantly beta dopamine is a sympathetic agent albuterol is a sympathetic beta2 and pro panel law is a sympathetic beta blocker medications used in airway management you have rapid sequence innovation and medication facilitated airway placement so you have sedative medications you have sedative hypnotic agents which is used in airway management and there are two ultra short acting sedative medications used to facilitate airway placement and that is uh atomidate or animate and it is uh preferred for its minimal effect on blood pressure it begins working in 30 to 60 seconds and peak is approximately 60 seconds it lasts about 5 minutes and it causes adrenal suppression if multiple doses are given", + "Ketamine": "and then you have ketamine so this causes profound disassociation and general amnesia it can maintain blood pressure and heart rate and it rises raises intracranial pressure it causes some degree of bronchiodilation and it may cause an emergent reaction of brief psychosis disorientation or hallucinations you have benzodiazepines and they have potential potent anti-seizure and sedative properties high doses for adequate sedation and some degree of seizure protection in patients with head injuries lower doses for reduction of anxiety flumasazole it's a benzodiazepine antagonist available in certain healthcare settings serious potential for life-threatening conditions and ser several contraindications it's risky minimal effectiveness of benzodiazepine if seizures occur following administration chemical paralytic agents provide muscle relaxation and bind with nicotinic receptor sites on muscle cells figure shows chemical paralytic medications binding with those receptor sites on muscle cells okay next we're going to talk about sexacholine", + "Sexacholine": "and it's a competitive depolarization paralytic agent it's preferred by many health care providers because of its rapid onset and relatively brief duration then you have non-depolarization paralytic agents and an immediate threat to life from depolarization and non-depolarization chemical agents if an artificial airway is not secured and then you have other airway medications so when upper airway edema is present the following medications may be used so corticosteroids or vasoconstrictors or bronchiodilators so medications used in the respiratory management we are going to talk about beta agonist", + "Beta Agonist Medications": "medications next the primary treatment for acute bronchiospasms associated with asthma copd and a variety of other conditions and it smooth muscles in the lower airways contract or relax in response to biochemical changes and external irritants so you have selective and that's target they target only the beta two receptor sites and then you have non-selective and they affect beta one and two albuterol is a selective beta two agonist medication typically nebulized or administered using an mdi for emergency treatment and then you have lev albuterol structurally similar to albuterol but fewer beta-1 effects okay so careful", + "Monitoring for Adverse Cardiovascular Effects": "monitoring for adverse cardiovascular effects should be done you have a muco kinetic or bronchiodilator medication so at your event so what happens is you administer only every six to eight hours and it's limited cardiovascular effects it causes brazo bronchiodilation and decreased mucus in the upper and lower airways and then corticosteroids so administered to reduce airway inflammation and provide oxygen and ventilation to reduce severity of respiratory compromise due to asthma or copd or allergic reactions and so some examples are solumedrol or decadron or prednisone they have immunosuppressant properties and many contra indications and adverse effects so you have to evaluate the potential risk and benefits for each patient leukotrine receptor at antagonists are reported to have exponentially more potent at causing bronchial constriction bronchoconstriction than histamines levels of leukotrienes are significantly elevated in patients with asthma and so leukotrine receptor antagonist medications are taken by patients with asthma and certain allergies on a long-term basis and that's medications like singulair so let's talk about medications affecting the cardiovascular system of course there's three components to that system you have the pump the plumbing and the blood alter the heart or change the tone of the blood vessels so you have anti-dysrhythmic medications and they target cells within the heart you have the ability to improve or correct abnormalities in the patient's cardiac rhythm and uh so there's groups of medications used to treat cardiac dysfunias and they're into four classes according to the mechanism all right so let's talk about these phase four cardiac cells are at breast and waiting for um the stimulus so the automaticity", + "Automaticity Phase": "phase 0 the phase begins when the cardiac muscle cells receive the impulse phase 1 sodium channels close while potassium exits phase 2 sodium and calcium slowly enter the cell phase three calcium channels slowly close and calcium leaves the cell during 0 1 2 and up to the middle of phase 3 no additional depolarization may occur because of external stimuli this is the absolute refractory period followed by a brief period for the potential stimulus to initiate depolarization this is known as the", + "Relative Refractory Period": "relative refractory period the figure shows the action potential in a cardiac muscle cell class one anti-discrimination medications slow the movement of sodium through the channels of certain cardiac cells procainamide suppresses activity of the atopic foci and slows conduction velocity lidocaine blocks sodium pumps in the purkinje fibers and ventricles resolving ventricular dysrhythmias and suppressing atopic foci class two those are anti-dysrhythmic medications and beta adrenergic blocking agents so completely inhibit the catecholine act activation of beta receptor sites they may be capable of beta-1 selectivity at therapeutic doses so toxic effects could be bradycardia hypotension and conduction delays they require extreme caution in patients with reactive airway disease and may cause massive conduction abnormalities when given with calcium channel blockers so stuff like low pressure it reduces the heart rate during myocardial ischemia and certain atrial tachycardias it requires monitoring of the heart rate and blood pressure and slowly administering the medication class three are anti-just rhythmic medications they prolong the absolute refractivity period by extending the duration of phases one two and three of the cardiac cycle they treat atrial and ventricle tachycardias stuff like amiodarone it is controversial treatment for worf pocket wolf parkinson's white and uh so you need to do this by the iv route and it may cause severe adverse cardiovascular effects and life-threatening pulmonary conditions", + "Class Four Antidisrespecting Medications Such as Calcium Channel Blockers": "class four antidisrespecting medications such as calcium channel blockers they have a variety of potential uses reducing blood pressure or controlling heart rate displace calcium to certain receptor sites and enter smooth muscle cells in place of calcium their slow conduction through the atrial ventricular node and decrease automaticity and decrease the velocity of cardiac contraction so verapamil and cartesim these agents are used to control heart rate in patients with afib and a flutter detalazam or cardizem has less effect on blood pressure rapamyl has a longer room temperature shelf life and costs less and medications are administered iv over two minutes verapamil and cartism require continuous electrocardiographic monitoring and frequent blood pressure monitoring adenosine it can be used to treat psvt and assist in diagnosing when the origin or pattern cannot be determined on the ecg because it's really fast it decreases cardiac conduction velocity and prolongs the effectively factory period rapid onset and brief duration the half-life is less than 10 seconds and it should be administered through a large bore proximal iv site followed by a 10 ml normal saline flesh and then continuous paper recording so you can see the change okay so additional cardiovascular meds", + "Cardiovascular Meds": "you have alpha adrenergic receptor agonist so these present or prevent catecholamines from reaching alpha receptors these medications lower blood pressure particularly this is the diastolic and they decrease systemic vascular resistance so patients are prone to orthostatic hypotension and they're prescribed for hypertension and large prostates and glaucoma so you have a caprice it's primarily an alpha 2 receptor agonist and it's given orally um ragatine and that's a catecholamine and simple pathomimetic can cause profound tissue necrosis if um infiltration occurs you have le betatol and that is an alpha 1 beta 1 and beta 2 and patients at risk for alpha stimulization should receive another alpha adrenergic agonist before receiving the beta talk", + "Angiotensin Converting Enzyme Inhibitors": "angiotensin converting enzyme inhibitors and these are known as ace inhibitors they alter the function of the angiotensin system and the the system that causes vasoconstriction and fluid retention in response to hypotension and hypo hyperfusion so they cause blood pressure to decrease and cardiac afterload to decrease and they're used for treating hypertension cardiomyopathy and congestive heart failure in patients taking these meds have chronic dry cough or experienced sudden life-threatening in angioedema so close monitoring and supportive treatment and they're also difficult endotracheal innovation patients okay so now we're", + "Anti-Collegiate Medications": "going to talk about the anti-collegiate medications used to treat allergic symptoms and we're gonna atropine we're gonna talk about and it's a competitive antagonist its effectiveness is related to the concentration at the receptor sites it's administered to exclude the possibility of vagal stimulization through episodes of bradycardia with an unidentified cause it's unlikely to be effective for the treatment of bradycardia caused by blocked cardiac conduction it's used before airway manipulation and life-saving antidote for anti-cholinergic inhibitor toxicity okay so the next group we're going to talk", + "Catecholamines and Sympathomimetics": "about is the catecholamines and sympathomimetics they're naturally occurring chemicals in the body that stimulate receptor sites in this sympathetic nervous system so um epi norepi and dopamine they're rapidly metabolized with a brief duration of action no natural sympathomimetic chemicals within the body they're sympathetic chemicals that mimic catecholamines and so various amphetamines albuterol phenyphedramine and cocaine they have a longer duration than catecholamines epi it is a catecholamine that stimulates the alpha beta 1 and beta 2 receptor sites it causes potent vasoconstriction increased heart rate contractility and cardiac output and it's also a powerful bronchiodilation can be administered iv io im subcutaneously endotracheally or via nebulizer and can dramatically increase the cardiac workload and myocardial oxygen demand and then nor epi which is levifed it's a catecholamine that has been commercially manufactured for use stimulates beta 1 and alpha receptor sites causes increased blood pressure cardiac contractility and heart rate indications include sepsis neurogenic shock and anaphylactic shock it's administered by a continuous iv infusion titrated according to the patient's response and can cause tissue necrosis if infiltration occurs dopamine it's used as a primary medication for hypotension refractory to volume resuscitation it's administered using a weight-based infusion calculation and there's a dramatic variation and clinical effects depending on the dose", + "Digitalis Preparations": "so next we're going to talk about digitalis preparations it's prescribed for treatment with chronic heart failure or certain rapid atrial dysrhythmias it acts by increasing the strength of the cardiac contractions which improves the cardiac output and slows conduction through the atrioventric ventricular junction may produce a wide variety of adverse reactions and commonly used dig precautions or preparations are lanoxin or digoxin direct vasodilator medications used for the management of uncontrolled hypertension congestive heart failure myocardial infarct or cardiac ischemia or cardiogenic shock and so nitro of course nitro bit or nitrostat it dilates veins of the coronary arteries it affects when administered sub-lingually by tablet or spray the peak is one to two minutes or um it begins and peak is four to ten minutes after following iv administration or um discontinuation begin almost immediately following iv administration so", + "Psychological Responses": "um the psychological responses relief of chest pain and decrease of blood pressure degradation of sublingual tablets and it binds with the plastic of containers and iv fluids and tubing and should not um be taken in patients taking other inhibitors used for erectile dysfunction nypride that is a potent iv vasodilator affecting smooth muscle of veins and arteries it's often used in conjunction with inotropic medications for management of cardiogenic shock it's also used for malignant hypertension in situations where intentional hypotension is desired so advisable iv infusion rates to maintain optimal blood pressure and cardiac output okay next we're going to talk", + "Diuretic Medications": "about diuretic medications and they're administered to correct fluid volume overload or manage congestive heart failure or improve respiration in patients with pulmonary edema potentially preserve kidney function to eliminate certain toxins and promote excretion of excess electrolytes the first one we're going to talk about", + "Furosemide": "is furosemide its uses are diuretic medication for management of hypertension congestive heart failure liver disease or kidney dysfunction careful consideration for administering the patients with hemodynamic instability and known electrolyte disturbances and administer by iv over one to two minutes per 40 milligram dose mannitol that's an osmotic diuretic it's used to decrease intracranial pressure associated with cerebral edemia it can target specific body tissues removing excess water from brain and eyes it draws water out of selected body tissues through the kidneys", + "Anti-Hypertensive Agents": "anti-hypertensive agents these agents are used to treat hypertension many diuretics are also used to as anti-hypertensive or in combination with the antihypertensives so beta blockers may be used in the treatment of hypertension patients with anti-hypertensives may have symptoms of hypotension and so orthostatic hypotension is the feeling of giddiness due to hypotension with a change in position the table shows commonly prescribed antihypertensive agents and other medications prescribed to treat and prevent heart disease", + "Blood Products and Medications That Affect the Blood": "okay so blood products and medications that affect the blood so manipulation", + "Manipulation and Enhancement of Characteristics of the Blood": "and enhancement of characteristics of the blood for therapeutic purposes", + "Blood Product Administration": "blood product administration so the average adult has five liters of blood constituting approximately seven to eight percent of the body weight blood is roughly five or fifty five percent plasma and water makes up approximately fifty percent of the total volume red blood cells account for approximately forty five percent of the volume trauma or a medical condition can alter the amount composition and performance of the blood so blood components the type specific to a particular patient cross match to a particular recipient and unmatched it most likely to be used in the pre-hospital setting almost always type o or rh negative during inter-facility patient transport paramedics may need to make a decision concerning what type to use if choice is not clear online medical control and sending physician will be", + "Resources": "available resources blood products require careful monitoring during administration and most blood products require spelt special filter iv tubing with packed red blood cells correct anemia is what they do resulting from blood loss or inadequate red blood cell production the rate of administration should be proportional to the rate of blood loss a unit of packed red blood cells contains approximately 225 to 250 milliliters of concentrated red blood cells patients at risk of volume overload require slow administration and careful monitoring patterned blood cells are typically administered over no longer than four hours per unit and they can be administered rapidly through commercial pressure infuser warmer or by using pressure bags for critical patients so units of packed red blood cells usually contain a some type of preservative and so hypokalemia may develop as a as this binds with calcium fresh frozen plasma this is used to treat impaired blood clotting often given following trauma hemorrhage or warfarin toxicity or other conditions it's considered consideration of the fresh frozen plasma when large volumes of blood components are administered compat compatibility with the blood patient's blood type but not rh compatible it requires adequate defrosting before administration", + "Cryoprecipitate": "cryoprecipitate that's a blood product that contains a concentrated absorbent of blood clotting factors without the additional volume present in the frozen um fresh frozen plasma and then there's platelets so it's used to correct the thrombocytopenia that's low platelet level in the blood and must be blood type and rh compatible medications that alter blood com performance so blood plate blood platelets combine with coagulation chemicals to terminate bleeding when clotting occurs in a blood vessel a thrombus is created okay transemic acid so it's a powerful medication intervention to promote blood clotting and reduce mortality and trauma patients with severe bleeding blood clot formation in response to an injury and bleeding so transamic acid", + "Transamic Acid": "it's a commercial preparation of amino acid in the body responsible for preventing breakdown of the fibrin clots significantly decreases patient mortality if administered within three hours of the traumatic event and current recommended doses is one gram in an iv infusion over 10 minutes", + "Anticoagulant Medications": "anticoagulant medications so they impair the function of clotting and coagulation chemicals in the bloodstream they enhance the function of substances in the blood that inhibit clot formation heparin so that is a an enhanced antithrombin 3 to inhibit blood coagulation and it prevents acute coronary syndrome or deep vein thrombosis or pulmonary emboli its compatibility of heparin and nitro and several other infusions potential to cause bleeding and thrombop cytopenia and other adverse effects okay so orphan or coumadin orphan is a common anticoagulant for treatment of prevention of blood clots it works by preventing the production of four different blood clotting factors that use vitamin k patients are at risk of life-threatening bleeding when warfarin levels are not adequately controlled following trauma or when any other hemorrhage occurs certain foods alcohol and a variety of medications can increase effects of warfam several treatment options are available if patients taking morphine develop severe bleeding and require an emergency surgery so there's anti-platelet medications and they are used to reduce platelet aggravation to prevent new thrombus formation and extension of an existing thrombus", + "Aspirin": "so aspirin it's an oral med it treats acute coronary syndrome and it is um indicated for treatment of stroke once presence of hemorrhage has been excluded okay so plavix it's an oral medication it inhibits platelet aggregation and um so it prevents potential platelet inhibition and administered iv infusion and adverse effects are bleeding", + "Fibrolytics": "fibrolytics they dissolve blood clots in arteries and veins administered for emergency treatment of acute myocardial infarct in a stroke administration in higher doses to open certain vascular catheters that have been occluded by the presumpt presumed blood clot can cause life-threatening hemorrhaging an avoidance of multiple iv attempts and unnecessary trauma in a patient who is likely candidate for thrombolytics okay so medications used for neurologic conditions so you have opiates which are narcotics and they act as analgesics in the pre-hospital setting they are effective at eliminating or reducing pain narcan is the powerful reversal agent", + "Opiate Analgesic": "opiate analgesic medications so stimulate opiate receptors in the body to relieve and prevent pain they're known to cause tolerance cross-tolerance and addiction and they can cause prevalence to take profound sensation respiratory depression and apnea when excessive doses are administered morphine sulfate that's used frequently in ems it's known to cause nausea and vomiting in up to 60 of patients then you have fentanyl that's generally not as prone to cause hypotension it does not have the same risk of nausea and histamine release as morphine and can be administered intra nasally", + "Opiate Agonist": "and then you have opiate agonist medications so narcan this is or naloxone this is used to reverse the effects of excessive opiate chemicals in the body its efficiency is dose dependent large doses are often required to reverse the effects of potent opiate chemicals and only administer enough to correct that life-threatening condition so you have dilatin that's administered to prevent seizure activity it's administered by iv infusion usually for 10 to 30 minutes and it decreases the potential for seizure activity by altering sodium channels and limiting cellular sodium and portions of the central nervous system all right so medications which affects", + "Medications Which Affects Affect the Gi System": "affect the gi system you have histamine 2 receptor antagonist they decrease acid secretions in the stomach prevent histamine from stimulating receptor sites in the parental cells in the stomach stuff like zantac and pepcid and tagament then you have anti-medic medications those are used to treat nausea and vomiting and um stuff like fenegrin these medications have anti-medic and anti-psychological properties so both medications can be given orally or iv and dystonic reactions are possible causing usually unusual muscle activity and significant patient discomfort many other potential adverse effects are possible okay so some miscellaneous medications used in the pre-hospital setting incur acetaminophen so tylenol it's an antiparetic so fever reducing medication it can be administered to um reduce discomfort in treating fever symptoms or to prevent febrile seizures in pediatric patients it's available as a tablet capsule liquid or rectal suppository", + "Calcium Preparations": "there's also calcium preparations so calcium can be used for or as the following an antidote to calcium channel blocker overdose or to prevent a mag magnesium toxicity and prevention of dysrhythmias during severe hyperchlaemia calcium is not indicated for route use during cardiac resuscitation okay", + "Dextrose": "dextrose so it's used for known or presumptive hypoglycemia it's administered through a large bore iv catheter and you have to continually observe for signs of infiltration initial dose for moderate to severe hypoglycemia is 25 grams of 50 dextrous solution for total volume of 50 ml children receive weight-based dosages of 25 percent destroy solution in infants are weight based of ten percent in diphyhydramine it's frequently used um by the ems providers for a variety of clinical situations it's a histamine one receptor antagonist prevents receptor activation of histamine released during various medical conditions it's used for treatment of anaphylaxis in conjunction with other medicines and interventions the sole treatment of mild allergic or medication reactions has mild sedative purposes and mild antitussive purposes it's typically administered by iv or im adverse effects generally limited mild sedation or palpations or anxiety possible toxicity and death following overdose then there's glucagon it's naturally occurring peptide manufactured commercially may be used for treatment of hypoglycemia it's useful when iv access cannot be attained in diabetic patients glucose production takes about five to twenty minutes following iv administration in 30 minutes following im dextrose is preferred for hypoglycemia okay in catacoralact this may be used as an alternative or adjunct to opiate at analgesic medications it's an nsaid that inhibits synthesis it's typically administered iv or im it can give you gi irritation or headache or pain at the administration site and no administration to patients with susceptible to that are susceptible to gi bleeding", + "Max Sulfate": "okay and then max sulfate so mag sulfate is an iv electrolyte medication used for emergency treatment of torsades or similar ventricular dysrhythmias correction of known or presumptive hypomag issemia and for cardiac arrest situations one to two grams of max sulfate can be given by slow iv push for one to two minutes max sulfate replaces magnesium deficiencies in the body and magnesium sulfate is essential for the movement of electrolytes it relaxes various smooth muscle tissues and toxic effects are treated by discontinuing the effusion and administering an iv calcium preparation", + "Sodium Bicarb": "then you have sodium bicarb it's an alkalizing agent it's used to raise the blood ph in patients with severe metabolic acidosis it stabilizes profound hyper hypercalcemia in an emergency situation provides cardiac cell membranes stabilization following a tricyclic antidepressant overdose promotes urinary excretion of chemicals and certain waste products and it replaces bicarbonate loss due to various medical conditions can be administered by rapid iv push or added to iv fluids for intermittent or continuous inflation infusion the effects are excessive administration so fluid volume overload or alkalosis or cerebral and pulmonary edema okay and the last medication we're going to talk about today is thymine it's a", + "Thymine": "commercial medication preparation of vitamin b1 it's used to correct a presumptive thymine deficiency before dextrose administration in patients who are malnourished or who consume alcohol on a long-term basis it's usually administered by iv in a pre-hospital setting iv push or added to iv fluids it's unlikely toxic and adverse effects when therapeutic doses are administered okay so that concludes chapter 13 principles of pharmacology lecture thank you for joining us today" + }, + { + "Introduction to Medication Administration": "hello and welcome to chapter 14 medication administration lecture this chapter begins with an overview of fluids and electrolytes balanced and imbalanced and the process of osmosis and diffusion next we will discuss the various types of iv solutions used in a pre-hospital setting and the techniques of iv therapy and interosseous infusion i will describe the mathematical principles used in pharmacology and for calculating medication dosages boluses and maintenance infusions and paramedics will administer medication in different forms and so we're going to talk about those different forms and routes for administering medicines okay so medication administration is what we're going to talk about we're going to talk about the routes of administration self-administered medication peer-assisted medication assist administer medications to the patient and within the scope of the practice of the paramedic administer medications to the patients all right so it is your responsibility", + "Administering Medications and Vascular Access": "to administer the appropriate medications and the appropriate dosage when needed and to determine the most effective route by which to administer them vascular access is often needed in emergency medicine for patients in hemodynamically unstable conditions and in need of an iv fluid in various medications or both many techniques are used in the pre-hospital setting cannulization of a peripheral extremity vein and that just means insertion of a catheter such as into the vein to allow for fluid flow then there's an external jugular vein cannulation there's interosseous access and long-term vascular access devices in critically ill or injured patients survival depends on your ability to obtain vascular access significant harm to the patient can result from improper technique or insufficient knowledge of medications", + "Medical Direction": "all right so when you're talking about gaining approval for medication and direction there's online direction and that is direct or medical control now paramedics must contact medical directors prior to performing certain procedures and you need to gather all the patient information prior to contact if you are not confident with a drug use indication contraindication or any other aspect of the medication administration use your protocols a drug formally a flip guide or a smartphone or tablet application or any other available resource okay beyond the resources available on your response unit consider medical control online medical direction is not just for approval of medications it's a general consultation of treatment modalities which um with which you are not confident so when in doubt just contact medical control", + "Ensuring Safe Medication Administration": "all right so ensure medications are administered accurately and safely use standing orders or online medical direction make conscious effort to avoid human factors that cause errors and follow the 10 rights of medication administration use a tool to verify the drug dose route name route of administration indication for administration contraindication drug concentration and volume to be administered never just guess at physicians orders and then you need to document so we're going to document the dose that we administered the quality administered during the administration the units of measure for the drug the volume administered to the patient also the name of the medication verify the spelling of the drug the route the rate and the rate is the bolus or infusion or other administration method and the time administered and who administered the drug who helped perform the medication check and the patient's response to the medication", + "Local Drug Distribution System": "okay so our local drug distribution system now we need to ensure all equipment on the ambulance is fully functional before responding to an ems call we need to verify and perform this verification will be performed during our check at the beginning of our shift we have to check all medications to make sure that they are not expired not damaged and readily available in the right quantity we are responsible for the documentation and the security of all controlled substances on the ambulance so we have to follow policy and procedures of the local drug distribution security and accountability system so medical asepsis is what we're going", + "Medical Asepsis": "to talk about next and this is the practice of preventing contamination of the patient using an aseptic technique it's the method of cleaning that prevents contamination of a site and when it's used when performing an invasive procedure it's accomplished through sterilization of equipment aseptic techniques and disinfectants we want a clean technique versus a sterile technique okay so some equipment has been sterilized and some medications have been packaged using sterile techniques sterile technique is deconstruction of all living organisms using heat gas or chemicals for a sterile field to exist we have to wear sterile gloves or a gown that covers you from the wrist to five centimeters approximately of the elbow okay we we had the we would have to wear sterile gloves using um numerical sizes we have to place sterile drapes around the procedure area and only sterile items and personnel may enter the sterile field now it may not be possible to maintain a sterile field in the in our environment so we need to practice medical asepsis to reduce risk of contamination and infection hand washing wearing gloves keeping equipment as clean as possible and for example the site on a patient's hand when it has been cleaned with iodine an alcohol before starting an iv line is said to be medically clean antiseptics and disinfectants antiseptics are used to clean before performing an invasive procedure they're capable of destroying pathogens and they're not toxic to living tissues most common examples of these are alcohol or rubbing alcohol iodine or chloropreps disinfectants are toxic to living tissues and they're that we use them only on non-living things", + "Standard Precautions and Contaminated Equipment Disposal": "okay so standard precautions and contaminated equipment disposal is what we're going to talk about next and the first one we're going to talk about is standard precautions so we treat any body fluid as being potentially infectious after an iv catheter or needle has penetrated the skin it's contaminated accidental needle sticks are common route for disease transmission we need to dispose immediately and properly so sharps uh is where any contaminated item that may cause injuries go so such as an iv im or subcu needles and catheters or broken ampoules or vials immediately dispose of any sharps in a puncture-proof sharps container and it should bear the biohazard logo and it should be readily accessible place at least two in the back of the ambulance and have a small sharps container in your jump kit follow your agency's exposure control plan", + "Body Fluid Composition": "right so cell cellular fluid composition and status so the body fluid composition the human body is composed of mostly water it provides an environment necessary for life and the body maintains a balance between intake and output of fluids and electrolytes when injured or ill the body may be unable to maintain this homeostasis", + "Abnormal States of Fluid and Electrolyte Balance": "so the first one we're going to talk about is dehydration and that's an inadequate total systemic fluid volume its signs and symptoms include decreases level of consciousness sterile hypotension tachypnea dry mucous membranes decreased urine output tachycardia poor skin turgor or flushed dry skin the causes of this are as dehydration vomiting gastrointestinal drainage infections metabolic disorders hemorrhage environmental emergencies high caffeine diet or insufficient fluid intake and then we have over hydration this occurs when the body's total systemic fluid volume increases it may occur in patients with impaired kidney function or who have been administered more fluid than their body can excrete younger than one month old kidneys are not fully developed yet signs and symptoms are shortness of breath puffy eyelids adeemia polyuria moist crackles and that's rails or acute weight gain and causes can be on monitored ivs and pediatrics kidney failure water intoxication in endurance sports or prolonged hypoventilation", + "IV Fluid Composition": "okay so let's talk about iv fluid composition each bag of iv solution is individually sterilized it co there's compounds and ions are identical to the ones in the body and alternating iv concentration can move water into or out of the fluid compartment in the body so let's talk about the operation of electrolytes a bodies or a patient's electrolytes can be come altered from excessive vomiting diarrhea dietary issues or medications taken regularly or administered by an ems crew so also blood loss or a variety of other injuries we want to understand the role of each electrolyte aids in selecting the appropriate iv solution okay this table shows the electrolyte composition of iv fluids okay so now let's talk about those types", + "Types of IV Solutions": "of iv fluids they can be categorized as either crystallized or colloid or as isotonic hypotonic or hypertonic and so let's talk about those five different types so you have crystalloid solutions and they are dissolved crystals in water just like they sound they're able to cross membranes and alter fluid levels best choice for pre-hospital care of injured patients needing body fluid replacement now it's a three to one replacement rule meaning three milliliters of isotonic crystalloid solution is needed to replace one milliliter of blood two-thirds will leave the vascular spaces in one hour you have to monitor urine output when heavy fluid resuscitation occurs and crystallized solutions cannot carry oxygen boluses should be given to maintain perfusion not to raise blood pressure increasing blood pressure may increase internal bleeding it and that interferes with homeostasis and of course the body's blood clotting mechanism blood pressure should be titrated to 90 millimeters of mercury unless otherwise noted the next solution we're going to talk about is colloid solutions and they contain molecules that are too large to pass out of the capillary membranes molecules remain in the vascular compartment this has a high osmolarity and it draws fluids from the interstitial and intracellular compartments into the vascular compartments it's used to treat edema it could cause dramatic fluid shifts and there's a danger to the patient if not given in a controlled setting it has a very short duration of action and low cost to benefit ratio okay so iv solutions are also categorized by their tonicity we have an uh the first one we're going to talk about is the isotonic solution and that's the same concentration of sodium as the cell so water does not shift no change in the cell shape when you have a hypertonic solution a greater concentration of sodium than the cell so water will be drawn out the cell may collapse from the increased extracellular osmotic pressure and then you have finally hypotonic solution and it's a lower concentration of sodium than the cell and the water will flow into the cell cell the cells can swell and could possibly burst from increased intracellular osmotic pressure so when it comes to isotonic solutions uh they have almost the same as molarity as serum or other body fluids so an example is normal saline so 0.9 of sodium chloride that's normal saline it expands the contents of the intravascular compartment and it does not shift fluid to or from the other compartments i we have to use with care to avoid fluid overloading though lactated ringers or lr solution is generally used for patients who have lost large amounts of blood it contains lactate and it should not be given to patients with liver problems it may be potentially detrimental if given during blood transfusions it's contra indicated for nitroglycerin nor epi proprofol and solumetrol infusions okay d5w or five percent dextrose in water is a unique isotonic solution and it's considered isotonic in the bag becomes hypotonic once administered though okay so that leads us into talking about hypotonic solutions solutions have a lower concentration of sodium than the cell serum they it begins to uh di dilute serum once in the vascular compartment so water pulled from the vascular compartment into the interstitial fluid compartment cells eventually swell and burst from increased intracellular osmotic pressure hydrate the cells while depleting the vascular compartment and it may treat hypoglycemic conditions and it can cause a sudden fluid shift from intravascular cells to cells it may lead to cardiovascular collapse and increase intracranial pressure it's dangerous for patients with stroke head trauma burns malnutrition or liver disease and it causes third spacing which is an abnormal shift into the serious linings okay 0.45 sodium chloride commonly referred to as half normal saline it's not common in pre-hospital settings and it may be encountered during inter-facility transport so for patients who have normal sodium levels but need fluid replenishment okay then we have the hypertonic solution and that has osmolarity higher than serum the solution has more ionic concentration than serum it pulls fluids and electrolytes from the inner cellular and interstitial compartments to intravascular compartments the cells may collapse from increased extracellular osmotic pressure it's um it helps stabilize blood pressure increases urine output and reduces edema but careful monitoring needs to be done to avoid fluid overloading so it should not be given to a diabetic ketoacidosis patient and patients at risk of cellular dehydration so three percent sodium chloride may be used per your ems protocols during intra facility transports it's used as a temporary measure to draw out fluid in an effort to reduce intracranial pressure until the patient can be taken into neurosurgery okay and then oxygen carrying solution so whole blood of course is the best replacement for lost blood it contains hemoglobin and uh basically synthetic blood substitutes are now being researched and field tested okay so techniques for administering", + "Techniques and Administration": "ivy fluid so iv therapy involves cannula cannulation of the vein with a catheter to access the patient's vascular system it's one of the most invasive techniques you will perform a peripheral vein cannula is cannulation involves accessing the veins of the periphery and the most important point to remember is to keep the iv equipment sterile so when you assemble your equipment you have to gather and prepare the equipment before you start the line then the following equipment will be available you need an elastic tourniquet aseptic wipe or solution some gauze tape or adhesive bandage an appropriate iv catheter iv administration set and a saline flush so ask yourself is the condition critical is the condition stable does the patient require fluid replacement or will the patient need medications iv solution is usually limited to two isotonic crystalloids normal saline or lactated ringers iv solution bags are wrapped in a sterile bag and get guaranteed sterile until the expiration date solution must be used within 24 hours once opened each bag has two ports there's an injection port for the medication and then there's an access port for the connecting the administration set iv bags come in different fluid volumes so when you want to choose your administration set an admission administration set moves fluids from the iv bag to the patient's vascular system contains a piercing spike protected by a plastic cover the set must be used or discarded once the spike is exposed and the seal surrounding the clamp cap is broken the number of package the number on the package indicates the number of drops it takes for a milliliter of fluid to pass through the orifice and into the drip chamber there are two sizes there's a micro drip set and that allows 60 drips per milliliter ideally for medication administration or pediatric fluid delivery it's easy to control fluid flow and then there's a macro drip set and this allows 10 to 15 drips per milliliter so as you could tell it's a much bigger opening it's ideal for fluid replacement so when you prepare your administration set you're going to verify the expiration date and check that the saline is for clear for clarity prepare the spike the bag over administration set so blood tubing has a macro drip administration and it's designed to facilitate rapid fluid replacement by a minimal infusion of multiple iv bags or iv fluid replacement combinations so there's a vultural or a micro drip set it fills about one to two hundred milliliters calibrated drip chamber able to administer only the amount wanted and its proximal collar clamp allows shut off of the drip chamber from the bag okay so when you choose an iv site you want to avoid areas of the vein that contain valves and bifurcations catheter will not pass through easily in the valves it's a small bump in the vein bifurcations are where two veins split into two the following criteria is used to choose a vein so locate the vein area that looks the straightest choose the vein that looks firm round and springs when palpated avoid veins that cross joints and also avoid any extreme extremity with a dialysis fistula limit iv access to distal areas of the extremity so you want to start distally and work proximally and any introduced fluid immediately below an open wound can enter tissue and cause damage okay so this figure shows common id sites on the upper and lower extremities bulging veins can roll from side to side so manual traction is needed to lock them in place you want to pull the skin over the vein taut with the thumb of the freehand flex the patient's hand stabilize the wrist and apply lateral traction to stabilize the veins in the forearm and anti-cubital areas cannulating the jugular requires a different approach of course consider the patient's option when selecting an iv site avoid extremity if it shows signs of trauma or injury or affection infection and look for track marks okay some protocols allow iv cannulation in the leg veins it can increase risk of venous thrombosis and pulmonary emboli however so when you choose the catheter the catheter should be based on the purpose of the iv line and the age of the patient and the location for the lime over the needle catheters now these are teflon catheters inserted over a hollow needle over the kneader catheters are preferred in the pre-hospital setting they're readily secured less cumbersome than the butterfly and allow for greater patient movement they do not need to be immobilized you don't have to immobilize the entire limb and uh the smaller the gauge the larger the diameter so butterfly catheters are hollow stainless steel needle with two plastic wings most common in phlebotomy and sometimes used for iv placement for scalp veins for pediatric patients and then intracatheter so it's a tube that connects the bloodstream with the puncturing needle it can be used in the pre-hospital setting for medication administration blood samples and hemodynamic monitoring newest needles retract after insertion to minimize the risk of a contamination stick and choose the largest diameter catheter for the vein that you have chosen so an 18 or 20 gauge catheter is usually a good size for adults so when you insert the iv catheter you want to consider it there are considerations for the technique keep the bevel side of the catheter up maintain adequate traction on the vein use a constricting band above the site and remove the band while assembling the iv equipment the most common constricting band is a latex-free iv tourniquet unlike tourniquets used for bleeding control these constricting bands stop only venous flow if visualizing or palpating iv site is difficult providers may choose to replace the constricted bands with a device that applies more pressure such as a larger diameter or denser band known as a penrose strain or a blood pressure cuff or a surgical hose in a pinch of course so you want to prep the site with alcohol or an iodine swab or a chloroprep do not touch the site after prepped apply lateral traction to the vein while holding the catheter bevel side up in your dominant hand insert at a 45 degree angle and push the catheter through the skin until the vein is pierced you should see a flash of blood in the catheter flash chamber drop the angle to 45 degrees and advance the catheter a few centimeters slide the sheath of the needle into the vein apply pressure to the vein proximal to the end of the indwelling catheter remove the needle dispose the needle into the sharps container okay so there is um ultrasound basically ultrasound ivs and those allow providers to see deeper veins that are not visible to the naked eye and may not be palpable so the process is it begins similar to the traditional iv insertion and you place the constricting band on the upper arm near the humeral neck and you apply sterile gel to the ultrasound transducer and arm place the transducer in your non-dominant hand and place the probe at the antecubita fossa run the probe up the humerus looking for a vein a brachial vein or a cephalic vein after identifying a vessel that is 1 6 of an inch or larger in diameter and half inch or less in depth begin to apply pressure to the vessel make sure that the vessel is a vein not an artery and hold the needle in your dominant hand and align the transducer so that the needle shadow is visible on the screen insert the needle through the skin at a 45 degree angle and visualize the needle tip on the screen advance the needle while watching the screen verify iv success with the presence of blood in the flash chamber and advance the catheter and needle withdraw the needle connect the device as you would a normal peripheral iv okay so when it comes to securing the line you want to tape the area to secure the catheter and tubing double back the tubing to create a loop this will act as a shock absorber if the line is accidentally pulled cover the insertion site with sterile gauze or secure with tape avoid circumferential taping around any extremity establish vascular access to correctly establish vascular access see skill drill 14-2 okay so if you ever have to uh change the iv fluid bag if if it becomes completely empty you want to change when there's 25 milliliters of fluid left so you don't ever want to let it go all the way down okay so replace the equipment if it becomes contaminated to change the iv fluid stop the flow of blood or fluid by closing the roller clamp prepare a new iv bag inspect the new bag of fluid for clarity and discoloration okay and ensure that it's not expired remove the piercing spike and insert it into the new bag do not touch the piercing spike port ensure that the drip chamber is filled and roll the roller clamp adjusting the fluid rate accordingly okay so when you want to disconnect the iv line you want to use the roller clamp to shut off the flow of course peel the tape back towards the iv site and stabilize the catheter do not remove the iv tubing from the hub of the catheter you just want to pull the catheter and iv line directly from the patient's vein and then apply pressure to stop the bleeding", + "Alternative IV Sites and Techniques": "so there are alternative iv sites and techniques a lot times in the field we'll use what's called a saline lock and this is to maintain active iv site without actually running fluids through the vein and it's composed of a male lure lock connector attaches to the hub of the iv catheter and then a female lure lock connector and it can connect to syringes or iv administration sets you want to attach to the end of the an iv catheter filled with approximately two milliliters of saline and also called intermittent sites okay so here is an alternative iv sites and techniques and one of the most uh popular alternatives is the external jugular or the ej vein and ej runs down and uh obliquely towards or backwards behind the jaw so pierce's deep fascia in the neck and large and easy to cannulate you can roll it though if it's not anchored okay so exhaust all other means of cannulalization by a peripheral vein before attempting an ej and risk include rapidly expanding hematomas or air emboli or actually puncturing the carotid artery so steps to cannulate the ej once you want to place the patient supine head down position turn the patient's head to the opposite side of the intended vena puncture feel carefully for the pulse do not penetrate or pierce if it's the carotid artery cleanse the site occlude the jugular vein with your finger align the catheter in the direction of the vein puncture midway between the jaw in the mid clavicular line stabilize the vein proceed canalization as you would for the peripheral vein and tape the line securely avoiding circumferential dressings", + "Considerations for Pediatric and Older Adult IV Therapy": "okay so these are pediatric iv therapy considerations so adult iv solutions and equipment can be used for pediatric patients um with some exceptions though so catheters the best gauges for over are over the needle catheters used for pediatrics are 20 22 24 and 26 and you can see the colors in the photo butterfly catheters though are ideal and can be used in the same location as over the needle catheters and can be used in visible scalp veins so explain your actions to the child or parent the youngest patients have fewer choices for iv sites hand veins are painful but remain the location of choice for peripheral iv lines critical to protect iv sites so ensure that the catheter hub and tubing connection are covered with a clear dressing so that they can be continually assessed techniques for starting the pediatric iv line include use a pen light to illuminate the veins through the back of the hand once the site is located graze a surface with the fingernail to mark location proceed with ivs insertion scalp vein canalization is unpleasant and can be difficult so it does not allow for rapid fluid infusion and tape a paper cup over the site to avoid direct pressure", + "Older Adult IV Therapy": "older adults iv therapy consideration so small catheters may be preferable um puncturing the vein may cause massive hematomas and tape may cause skin damage so use smaller catheters like a 20 or 22 or 24 gauge be careful using macro drips and because it can allow for rapid infusion of fluids and that could lead to fluid overload locations consider poor vein elasticity avoid spider veins and do not use varicose veins they are completely closed off", + "Factors Affecting IV Flow Rates": "okay next we're going to talk about some factors affecting iv flow rates so perform the following checks after completing an iv administration and whether there's a problem so you want to check the iv fluid check the administration set so remember macros will deliver fluid rapidly and micros will deliver controlled flow check the height of the iv bag check the type of the catheter that you use check that the constricting band has been removed check the entire line to ensure is not clamped at any point and check the position of the iv lamp", + "Local IV Site Reactions and Complications": "so there's problems that can occur with iv therapy and it can include redness and we could possibly be infiltration or thrombo thrombophletis so systemic complications could be allergic reactions or circulatory overload air embly or catheter shear so local iv site reactions and local complications this could be infiltration and that is the escape of fluid in the surrounding tissues it causes localized area of edema and it could cause iv it could be could include iv catheter passes through the vein and out the other side and the or the patient could be moving excessively or a catheter is inserted too shallow so signs and symptoms include edema at the catheter site patient might complain of tightness or burning pain around the iv site if infiltration occurs you have to disconnect the iv line re-establish an iv line in the opposite extremity or more proximal location in on the same extremity apply direct pressure of the swollen area and do not wrap tape around the entire extremity occlusion is the physical blockage of a vein or catheter so the first sign is a decreasing drip rate or blood in the iv tubing and it may develop because of the position of the catheter within the vein or the patient's blood pressure overcoming the flow to determine whether the iv line should be reestablished use a syringe of clean iv fluid to add pressure to the line gently apply pressure to the plunger to disrupt the occlusion and release the re-establish the flow discontinue administration or re-establish iv in the opposite extremity or a proximal location on the same extremity and then you could have a vein irritation so some patients report the saline is bothering them observe the patient carefully for an allergic reaction and often caused by too rapid of an infusion rate if redness at the iv occurs discontinue the line and save the equipment for analysis re-establish the line in the other extremity with new equipment okay so thrombophlebitis is inflammation of the vein it may occur in association with venous cannibalization and it's frequently caused by lapses in aseptic techniques commonly seen in patients who abuse drugs patients who receive long-term iv therapy or excessive motion of the iv needle after been placed manifest in pain and tenderness and does not appear until several hours after iv drug therapy stop the infusion and discontinue the iv at the site and apply a warm compress and it can be prevented by disinfecting the skin over the venapuncture site wearing gloves not touching the or contaminating the site covering the puncture site with sterile dressing and anchoring the catheter and tubing to prevent motion a hematoma is an accumulation of blood in the tissue surrounding the iv site often caused by vein perforation or improper catheter removal blood can be seen pooling around the iv site it's common in patients with a history of vascular disease or taking certain medications or drinking alcohol stop and apply direct pressure if a hematoma develops while inserting a catheter evaluate the iv flow if the if a hematoma develops and apply pressure if a hematoma develops as the result of discontinuing the iv nerve tendon or ligament damage so it can be caused by improper identification of an anatomic structure around the iv site injury results in the sudden or severe shooting pain in the patient remove the catheter and select another iv site and an arterial puncture so there's a risk it's high near the jugular vein bright red blood will spurt back through the catheter withdraw the catheter and apply direct pressure for at least five minutes or until the bleeding stops to avoid check for a pulse in any vessel you intend to cannulate", + "Systemic Complications": "so usually involve other body systems and can be life-threatening with systemic complications and do not remove iv lines that have been established so so when we talk about pyrogenic reactions this is foreign proteins capable of producing fevers it's characterized by abrupt temperature elevation with severe chills backache headache numbness weakness nausea and vomiting reaction begins within 30 minutes after iv fusion has been started stop the effusion immediately and can be avoided by inspecting iv bag before use when it comes to circulatory overload healthy adults can handle about two to three extra liters of fluid problems occur in patients with cardiac pulmonary or renal dysfunction though it's commonly caused by failure to readjust the drip rate after flushing an iv line after insertion so use an iv delivery device for patients at risk and the signs and symptoms include dyspnea jvd hypertension crackles of course that's rails when you heard evaluating breast sounds or acute peripheral edema so when you treat so to treat you want to slow the iv rate raise the patient's head administer high flow oxygen and monitor vital signs and breathing adequacy and also consider cpap when you talk about some complications you also have to talk about air emboli so healthy adults can handle about up to 200 ml of air introduced into the circulatory system but ill patients cannot properly flushing an iv line will help eliminate the likelihood of an air emboli replace empty iv bags with full ones signs and symptoms are respiratory distress with unequal breath sounds cyanosis loss of consciousness or respiratory rest to treat place the patient on his or her left side with head down administer high flow to transport to the closest facility and assist with ventilations if needed the next systemic complication we're going to talk about is a vague vasovagal reaction and it's caused from anxiety concerning needles or the sight of blood and it may drop the blood pressure and the patient may collapse so patients will present with anxiety or diaphoresis nausea or sinkable episode treatment includes you want to put the patient in the shock position apply high flow to monitor vital signs and then establish the iv line and then we're going to talk about the catheter shear neck so this occurs when part of the catheter is pinched against the needle and the needle slices through the catheter creating a free flowing segment treatment involves surgical removal of that tip so if you suspect a catheter shear put the patient in a left lateral recumbent position legs down and head elevated catheter hubs are um are retro opaque which they appear to be white white on the radiograph because they appear to be white it aids in diagnosing catheter shear so signs and symptoms include dipsnia shortness of breath or diminished breath sounds and symptoms mimic presentation of an air emboli", + "Obtaining Blood Samples": "okay so we're going to talk about obtaining blood samples next and to obtain blood samples at the same time you start an iv line the following equipment will be needed when starting an iv line so you need a 15 or 20 ml syringe an 18 or 20 gauge needle and self-sealing blood tubes blood tubes should be filled in the following order so the mnemonic is red blue gives life so a red blood gives life so red it contains no additives intended to clot if the blood typing is needed blue contains thromp prothom thrombin and so of course that will help with clotting green contains heparin and it determines blood's electrolyte and glucose levels and lavender contains sodium citrate and that determines the complete blood count after the iv is in place occlude the catheter and remove the constricting band you're going to attach a 15 or 20 ml syringe to the help of the iv and draw the necessary blood remove the constricting band while drawing the blood remove the syringe after blood has been obtained and attach iv tubing and begin infusion attach an 18 or 20 gauge needle to the syringe and fill the tubes immediately dispose of the syringe and needle if iv therapy is not indicated but blood samples are required you can use a vacutainer and so it's an 18 or 20 gauge sampling needle and so the steps are apply the constricting band and locate the vein prep the vein just as you would for an iv line insert the needle into the vein remove the constricting band and insert the blood tubes remove the needle and apply direct pressure dispose of the needle and label the tubes you want to label it with the patient's name date time and your name here's a good picture of a vacutainer that we just talked about turn the blood tubes back and forth to mix the anticoagulant and blood evenly do not shake the red tube which is meant to clot blood tubes must be at least three-fourths full to be viable for testing", + "Blood Transfusions": "okay and then blood transfusion so blood type is identified by obtaining a type and cross match from the patient's blood work bracelet will be based on the placed on the patient to identify the blood type blood to be transferred must be checked against the bracelet and verified by two advanced life support providers verification includes the patient's name patient's medical record number the product that is being transfused the number of the product being transfused and and rh type of the product in the emergency medical settings the patient's blood type and rh factor may not be known the hospital will have type o blood available for transfusion if your crew is expected to switch out units during the transport then verify the type and rh factor before leaving anytime you accept a transfer involving a blood transfusion ensure the patient has at least one available vascular site that does not have blood running if the transfusion reaction occurs then any iv lines that have blood transfusion should be disconnected blood being transfused is administered through specific blood tubing and mixed with normal saline you want to assess vital signs every five minutes and monitor the patient for any signs of any type of reaction such as tachycardia hives airway compromise wheezing chest pains or signs of impending doom", + "Intraosseous Infusion": "okay next we're going to talk about io infusions or inner osseous and that means within the bone interosseus or io infusion is a technique of administer fluids blood and blood products and medications into the io space of the proximal tibial tibia humeral head or sternum long bones consists of the shaft which is the difficulties the ends of this epiphyses and the growth plate which is the epithelial plate when the patient is in a hemodynamically compromised condition peripheral veins often collapse iv access difficult if not impossible so io remains space remains patent quickly absorbs iv fluids and medications and anything that can be given via iv route can be given via io route historically reserved for children under the six when iv access could not be obtained within three attempts or 90 seconds but now it's approved as a means to establish vascular access in critically ill or injured adults and as i said earlier there are three common sites that we use for the i o insertion and this is the sternum humerus or prox proximal tibia", + "IO Sites": "and the photos right here show those common i o sites okay so we're going to talk about the humeral io and to locate the humeral io you want to palpate the arm or manipulate the arm and palpate the humeral head place the patient's hand over his or her abdomen place the ulnar aspect of one of your hands vertically over the axial near the humeral head that will be used for the insertion okay so place your thumbs together palpating up the surgical neck to the humeral head okay and then next we're going to talk about the sternum so identify the sternal iocide by palpating the sternal notch and using the i o devices adhesive target the device location is near the chest compression landmarks however the device does not impede chest compressions okay the flat bone of the proximal tibia is located medial to the tibial tuberosity that's the bony prominence just above the knee okay you must feel the leg to know the difference between the first and second landmarks to locate the proximal tibia i o site palpate the tibial tuberosity then for adults you're going to palpate two centimeters medially and for pediatric patients it's just one to two centimeters distal to avoid the epithelial plate for the distal io site use palpation as well okay so identify the medial menialis then for adults palpate two to three centimeters above the site for pediatric patients palpate one to two centimeters above the site", + "Equipment for IO Infusion": "okay so equipment for the i o infusion use of the devices require special training there are manually inserted i o needles and this consists of a solid bore needle inserted through a sharpened hollow needle and it's pushed into the bone via screwing and twisting once the needle pops through the bone a solid needle is removed the hollow needle remains these needles need to be needles rest at a 90 degree angle to the bone and they're easily dislodged and require careful immobilization and then there is this fast so it's first access for shock and trauma and do not use this in children its design elements allow for io placement in the sternum the infusion tube and subcutaneous portal target and strain relief patch there's a protective dome and it can be used during cardiac arrest while chest compressions can coincide with the fast io use mechanical cpr must be paused during the insertion phase so mechanical cpr can continue once the fast device is stabilized sternal placement enables ease of locating the manubrum so the original device fast one consists of 14 gauge infusion tube that and 10 stabilization needles fast responder is an updated device it's partially pre-assembled has a safety lock and requires less pressure the easy i o now this is uh this features a handheld battery powered driver with an attached i o needle it inserts the io needle into the proximal tibia of adults and children and humeral head of adults when iv access is difficult or impossible determining factor in the needle size selections is the amount of subcutaneous tissue present over the insertion site and so you could see on this slide you could see the needle determination criteria so pink is from 3 to 39 kilograms blue is a greater than 40 kilograms and 45 or the yellow is excessive subcutaneous tissue and humeral io for the humeral io insertion all of the needles are eight or 15 gauge needles okay the bone injection gun or big this is a spring-loaded device it inserts io needle into the proximal tibia of adults and children in the humeral head in adults it comes in an adult size and pediatric sizes uses a safety lock as a stabilization device once the device has been inserted and to remove the device use a the stabilization device as the removal tool and then there's this new intraosseous device or nio and it's placed in the proximal tibia of the adult the humeral head is an alternative site for this device it's a spring-loaded device and it contains neither drill nor battery and a pediatric version or an niop is also available this device is a adjustable dial allowing for the provider to adjust by age and depth", + "Performing IO Infusion": "okay so when you perform the i o infusion you want to if you you're using the easy io you want to follow the steps on skill drill 14-3 to attach the fast device we're going to talk about the steps right now so you want to align the adhesive target on the patient and prepare the site to insert the device into the manubrum so prepare the insertion site on the patient's manubrum you're going to position yourself behind the patient's head place two hands on the fast device and align stabilization needles with the target and apply approximately 45 pounds of pressure until you feel the insertion the infusion tube separate from the fast introducer so discard the stabilization needle in the sharps container and attach the iv tubing to the insertion tube's lure lock aspirate the blood and part particles of bone marrow to ensure proper placement slowly inject the iv solution to ensure proper placement of the needle adjust the flow rate and place the protective dome and begin using the device", + "Potential Complications of IO Infusion": "okay so there are complications of iv infusions and it's the same complications as you would have with the iv therapy as well as some others extravestation occurs when the io needle rests outside the bone rather than inside the io space iv fluids will leak into the soft tissues it will reduce the risk using you could reduce the risk using the proper technique remember you want to insert the needle at the 90 degree angle to the bone if if you suspect that the infusion does not run freely or the site becomes ademius discontinue the infusion immediately and reattempt in the opposite leg and then there's osteomyelitis is it's an infection of the bone and muscle caused by infection and it failure to identify the proper anatomic landmark can damage the growth plate proper technique can cause a fracture if you're too forceful or if there's too large of the io needle through and through insertion also can occur if the io passes through both sides of the bone and stop inserting when you feel that pop a pulmonary emboli or pe can occur if particles of bone fat or merrell find their way into the systemic circulation patient will experience shortness of breath pleuric chest pain and cyanosis", + "Contraindications for IO Infusion": "and then a functional iv line is available fracture of the bone intended for i o cannulization osteoporosis osteogenesis which is an imperfecta and bilateral knee replacements and prosthetic limb are contraindications of the io infusion okay so next we're going to talk about medication administration so you want to understand how medications affect the human body before you administer them you need to be familiar with the mechanism of action indications contraindications side effects routes of administration pediatric and both adult doses and then the antidotes the first rule of medication is to do no harm you want to ensure a proper or particular drug is clearly indicated to treat the patient's condition and understand basic math to calculate approximate dosage", + "Mathematical Principles Used in Pharmacology": "so there's mathematical principles when we use pharmacology so let's do a mathematics review fractions represent a portion of a whole number this is expressed as a numerator so the top number represents the portion available over the denominator and that's the total quantity decimals distinguish numbers that are greater than zero from numbers that are smaller than zero whole numbers are on the left side of the decimal fractions of numbers are on the right side of the decimal invert fractions two decimals by dividing the numerator by the denominator dividing or multiplying by 10 can easily be done by remembering a calculation method when dividing move the decimal point to the left when multiplying move the decimal point to the right percentages are part of 100 and use the percentage symbol written as a fraction with a denominator being 100 convert decimals to percentages by moving the decimal over two places the metric system is a decimal system based on multiples of ten measures length volume and weight meter is the length liter is the volume and gram is the weight prefixes demonstrate the fraction of the base being used so micro milli senti and kilo drugs are supplied in a variety of weights and volumes you will be required to convert weights to volumes you will be required to convert larger units of weight to smaller ones and vice versa and you will be required to convert larger units of volume to smaller ones and vice versa drugs are packaged in various units of weight and volume usually comprise only a fraction of packaged form conversion required to fulfill drug requests okay so volume conversion the pre-hospital setting uses two measurements of volume milliliters and liters one liter equals one thousand milliliters so converting milliliters to liters divide the smaller number by 1000 or move the decibel point three places to the left so convert liters to milliliters you want to multiply the liter by 1000 or move the decimal place point three places to the right weight conversion okay to convert a larger unit of weight to a smaller one multiply the larger by 1000 or move the decimal point three places to the right the to convert the larger unit of weight to a larger one or the smaller to a larger divide the larger by 100 1000 or move the decimal point three places to the left one gram equals one thousand milligrams or one milligram equals one thousand micrograms when you convert pounds to kilograms for a patient who do not know their weight in pounds or who are unresponsive estimate the patient's weight in pounds and convert pounds to kilograms there are two formulas for converting pounds to kilograms you could divide the patient's weight in pounds by 2.2 one kilogram equals 2.2 pounds divide the patient's weight in pounds by 2 and subtract 10 of that number temperature conversion so on a celsius scale water freezes at zero and water boils at 100 on the fahrenheit scale water freezes at 32 and boils at 212. normal body temperature is 98.6 or in fahrenheit it's 37 celsius to convert fahrenheit to celsius you're going to subtract 32 then multiply by .555 to convert celsius to fahrenheit you're going to multiply by 1.8 then add 32. okay so when you calculate medication dosages it's based on three factors the desired dose and that's the amount of drug ordered by the physician this is expressed as standard dose or specific number of micrograms milligrams or grams then there's drug concentrations so total weight of a drug contained in a specific amount of volume it may be printed on the label of a drug container some containers list the total weight and total volume separately so you have the volume on hand the volume of solution that the drug is contained in the weight of the drug is present in one milliliters will tell you its concentration so total weight of the drug by the total volume of milliliters okay if the label can list the concentration of the drug as a percentage so the number of grams present in one ml 100 ml so divide the numerator numerator by the decimal denominator by 100 and then finally you have the volume to be administered so the volume to be administered is the desired dose by the concentration of the drug at hand and that's going to equal the volume to be administered okay some medication doses are based on the patient's weight in kilograms so add one step it this adds one set to the firm formula because you have to convert the patient's weight to from pounds to kilograms and remember one kilogram is equal to 2.2 pounds so calculating fluid infusion rates you want to adjust the flow rate of the iv or io catheter according to the patient's condition as dictated by medical control you must know the volume to be infused the period over which it is to be infused and the properties of the administration to calculate the flow rate okay when you're calculating the dose and rate for the medification infusion so non-bait weight non-weight based medication infusions you may need to begin a continuous infusion to maintain a therapeutic blood level of a drug to prevent a recurrence of a condition infusions are usually ordered to be administered over a specific period now that's usually typically per minute to calculate this you know the following information you want to know the desired dose properties of the administration set that you're going to use and if you are using an infusion pump okay so you use the formula same formula to calculate a drug dose as previously discussed to calculate the desired dose to be administered continuously you have to know the number of drops you're going to use the drip set so whether it's a micro or a macro weight based medication infusions to calculate the iv drip rate you're going to use the previously discussed formula but factor in the patient's weight in kilograms and then of course there's pediatric drug dosages there are many methods to determine the right dose of medication for pediatric patients length based resuscitation tape measures or pediatric wheel chart also a field ems guide with tables and charts can be used but most drugs used in the pediatric emergency medicine are based on the child's weight in kilograms calculations are the same for pediatric medicines as they are for adults okay internal medications are those given through the digestive or intestinal tract so oral medications include capsules or time release capsules lodges pills tablets elixirs emulsions suspensions and syrups these drugs are absorbed at a slow rate the slowest almost and po by mouth medication may need to be started early so to administer you may use a medic medicine cup or a medicine dropper teaspoon oral syringe or a nipple check for indications contraindications and precautions and review the 10 rights prior to administration when administering an oral med you need to take standard precautions determine the need for medication follow history including allergies follow standing orders or contact medical control and check the medication to ensure it's correct not cloudy or discolored and not past its expiration date and determine the appropriate dose instruct the patient to swallow a pill or tablet with water monitor the patient's condition and document the medication given route time administration and the response of the patient orogastric or nasogastric tube medication administration so gastric tubes are occasionally inserted in the pre-hospital setting do this to depress the stomach perform gastric lavages or establish a route for internal medication administration common during inter-facility transports and most common solution administered is a feeding tube to administer medications via the gastric tube after the tube has been inserted you want to see skill drill 14-4 use warm water for injections and a saline or solution at room temperature could place the patient in hypothermia if it's too cold and then there's rectal medication administration so medication absorption is rapid and predictable it bypasses the first past metabolism some medication available in suppository form and drug mixed in a firm base that melts to body temperature and is shaped to fit the rectum that's a suppository to administer drugs regularly rectally take standard precautions determine the needle for the medication obtain a medical history including allergies follow standing orders or contact medical control determine the appropriate dose and ensure that the it's the right medication no cloudiness or discoloration and that medicine is not expired use a water-soluble gel for lubrication and insert into the rectum one to 1.5 inches tell the patient not to bear down modifications may be needed for liquid form you may use a nasopharyngeal airway or small endotracheal tube or large bore iv or commercial device lubricate the end of the delivery device and insert it 1 to 1.5 inches into the rectum tell the patient not to bear down push medication through the tube with needleless syringe remove and dispose of the tube and monitor the patient document the medication route time administration and response of the patient so the para internal route is any route that other than the gastrointestinal tract right so this includes the intradermal subcutaneous intramuscular intravenous intraosseous or percutaneous right so medications are absorbed into the central nervous system faster and at a predictable rate syringes and needles are what we're going to talk about next so there's a variety of needles and syringes that are used they may be pre-packaged with the needle attached or they may be packaged separately syringes consist of a plunger and body and barrel flange and a tip the most syringes are marked with 10 calibrations per milliliter on one side the other side is marked in minimums they vary from 1ml to 60 ml hypodermic needles vary from 3 8 to 2 inches in length and for standard injections so the gauge refers to the diameter and we mentioned this earlier the smaller the number the larger the diameter common needle gauges is 18 to 26 proximal end of the needle is the hub it attaches to a standard fitting on the syringe and the distal end is beveled okay so we're going to talk about packaging and first one we're going to talk about is the ampoules and this is a breakable sterile glass container you carry one it carries one dose of the medication and to correctly draw the medication from this ampule we'll see skill drill 14-5 then after the ampoules are vials it's a glass or plastic bottle with a rubber stopper on the top they contain single or multiple doses determine how much of the drug is needed and how much is in the bottle a single dose may require the whole vial draw only what is needed from a multiple dose vial removing the cover makes it no longer sterile some medications and vials may need to be reconstituted this involves injecting sterile water into the powder um or from one vial into another okay so it makes a solution for injection shake the vial vigorously or a mixo vial is a single vial divided into two compartments as you could see on the slide by a rubber stopper to recon constitute it squeeze the vials together and shake vigorously and this is uh solumedra on the slide the to correctly draw the medication from this file see skill drill 14-6 and then of course you have the best types of medication packaging and that's pre-filled syringes and it's packaged in a tamper-proof box there are two types separated into a glass drug cartridge and syringe pre-assembles pre-filled syringes okay so places may contain sharps or pieces may contain sharp so dispose of them properly to assemble the two-part pre-filled syringe just pop off the yellow caps from one syringe and or from the drug cartridge and syringe insert the drug cartridge into the barrel of the syringe and screw them together remove the needle cover and expel air in the manner previously described and follow medication delivery instructions and then you could have a single dose medication cartridges that insert into a reusable syringe those are also available push-dose pressers so some vasopressors are available for administration in a small bolus format they generally reserve for patients with transient hypotension or for ems systems with short transport times at b are commonly or are currently available in a push dose format it's becoming a popular substitute for dopamine in many ems systems using push dose epi involves mixing the appropriate concentration so you want to use a 10 ml saline flush to waste 1 ml you use a blunt tip needle and draw a point or 0.1 milligrams of epi of 1 to 10 000 pre-fill the result will concentrate of 0.1 milligrams or one microgram per tumour 10 ml typically dosing is 10 to 20 micrograms every two to five minutes as needed or until an infusion is indicated intradermal medication administration so intradermal injections involve administering a small amount of medication into the dermal layer uses a 1 ml syringe and a 25 to 27 gauge needle avoid areas containing superficial blood vessels most common indications used are anterior forearm and the upper back medications have a slow absorption rate minimal to no systemic distribution medications remains local local at that area to administer medication intradermally take standard precautions of course determine the need for the medication obtain history including drug allergies follow standing orders or contact medical control we're going to always check the medication to ensure it is correct not cloudy or discolored not expired and the appropriate dosage advise the patient of the potential discomfort and explain the procedure assemble and check the equipment alcohol preps 1 ml syringe with a 25 to 27 gauge needle and the correct dose of the medication cleanse the area for the injection and pull skin taut with your non-dominant hand insert the needle at a 10 to 15 degree angle with the bevel up slowly inject the medicine and look for a wheel so a wheel is a small bump indicating that the medication is pooling in the intradermal tissue remove the needle and immediately dispose of it in the sharps monitor the patient's condition and document the medication route given administration time and response of the patient and then there's the subcutaneous medication administration so subcutaneous or sc injections are given into the loose connecting tissue between the dermis and muscle layer you want to use a 24 to 26 half inch to one inch needle common sites include upper arms anterior thighs and abdomen to correctly administer a medication via subcutaneous route we're going to see skill drill on 14-7 and this figure shows the angle of subcutaneous injection and common sites for that subcutaneous injection and then there's the im or i intramuscular medication administration and they are given by penetrating a needle through the dermis and subcutaneous muscle into the muscle layer it allows for a large volume of medication and potential to damage the nerves though exists so common sites include the lateralis muscle and that's a large muscle on the lateral side of the thigh the rectus femoris muscle that's the large muscle on the anterior side of the thigh the glute and that's the buttocks and then the deltoid muscle that's the muscle on the upper arm that covers the shoulder to correctly administer the medication via im route we are going to use skill drill 14-8 and the figure shows common sites for intramuscular injections okay next we are going to talk about the iv bolus medication administration iv route places drugs directly into the circulatory system we know this is the fastest route of administration it bypasses most barriers of drug absorption direct injection of drugs with a needle and syringe into the iv line and a bolus is a single dose given by the iv route the smaller large quality quantity of the drug it can be delivered rapidly or slowly some medications require initial bolus followed by continuous iv infusion to correctly administer a medication via iv bullish route we want you to see skill drill 14-9 saline locks are used for patients who are not in need of iv fluid but they do need some medication therapy so to administer medication through the saline lock we're gonna do all the same procedures take the standard precautions obtain the need obtain history follow the standing orders check the medication to ensure that it's not cloudy or discolored expired or incorrect amount of concentration and concentration i explain the procedure to the patient we're going to assemble the needle assemble the needed equipment and drop the medication a 20 ml of normal saline needed to use as a flush of course we're going to cleanse the injection port with alcohol and remove the protective cap insert the needle into the port and screw the syringe onto the port clamp off the iv tubing to prevent black flow pull back slightly on the syringe plunger to observe for blood return if the blood appears watchful infiltration if resistance is felt or if the patient reports discomfort discontinue and then establish a new site place the needle and sharps into or syringe into a shop's container okay and so this is just talking about clean the port insert the needle flush the needle talking about doing the flush and then of course you're going to monitor the patient's condition and document the medication route the medication that's given the type of administration and the response of the patient adding medication to the iv bag is what we're going to talk about next you want to check the fluid in the iv bag for discoloration and ensure it's not expired okay so check the drug and name and concentration compute the volume of the drug to be added to the iv bag and draw up that amount in a syringe and then you're going to inject that medication into the iv bag via that rubber stopper you could see the rubber stopper on the slide right there withdraw the needle and dispose it in the sharps container you need to agitate the iv bag to ensure the drug is mixed into the solution label the iv bag with the name of the medication that was added the amount added concentration in the iv bag the date and time in your name and attach the iv administration set and prepare the iv bag okay another way that you could administer medication is through a thing called an iv piggyback so when you do this you have a primary line that's iv administration set that is connected directly to the hub of the iv catheter okay when performing continuous infusion you want to take the distal tip of the drip set and connect it to the port of the primary line and that's the line connected to the continuous infusion in the piggyback so you're going to have multiple lines and that can be piggybacked label the lines to ensure there is no interactions and follow the steps in skilder 14-10 to perform an iv piggyback infusion you want to use an electro-mechanical infusion pump sometimes and so you use them when you're administering a medication maintenance infusion or delivering iv fluid maintenance infusions in children and older adults there are benefits and they deliver the rates set by the pump without deviating and you could calculate the amount of fluid infused and amount remaining but there are problems they can lack uniformity among manufacturers and air can trap in the lines causing the pump to stop and alarm to sound okay and so on the slide you can see two two separate infusion pumps and they may be designed to accommodate iv tubing to regulate the flow of fluids and needless syringes on them as well they may have multiple chambers for multiple medications and some pumps have medication databases that calculate medication rate by desired dose and patients weight and so iv infusion pumps come in a wide variety of configurations i o medication administration so fluid does not flow well into the bone um and so use a large syringe to infuse the fluid a pressure infusion device as a sleeve placed over on the iv bag and inflate to force the fluid from the iv bag potential for compartment syndrome if the fluid leaks out of the bone and to correctly administer a medication via the io route see skill drill 14-11 and then there's the percutaneous medication administration so with the percutaneous route of administration medications are applied to and absorbed through the skin and mucous membranes a transdermal medication administration so typically it's applied topically so on the surface of the body useful for sustained release of certain medications we use this with nitro paste right now and delivery includes patches or creams lotions and pastes too much medication or thin non-contact skin may increase the speed of absorption or thick skin or scar tissue may decrease the speed of absorption so to apply um you want to perform the following steps of course standard precautions determine the need obtain the history follow standing orders or contact medical control check the medication to ensure it's correct unexpired and appropriate explain the procedure clean and dry the area apply the medication in accordance with the manufacturer's specifications and monitor the patient and document the medication route time and patient response sublingual medication administration so that is under the tongue it's very vascular under the tongue and the medication is rapidly absorbed drugs may also be injected under the tongue and useful for drug addicts if it is difficult to find a suitable vein to correctly administer sublingual medication c skill drill 14-12 and then there's bucal medication administration so the buccal region lies in between the cheek and gums medication comes in the form of tablets or gel and to administer medication via bucal route you're going to take all the standard precautions um determine the need obtain the history follow the orders explain to the patient place medication between the patient's cheek and gum or ask the patient to do so advise the patient to allow the tablet to dissolve slowly rather than to chew or swallow it and then of course you have to monitor the patient's condition and document the medication given route administration time and the response of the patient there's also ocular medication administration those are drops or ointments and are commonly administered via the ocular route typically administered for pain relief allergies or infections medication administered via ocular route is rare in the pre-hospital setting in hospitals and in some pre-hospital systems providers use bottles to squeeze the prescribed amount of drips or drops into the eye or a morgan lens can be used for some ophthalmolic medications particularly local anesthetics okay so you're going to take standard precautions confirm prescription have the patient tilt the head and look up expose the conjunctiva by gently pulling down on the lower eye without touching the eyeball administer the medication using an eye dropper and advise the patient to close their eyes for one to two minutes document of course the medication name dose in the administration time and then you have the oral medication administration and that's administered via the ear canal to assist the patient with the oral medication administration you want to take standard precautions confirm prescription place the patient on side with affected ear facing up expose the ear canal by pulling the ear back and up and back in adults or down and back in infants and children administer medication with a medication dropper and document the medication name dose and administration time and then there's intranasal medications and these intranasal medications include nasal spray for congestion or solutions to moisten the nasal mucosa they rapidly absorb a rapid onset and perform with a mucosal atomizer device that's a mad device it attaches to syringe it gets spray medication into the nasal mucosa and typically requires about 2 to 2.5 times the dose of iv medications follow local protocol or consult medical control and to administer a medication via the intranasal route follow the steps and skill drill 14 14-13 and then of course there's our inhalation route and it could be a nebulizer or a meter dose inhaler the most common medications via inhalation is of course oxygen you want to check your drug reference guide or packaged prior to administration a patient with a history of respiratory problems will have a meter dose inhaler and mdi administered by the patient but the patient may ask for assistance of course and it can be delivered through the mouthpiece held by the patient or by a mask okay liquid bronchiodilators may be aerosolized in nebulators nebulizers for inhalation most common method of administration of it held medications in the pre-hospital setting it may allow blow by administration or nebulize mask and to administer a medication via a small volume nebulizer see skill drill 14-15 in your book the patients are breathing inadequately they may be unable to effectively inhale medicines so you have to assist with a bag valve mask attach a small volume nebulizer to the ventilation device place a short piece of corrugated tubing between the bag and the mask or endotracheal tube when using cpap most manufacturers have a nebulizer that is designed to work with their device and then of course endotracheal medication administration certain resuscitative medicines can be administered down the endotracheal route you want to administer two to two and a half times the standard iv dose and there's only four medications that are accepted for administration and you can remember the pneumonic lean okay lean that's lidocaine epi atropine and narcan and narcan that's contraindicated for neonates of course so check your local protocols prior to administration then you have long-term vascular devices and these are patients who are receiving antibiotics or chemo or regular blood draws or hemodialysis usually patients are up front and will request a peripheral line is not used there are two types it's there's the non-tunneling and then they have implanted most protocols do protocols only allow access during critical events and they're usually preserved with heparin most non-tunneling devices have been inserted by direct venipuncture most commonly encountered in pre-hospital settings include peripheral insertion catheters central catheters or picc lines these are used for long-term medication administration such as chemotherapy frequent venous sampling or or sometimes a total parental nutrition so insert by pic nurses of can be left in place for about six to eight weeks may have single double or triple luminum and midlines are inserted into the anacubital vein distal end of the midline is proximal end of the extremity those can be used for four weeks and then central venous catheters are used in an emergency of course large bore iv catheters and they sit near the vena cava to correctly access a tunneling device see skill drill 14-16 implanted vascular access devices are implanted in surgery sutured under the skin you could palpate them they're not exposed to the environment their self-sealing core is inserted in a stainless steel titanium or plastic shell connected to a catheter and they can be used for long-term medication administration av fistulas are used for a variety of disorders and they are created by connecting a vein in an artery they are used for hemodynamics require a unique skill set to access this figure shows the steps of accessing an implanted vascular access device okay so rates of medication absorption and drugs are absorbed at a speed directly related to the route of delivery drugs injected into the bloodstream gain access fastest oral meds take longer because of they they have to be absorbed first and so the table on this slide shows medication routes and rates of absorption ioiv fastest and topical slowest okay and this table shows examples of specific medicines okay so this concludes chapter 14. thank you for joining us this evening and we hope that you join us for another lecture" + }, + { + "Introduction to Vascular Access and Medication Administration": "chapter 13 vascular access and medication administration before administering medication to a patient it's important to understand its effects on the body this involves comprehending the medication's mechanism of action indications for use contraindications routes of administration dosage and potential adverse reactions additionally it's necessary to be aware of the procedures to follow in case of an ad ver reaction the primary principle in medicine is first Do no harm ensure that the medication administered is specifically indicated for the patient's condition a thorough assessment of the patient will help confirm that only beneficial medications are given IV therapy is one of the most invasive procedures that an aemt must learn requiring extensive training and practice Mastery of IV techniques is necessary for many Advanced life support procedures medical conditions disrupt the body's homeostatic balance therefore it's essential to fully assess the patient's condition and address any life-threatening injuries or illnesses that could affect homeostasis B basic math skills are necessary to calculate the correct medication dose errors in drug Doses and flow rate calculations are frequent sources of confusion adverse reactions including potentially fatal outcomes may result from administering an incorrect drug or dose delivering the medication via an incorrect route or infusing it too rapidly or too slowly medication administration is regulated by local protocols and or online medical Direction most EMS services are equipped with drug boxes containing a range of medications including cardiac agents pain relievers anti-convulsants anti Medics and Other Drugs specific to their service standing orders May permit the administration of certain certain medications prior to physician contact local policies and procedures are established to provide guidance in various situations an AM emt's responsibilities related to drug orders include confirming the rights of medication administration the right patient the right medication and indication the right dose the right route the right time the right education the right to refuse the right response and evaluation and the right documentation the procedure for administering medication involves several steps first obtain an order from medical control it is essential to be knowledgeable about each medication carried on the ambulance to ensure safe patient care this includes understanding the indications contraindications therapeutic effects side effects and appropriate dosages of each medication additionally be aware of when and when not to administer each Med including knowing which medications require specific intervals for repeated Doses and the correct intervals for administration ensure that medical control fully understands the situation before administering medication this involves providing a comprehensive overview of the patient's condition including relevant history and current symptoms the decision to administer medication should consider several factors about the patient their age which can influence drug metabolism and dosage their weight which impacts the appropriate dosage their overall clinical status including any immediate health concerns their allergy history to avoid adverse reactions any concurrent medical conditions that might affect drug efficacy or safety and other medications that the patient may be taking which could lead to drug interactions it is essential to provide complete and accurate information about the patient to the physician in order to ensure that the medication decision was well informed and tailored to the patient's needs additionally verify the identity of the patient especially in situations with multiple patients in order to prevent errors when assisting a patient with medication confirm that is specifically prescribed for them and is not intended for someone else this ensures the medication A's appropriateness and safety for the patient's unique condition and avoids potential complications ensure you fully understand the physician's orders before proceeding with medication administration you must repeat any orders for btim to confirm their accuracy and to prevent errors ask about any medication allergies the patient might have in order to AV avoid adverse reactions verify the medication and the prescription details paying close attention to the concentration printed on the label before administering the medication read the label at least three times to make sure that you have the correct drug first check the label when the medication is still in the drug box to confirm that it matches the prescribed drug second review the label again while preparing the medication for administration finally check the label once more just before administering the medication to the patient in order to double check that no errors have occurred during preparation confirm the medications form dose and route to ensure they match the physician's orders also inspect the expiration date and condition of the medication in order to verify that it's still safe to use make sure that the medication is compatible with any other medications or Solutions it may be combined with if the medication is administered through an IV line verify its compatibility with the IV solution if you notice any cloudiness or precipitate forming over the medication immediately clamp the tubing to prevent further infusion replace the contamin ated tubing with a new Administration set to maintain the Integrity of the IV therapy and prevent potential complications dispose of any syringes and needles safely to prevent needle stick injuries and ensure proper Waste Management monitor the patient closely for any potential adverse side effects that may arise from the medication document all actions taken including the medic administered dosage time and the patient's response do this on the patient care report in order to maintain accurate and comprehensive medical records on the screen you can see the medications that most aemts are authorized to administer of course this will vary depending upon the service provider that they are working for", + "Understanding Electrolytes and Their Role": "electrolytes are ions that carry a positive or negative charge and their proper balance is vital for numerous physiological functions atoms which are the basic units of matter possess electrical charges that can combine to form molecules when two or more atoms bond together they create molecules molecules that contain carbon atoms are known as organic molecules while those that do not contain carbon are classified as inorganic molecules inorganic molecules when dissolved in water dissociate into their charge components creating electrolytes these electrolytes include ions such as sodium potassium calcium chloride which are essential for various bodily functions because these ions are reactive their concentration and balance must be carefully regulated to prevent potential disturbances or harmful effects water in the body plays a crucial role in maintaining the balance and stability of electrolytes it acts as a solvent helping to dissolve electrolytes and ensure that they are distributed throughout the the body this distribution allows electrolytes to participate in critical metabolic processes such as nerve impulse transmission muscle contraction and maintaining fluid balance proper hydration and electrolyte management are necessary to support these functions and overall health cat ions are electrolytes with an overall positive charge while anion are electrolytes with an overall negative charge sodium is a principal extracellular cation that is important for regulating the distribution of water throughout the body it plays a major role in maintaining adequate cellular profusion by influencing blood volume and pressure sodium is also a key component of the circulating buffer system which helps maintain acid base balance in the blood the sodium potassium pump is a critical cellular mechanism that actively transports sodium ions out of the cell and potassium ions into the cell this process is essential for maintaining the appropriate concentrations of these ions inside and outside of the cell which is needed for normal cell function the activity of the pump is enhanced by insulin and epinephrine insulin helps promote the uptake of potassium into the cells while epinephrine stimulates the pump's activity and facilitates transport of both sodium and potassium ions hypokalemia or low potassium levels in the blood can significantly impact various bodily functions potassium is vital for normal muscle function including the skeletal muscles a deficiency in potassium can lead to muscle weakness cramping and decreased muscle function additionally low potassium levels can cause GI disturbances such as constipation as potassium is essential for proper muscle contractions in the GI tract furthermore hypokalemia can affect cardiac function potentially leading to arrhythmias or other heart related issues due to the critical role potassium plays in maintaining the electrical stability of the heart on the other hand hyperemia or high potassium levels can have severe effects on the body elevated potassium levels can lead to hypers stimulation of neural cells affecting nerve signal transmission and potentially causing abnormal muscle contractions or cardiac arrhythmias the most serious consequence of hyperkalemia is cardiac arrest as high potassium levels can disrupt the normal electrical activity of the heart leading to potentially life-threatening conditions managing potassium levels is therefore essential for maintaining proper physiological function and preventing these serious complications calcium is a principal cation necessary for several vital functions including bone growth heart muscle contraction nerve function cell membrane stability and blood clotting hypocalcemia can lead to overstimulation of nerve cells resulting in symptoms such as skeletal muscle cramps abdominal cramps carpopedal spasms hypotension and and Vaso constriction in contrast hypercalcemia can decrease nerve cell stimulation which may lead to skeletal muscle weakness lethargy a taxia or lack of muscle coordination vasod dilation and hot flush skin bicarbonate levels play a key role in regulating the body's acid base balance affecting conditions such as acidosis and alkalosis chloride is crucial for maintaining stomach pH and regulating extracellular fluid levels while phosphorus is essential for the formation of a Denine triop phosphate or ATP which is a critical molecule for energy transfer within the cells", + "Fluid Balance and Movement in the Body": "body fluids are essential for various physiological processes and are made up of water and dissolved elements in a solution which describes body fluids there are two primary components the solvent and the solute the solvent is the fluid that dissolves other substances with water being the main solvent in body fluids water facilitates the dissolution and transport of various solutes within the body solutes are the particles or substances that are dissolved in the solvent and include electrolytes nutrients gases and waste products they are crucial as well for maintaining bodily functions such as nutrient transport waste removal and the regulation of acid base balance the combination of solvent and solute creates a solution that supports the proper distribution and interaction of substances within the body which is vital for maintaining homeostasis and overall health fluid and electrolyte movement across cell membranes involves maintaining balance in two primary aspects the balance of compounds and the balance of electrical charges the balance of compounds refers to the distribution of substances such as ions neutr nuut and waste products on either side of the cell membrane these substances move from areas of higher concentration to areas of lower concentration through a process known as diffusion which helps to equalize their concentrations across the membrane the balance of charges involves the distribution of positive and negative ions to maintain electrical neutrality the difference in charge across the membrane known as the membrane potential influences how ions move for example positively charged ions may move toward areas with a more negative charge the movement of materials is also dependent on the permeability of the cell membrane which determines whether a substance can pass through the membrane's permeability is influence infuenced by its structure and the presence of specific channels or transport proteins some membranes are selectively permeable allowing only certain ions or molecules to cross While others actively transport substances against their concentration gradient using energy or active transport these processes collectively ensure that cells maintain their internal environment regulate ion concentrations and support physiological functions such as nutrient uptake waste removal and electrical activity that's necessary for nerve and muscle function", + "Processes of Diffusion, Filtration, and Active Transport": "diffusion is the process by which compounds or charges that are concentrated on one side of a cell membrane move across the membrane to an area of lower concentration this movement occurs naturally to achieve equilibrium where the concentration of substances is balanced on both sides of the membrane filtration is a type of diffusion utilized by the kidneys to cleanse the blood in this process water carrying dissolved compounds is pushed across the cell membranes of the kidney tubal the dissolved compounds are then trapped allowing the kidneys to remove waste products and excess substances from the blood while retaining the necessary components active transport is a method used to move compounds across cell membranes to create or maintain an imbalance of charges this process requires energy typically in the form of a Denine triop phosphate to transport substances against their concentration gradient an example of active transport is a sodium potassium pump this pump moves sodium ions out of the cell and potassium ions into the cell contributing to the cell's resting membrane potential and the generation of electrical signals necessary for the processes of depolarization by using ATP the pump actively transports these ions maintaining the necessary concentration gradients and charge imbalances across the membrane", + "Osmosis and Tonicity": "osmosis is the movement of water across a cell membrane in response to differences in solute concentrations on either side of the membrane when there are varying concentrations of solutes such as sodium on each side of the membrane water moves to balance these concentrations for instance increasing the concentration of sodium in the extracellular fluid reduces the water concentration in that fluid consequently water moves out of the cell to dilute The increased sodium concentration and Achieve equilibrium this movement of water creates osmotic pressure where the increased yet balanced volume of water exerts pressure against the cell wall helping to maintain proper cellular function and fluid balance tonicity describes the effects of osmotic pressure on a cell would Expos to different solutions an isotonic solution has the same concentration of sodium and other solutes as the cell's internal environment resulting in a no net mve mement of water into or out of the cell essentially the cell retains its shape and volume however a hyperonic solution we have a higher concentration of sodium compared to the cells interior which causes water to move out of the cell leading to cell shrinkage or crenation conversely a hypotonic solution has a lower concentration of sodium than the cell's interior causing water to move into the cell now this influx of water can result in the cell swelling but it can also result in Lis if excessive meaning that the cell bursts and is destroyed", + "Fluid Compartments and Regulation": "water in the body exists in two main compartments intracellular and extracellular the levels of water in these compartments are continuously shifting due to various physiological processes but homeostatic mechanisms work to restore and maintain balance the vascular system which includes your blood vessels functions as a fluid Highway and also contains cells this system can be considered an additional fluid compartment contributing to the overall distribution and regulation of body fluids the extracellular compartment of the body is divided into two main subcompartments intravascular and interstitial intravascular fluid is the water portion of the circulatory system that surrounds the blood cells within the blood vessels in contrast the interstitial fluid is found outside the vascular system system filling the spaces between cells and acting as a buffer between the vascular and intracellular compartments together with intracellular fluid these three fluid compartments account for approximately 60% of the body's total weight extracellular fluid includes all fluid outside the cells and serves as a conduit for transferring gases and nutrients between the vascular and intracellular compartments its levels are regulated by sodium concentrations interstitial fluid which represents about 16% of total body weight occupies the microscopic spaces between cells and consists of a gel-like protein that helps evenly distribute water throughout the interstital compartment facilitating the movement of water between cells and the vasculature profusion in the capillaries is driven by high hydrostatic pressures and osmotic forces within the capillary beds hydrostatic pressure pushes fluids and nutrients out of the blood and into the surrounding tissues while osmotic pressure primarily due to the presence of plasma proteins draws fluids back into into the capillaries from the interstitial space this balance ensures that tissues receive adequate nutrients and that waste products are efficiently removed intracellular fluid is the fluid contained within all body cells it plays a critical role in cellular function and homeostasis the presence of large proteins within the cell such as albumin or or other intracellular proteins creates an osmotic gradient that attracts water into the cell this influx of fluid helps to maintain cell turer and supports various cellular processes sodium ions that enter the cell driven by concentration gradients are actively transported out by the sodium potassium pump again this pump uses ATP to move those sodium ions out of the cell and bring potassium ions in this active transport is essential for maintaining the appropriate balance of ions inside and outside the cell preserving cellular integrity and preventing cellular Lis fluid balance is important for maintaining cellular function and overall homeostasis water surrounds all cells and plays a role in cellular metabolism and the regulation of internal environments the body manages the balance between intracellular and extracellular fluid by adjusting water retention and elimination this is achieved when the intake of fluid equals the output ensuring stable fluid levels within the body the maintenance of the internal envir M of cells is regulated by feedback systems that monitor and adjust fluid levels ionic concentrations and other variables to ensure proper cellular function and overall equilibrium", + "Dehydration and Overhydration": "dehydration is characterized by a depletion of the body's total systemic fluid volume and is more common among older adults and young children it may develop over days and can result from various medical conditions when fluid is lost from the vascular compartment the body compensates by shifting interstital fluid into the vascular area this shift causes fluid to move from the intracellular to the extracellular compartments this leads to a total systemic fluid deficit signs and symptoms of dehydration include include decreased levels of consciousness orthostatic hypotension dry mucus membranes tardia poor skin turer flushed and dry skin and decreased urine output common causes of dehydration include diarrhea vomiting GI drainage Hemorrhage insufficient fluid or fluid intake and infection overhydration is characterized by an increase in the body's total systemic fluid volume this excess fluid initially fills the vascular compartment and then filters into the interstital compartment it may even eventually move into the intracellular compartment this fluid overload can lead to severe complications including potential fatal outcomes if not managed properly signs and symptoms of overhydration include shortness of breath puffy eyelids edema polyurea crackles and acute weight gain common causes of overhydration include unmonitored IV lines kidney failure prolonged hypoventilation all of which can impair fluid balance and exacerbate fluid retention", + "IV Fluid Composition and Types": "IV fluid composition involves Solutions where compounds and ions are dissolved to match those found in the body each IV solution consists of a specific concentration of solute and solvent sodium is often used as a reference point to determine a solution's tenic with the concentration of sodium in the body cells being approximately 0.9% a commonly used IV fluid is normal saline which contains sodium chloride at this concentration by altering the sodium concentration in the IV solution water can be directed into or out of different fluid compartments within the body thereby influencing fluid balance and distribution IV Solutions are categorized as either crystalloid or colloid based in their composition and they are further classified as isotonic hypotonic or hypertonic according to their tonicity crystalloid Solutions are composed of dissolved crystals in water with compounds that quick l dissociate in the solution these Solutions are particularly effective for prehospital care in patients experiencing fluid loss due to injury they are governed by the 3:1 replacement rule which dictates that 3 MLS of isotonic crystalloid solution is needed to replace 1 ml of lost blood unlike colloid Solutions crystalloids do not carry oxygen and therefore are not suited for oxygen transport when administering crystalloids boluses of 250 mLs are typically used to maintain profusion as evidenced by the presence of radial pulses but this does not necessarily restore blood pressure increasing blood pressure through the use of these IV Solutions can dilute the remain in blood volume and potentially worsen internal bleeding by disrupting the normal hemostatic process colloid Solutions contain large molecules typically proteins that are too substantial to pass through capillary membranes thereby remaining in the vascular compartment these Solutions exhibit very high osmolarity which draws fluid from the the interstial and extracellular compartments into the vascular system this property makes colloid Solutions effective in reducing edema while simultaneously expanding the vascular compartment however their ability to shift fluid can lead to significant and sometimes dramatic fluid redistributions in the body", + "Tonicity and IV Solutions": "IV Solutions are categorized based on their tenic which influences how they affect fluid movement between body compartments isotonic Solutions such as normal saline and lactated ringers have an equal concentration of solute compared to the body cells and extracellular fluid helping to maintain fluid balance and often use for hydration and volume replacement hypotonic Solutions like e5w have a lower concentration of solutes than the body cells causing fluid to move into the cells and addressing cellular dehydration but potentially risking cellular swelling hypertonic Solutions including 3% saline certain blood products and albumin have a higher concentration of solutes compared to the body cells drawing fluid out of the cells and interstitial spaces into the vascular compartment these Solutions are useful for managing edema and expanding blood volume though they may also pose risks due to significant fluid shifts isotonic Solutions which are characterized by having nearly the same osmolarity as serum and other body fluids effectively expand the intas ular compartment without significantly altering the fluid distribution between those compartments this means that these Solutions stay predominantly within the vascular system minimizing the movement of fluid to or from other areas it's important to manage the volume carefully to avoid fluid overload particularly in patients with hypertension or heart failure those patients who are at higher risk for such complications in clinical practice lactated ringer solution is frequently used for patients who have lost substantial amounts of blood providing essential electrolytes in fluid replacement D5W is unique among isotonic Solutions because while it remains isotonic before Administration the dextrose is quickly metabolized by the body once infused in this process converts the solution into a hypotonic state potentially causing a shift of fluid into the cells and affecting fluid balance hypotonic Solutions have a lower concentration of sodium compared to the cells these Solutions hydrate the cells by promoting the movement of water from the vascular compartment into the cells which can lead to a reduction in the fluid volume within the vascular system they are sometimes used in specific clinical situations such as for patients undergoing dialysis who experience cellular dehydration due to diuretic therapy or for individuals with hyperglycemic conditions like diabetic keto acidosis where High serum glucose levels draw fluid out of the cells however these Solutions do carry significant risks including the potential for a rapid and dangerous fluid shift from the intravascular space into the cells which can lead to complications they are particularly risky for patients with stroke or head trauma as well as those with Burns trauma malnutrition or liver disease due to their compromised fluid balance and potential for exacerbating underlying conditions hypertonic Solutions have an osmolarity higher than that of serum and contain a greater ionic concentration these Solutions work by shifting body fluids into the vascular Space drawing fluid and electrolytes from the intracellular and interstial compartments into the intravascular compartment this mechanism can help stabilize blood pressure increase urine out put and reduce edema however hypertonic Solutions are rarely used in prehospital settings due to the need for careful monitoring to prevent fluid overload they should not be administered to patients in diabetic keto acidosis are those at risk of cellular dehydration as the movement of fluid out of the cells could exacerbate their condition", + "IV Equipment and Site Selection": "when administering IV fluids it's crucial to maintain sterility of all equipment to prevent infection Begin by gathering and preparing all necessary equipment before starting the procedure this should include an elastic constricting band to help identify veins an antiseptic wipe or solution to disinfect the site Galls for managing any bleeding and tape or an adhesive bandage to secure the catheter in place you'll also need an appropriately sized IV catheter IV extension set a saling flush for clearing the catheter and an IV Administration set to deliver the fluids ensuring that all these items are prepared in advance helps streamline the process and minimizes the risk for complications when choosing an IV solution first assess the patient's condition to determine their specific needs consider whether the patient's condition is critical or stable and if fluid replacement is necessary each IV solution bag is enclosed in a protective stero plastic bag to maintain stability at the bottom of each bag there's an access port for connecting the administration set which should be protected by a removable pigtail the serves as a two point of no return to ensure the stability of the access point IV solution bags are available in various fluid volumes allowing selection based on the required volume for the patient's treatment choosing an Administration set involves selecting the appropriate device to transfer fluid from the IV bag to the patient's vascular system the administration set features a piercing Spike that is initially protected by a plastic cover to maintain stability until use these sets come in various sizes to accommodate different clinical situations in patient needs most drip sets are labeled with a number on the package which indicates how many drops are required for 1 mm of fluid to pass through the orifice and into to the drip chamber this helps in regulating the flow rate and ensuring accurate fluid delivery drip sets are available in two primary sizes each suited for different clinical needs micro drip sets which allow 60 drops per milliliter feature a small needle-like orifice inside the drip chamber these are ideal for precise medication administration or for delivering fluids to Pediatric patients due to the ease of flow control in contrast macro drip sets allow for 10 to 15 to 20 drops per milliliter and have a larger opening between the piercing Spike and the drip chamber they are best suited for Rapid fluid replacement due to their higher flow rate blood sets are a specialized type of macro drip set that's designed to facilitate rapid fluid replacement by enabling the manual infusion of multiple IV bags or combinations of IV and blood products many blood sets come equipped with dual piercing spikes allowing two bags of fluid to be hung simultaneously for the same patient when choosing an IV site it's important to follow specific criteria to ensure successful catheter placement and optimal fluid administration first locate a vein that appears straight as this facilitates easier catheter insertion select a vein that feels firm and round or springy or spongy upon palpation indicating a well-filled vessel avoid veins that cross joints as these areas are more prone to movement it may lead to complications or discomfort during or after the procedure When selecting an IV site it is also important to avoid extremities showing signs of trauma injury infection or edema as these conditions can complicate catheter placement and increase the risk of complications additionally steer clear of extremities with a dialysis fistula as using these veins can disrupt the dialysis access avoid selecting an extremity on the same side as a prior myectomy or lyth node dissection surgery as these areas may be more susceptible to infection and complications due to altered lymphatic drainage when choosing an IV site pay close attention to areas of the vein with tra marks as these May indicate sclerosis from frequent punctures or culations for patients in critical condition it's advisable to start with veins located at the anticubital fossa or higher for easier access begin the search for a vein distally and work proximately to optimize vein selection be aware that large protruding arm veins may move side to side during canulation increasing the risk of missing the vein and causing infiltration to stabilize hand veins pull the skin over the vein taut with your thumb while the patient's hand is flexed for wrist veins Flex the wrist and pull the skin taut over the vein applying lateral traction with your free hand can help stabilize veins in the forearm and anticubital areas it's also helpful to ask the patient if they know of an effective IV location from past experiences when culating leg veins exercise caution due to the increased risk of infection Venus thrombosis and potential pulmonary embolism", + "IV Catheter Selection and Insertion": "when choosing a catheter the most common options are the over the needle catheters or angio caths and Butterfly catheters the selection should be based on the specific requirements of the administration the patient's age and the site of insertion for instance over the needle catheters are generally preferred for long-term infusions or larger veins while butterfly catheters may be used for short-term access or in smaller veins over thee needle catheters are sized by their diameter we refer to this as the gauge and they can be used for all adults and most children for long-term IV Therapy when inserting the IV catheter regardless of the technique used keep the beveled side of the catheter facing up this orientation helps to ensure proper entry into the vein additionally maintain adequate traction on the vein throughout the canulation process to stabilize it and facilitate successful catheter placement to insert the IV catheter start by applying a constricting band above the selected site avoid leaving the constricting band on while assembling the IV equipment these bands can be made from various materials including a pinrose drain a blood pressure cuff gloves or surgical tubing once you've chosen your site prep it with an alcohol swab iodine swab or chlorhexadine taking care not to touch the sight afterwards apply gentle downward or lateral Al traction on the vein with your free hand while holding the catheter with the bevel Side Up in your dominant hand establish an insertion angle of approximately 45\u00b0 and Advance the catheter through the skin until the vein is pierced then lower the angle to about 15\u00b0 and Advance the catheter to a few more millimeters to ensure the catheter sheath is within the vein Slide the sheath off the needle and into the vein avoid advancing the needle too far to prevent lacerating the back wall of the vein once the catheter is fully in place apply pressure to the vein just proximal to the end of the IND dwelling catheter remove the needle and very importantly dispose of it in the sharps container when drawing blood providers should do so before administering any fluids or medications if you encounter difficulty drawing blood prioritize establishing the IV line before proceeding to assist with blood collection a vacutainer can be connected to the catheter in the absence of a vacutainer setup a 15 to 20 ml syringe can be used to draw blood from the IV site you should always follow your local protocols regarding the types of blood tubes required however you should always ensure that each tube is labeled with the patient's name the date the time and your name to secure the IV line effectively tape the area to ensure that the catheter and tubing are firmly anchored this will reduce the risk of dislodgment if the line is pulled suddenly it's a good idea to tear the tape before beginning IV Administration in order to avoid any delay or complications create a loop in the tubing by doubling it back this Loop acts as a shock absorber helping to prevent accidental dislodgment if the line is inadvertently tugged avoid wrapping tap circumferentially around the extremity as this can impede circulation to change an IV bag first ensure that the current bag does not become completely empty ideally you should replace it when there's about 25 MLS of fluid left this process should be performed with sterile technique to maintain infection control Begin by stopping the flow of fluid from the depleted bag by closing the roller clamp next prepare the new IV bag by removing the pigtail from the piercing Spike port and inspect the new bag for clarity discoloration and an expiration date remove the piercing Spike from the depleted bag and insert it into the port of the new bag taking care not to touch the spike itself to maintain sterility finally ensure the drip container is filled properly then open the roller clamp and adjust the flow rate to the prescribed level to discontinue an IV line first close the flow of fluid by shutting off the roller clamp then carefully peel back the tape securing the C catheter working toward the IV site stabilize the catheter as you loosen any remaining tape but do not remove the IV tubing from the catheter Hub fold a 4 in by 4in piece of gauze and place it over the insertion site hold the gauze in place while you gently pull back on the Hub of the catheter as you remove the catheter and IV lime from the patient's vein apply pressure to the site with gauze to control any bleeding", + "Saline Locks and External Jugular IV Lines": "saling locks also known as intermittent sites or ints are used to maintain an active IV site without continuous fluid infusion they're primarily used for patients who do not require ongoing fluids but might need quick access for medication delivery this method is particularly useful for patients with conditions such as heart failure or pulmonary edema a saline lock is attached to the end of an IV catheter and is filled with approximately 2 MLS of normal saline the saline remains in the port which prevents clotting and keeps the access site sealed without the fluid entering the vein this setup eliminates the need to reestablish an IV line each time medication or fluids are required external jugular IV lines provide an alternative Venus access through the external jugular veins of the neck to facilitate catheter insertion apply GLE pressure by placing a finger or the edge of a tongue depressor on the vein just above the clavicle this will help fill the vein if located the vein proves challenging positioning the patient sepine can assist in enhancing Venus return the catheter is inserted midway between the angle of the jaw and the midclavicular line using a technique similar to that of a standard IV line", + "Troubleshooting IV Therapy": "when troubleshooting IV Therapy Begin by checking the IV fluid to ensure it is not expired is properly connected and is Flowing correctly without contamination inspect the administration set for any kinks clogs or leaks and confirm that is correctly assembled and connected to both the IV bag and the catheter verify that the IV bag is at the appropriate height to ensure proper fluid flow if it is too low the fluid delivery may be inadequate assess the type of catheter used to make sure it's suitable for the patient's condition and the duration of therapy and ensure it's correctly placed and not dislodged lastly confirm that the constricting band was removed before starting the infusion and that it was not left on for too long as this could impact blood flow and vein integrity local IV site reactions can occur and typically require immediate action to address in the event of a local reaction the administration should be discontinued and a new IV line should be established in the opposite extremity providers should document the event as this is essential for accurate medical records and follow-up care one common local reaction is infiltration where fluid escapes from the vein into the surrounding tissue this results in localized swelling and discomfort infiltration may occur if the IV line has passed completely through the vein and out the other side this could also happen if there is an excessive patient movement if the securing tape has become loose or dislodged or if the catheter was inserted at too shallow of an angle and has only entered the fascia surrounding the vein infiltration can present with several signs and symptoms including swelling at the catheter site continued IV flow even after uding the vein above the insertion point and patient complaints of tightness and pain around the sight to correct infiltration the administration should be discontinued immediately and the IV line should be reestablished in the opposite extremity or at a more proximal location on the same extremity apply direct pressure to the swollen area to minimize further swelling or bleeding into the tissue it's also important to avoid wrapping tape around the extremity for direct pressure as this can actually exacerbate the problem thrombo fitis is characterized by the inflammation of the vein and is not commonly encountered with emergency prehospital patients it can present with symptoms such as fever tenderness and red shaking along the affected vein hardening of the vein may occur if it has been repeatedly punctured common causes of thrombo fitis include localized irritation and infection from nonsterile equipment prolonged IV Therapy irritating IV Solutions and two rapid infusion rates if redness and symptoms of thrombophob bitis develop at the IV site it's essential to discontinue the infusion and save the equipment for later analysis the IV line should be reestablished in the opposite extremity using new equipment to prevent any potential contamination from the previous setup occlusion refers to a physical blockage of a vein or catheter that can impede the flow of IV fluids this issue may arise if the flow rate is insufficient to keep the fluid moving out of the catheter tip leading to the the formation of a clot if blood enters the catheter early signs of occlusion include a decreased strip rate or the presence of blood in the IV tubing common causes of occlusion include a positional IV site proximity to a valve patient movement or the IV bag nearing empty which can cause the blood pressure to overcome the flow and back up into the line to address occlusion it's important to assess the IV site reposition the catheter if necessary and ensure the IV bag is properly filled if you encounter blood in the line do not under any circumstances flush the blood back into the vein you should discontinue the line clear it out and reconnect to determine whether an IV line should be reestablished due to occlusion use a syringe filled with saline to apply pressure to the line gently press the plunger to attempt to disrupt the occlusion and restore flow if flow is successfully reestablished confirm that the line is clear and that the flow rate is adequate if the occlusion cannot be resolved discontinue the current IV Administration and establish a new IV line in the opposite extremity or at a more proximal location on the same extremity a hematoma is an accumulation of blood in the tissues surrounding an IV site typically resulting from vein perforation or improper catheter removal this condition can cause visible pooling of blood around the IV site accompanied by tenderness and pain if a hematoma develops during catheter insertion stop the procedure and apply direct pressure to minimize bleeding if this occurs after a successful catheter insertion assess both the IV flow and the hematoma if the hematoma appears controlled and does not affect the IV flow monitor the site and leave it in place if a hematoma forms upon removal of the IV line apply direct pressure to control the bleeding nerve tendon or ligament damage can occur if anatomic structures around the IV site are not properly identified this risk is higher when choosing an IV site near joints symptoms of such damage include sudden severe shooting pain and numbness in the extremity if nerve tendon or ligament damage is suspected immediately remove the catheter and choose another site arterial puncture is indicated by bright red blood either spurting from the catheter after the needle is removed or backing up into the IV tubing in bag in the event of an arterial puncture stop Administration immediately and apply direct pressure to the site with Galls for at least 15 minutes systemic complications can arise from reactions or issues related to IV insertion and may pose significant risks including life-threatening conditions if the IV line is established and patent it should generally remain in place allergic reactions while often minor can escalate to sever your anaphylaxis and must be addressed with urgency these reactions might be linked to an individual's unexpected sensitivity to medications that were administered through the IV site systemic complications from IV Therapy can be severe and require prompt action common signs and symptoms of an allergic reaction include twitching shortness of breath edema of the face and hands ticaria bronchospasm wheezing and potentially an aaxis if such a reaction occurs discontinu Administration immediately and remove the solution keep the catheter in place for emergency medication access notify medical control promptly and ensure the patient's Airway is open air embolis is a serious systemic complication in which an air bubble obstructs blood flow to prevent this ensure the IV line is properly flushed and replace empty IV bags with full ones to avoid air introduction signs of an air embolis may include cyanosis symptoms of shock loss of consciousness and respiratory arrest if a patient shows signs of respiratory distress or unequal breath sounds consider an air embolis in such cases position the patient on their left side with their head down and transport them rapidly to the nearest appropriate facility it's also not a bad idea to be prepared to assist with ventilation if the patient's breathing becomes compromised catheter Shear occurs when a part of the catheter is pinched against the needle causing the needle to slice through the catheter and create a free floating segment this segment can travel through the circulatory system potentially blocking other vessels and leading to Serious conditions such as Mi stroke or pulmonary embolis treatment typically involves the surgical removal of the sheared tip catheter hubs are ready opaque to assist in diagnosing this issue it's important to never rethread a catheter if a patient exhibits symptoms such as sudden dnia or shortness of breath particularly if they have a pulmonary artery occlusion treat them the same as an air embolis Circ overload occurs when patients with cardiac pulmonary or renal dysfunction are unable to handle the increased volume of fluids in trauma patients excessive fluid resuscitation can disrupt clot formation and exacerbate bleeding one common cause is failing to adjust the drip rate after flushing the IV line always monitor IV bags to maintain the current drip rate symptoms of circulatory overload include trouble breathing jugular vein distension increased blood pressure and crackles heard on oscilation acute peripheral edema may also indicate overload to manage the situation slow the IV rate raise the patient's head to alleviate trouble breathing administer high flow oxygen and monitor Vital Signs and breathing phaso vagal reactions can occur in patients who experience anxiety related to needles or the sight of blood this reaction leads to vasod dilation which results in decreased blood pressure and possible patient collapse symptoms include anxiety diaphoresis nausea and snle episodes to manage a patient experiencing a Vaso vagal reaction position them according to shock management protocols apply high flow oxygen monitor Vital Signs and establish an IV for potential fluid resuscitation", + "Pediatric and Geriatric IV Therapy": "when performing IV therapy on pediatric patients catheter selection and insertion techniques require special considerations pediatric catheter come in various sizes with 20 22 24 or even 26 over the needle catheters being preferred based on the patient size and the available veins butterfly catheters are often ideal due to their precision and ease of use in young infants scalp veins are commonly utilized for IV access due to their accessibility and si in pediatric IV Therapy the choice of IV locations varies with the age and size of the patient for younger children there are fewer suitable IV sites hand veins though painful and challenging to manage are often the preferred site for peripheral IV lines due to their accessibility proper protection of the IV site is essential once it's established in order to prevent complications utilizing a pin light can Aid in visualizing veins on the back of the hand scalp vein canulation while sometimes necessary can be very distressing for both the child and their parents to secure a scalp vein it is helpful to tape a paper cup over the site which prevents direct pressure on the butterfly catheter and helps keep the site protected in geriatric IV Therapy it's often preferable to use smaller catheters unless rapid fluid replacement is required older adults may have fragile skin and veins due to medications making them more susceptible to complications such as hematomas from even minor punctures Additionally the the use of tape can exacerbate skin damage for greater comfort and to minimize the risk of extra vation smaller catheters such as 20 22 or 24 gauge are recommended When selecting these IV sets caution is advised with macro drips as they can cause edema if not monitored carefully additionally fluid overloading can be particularly serious for both geriatric and pediatric patients so it's crucial to monitor fluid administration closely When selecting an IV site for geriatric patients consider the potential for reduced vein elasticity due to aging as tissues lose elasticity over time veins can become less resilient avoid using small spidery veins that that are difficult to navigate and may weave unpredictably steer clear of varicose veins as they often have impaired circulation and therefore are not suitable for IV access", + "Intraosseous Infusion": "intra OAS infusion is a medical procedure used to deliver fluids blood blood products and medications directly into the intra space which is the cavity within the bone marrow this technique is typically employed in emergency situations when intravenous access is challenging or simply impossible common sites for Io infusion include the proxi tibia the humoral head or the sternum this procedure provides an effective alternative route for fluid and medication administration especially in critically ill or traumatic injury patients IO infusion involves administering fluids blood and medications inside the in oous space of long bones the structure of long bones includes a central Shaft or the diaphysis the ends epiphysis and a growth plate the Epic cial plate the Inner oia Space encompasses the spongy cancellus bone within the epiphysis and the medullary cavity of the diaphysis the space is often referred to as a non-collapsible vein due to its reliability in emergencies keep in mind that any substance you can administer IV can also be given via the io route that's why IO infusion is particularly useful when IV access is difficult or impossible the common IO infusion sites include the sternum proximal humoris proximal tibia and the distal tibia for accessing the humoral IO site it is necessary to manipulate the patient's arm and palpate the humal head each site provides a reliable access point for fluid and medication administration to identify the sternal iOS site palpate the sternal notch and use the adhesive Target provided by the io device for accurate placement the sternal iio side is known for its extremely rapid flow rate making it a valuable option in urgent situations to locate the proximal tibia iio site palpate the tibial tuberosity and then move 2 cm medially for the distal tibia iio site identify the medial malis and palpate 2 to three CM above it these sites are used for Access mainly during car CC arrest as it allows the compressor and the ventilator to do their job without interference from the provider pushing medications several options are available for Io infusion including manually inserted IO needles the fast one easy IO the bone injection gun and the new inner ocus nio device the use of these devices requires specialized training and a thorough understanding of their features functionality and clinical application manually inserted devices were the original devices used primarily for establishing access in children and continue to be widely used in the prehospital setting these needles consist of a solid boring needle known as a trocar inserted through a sharpened Hollow needle the io needle is Advanced into the bone with a screwing or twisting motion once the needle penetrates the bone the solid needle is removed and IV tubing is attached to the catheter fast devices the first intra oous devices that were approved for use in patients 12 years and older feature several design elements that facilitate IO placement in the sternum these elements include an infusion tube and subcutaneous portal an introducer a Target or strain relief patch and a protective Dome the fast devices are versatile and can be used during Cardiac Arrest situations providing rapid access to the vascular system and critical conditions here we have the original external IO device known as the fast one it features a 14 gauge infusion tube and 10 stabilization needles there is an updated version known as the fast responder and it offers an improved design and functionality to remove either one of these devices you you grab the insertion tube firmly and pull steadily in one continuous motion until the device becomes dislodged the EAS iio is a handheld battery powered driver designed for inserting IO needles into the proximal or distal tibia and the humal head it's equipped with a universal battery powered driver that accommodates various sizes of needles based on the patient's needs when inserting the needle ensure that at least one of the hash mark is visible after insertion to remove it attach a 10 mL syringe to The io's Lure lock twist the syringe clockwise and pull the device out in one swift motion the bone injection gun or big is a spring-loaded device designed for inserting IO needles into the proximal tibia of both adult and pediatric patients it features different depth settings for adult and Peds after insertion the big uses a safety lock as a stabilization device the new intra Aus device or nio is used primarily in the proximal tibia of adult patients though the humoral head is also an option the spring-loaded device does not require a drill or battery for insertion to use it unlock the safety cap apply downward pressure with the dominant hand and use the other hand to pull up the trigger Wings deploying the device the nio device is then pulled up in a rotating motion while holding the needle stabilizer against the skin after removing the introducing tro car lure lock tubing can be attached to perform an IO infusion with a fast one device start by aligning the adhesive Target on the patient and preparing to insert the device into the manubrium next prepare the the insertion site on the patient's manubrium to attach a fast one device position yourself behind the patient's head and place both hands on the device align the stabilization needles with the adhesive Target on the manubrium apply pressure until you feel the infusion tube separate from The Fast One introducer to complete the fast one device attachment discard the stabilization needle in a Sharps container and attach the IV tubing to the insertion tube's lure lock aspirate blood and bone marrow particles to confirm proper placement then slowly inject the IV solution to ensure correct placement adjusting the flow rate as needed lastly place the protective Dome and begin using the device potential complications of IO infusion are relatively low when the technique is used correctly however there are issues that can arise extra vation occurs when the io needle fails to properly reside in the io space causing fluid to accumulate in the surrounding soft tissues this R can be minimized by using proper insertion techniques signs include difficulty in free fluid flow and Rapid sight edema if undetected it can actually lead to compartment syndrome osteomyelitis which is inflammation of the bone and surrounding muscle due to infection is another potential complication failure to accurately identify anatomical landmarks during IO insertion can lead to long-term bone growth abnormalities in children fractures may occur if the insertion technique is overly forceful or if an IO needle is too large for the patient's age or size as used through and through insertion happens when the io needle punctures both sides of the bone if a patient show signs of acute shortness of breath pic chest pain and cyanosis you should suspect a pulmonary embolism IO infusion is contraindicated under several conditions if a functional IV site is already available IO canulation is not indicated additionally IO infusion should not be performed if the bone intended for canulation is fractured or if the patient has osteoporosis or osteogenesis imp perfecta both of which will compromise bone Integrity bilateral knee Replacements or the presence of a prosthetic limb at the intended IO site also contraindicate the use of an IO infusion", + "Mathematical Principles for Medication Dosage": "mathematical IAL principles are essential for calculating accurate medication dosages fractions are expressed as a numerator the portion available over a denominator the total quantity decimals on the other hand distinguish between numbers greater than zero and those smaller than zero with whole numbers appearing to the left of the decimal point and fractional parts to the right fractions can be converted to decimals by dividing the numerator by the denominator when dealing with multiplication or division by 10 remember that dividing a number by 10 requires moving the decimal point one place to the left while multiplying by 10 involves moving it one place to the right for instance multiplying 20 by 10 involves placing the decimal point in a 20.2 and moving it one space to the right to get 2.0 percentages represent a part of 100 and are denoted by the percent symbol they can be expressed as fractions with a denominator of 100 and be converted from decibels by moving the decimal point two places to the right the metric system is a decimal base system used for measuring length volume and weight it operates on multiples of 10 making conversions straightforward the basic units are the meter for length the liter for volume and the gram for weight prefixes in the metric system indicate the fraction of the base unit being used allowing for easy scaling and conversion between units commonly used prefixes in the metric system from smallest to largest include micro which represents 0.000000001 or 1 millionth Millie representing 0.001 or 1,000th CTI which stands for 0.01 for 100th and kilo denoting a th000 or 1,000 the volume and weight of the medication to be administered are typically only fractions of the total amount for volume conversion 1 lit equals 1,000 milliters so to convert milliliters to liters divide the volume by a th000 or move the decimal point three places to the left for example 100 ml divided 1,000 equals 0.1 L conversely to convert liters to milliliters multiply the liters by a th000 or move the decimal point three places to the right for instance 1.5 L multiplied by 1,000 equals 1,500 milliliters for weight conversion to convert grams to milligrams multiply The Weight by a th000 or move the decimal point three places to the right so for 2 G multiply that by 1,000 to get 2,000 migs to convert milligrams to gr divide by a th000 or simply move the decimal point through places to the left for instance 500 mg / 1,000 equals 0.5 G to convert pounds to kilog you can use either of the following methods first divide the weight in pounds by 2.2 since 1 kilogram equals 2.2 lb for instance a weight of 154 lb would convert to approximately 70 kg alternatively divide the weight by two and then subtract 10% of that value so with our same problem of 154 PBS if you were to divide it you would get 77 10% of 77 is 7.7 which would give you 69.3 kg to calculate the drip rate for IV fluids use dimensional analysis if you need to give 250 MLS of normal saline over 90 minutes using a macro drip at 10 drops per ML and you can find the rate like this set up the calculation by multiplying the drip factor or 10 drops per ml by the total volume of 250 MLS and then divide by the infusion time is 90 minutes this will give you 10 drops over 1 ml time 250 MLS over 90 minutes then we simplify cancel out the units and calculate this leaves you with 2500 over 90 which gives you approximately 27.78 drops per minute from there simply round the result to the nearest whole number of approximately 28 drops per minute to calculate medication doses you need to consider three main factors first determine the desired dose which is the amount of medication ordered by The Physician expressed as a specific number of grams or milligrams per kilogram of body weight second understand the medication concentration which indicates how much medication is contained in a specific volume of solution this is calculated by dividing the total weight of the medication by the volume of the solution for instance if the order is for dextrose at 25 G per 50 millit the concentration would be 0.5 G G per milliliter lastly identify the volume to be administered which is the amount of solution needed to deliver the desired dose to the patient to calculate the volume to be administered use the formula volume to be administered equals desired dose in milligrams divided by the concentration on hand or milligrams divided by milliliters ensure that the units of the desired dose match the units in the concentration on hand fraction if you need to administer 12.5 gam of dextrose and you have a pre-filled syringe of 25 gram of dextrose in 50 milliliters follow these steps first calculate the concentration on hand so 25 G / 50 millit equal 0.5 G per Miller then determine the volume to administer 12 point G is the desired dose divided by 0.5 G per milliliter or your concentration which equals 25 mlit thus you'd administer 25 mlit which is essentially half of the 50ml syringe for weight-based medication dosages the calculation depends on the patient's weight in kilograms since 1 kilogram equals 2.2 PBS adjust the dose according to the patient's weight this method is commonly used for Pediatric dosages of medications such as dextrose epinephrine or noox when administering pediatric doses utilize length-based resuscitation tapes and refer to field guides with tables or charts for accurate dosing although the principles of calculating drug dosages and medication infusions are the same for children as they are in adults pediatric Doses and volumes are typically smaller" + }, + { + "Introduction to Pharmacology": "chapter 12 principles of pharmacology aemts are responsible for administering specific medications to patients and assisting them in self administering other drugs understanding the drug profile which encompasses all pertinent details about a medication is essential this information is typically found on the package insert and is also detailed in various pharmaceutical Publications while it's important to read on medications that you may be administering aemts must have a general knowledge and a good understanding of the pharmacodynamics of the medications that they're administering pharmacology is the study of the properties and effects of drugs and medications on the body drugs are chemical agents that are utilized in the diagnosis treatment and prevention of disease diseases medications are specific chemical substances that are employed to treat or prevent diseases or leviate pain the dose refers to the amount of medication that is administered the action describes the therapeutic or the intended effect that the medication is expected to have on the body for instance when we administer 400 mg of ibuprofen po the intended therapeutic effect is that it will inhibit swelling and help control pain unintended effects are undesirable outcomes of medication that generally pose minimal risk to the patient UNT effects are adverse outcomes that can be harmful while toxicity refers to the potential of a substance to cause health hazards to an individual or organism an unintended effect would be patients experiencing an allergic reaction to aspirin an unor effect would be a patient taking ibuprofen and going into anaphylactic shock and toxicity would refer to a patient overdosing on Tylenol and ending up on dialysis.", + "Indications and Contraindications": "indications are the therapeutic uses for a particular medication for example nitroglycerin is indicated for the treatment of angina pectoris contraindications are situations where a medication should not be administered because it may harm the patient or have no beneficial effect a good example of this is that aspirin is contraindicated in patients with active GI bleeding as it may exacerbate their condition.", + "Sources of Medications": "medications are derived from four primary sources animal Origins plant sources minerals and synthetic compounds drugs obtained from animals could include various biologics and hormone preparations plant sources are numerous and include those extract Ed from herbs and other Botanical substances mineral-based drugs are derived from inorganic elements while synthetic compounds are chemically manufactured to produce specific therapeutic effects.", + "Drug Naming Conventions": "the trade name also known as the brand name is assigned to a medication by its manufacturer and is written with an initial capital letter a medication may have multiple trade names depending on how many companies produce it the generic name is typically the original chemical name of the medication proposed by the first manufacturer and approved by the FDA in the United States pharmacopia or USP all medications authorized for use are listed under their generic names the chemical name provides a precise description of the medication's chemical composition and molecular structure the official name is a designation given to a medication by the USP generally consisting of the generic name followed by USP for the medication beome methanone di appropriate various names would include the chemical name 9 chloro 11 beta 1721 trihydroxy 16 beta methyl pregna 14 dine 320 Don 1721 di appropriate the generic name becko methone di appropriate the trade name vanceril and the official name beckam methasone di appropriate USP for those who are wondering this is a corticosteroid drug with anti-inflammatory and vasoconstrictive effects it's used to treat chronic inflammatory processes such as asthma allergic rinitis and corticosteroid responsive dermatosis.", + "Prescription and OTC Medications": "prescription medications are dispensed by pharmacists based on a physician's order overthe counter medications or OTC meds can actually be purchased directly without a prescription of course just because a medication is available OTC doesn't mean that it can't be dangerous especially if taken incorrectly or at high doses.", + "Sources of Drug Information": "sources of drug information include the US FDA Center for drug evaluation and research The physicians's Desk Reference and hospital formularies all of which specify the drugs used in a particular facility additionally drug inserts and various online resources provide detailed information providers should be knowledgeable about these references and field resources especially cons concerning medications encountered in prehospital care.", + "Regulations and Laws in Pharmacology": "the manufacturer of pharmaceuticals in the United States as well as in many other countries is governed by a range of laws and regulations that are designed to protect consumers these regulations prevent manufacturers from making false claims about the benefits of drugs and prohibit companies from providing advice on Drug Administration directly to patients these regulations also mandate the disclosure of information regarding side effects and potential harmful effects additionally they set standards to ensure that drugs are produced by different manufacturers are consistent in strength and Purity these standards are detailed in the USP and the national for formulary several federal laws have been enacted to safeguard patients from unsafe substances and unethical practices by manufacturers and Distributors the Pure Food and Drug Act of 1906 was the first federal drug related legislation in the United States it was designed to protect the public from Foods medication and alcoholic beverages that could be mislabeled poisonous or otherwise harmful the food drug and cosmetic Act of 1938 amended in 52 and 62 introduced several key regulations it required drug manufacturers to label their products to indicate whether they contained potentially bad habit forming substances and to incl include warnings about possible side effects this act also established that FDA the Food and Drug Administration as well as mandating that dangerous drugs could only be dispensed with the prescription the Harrison narcotic Act of 1914 regulated the import manufacture prescription and sale of several non-narcotic drugs as well as cocaine opium and their derivatives it required meticulous recordkeeping for the dispensing of controlled substances and mandated the registration of Distributors such as pharmacists violations including illegal possession or distribution of controlled drugs could lead to fines and imprisonment the narcotic Control Act of 1956 increased penalties for violations of the Harrison narcotic Act made the possession of heroin illegal and prohibited the acquisition and transportation of marijuana the Controlled Substances Act of 1970 provides comprehensive legislation addressing both narcotic and non-narcotic drugs with potential for abuse it outlines requirements for registration procurement storage distribution and recordkeeping of these substances and establishes penalties for non-compliance drugs are classified into five schedules based on their potential for abuse schedule one includes substances with the highest abuse potential and severe dependency risk while schedule five contains drugs with the lowest abuse potential.", + "Drug Standardization and Approval": "Federal legislation also addresses the standardization of doses to ensure consistency in medication standardization guarantees that when patients take a medication with a specified amount of the active ingredient They will receive the exact amount for a drug to Bear a USP label the amount of active ingredients Must Fall within 95 to 105% of the quantity stated on the label the FDA enforces the food drug and cosmetic act and is responsible for determining the safety and efficacy of drugs before they are permitted on the US market it also oversees the safety and effectiveness of vaccines used in the United States the DEA implements the Controlled Substances Act which includes registering Physicians that are authorized to dispose of Controlled Substances the FTC monitors drug advertising to ensure it is not misleading or inappropriate and provides recommendations to the FDA concerning direct to Consumer advertisements the drug approval process is extensive and can span several years on average it takes about 9 years for a drug to be developed tested and approved during this period manufacturers may discover that the drug does not perform as intended or is too hazardous for human use before a drug can be approved for distribution it must undergo animal studies and clinical trials in humans animal studies are conducted to understand the Drug's properties and and to identify which tissues and organs may be affected by the drug the law requires testing in at least two animal species following the successful completion of animal studies an investigational new drug can proceed to clinical trials involving human subjects clinical trials are conducted in multiple phases to ensure the safety and eff efficacy of a new drug phase one involves testing the new drug in healthy volunteers to compare human data with animal data determine safe dosages and assess the overall safety phase two is performed with a specific patient population typically consisting of 50 to 300 patients in these studies one group receives the drug while another receives a placebo in double blind trials this phase evaluates the Drug's efficacy and safety as well as helps identify the most effective formulation phase three expands the study to a larger Patient Group often several thousand individuals and usually lasts several years it assesses the drugs efficacy and monitors the nature and frequency of side effects stage four involves applying to the FDA for approval to market the drug this phase compares the new drug with existing treatments and examines long-term efficacy and cost Effectiveness.", + "Drug Storage and Security": "drug storage and security for Controlled Substances require careful measures to prevent theft and ensure proper management drug container ERS or boxes should be locked and secured within the ambulances policies should dictate how drugs are secured stored distributed and accounted for for Controlled Substances such as narcotics records must be kept separate from other documentation due to strict DEA regulations in the event of loss or theft of these drugs immediate notification to the supervisor and law enforcement is required all medications should be stored in a temperature controlled environment to maintain their potency factors such as temperature light moisture shelf life and exposure to air can affect the efficacy of medications expired controlled medications must be destroyed with the destruction witnessed by two employees and documented on appropriate forms.", + "Considerations for Special Populations": "when administering medications to a female of childbearing age it is important to first determine if she might be pregnant the expected benefits of the medication should be weighed against potential risks to the fetus as both prescription and OTC drugs can pose risks for The Unborn or newborn the teratogenic drug is one that poses a risk to the normal development or health of the fetus pregnancy induces physiological changes that affect drug processing potentially increasing the risk of harm drug metabolism in the liver May decrease while the rate of drug excretion may increase the FDA has replaced the previous category system the a b c d and x with a more detailed narrative summary system that provides information on prescribing during pregnancy lactation and reproductive risks medications approved after June 2015 are listed with this updated narrative summary many drugs with unknown effects during pregnancy are still used one example is epinephrine while it is known to be essential in emergency situations such as in the treatment of anaphylaxis or severe asthma exacerbations it effects on pregnancy are not fully established despite the unknown risks epinephrine may be used in life-threatening emergencies during pregnancy if it is deemed necessary for the patient's immediate health in non-life-threatening situations pharmacologic treatments for pregnant patients should be generally delayed until they reach the hospital in cases of uncertainty it's advisable to consult medical control for guidance medications can have varying effects on pediatric patients while infants exhibit reduced metabolic capacity with an incomplete GI tract that can slow the absorption and delay of elimination of oral medications as a result the same medications might be more potent in infants compared to adults conversely older children may metabolize some medications more quickly than adults potentially requiring higher doses or more frequent Administration to achieve the desired therapeutic effect an example of a medication that has different effects in pediatric patients is acetaminophen in young infants the reduced metabolic capacity and incomplete development of the GI tract can slow the absorption of oral medications and delay their elimination making the drug potentially more potent in contrast older children can metabolize acetam minin more rapidly often necessitating relatively higher doses or more frequent Administration compared to adults in order to achieve the desired effect in geriatric patients changes in pharmacokinetics can resemble those observed in young children hepatic functions and GI activity may slow affecting the absorption and elimination of medications additionally older adults often take multiple medications which can interact with each other and alter their effects this can lead to unintentional overdoses or MISD dooses due to complex medication regimens.", + "Legal and Ethical Responsibilities": "you are legally morally and ethically responsible for every drug you administer ensuring that Drug Administration is both safe and therapeutically effective is essential always keep a field guide or other reference readily available and adhere to the standardized National guidelines when administering drug therapy an example is administering the lockone in an emergency situation for an opioid overdose you are responsible for ensuring that Naran is administered correctly according to established guidelines which includes verifying the dosage the route of administration and monitoring the effect for efficacy and adverse effects keeping a field guide handy helps in confirming the appropriate dosage and procedure while adhering to standardized guidelines ensures that the administration is both safe and effective.", + "Drug Classification Methods": "drugs can be classified based on their effects on specific body parts or conditions with many drugs fitting into more than one category they are primarily classified into three methods by body system class of agent and mechanism of action the body system classification groups drugs according to the body system they affect such as the cardiovascular or respiratory systems the class of agent categorizes drugs based on their chemical properties or therapeutic use such as antibiotics or anti-hypertensives the mechanism of action classification organizes drugs according to how they produce their effects such as by blocking receptors or inhibiting enzyme activity.", + "Nervous System and Drug Effects": "the nervous system is the body's principal control system and is composed of the central nervous system and the peripheral nervous system the CNS includes the brain and spinal cord while the pns s encompasses all nervous tissues outside of the CNS the pns contains the autonomic nervous system which manages all automatic or involuntary functions the ANS is further divided into the sympathetic and parasympathetic nervous systems the sympathetic nervous system is responsible for the body's response to shock or stress and we often refer to it as the fight ORF flight response this system triggers an adrenic response leading to the release of hormones such as epinephrine and norepinephrine it results in physiological changes such as an increased heart rate elevated blood pressure dilation of pupils and reduced digestive activity with blood shunted from the extremities to vital core organs in contrast the parasympathetic nervous system promotes relaxation and controls autonomic functions during non-stressful times often referred to as the rest and digest state it counteracts the sympathetic nervous system facilitating a state of calm and restoring normal bodily functions after stress hormon released during sympathetic nervous system stimulation produce their Effects by binding to adrenic receptors which are specialized proteins located on the surface of target cells these receptors are divided into four main types Each of which are associated with different physiological responses alpha 1 receptors are primarily found in smooth muscle cells such as those in the blood vessels when activated alpha 1 receptors cause Vaso constriction which increases blood pressure by narrowing the blood vessels they also contribute to the contraction of other smooth muscles such as those in the bladder and the eye leading to effects such as pupil dilation and increased bladder tone Alpha 2 receptors are located both pre synaptically and post synaptically pre synaptic Alpha 2 receptors inhibit the release of norepinephrine and other neurotransmitters which can lead to a reduction in sympathetic outflow and a decrease in blood pressure post synaptic Alpha 2 receptors on the other hand are involved in various functions including the inhibition of insulin release and mod ation of neurotransmitter release in the central nervous system beta 1 receptors are found mainly in the heart and play a critical role in increasing heart rate and the force of contraction activation of these receptors enhances cardiac output by increasing both the rate and strength of the heartbeats beta 1es are also present in the kidneys where they influence the release of renin a hormone that's involved in regulating blood pressure beta 2 receptors are primar located in the lungs smooth muscles and in the uterus activation of beta 2 leads to Bronco dilation which helps to open the Airways of the lungs making breathing easier in addition they facilitate vasod dilation and reduce uterine contractions which can be beneficial in managing Asthma as well as preventing premature labor each type of adrenic receptor contributes to the overall physiological response by mediating specific effects that help the body cope with stress or maintain homeostasis.", + "Sympathomimetics and Sympatholytics": "drugs that influence the sympathetic nervous system are classified into two main categories sympathomimetics and sympatholytics sympathomimetics mimic the effects of the sympathetic nervous system hormones such as epinephrine and norepinephrine by stimulating adrenic receptors this results in physiologic responses such as increased heart rate Vaso constriction and Bronco dilation these drugs are useful in conditions where enhancing the sympathetic response is beneficial such as in the treatment of asthma with beta 2 agonists in contrast sympatholytics also known as anti- adrer inhibit the sympathetic nervous system by blocking adrenic receptors this leads to reduced heart rate lower blood pressure and decreased anxiety sympatholytics are employed in managing conditions where reducing sympathetic activity is advantageous such as treating hypertension or certain arrhythmias antagonists are drugs that counteract the effects of other substances by binding to receptors and blocking their activation by preventing the action of agonists or indogen substances antagonists inhibit their physiological effects in contrast agonists bind to specific receptors and activate them leading to a response these drugs mimic the action of natural substances in the body enhancing or initiating physiological processes medications can vary in their effects depending on whether they stimulate multiple types of adrenic receptors or are selective for specific ones some drugs have the ability to activate both Alpha and beta receptors which can lead to a broad range of physiological responses for instance these medications may be used in situations where multiple systems need to be influenced simultaneously beta blockers are a specific class of drugs that block beta beta adrenic receptors they are commonly employed to manage conditions such as hypertension and certain types of arrhythmias by blocking beta 1 receptors in the heart beta blockers help reduce heart rate and blood pressure thereby aiding in the control of blood pressure and stabilization of heart rhythms in contrast drugs that antagonize beta 1 receptor are used in emergency situations like cardiac arrest and hypotension these medications stimulate beta 1 receptors in the heart increasing heart rate and force of contraction to improve cardiac output in blood pressure beta 2 selective drugs are designed to Target beta2 receptors predominantly found in the lungs these drugs are used primarily for their Bronco dilator effects which help open the Airways and ease breathing they are preferred in treating conditions like asthma because they have minimal effects on the heart compared to non-selective Beta agonists this selectivity reduces the risk of unwanted cardiovascular side effects while providing effective relief of respiratory symptoms.", + "Parasympathomimetics and Parasympatholytics": "drugs that affect the parasympathetic nervous system are known as parasympathomimetics or cenic medications these drugs enhance the effects of the parasympathetic nervous system by acting as agonists to coleric receptors they may work directly on these receptors or indirectly by increasing in acetycholine levels a neurotransmitter that facilitates parasympathetic signaling excessive col energic activity can lead to a set of symptoms referred to as sludge which includes salivation and sweating excessive lacrimation or tearing frequent urination defecation drooling diarrhea gastrointestinal upset cramps emesis and muscle twitching with meosis or pupil constriction these symptoms reflect an overreaction of the parasympathetic nervous system exposure to certain hazardous substances such as specific fertilizers insecticides and nerve agents like VX and sarin gas can induce SL sudum symptoms due to their effects on coleric receptor activity or their inhibition of acetylcholine estras which is the enzyme that's responsible for breaking down acetycholine parasympatholytics also known as anti-cholinergic medications function as antagonists to the parasympathetic nervous system by blocking the action of acetylcholine at colonic receptors these drugs interfere with the activation of muscarinic and nicotinic receptors which are key components of the parasympathetic signaling pathway atropine is one of the most well-known and frequently used parasympatholytics by binding to and inhibiting muscarinic receptors atropine prevents acetycholine from exerting ing its effects leading to several physiological responses these include a reduction in secretions from salivary gastric and sweat glands which can be beneficial in conditions where excessive secretions are a concern atropine also increases heart rate by blocking the vagal effects that normally slow down the heart making it useful in treating bra cardia additionally it relaxes smooth muscles including those in the GI tract and urinary tract which can help alleviate symptoms such as spasms and cramps parasympatholytics through their action in both muscarinic and nicotinic receptors play a critical role in various clinical situations as they can be used to manage conditions such as COPD by dilating Airways or to counteract the effects of excessive parasympathetic activity as seen in certain poisoning cases that being said due to their broad effects these medications can also lead to side effects such as dry mouth blurred vision constipation and urinary retention thus they should be used carefully to balance the therapeutic benefits with potential adverse effects.", + "Analgesics and Opioid Medications": "analgesics are medications that are designed to relieve pain and induce analgesia providing relief from discomfort among these opioid agonists represent the most common class of analgesics derived from or similar to compounds found in the Opium plant opioid agonists work by binding to opiate receptors in the CNS this binding action prevents neurons from transmitting pain signals thus alleviating pain as CNS depressants these medications can have sedative effects fentanyl is a notable example of a rapid acting highly potent opioid Agonist with a relatively short duration of action making it effective for quick pain relief but requiring careful dosing and monitoring due to its potency nonopioid analgesics which provide pain relief and often reduce fever work by modifying the production of prosta Landin and Cox enzymes both of which are involved in the inflammatory response and pain sensation this class of medications includes three primary forms cicat non-steroidal anti-inflammatory drugs and Par aminophenol derivatives cicat such as aspirin specifically Target Cox one enzymes reducing platelet aggregation and inflammation non-steroidal anti-inflammatory drugs such as ibuprofen are used to alleviate pain inflammation and fever through the inhibition of both Cox one and Cox 2 enzymes par aminophenol derivatives including aaminin provide analgesic and antipyretic effects but do lack significant anti-inflammatory properties and do not inhibit Cox enzymes to the same degree as ineds opioid antagonists are medications used to reverse the effects of opioid drugs particularly their depressant effects on the central nervous system an example of an opioid antagonist is nxone which can rapidly counteract the life-threatening effects of opioid overdose which include respiratory depression opioid Agonist antagonists on the other hand possess both antagonistic and agonistic properties these drugs are designed to alleviate pain while minimizing the risk of respiratory depression and dependence that is commonly associated with opioid agonists by activating certain opioid receptors to relieve pain and simultaneously blocking other receptors these drugs provide pain relief without the same potential for addiction or severe respiratory side effects nuban is a great example of one of these drugs.", + "Sedatives and Hypnotics": "anti-anxiety sedative and hypnotic drugs are used to help patients sleep through medical procedures by inducing sedation and hypnosis these medications are crucial for managing anxiety and ensuring patient Comfort during invasive procedures benzo diazines are among the most commonly used drugs for this purpose they are effective in preparing patients for procedures by providing sedation and reducing anxiety other cases of medications in this category include barbituates which are also used for Sedation but are less commonly used today due to their potential for dependence and overdosing opioid agonists can have sedative effects and are sometimes used in combination with other agents for their analgesic properties non-b barbituate hypnotics offer an alternative for inducing sleep with a lower risk of dependence compared to barbituates finally disassociative anesthetic agents can provide sedation and analgesia while inducing a state of disassociation which is useful in certain types of procedures.", + "Anti-Convulsants and Stimulants": "anti-convulsants are medications used to manage and prevent seizures they're thought to work primarily by inhibiting the influx of sodium ions into cells this action decreases the cell's ability to depolarize and propagate electrical signals which helps prevent the onset of seizures and reduces their frequency by stabilizing neuronal membranes and limiting excessive neuronal activity anti-convulsants effectively control various types of seizures and are a key component in epilepsy management stimulants exert their Effects by exciting the central nervous system they increase the levels of excitatory neurotransmitters while decreasing those of inhibitory neurotransmitters which leads to heightened weightfull include caffeine cocaine and both prescription and elicit amphetamines these substances work by increasing the release of dopamine and nor epinephrine which contribute to increased alertness and energy however stimulants can also raise heart rate and blood pressure leading to teac cardia and hypertension high doses of stimulants may actually cause adverse effects such as nervousness irritability Tremors and headaches additionally they can induce seizures and psychosis withdrawal from stimulants can lead to symptoms such as fatigue depression and Cravings making discontinuation challenging for some individuals.", + "Depressants and Psychotherapeutic Drugs": "depressants are a class of medications designed to slow brain activity offering therapeutic benefits for various conditions they are commonly prescribed to manage anxiety muscle tension pain insomnia stress panic attacks and seizures by reducing neural excitability and promoting relaxation additionally some depressants are used as anesthetics inducing and maintaining anesthesia during medical procedures by further suppressing Consciousness and reducing brain function common examples include aapam which is used for anxiety and as a pre-anesthetic valum which addresses anxiety muscle spasms and seizures Xanax which manages panic attacks and generalized anxiety disorder and ambient which is prescribed for short-term insomnia to promote sleep these medications work by enhancing the effect of neurotrans transmitters such as Gaba which inhibit brain activity despite their efficacy depressants must be used cautiously due to their potential for dependence tolerance and side effects especially with long-term use or in combination with other CNS active substances psychotherapeutic drugs primarily function by blocking dopamine receptors in the brain which help in treating mental health conditions such as schizophrenia and depression however their use can lead to several side effects extra predial symptoms are common including involuntary movements trimers rigidity muscle contractions restlessness and changes in breathing and heart rate other side effects may include or orthostatic hypotension sedation and sexual dysfunction depression is typically managed with Selective serotonin reuptake Inhibitors or ssris monoamine oxidase Inhibitors or maois or tricyclic antidepressants each of these medications Works through different mechanisms to alleviate symptoms of depression but all of them carry risks and side effects that must must be carefully monitored.", + "Cardiovascular Drugs": "drugs affecting the cardiovascular system are categorized based on their impact on Specialized cardiac cells these effects are classified into several categories chronotropic drugs that influence heart rate inotropic drugs that modify the force of cardiac contractions and dromotropic drugs that affect the velocity of of electrical conduction through the heart each of these effects can either be positive or negative depending on the specific drug and its application cardiac glycosides which are derived from Plants work by blocking certain ionic pumps in cellular membranes which indirectly raises intracellular calcium concentrations although effective for treating conditions like heart failure cardiac glyc Ides can cause numerous side effects necessitating careful monitoring during treatment anti-arrhythmic medications are essential for managing irregular heart rhythms and can affect cardiac tissue in various ways they are categorized based on their mechanisms of action sodium channel blockers for example work by slowing the conduction of electrical impulses through the heart which leads to a negative dromotropic effect this action helps stabilize abnormal heart rhythms by preventing rapid and irregular electrical signals from propagating beta blockers reduce the stimulation of beta adrenic receptors which are involved in the body's fight ORF flight response by blocking these receptors beta blockers decrease the influence of adrenaline and other stress hormones on the heart helping to control the heart rate and to reduce arrhythmias potassium channel blockers increase the heart's contractility which is known as a positive inotropic effect by affecting potassium channels these medications help in prolonging the refractory period of cardiac cells thus helping to maintain normal heart rhythm calcium channel blockers on the other hand decrease the force of cardiac contractions and reduce the heart's automaticity or the ability of the heart to generate electrical impulses on its own they also slow down the conduction velocity through the heart's electrical Pathways resulting in a negative dromotropic effect this combined action help helps manage arrhythmias by reducing the speed and strength of electrical conduction within the heart.", + "Anti-Hypertensive Medications": "anti-hypertensive medications Encompass several classes each targeting different mechanisms to lower blood pressure diuretics for instance promote the excretion of excess salt and water through the kidneys thereby reducing total fluid volume in the body this decrease in fluid volume lowers preload and stroke volume contributing to lower blood pressure vasodilators work by relaxing the smooth muscles of arterioles and veins which helps to widen blood vessels and to reduce blood pressure sympathetic blocking agents including beta blockers and adrenic Inhibitors reduce the effectss of beta adrenic stimulation by blocking these receptors these medications help to lower heart rate and blood pressure Angiotensin converting enzyme or ACE inhibitors Target the renin Angiotensin aldosterone system suppressing the conversion of angiotensin 1 into Angiotensin 2 this action results in Vaso dilation and reduce blood pressure additionally calcium channel blockers possess both anti-is rythmic and anti-hypertensive properties they work by inhibiting calcium influx into cardiac and smooth muscle cells which reduce heart rate myocardial contractility and blood pressure.", + "Blood Clotting and Thrombotic Management": "anti-coagulants fibr linic and blood components play crucial roles in managing blood clotting and Ving thrombotic events anti-platelet agents function by interfering with platelet aggregation which helps to prevent the collection of platelets and further buildup of these cells they do not dissolve existing platelet clumps but they do prevent new ones from forming anti-coagulant drugs on the otherand work by inhibiting the coagulation process to prevent the formation of thrombi these medications may be prescribed long term as a preventative measure against clot formation it's essential to be aware of anti-coagulant use especially in patients with traumatic injuries as these drugs can hinder necessary blood coagulation and complicate efforts to control bleeding fibr linic agents are used to dissolve existing thrombi which helps to prevent them from breaking off and traveling through the bloodstream these agents are critical for treating conditions such as acute myocardial infarction or stroke where rapid thrombus dissolution is necessary to restore normal blood flow and prevent further complications.", + "Respiratory System Drugs": "drugs affecting the respiratory system play a vital role in managing various respiratory conditions and emergencies oxygen is the most frequently used medication in the prehospital setting with both appropriate and inappropriate uses and potential side effects OTC decongestants are commonly utilized during cold and influenza Seasons to relieve nasal congestion during allergy season patients often take anti-histamines to alleviate symptoms however there have been instances of overdose involving decongestants such as pseudo aedin antitussives like dextrorphan and antihistamines such as Dien hydramine in many respiratory emergencies sympathomimetic medications are employed these drugs stimulate beta 2 receptors which are particularly beneficial for patients experiencing respiratory distress xanthines used as a second line treatment help relieve Airway constriction by relaxing smooth muscles of the bronchioles and increasing blood flow they also stimulate the central nervous system caffeine is a well-known example of a xanthane and a CNS stimulant additionally corticosteroids are used to suppress the inflammatory response in the Airways providing relief in conditions that are characterized by inflammation and swelling.", + "Pancreatic and Immunologic Drugs": "drugs affecting the pancreas are critical for managing blood glucose levels in individuals with diabetes a variety of hypoglycemic medications are available each with different mechanisms of action some of these drugs act directly on the pancreas While others modify how insulin is utilized ized in the body sualin nurius for example increase insulin secretion from the pancreatic beta cells helping to lower blood glucose levels in contrast other oral hypoglycemic agents such as thoomin diones and biguanides work by enhancing insulin sensitivity improving the body's response to insulin and aiding in better gluc glucose control drugs affecting the immunologic system play a role in managing conditions where the immune system is either overactive or misdirected immunosuppressant medications are commonly prescribed to patients undergoing an organ transplant or those with autoimmune diseases these medications are designed to inhibit the body's immune response in two key ways first by preventing the immune system from attacking a transplanted organ and second by reducing the immune systems attack on the body's own tissue in autoimmune conditions immunosuppressants work by targeting and inhibiting lymphocytes and te- cells which are crucial components of the immune system involved in these processes.", + "Vitamins, Minerals, and Fluids": "vitamins and minerals play Vital roles in maintaining Health by supporting normal metabolism growth development and cellular function these essential nutrients help the body function optimally and prevent deficiencies that can lead to various health problems supplements can be taken for two primary reasons to replace deficiencies and to serve as a preventative measure replacing the deficiencies is critical for individuals who may not obtain sufficient nutrients through diet alone such as those with specific medical conditions or dietary restrictions preventative supplementation helps maintain Optimal Health and may reduce the risk of developing certain conditions in the prehospital setting thamin is particularly significant as it is critical for carbohydrate metab abolism and helps convert carbs into energy this function is vital for patients with alcohol use disorders as chronic alcohol consumption can impair thyine absorption and utilization leading to deficiencies thamin deficiency can cause serious conditions such as wariki corov syndrome which presents with symptoms including confusion Axia and memory disturbances therefore administering thamin in emergency situations involving individuals with alcoholism or related conditions is essential to prevent or address these potentially severe complications fluids and electrolytes are essential for maintaining the body's balance and ensuring proper physiological function crystalloid Solutions are a primary type type of intravenous fluid used in Medical Treatments and are classified based on their tonicity isotonic Solutions which have a similar osmotic pressure to that of the body cells are used as stable mediums for medication administration and effective fluid and electrolyte replacement examples include normal saline and lactated ringers hypertonic Solutions with a lower osmotic pressure than body fluids are used to draw fluids from the intracellular space into the bloodstream providing nutritional support or managing severe fluid imbalances such as 3% saline hypotonic Solutions with a lower osmotic pressure than body fluids help replenish intracellular fluids and are beneficial in hydration situations but not for hypo of lmia an example is 0.45% saline additionally colloid Solutions may be administered containing larger molecules that remain in the vascular compartment to increase oncotic pressure thus helping maintain blood volume and pressure they are used for Rapid volume expansion in cases of severe blood blood loss or shock with examples including hydroxyethyl starch and dextran.", + "Drug Forms and Administration Routes": "Drug forms play a crucial role in determining how a medication is administered and how it will act within the body the form of medication often dictates its route of administration which is essential for achieving the desired therapeutic effects the choice of drug form ensures the proper route for the medication controls the timing of its release into the bloodstream and influences its effects on target organs or body systems for example oral tablets are designed for ingestion and absorption through the digestive tract while intravenous Solutions provide immediate entry into the bloodstream each drug is specifically designed to optimize the medication Effectiveness and safety according to its intended use solid drugs commonly used for oral Administration in adult patients come in several forms each with specific characteristics capsules are gelatin shells filled with either powdered or liquid medication which dissolve in the stomach to release tablets are SOL solid forms often containing additional materials mixed with the active ingredient and compressed under high pressure they may dissolve quickly with liquid be absorbed rapidly when taken sublingually or be ground into a powder to enhance absorption pills are solid medications shaped into balls or ovals intended for swallowing suppositories which are inserted into the rectum dissolve and absorb there but are not administered by aemts each drug form is tailored to optimize medication delivery and Effectiveness based on its intended use and the patient's needs liquid drugs come in several forms each tailored to specific therapeutic needs and routes of administration Solutions are homogeneous mixtures in which one or more substances are fully dissolved in a solvent these mixtures remain stable and uniform meaning they can't be separated by filtration or settling and they can be administered via various routes including oral intravenous and topical suspensions or formulations or fine particles of a medication are dispersed throughout a liquid these particles are not dissolved but suspended in the liquid medium requiring shaking or stirring before use to ensure even distribution a common example is activated charcoal which is used in poisoning cases to absorb toxins entur spirits and elixir are liquid medications that include alcohol in their preparation tenters are alcoholic extracts of plants or other substances Spirits are alcoholic Solutions with a high concentration of active ingredients and elixir are sweetened liquid preparations that contain alcohol these forms help dissolve and preserve certain drugs enhancing their stability and absorption syrups are aquous solutions with a higher sugar content used to mass the taste of medications and improve taste the sugar content also acts as a preservative extending the shelf life of the syrup and aiding in medication adherence emulsions are mixtures where two imis liquids such as oil and water are combined with the help of emulsifying agents this creates a staple product that allows for the administration of medications that would otherwise separate providing the means to deliver lipophilic or fat loving drugs in a liquid form emulsions are commonly used with both oral and intravenous drug formulations metered dose inhalers are compact spray canisters designed to deliver medications directly to the lungs via the mouth they are engineered to provide a consistent and precise dose of medication with each use ensuring that patients receive the intended amount of the drug to ensure proper delivery of the medication mdis must be shaken vigorously before use as the medication is often a suspension that needs to be evenly distributed within the canister this shaking helps mix the medication thoroughly and prevents the particles from settling mdis are commonly utilized by individuals with respiratory conditions such as asthma and empyema they are particularly effective for these patients as they deliver medication directly into the Airways providing quick relief from symptoms and helping to manage chronic respiratory issues topical medications are applied directly to the surface of the skin and affect only the area where they are applied these medications come in various forms each with different rates of absorption lotions for instance are the most rapidly absorbed topical medications they spread easily over large areas of skin and are exemplified by calamine lotion which is used to relieve itching and irritation creams are absorbed more slowly than lotions but faster than ointments they have a medium consistency allowing for relatively quick absorption an example is hydrocortisone cream known for its anti-inflammatory properties ointments have the slowest absorption rate among topical medications They are thicker and more imalent creating a barrier that retains moisture and allows for a gradual release of the medication Neosporin first aid ointment is a common example used to prevent infection in minor cuts and abrasions transcutaneous medications which are also known as transdermal medications are designed to be absorbed through the skin and can affect other areas of the body beyond the state of application these medications are typically intended for systemic effects meaning they influence the entire body rather than just the local area where they are applied examples include nitroglycerin which is used for managing angina and heart conditions as well as fentanyl a potent opioid used for pain management transdermal systems offer a controlled and steady release of medication over time making them a convenient option for continuous therapeutic effects gels are semi-liquid substances that can be administered orally through capsules or plastic tubes they have a consistency similar to pastes or creams but are typically transparent an example of a gel used in medical settings is oral glucose which provides a rapid source of glucose to raise blood sugar levels in patients experiencing hypo glycemia gases are most often delivered in an operating room setting with oxygen being the most commonly used gas nitrous oxide another example serves as an analgesic and is administered via inhalation through a mask it is known for its euphoric effects providing pain relief and a sense of well-being during procedures the route of administration significantly influences the onset of action and the therapeutic response of a drug interal drugs which are administered along any part of the GI track include oral and rectal routes oral medications can take up an hour to be absorbed depending on various factors rectal Administration is not to Ty Ally used by aemts with the possible exception of D50 if permitted by local protocols parenteral drugs are administered through any other route than the GI tra providing various options for medication delivery based on urgency and patient condition intravenous or IV injections are the fastest method delivering medications Direct into the bloodstream for immediate effect but this is not suitable for all drugs intra OAS or IO injections are used to access the bloodstream through the bone marrow particularly in patients who are unresponsive due to Cardiac Arrest or severe shock and are frequently utilized in children with difficult IV access subcutaneous injections are absorbed more slowly and offer longer lasting effects but may be less effective in patients with poor peripheral profusion intramuscular or IM injections are absorbed quickly due to the vascular nature of muscle tissue though they can pose risks such as muscle damage and inconsistent absorption sublingual or SL Administration involves placing medication under the tongue where it rapidly enters the bloodstream through the oral mucus membranes offering a faster action than the oral route and avoiding the digestive system chemicals bual Administration is similar with medication placed between the cheek and gums often used for glucose gel transcutaneous or transdermal routes involve absorption through the skin while intranasal or I in administration uses a mucosal atomizer device or mad to deliver medication as a spray providing quick absorption inhalation involves aerosolizing drugs which are then inhaled into the lungs with forms including aerosols fine powders and sprays commonly used for nebulized medications and meter dose inhalers.", + "Pharmacokinetics and Pharmacodynamics": "pharmacokinetics involves four primary stages absorption distribution metabolism and excretion drugs modify existing functions of tissues and organs but they do not create new functions generally just producing multiple actions rather than a single effect the effectiveness and duration of a medication are influenced by factors such as the dose route of administration and the patient's clinical status the onset and peak of a drug are related to its absorption and distribution while a minimum concentration at specific sites is necessary for therapeutic effects the duration of action is mainly linked to metabolism and elimination drug absorption is affected by various factors including the nature of the absorbing surface blood flow to the administration site drug solubility pH concentration dosage form route of administration bioavailability diffusion osmosis and filtration once administered drugs quickly move from the vascular space into the interstitial fluid with blood flow to specific areas determining the amount reaching different parts of the body some areas like the brain and placenta are less accessible to certain drugs biotransformation involves the chemical alteration of substances within the body primarily occurring in the liver drug elimination or excretion involves the removal of waste products which can occur in their original forms or as metabolites the main organs of excretion include the kidneys intestines lungs sweat glands and mamory glands the rate of elimination varies based on the drugs concentration in the body and the condition of the excretion or or an poor elimination as seen in patients with shock or the elderly can lead to drug accumulation and potentially toxic effects if additional doses are given pharmacodynamics refers to the study of how a medication produces its intended response also known as the mechanism of action it encompasses the processes by which drugs exert their effects on the body including the interaction between the drug and its Target receptors or enzymes this field also considers factors that may alter the intended response such as variations in individual patient characteristics or concurrent use of their medications additionally pharmacodynamics includes the assessment of side effects and any unexpected effects that may arise from Drug Administration the mechanism of action of a drug involves several key steps and factors for a drug to produce its intended effect it must reach appropriate concentrations at a Target site the magnitude of the response is influenced by both the dose and the time it takes for the drug to travel through the body medications can act through various mechanisms they may bind to specific receptor sites change the physical properties of cells chemically interact with other substances or alter normal metabolic pathways once a drug binds to its receptor it initiates a series of chemical changes that lead to the desired effect understanding these mechanisms is critical for optimizing therapeutic outcomes and managing potential side effects the drug response relationship examines how the amount of medication administered correlates with the response it elicits it's crucial to understand the onset of action duration of action and termination of action when administering a medication these factors significantly influence the therapeutic index which is the ratio of a Drug's lethal dose for 50% of the population or ld50 to its effective dose for 50% of the population ed50 the therapeutic index provides an indication of a medication's margin of safety helping to balance efficacy and risk Additionally the the therapeutic threshold is the minimum concentration of a drug that's required to produce the desired therapeutic response.", + "Medication Interactions and Errors": "medication interactions can be influenced by a variety of factors an interaction occurs when the actions of a drug are altered by another chemical substance which can include another prescription medication herbal or OTC medications nicotine dietary components or any other substance the patient is exposed to as a provider it's important to be aware of potential interactions between prescribed medications and any self-administered drugs the patient may be taking this includes understanding poly Pharmacy interactions with food or alcohol and taking note of warning label r on prescription bottles that indicate possible substances that may cause interactions predictable responses to medications such as side effects are actions of a drug that differ from the undesired therapeutic effects these side effects may still occur even when the medication is administered correctly and under appropriate conditions iatrogenic responses are adverse conditions unintentionally induced by treatment such as a urinary tract infection following catheter insertion unpredictable responses are those that are not anticipated based on the Drug's known effects allergic reactions are the most common of these involving an immune response to the medication serum sickness a delayed hypers sensitivity reaction and idiosyncrasy a unique response specific to an individual are other examples tolerance occurs when there is a reduced response to a drug over time necessitating higher doses for the same effect cross tolerance May develop where tolerance to One Drug results in tolerance to others within the same class a refractory condition does not respond to treatment and cumulative effects can occur with successive doses of a medication leading to increased or unintended effects drug dependence involves a need for a drug to function normally while habituation refers to physical tolerance and psychological dependence drug interactions May alter the response of one medication due to the presence of another with drug antagonism blocking or diminishing effects summation effect combining the effects of similar drugs and potentiation enhancing one Drug's effect by another interference involves a direct biochemical interaction between two drugs reducing medication errors is critical especially in stressful life-threatening situations where decisions are often made from memory to minimize these errors it's essential to adhere to the rights of medication administration these rights include ensuring the right patient receives the medication verifying the right medication and its indication and administering the correct dose via the appropriate route at the right time additionally providing proper patient educ Med ation respecting the patient's right to refuse medication and evaluating the response to the medication are key accurate documentation of all medication related actions is also crucial to maintain safety and efficacy to further reduce medication errors it's important to use current reliable medication reference sources whenever administering unfamiliar medications or when considering unusual doses or routes of administration additionally having a partner verify the volume in a syringe or the calculations for weight-based medications can help ensure accuracy and prevent mistakes before administering any medication evaluate the patient for potential allergies or hyp sensitivity to the medication this helps to avoid adverse reactions it ensures the patient safety Additionally the institute for safe medication practices has developed a list of medication abbreviations that are prone to causing errors familiarizing yourself with this list can help prevent miscommunication and mistakes related to medication administ ation.", + "Scope of Medication Administration": "you may administer a range of medications including oxygen oral glucose glucagon and intravenous dextrose Solutions other IV fluids you might use include D5W normal saline and lactated ringers Additionally you can administer epinephrine either intramuscular or subcutaneously MDI medications such as Albuterol and nebulized albuterol nitroglycerin can be given in the form of spray tablets or paste while nitrous oxide is also within your scope nxone and aspirin are other medications that you may administer you are authorized to administer or assist with these medications only under specific conditions either a licensed physician gives you a direct order to administer the medication or your local medical protocols permit you to do so this includes following standing orders for medication use in defined situations as outlined in your local medical protocols.", + "Conclusion and Best Practices": "medication administration is a critical aspect of patient care encompass ing a variety of drug forms and routes drugs can be delivered in different forms including solids like tablets capsules and suppositories liquids such as Solutions suspensions and syrups and gases Like Oxygen and nitrous oxide each form is designed for specific routes and purposes such as oral intravenous intramuscular or transdermal to ensure effective delivery and absorption the choice of form and Route directly impacts the Drug's onset duration and overall effectiveness pharmacokinetics and pharmacodynamics are essential in understanding how drugs work within the body pharmacokinetics involves the absorption distribution metabolism and excretion of drugs determining how they reach and affect their target sites factors such as drug concentration pH and route of administration influence this process pharmacodynamics on the other hand focuses on the drugs mechanism of action and the relationship between drug dose and its therapeutic effects this includes understanding how medications interact with receptors alter metabolic pathways and produce the desired effects to reduce medication errors it's crucial to adhere to best practices and guidelines this includes verifying patient allergies using reliable references for unfamiliar medications and confirming calculations with a partner familiarity with common drug interactions and understanding predictable and unpredictable responses es such as side effects and allergic reactions help prevent adverse outcomes medications such as oxygen glucose and nitroglycerin may be administered under specific conditions set by local protocols or physician orders emphasizing the importance of following established guidelines to ensure patient safety and effective treatment" + }, + { + "Introduction to Critical Care Pharmacology": "chapter eight Critical Care\n\nIntroduction pharmacology introduction pharmacology defined as the comprehensive exploration of medication preparation uses and actions is significant in the realm of pre-hospital and critical patient care Critical Care transport professionals bear the responsibility of possessing a profound understanding of pharmacology in its entirety ensuring the administration of medications aligns with the goal of optimal patient care while concurrently avoiding potential harm or fatality this chapter presents a concise review of fundamental pharmacological principles presupposing a foundational comprehension of the subject in the dynamic landscape of medical advancements where novel medications and treatment approaches continually surface a judicious equilibrium between integrating new information and adhering to established treatment strategies becomes imperative providers are urged to navigate their practice in alignment with local regulations policies and protocols emphasizing the necessity of Consulting reliable up-to-date sources when engaged in the administration of any", + "Pharmacology and Medication Information": "medication pharmacology and medication information critical care providers are tasked with a constant commitment to staying a breast of the ever evolving landscape of newly approved medications and contemporary research findings in the field of pharmacology the acquisition of accurate and upto-date information is instrumental in ensuring the efficacy and safety of patient care various resources available in both traditional print and modern electronic formats serve as conduits for this Essential Knowledge educational institutions industry organizations independent publishing companies and the vast expanse of the internet alongside specialized software like Epocrates collectively furnish a comprehensive spectrum of information sources for providers in navigating this diverse array of resources providers are urged to exercise Prudence by engaging in careful scrutiny of the selected sources to ascertain their accuracy and reliability this diligent approach to information gathering fortifies the foundation upon which critical decisions regarding medication administration are made through painstaking research providers can confidently integrate the latest pharmacological iCal insights into their practice fostering an environment where patient care is enriched by the application of reliable and contemporary medical", + "A Practical Approach to Medication Administration": "knowledge a practical approach to medication administration several considerations come into play When selecting the appropriate medication for a specific medical condition and various factors influence this decision-making process particularly in the context of critical care patient transport the availability of the optimal medication may not be guaranteed during patient transport as professionals typically do not routinely carry a comprehensive array of specialized medications to mitigate this challenge it is imperative for providers to ensure that they have obtained sufficient quantities of any specialized medication from ascending facility before commencing transport this includes anticipating transport time and incorporating an additional amount to accommodate potential delays thereby maintaining a safety margin in addition to medication availability the scope of practice and monitoring capabilities of the transport team must be considered When selecting a medication this includes an assessment of the clinical status of the patient where immediate life-saving interventions may take precedence over routine medication administration in instances where safety or operational priorities such as those related to the mode of Transport supersede the urgency of medication administration decision-making processes need to be in place these multifaceted considerations underscore the complexity involved in medication selection during critical care patient transport or careful evaluation of various elements ensures the delivery of optimal and safe patient care before the administration of any medication consideration of specific factors related to that drug helped to ensure patient safety and treatment efficacy the healthc care provider must evaluate the indications while simultaneously performing an assessment of contraindications in an attempt to identify circumstances or patient characteristics where the medication may be deemed inappropriate or pose an unacceptable risk understanding the pharmacodynamics of a medication its mechanism of action and effects on the body provides critical insights into its therapeutic potential furthermore a comprehensive grasp of pharmacokinetics which involve the drugs absorption distribution metabolism and excretion is imperative for optimizing dosage regimens and minimizing the risk of toxicity potential adverse effects ranging from mild to severe demand careful consideration to anticipate and manage any unted reactions that may occur this methodical evaluation of medication specific factors forms the foundation for informed clinical decision-making enabling Health Care Providers to tailor treatments to individual patient needs while mitigating potential risks and optimizing therapeutic", + "Pharmacokinetics": "outcomes pharmacokinetics pharmacokinetics a branch of pharmacology examines the intricate processes governing the actions of medications within the human body focusing specifically on the temporal aspects of absorption distribution metabolism also known as biotransformation and elimination in the context of medication absorption this process occurs either immediately or shortly after Administration and the route of administration plays a decisive role in determining the speed and extent of absorption intravenous intra oous intramuscular subcutaneous oral inhaled transdermal nasal and rectal routes present divers Avenues of drug delivery each with its own set of considerations notably some routes such as ocular intraarterial odic epidural and vaginal are not typically performed by Critical Care paramedics the selected route significantly impacts the bioavailability of a medication with intravenous administration offering 100% % bioavailability while oral Administration ranges from 0% to 100% contingent on the specific substance the differences in bioavailability underscore the critical concept that a dose of a medication may be safe when given orally but could be toxic or even lethal when administered intravenously moreover alternative routes such as nasal sublingual and rectal Administration may present safe alternatives to intervenous delivery in certain situations distribution exhibits High variability subsequent to the absorption of medications the bloodstream serves as the primary conveyance for distribution facilitating the dispersion of substances throughout the body the process of distribution is influenced by various factors including the size of the molecule ionization properties affinity for binding to tissues or plasma proteins lipid or water solubility and the capability to penetrate Target tissues the presence of physiological barriers such as the placental and blood brain barrier act as a regulatory mechanism limiting the distribution of certain substances into fetal and brain tissues respectively highly lipid soluble medications demonstrate a propensity to readily Traverse these barriers while Others May simply exhibit minimal or no penetration the concept of the first pass effect which is observed with orally administered medications underscores the reduction in medication concentration as it passes to the liver before entering systemic circulation also known as first pass metabolism this phenomenon significantly influences a Drug's bioavailability Which shapes its therapeutic efficacy routes of elimination play a role in concluding the pharmacokinetic journey the kidneys and urinary system stand as the principal routes for elimination with additional Pathways including excretion via the lungs sweat saliva stool and breast milk biotransformation predominantly unfolds in the liver although various body tissues and cells possess the capacity for this transformative process the liver housing an array of enzyme systems assists in biotransformation with the cytochrome p450 system emerging as the primary pathway responsible for these metabolic conversions this can lead to four potential events the conversion of an active drug into an inactive metabolite the transformation of an active drug into an active metabolite the generation of a reactive metabolite with heightened potential for action or toxicity and the conversion of a poorly active substance into an active and potentially harmful toxic form the complexity of biotransformation introduces challenges in clinical settings particularly when dealing with active or reactive metabolites necessitating special considerations in medication selection genetic polymorphism can influence the cytochrome p450 system impacting the efficiency and speed of biotransformation additionally Associated medications and external agents such as nicotine grape fruit juice and certain vegetables like broccoli can either inhibit or induce the the cytochrome p450 system further complicating the biot transformation process moving to the phase of elimination substances or medications undergoing this process follow either a zero order or first order elimination pattern zero order elimination involves a fixed amount of substance being eliminated over a given time period earr perspective of its plasma concentration conversely first order elimination reflects a proportionate decrease in substance concentration over time medication half- lives representing first order kinetics and achieving a medication steady state where the rate of administration equals the rate of elimination are crucial Concepts especially in the context of antibiotics and anti-coagulants factors influencing both biotransformation and elimination incompass profusion as well as liver and kidney status metabolism the manner and extent of absorption and chronic exposure to specific medications or chemicals understanding biotransformation is essential in tailoring Health Care interventions particularly in medication management for example consider a patient with a known genetic polymorphism affecting the cytochrome p450 system this individual May metabolize certain medications at a slower or faster rate than the general population impacting drug efficacy and potential toxicity in a clinical scenario a healthc care provider aware of this patient's genetic pre disposition can adjust medication dosages accordingly for a drug primarily metabolized by this system such as deltm or halol the provider May opt for a lower initial dose to avoid potential adverse effects associated with slower metabolism conversely if the patient metabolizes a drug rapidly necessitating a higher dose for therapeutic efficacy the healthcare provider provider can then adjust a treatment plan", + "Pharmacodynamics": "accordingly pharmacodynamics in exploring the theories of drug action four fundamental mechanisms delineate the ways in which chemicals interact with the body to achieve specific therapeutic goals firstly medications May bind with receptor sites on specific cells either promoting or inhibiting particular cellular activities based on the nature of the interaction secondly drugs can induce the physical properties of cells thereby altering their functioning and contributing to the overall pharmacological response moreover medications May engage in direct inter interactions with other chemicals within the body resulting in the alteration or limitation of the effects of these substances or facilitating their removal this interaction emphasizes the interconnectiveness of drugs within the physiological milu lastly drugs May alter metabolic pathways affecting the intricate biochemical processes within cells to achieve desired therapeutic outcomes this diverse spectrum of mechanisms showcases the versatility of pharmacodynamics in modulating cellular activities and biochemical Pathways to elicit specific and targeted physiological responses when a medication molecule attaches to a receptor site it elicits one of two primary effects demonstrating the role of receptor interactions in pharmacotherapy firstly the medication May stimulate the receptor site functioning as an Agonist and activating the cellular response associated with that particular receptor conversely the medication may act as an antagonist blocking the receptor site from being stimulated by endogenous substances or other medications this dichotomy in the effects forms the basis for modulating physiological responses in various clinical scenarios notably certain medications exhibit a dual nature as Agonist antagonists meaning they can both stimulate and block receptor sites depending on the specific context and conditions within the body the effectiveness of medications binding to two receptor sites is contingent on the availability of these sites the number of receptors is inconsistent and can be influenced by multiple factors these include the actual number of receptor sites present in the body the number already occupied by endogenous chemical mediators and the number occupied by other concurrently administered medications this variability underscores the complexity of pharmacodynamics and emphasizes the importance of understanding the dynamic interplay between medications and receptors in optimizing therapeutic outcomes the drug response relationship encapsulates the dynamic interplay between a medication and its effects within the body delineated by several key temporal and quantitative parameters upon Administration the onset of action signifies the period required for the concentration of the medication at the Target tissue to attain the minimum effective level concurrently the duration of action reveals the time frame during which the medication is expected to remain Above This minimum effective level in influencing the overall therapeutic efficacy the termination of action represents the interval from the point where the concentration Falls below the minimum level to the subsequent elimination from the body marking the conclusion of the Drug's impact Central to understanding the drug safety and efficacy profile is the therapeutic index expressed as the ratio of a Drug's lethal dose for 50% of the population or ld50 to its effective dose for 50% of the population known as ed50 this ratio serves as a critical determinant of a medication's margin of safety gauging the relative safety of a drug by assessing the range between its therapeutic and toxic dosages Additionally the concept of Half-Life provides insights into the temporal aspects of drug elimination it denotes the time required for the body to eliminate half of the administered drug notably a medication is typically considered eliminated after about five Half Lives emphasizing the importance of this parameter in determining appropriate dosing intervals and avoiding potential accumul ulation which can lead to toxicity factors influencing drug responses Encompass a multifaceted interplay of variables each demanding careful consideration age stands out as an important determinant with older adults exhibiting heightened sensitivity to drug effects often necessitating smaller dosages than their younger counterparts determining appropriate medication doses in the elderly is further Complicated by factors such as declining renal function decreasing muscle mass alterations in body water content relative to fat content and changes or reductions in specific neurotransmitters in contrast pediatric medications typically possess an increased metabolic rate compared to adults in other individuals leading to variations in drug responses certain medications May elicit different effects based on age exemplified by sedative hypnotic agents having a more profound or prolonged impact on older patients while pediatric patients may experience paradoxical drug reactions where in sedative agents induce hyperactivity and even agitation weight is another Factor influencing drug responses requiring precise dosage calculation dosages are often expressed in milligrams or micrograms per kilogram of the patient's body weight depending on the drugs pharmacokinetics and pharmacodynamics doses may be based on total or actual body weight ideal body weight or adjusted body weight calculating ideal body weight involves specific formulas considering height and gender M's ideal body weight is calculated by using 106 PB for the first 5T of height and adding six additional pounds for each inch for women the ideal body weight calculation starts with 100 lb for the first 5 fet of height and then adding five PBS for each additional inch sex differences also contribute to variations in drug responses primarily due to General disparities in body mass between males and females recognizing and accounting for these factors in drug prescription at Administration is imperative for healthc Care Professionals to optimize therapeutic outcomes and ensure patient safety across diverse demographic groups the environment shapes drug responses encompassing both physiological and psychological stresses imposed on the patient psychological factors such as stress and emotional states can significantly influence how a patient responds to a medication additionally physiologic stresses such as those induced by environmental factors like seasonal allergies can alter the body's response to medications the time of medication administration often considered in relation to meals is yet another Factor influencing drug responses the presence or absence of food in the GI tract can imp impact the absorption and bioavailability of certain medications this consideration is especially pertinent for drugs that require specific conditions for optimal absorption or those that may cause gastric irritation furthermore the overall condition of the patient serves as a fundamental determinant of drug responses patients in varying states of Health such as those in shock or suffering from hypothermia exhibit altered physiological conditions that can impact the pharmacokinetics and pharmacodynamics of administered medications in patients experiencing shock for example there may be alterations in blood flow affecting the distribution and elimination of drugs likewise hypothermic patients may experience changes in metabolism potentially influen infuencing the pharmacokinetic profile of medications genetic factors wield a substantial influence on a patient's response to medications impacting both pharmacokinetics and Dynamics variations in a patient's genetic makeup can lead to specific enzyme deficiencies such as glucose 6 phosphate dehydrogenase deficiency or G6 PD which contraindicates the administration of oxidant medications or sulphamides additionally genetic predispositions play a role in conditions like primary pulmonary hypertension and CLE cell disease where the patient's genetic profile significantly shapes the pharmacological response and potential complications associated with drug therapy pregnancy introduces a unique set of considerations in drug therapy as medications Traverse from the pregnant woman's bloodstream into the placenta subsequently affecting the developing fetus the physiological changes associated with pregnancy including altered respiration hemodilution and modified hemodynamic parameters further compound the complexity of drug responses catac colomines for instance may have adverse effects on placenta profusion necessitating careful consideration in medication choices for pregnant patients psychological factors are integral considerations particularly when administering medications for analgesia and sedation patient positioning temperature regulation and proactive communication are important in managing psychological aspects to potentially decrease the overall amount of medication require required patients with psychiatric disorders May exhibit unique responses to medications and certain drugs such as Bodines can induce paradoxical reactions in specific populations emphasizing the importance of tailoring drug therapy to individual patient characteristics and needs the critical care trans support professional must be prepared to encounter predictable responses to medications extending beyond the intended therapeutic effects to Encompass potential side effects anticipating and evaluating these side effects is Paramount to assessing the overall risk benefit ratio associated with a particular drug regimen the provider should weigh the benefits of the medication against the potential risks posed by its side effects considering individual patient characteristics and clinical context what may be a tolerable side effect for one group of patients could have life-threatening implications for another particularly those deemed high risk or critically ill furthermore the concept of atrogenes underscore the inadvertent induction of adverse conditions in patients with a direct consequence of medical treatment an example is the development of a urinary tract infection subsequent to the insertion of an indwelling catheter this unintended consequence highlights the importance of vigilance and proactive measures in patient care to mitigate the risk of atrogenes unpredictable responses to medications present a multifaceted challenge in the critical care setting where the most common predictable reaction is an allergic response providers must remain Vigilant anticipating the possibility of allergic reactions with any administered drug notably antibiotics with a penicillin base carry a higher risk for allergic responses moreover the presence of Aller allergies to bananas or avocados may serve as indicators of a latex allergy highlighting the interconnected nature of allergic responses and the need for comprehensive patient Assessments in rare instances patients May exhibit completely unique or idiosyncratic responses unrelated to the pharmacologic action or dosage of a medication additionally prolonged use of a medication can lead to tolerance where patients require higher doses to achieve the same therapeutic effect the cross tolerance phenomenon is often observed in patients taking multiple pain medications while tachy filis represents a rapid onset of Tolerance and Drug dependence manifests as significant withdrawal symptoms upon discontinuation the cumulative effect introduces the risk of increased response when a medication is administered in successive doses potentially resulting in either super therapeutic or non-therapeutic effects unanticipated drug interactions further complicate the landscape of unpredictable responses emphasizing the importance of a thorough medication history and Vigilant monitoring for potential adverse effects a summation effect emerges when two drugs with similar effects are administered doubling the response exhibited by the patient this phenomenon can manifest in various ways including synergism where the combined effect is greater than the sum of individual effects potentiation where One Drug enhances the effect of another interference where One Drug diminishes the effect of another and inhibition where One Drug hinders the action of another", + "Avoiding Medication Errors": "avoiding medication errors medication errors represent a pervasive challenge in the field of medicine and they often stem from lapses in the selection Administration or monitoring phases of drug therapy providers should work hard to avert such errors and Ensure patient safety through using a comprehensive approach the provider must adhere to a meticulous checklist ensuring that the right patient receives the right medication for the right indication at the right dose through the right route and at the right time this encompasses aspects like providing the right education to the patient respecting the right to refuse treatment conducting a third evaluation of the patient's response and documenting the entire process accurately in addition to their own responsibilities Critical Care transport providers are tasked with evaluating medication decisions made by the staff at sending facilities to identify potential errors confirming the accuracy of any medication infusion that is continued during transport is vital involving an assessment of proper labeling and compatibility of infusion lines issues such as line incompatibility can have profound implications for the integrity and effectiveness of medication administration during", + "Medication Management": "transport medication management certain medications are sensitive to environmental factors such as extremes in temperature exposure to direct sunlight or excessive humidity these conditions can often lead to a decrease in the potency of medications ensuring optimal storage conditions involves Consulting the drugs package insert or referring to the United States pharmacopia for specific guidelines preventative measures include avoiding direct sunlight and storing medications within a temperature range of 59\u00b0 f to 86\u00b0 F to preserve their chemical stability in the context of critical care transport special consideration must be given to medication storage within transport Vehicles each healthc care department requires a written protocol or procedure detailing the specific spefic handling of medication fluid or dilutent storage and handling to maintain the Integrity of these substances during Transit security is Paramount when dealing with controlled medications the majority of which are prescription drugs subject to additional regulations the US Drug Enforcement Administration or DEA necessitates stringent control measures the minimum requirements for the storage of Controlled Substances include the use of securely locked substantially constructed cabinets with no indication of their purpose additionally a controlled substance disposition record must be maintained and any expired Controlled Substances should be promptly returned to their respective agency or departmental officer these measures are essential not only to comply with regulatory guidelines but also to prevent unauthorized access and misuse of controlled medications ensuring patient safety and Regulatory", + "Specific Medications Used in Critical Care Transport": "Compliance specific medications used in critical care transport this section serves as an overview of common medications frequently utilized by Critical Care transport professionals while it provides a foundation it's important to acknowledge that the scope of clinical practice May introduce providers to a broader array of medications necessitating the development of a comprehensive strategy for the safe administration of any drug required in specific patient scenarios we must recognize that not every medication or medication class detailed here will be directly applicable to Providers exclusively engaged in critical care transport for specialized populations such as high-risk obstetric or neonatal cases vasopressors represent a class of medications employed in critical care settings to induce Vaso constriction thereby elevating arterial blood pressure the mechanism of action revolves around the stimulation of generic receptors involved in Vaso constriction some vasopressors also exhibit inotropic activity enhancing myocardial contractility these medications are indicated in distributive shock States once any fluid volume deficits have been addressed rest as they help restore vascular tone and systemic blood pressure despite their therapeutic benefits vasopressors come with significant side effects that demand careful consideration one notable risk is tissue necrosis resulting from extra vation where the medication leaks from the intended vascular p pathway into surrounding tissues Additionally the vasoconstrictive effects of these medications can lead to eskema potentially compromising blood flow to vital organs the use of vasopressors requires a nuanced understanding of their pharmacodynamics and potential complications emphasizing the importance of precise Administration and Vigilant monitoring to mitigate adverse effects and optimize therapeutic outcomes in critically ill patients pheno nephrine an alpha1 Agonist binds to and stimulates alpha1 receptors inducing systemic arterial Vaso constriction caution is warranted when administrating to patients with coronary artery disease as it may precipitate or worsen myocardial esea additionally patients with bre cardia should avoid phenylephrine as it may further decrease heart rate its infusion rate typically ranges from 40 to 60 micrograms a minute with the need for Rapid titration or bolus doses to achieve the desired blood pressure response especially in cases of vasomotor tone loss without simultaneous myocardial impairment norepinephrine a beta 1 and alpha1 Agonist is commonly employed for blood pressure control in cardiogenic or septic shock it is the firstline phase oppressor in septic shock patients who remain hypotensive after fluid challenges however Administration may result in arrhythmias tacac cardia hypertension and decreased perip pereral blood flow nor epinephrine rapid onset and short half-life necessitate continuous infusion to maintain its effects epinephrine an alpha beta Agonist stimulates alpha 1 beta 1 and beta 2 adrenic receptors causing bronchial smooth muscle relaxation cardiac stimulation and vasod dilation it is indicated for various conditions with infusion doses ranging from 0.05 to 0.5 micrograms per kg a minute epinephrine should be infused through a Central Access line to minimize adverse effects like tacac cardia anxiety arhythmia and lisia vasopressin a naturally occurring antidiuretic hormone is used for refractory distributive shock it acts on V1 receptors increasing systemic vascular resistance and mean arterial pressure vasopressin infusions ranging from 0.01 to 0.1 units per minute are employed for conditions like septic shock with effects seen in less than 15 minutes adverse reactions include brto cardia decreased cardiac output hyponatremia and tissue esema methylene blue an antidote for met hemoglobinemia is also used in critical care for vasopressor refractory hypotension acting as a nitric oxide inhibitor it blocks Vaso relaxation its dosing strategies vary and careful monitoring is required due to potential adverse effects like urine discoloration and interference with pulse oxymetry readings push dose pressors including epinephrine and phenol nephrine are used in critical care for refractory hypotension administered in small Alo quats they are indicated when conventional vasopressors fail to produce the desired blood pressure increase close patient monitoring is essential for safety Angiotensin 2 a relatively new medication supports blood pressure and distributive shock acting on the renin Angiotensin aldosterone system it causes Vaso constriction and water retention however due to significant thrombosis risk and higher costs its use is limited however providers may still encounter patients on active infusions inotropes are medications that can exhibit positive or negative inotropic effects influencing the force of myocardial contractility positive inotropic medication s increase myocardial contractility and are commonly used in patients experiencing cardiogenic shock the selection of an inotrope depends on the specific diagnosis and provider preference and the mechanisms of action can vary inotropic medications may have side effects ranging from headaches to Arias dopamine was historically popular for its theorized positive inotropic effects by stimulating beta 1 receptors however it also stimulates alpha 1 receptors at higher doses causing peripheral Vaso constriction dopamine affects dopamine ergic receptors Increasing myoc cardio contractility and cardiac output while it was once used as a firstline vasopressor in fluid refractory hypotension recent evidence suggests potential harm and norepinephrine is now considered Superior especially in sepsis dopamine May promote renal esea and has been associated with acute renal failure infusions are titrated from 1 to 20 microgr per kilo per minute administered through a central line line and any extra vation should be treated aggressively dobutamine is used in the treatment of cardiac decompensation secondary to heart failure it stimulates beta 1 receptors increasing myocardial contractility in heart rate while also causing vasod dilation through beta 2 effects despite its vasod diil and inotropic effects making it ideal for heart failure its utility is limited in patients with hypotension infusions are typically started at 5 micrograms per kg per minute and can be increased in increments every 10 minutes to a maximum of 20 micrograms per kg per minute dobutamine has a short duration of action and does not pose the same risks of tissue damage as other inotropes mil Renown a phoso dionas 3 enzyme inhibitor is used as an inotropic agent for patients in cardiogenic shock or Advanced stages of heart failure it is employed in patients who fail to respond to debam those with inst stage heart failure not eligible for transplantation and those with postop operative pulmonary hypertension infusions are initiated at 0.125 to 0.75 micrograms per kg per minute its onset of action is 5 to 15 minutes with a halflife of 2.3 to 2.4 hours extending to 20 hours in patients with renal failure major side effects include hypotension and arrhythmias usually ventricular in nature vasodilators are pharmacological agents that induce vasod dilation resulting in the lowering of mean arterial pressure the mechanism of action for vasodilators involves the reduced relaxation of smooth muscle in the walls of blood vessels this relaxation leads to an increase in the diameter of the blood vessels reducing resistance to blood flow and subsequently lowering blood pressure the selection of specific vasod dilators is based on the indication for use individual patient response and considerations of cost Effectiveness one notable aspect of vasodilator therapy is the potential occurrence of hypotension which is both the most common and most dangerous side effect associated with these medications the excessive drop in blood pressure can compromise profusion to vital organs and tissues leading to adverse outcomes careful monitoring of blood pressure and patient response is essential during vasod dilor Administration with adjustments made as needed to avoid hypotensive episodes and ensure optimal therapeutic effects sodium Nitro pride is an arterial and Venus dilator known for its vasod dilating effects resulting from the breakdown of nitric oxide which acts directly on vascular smooth muscle it finds application in treating acute hypertension and acute decompensated heart failure with therapeutic effects manifesting within 2 minutes sodium Nitro proside in severe heart failure can increase cardiac output initial dosing starts at 0.25 to 0.5 micrograms per kg per minute titrated in increments of 0.5 to 1 microgram per kg per minute every 3 to 5 minutes with a usual dose range of 0.25 to three nitroglycerin acts through the relaxation of vascular smooth muscle reducing preload and peripheral vascular resistance used for ES schic chest pain its infusions begin at 10 micrograms a minute titrated every 3 to 5 minutes hydrazine a direct arterial vasodilator acts on arteriolar smooth muscle and is employed in hypertensive emergencies administered as an IV dose of 10 to 20 milligrams every 4 to 6 hours clevidipine a calcium channel blocker reduces mean arter IAL blood pressure by decreasing systemic vascular resistance administered for short-term treatment of hypertension this drug is titrated by doubling the dose every 90 seconds nicardipine another calcium channel blocker for short-term hypertension treatment selectively affects vascular smooth muscle infusions start at 5 milligrams an hour and are titrated every 50 15 minutes with a maximum recommended dosing of 15 mg per hour both of these drugs may present side effects including teoc cardia and irritation at the infusion site sedatives Aesthetics analgesics anticho and anti-convulsants are medications that with the exception of antipsychotics primarily exert their effects on the nervous system typically depressing nervous system activity sedatives encompassing anxiolytics and hypnotics function as CNS depressants or relaxants inducing a calming or sleep inducing effect anesthesia involves the induction of a state of unconsciousness through anesthetics facilitating medical procedures or surgeries analgesics on the other hand are medications aimed at providing relief from pain acting through various mechanisms to alleviate discomfort anti-convulsants play a role in halting seizure activity often prescribed to individuals with epilepsy or other seizure disorders it is no noteworthy that many medications within the sedative anesthetic analgesic and anti-convulsive categories may have cross classifications depending on the dose and indication a single medication may be considered a member of multiple classes the mechanisms of action of these medications vary widely reflecting their diverse roles in managing conditions such as anxiety pain and and seizures understanding the distinct mechanisms of action for each class is essential for healthc Care Professionals to appropriately prescribe and administer these medications based on individual patient needs and medical context while these drugs exhibit a broad range of side effects the most significant and potentially perilous adverse effect common to all CNS depressants is the occurrence of unrecognized respiratory depression respiratory depression involves a decrease in the rate and depth of breathing leading to inadequate oxygen intake and potential complications such as hypoxia monitoring and promptly recognizing respiratory depression are important aspects of patient safety during the administration of these medications waveform capnography has emerged as the gold standard of care for monitoring respiratory function and prly detecting signs of respiratory depression this monitoring method measures the concentration of entitle CO2 in each breath providing realtime data on the patient's ventilatory status capnography allows healthc Care Professionals to assess the effectiveness of ventilation detect hypoventilation or apnea and identify early signs of respiratory compromise in the context of CNS depressants especially during procedures involving sedation or anesthesia continuous waveform capnography ensures Vigilant monitoring of respiratory parameters timely recognition of changes in the capnographic waveform such as a sudden decrease or absence of CO2 can alert healthc care providers to respiratory depression allowing for prompt intervention to prevent complications and ensure patient safety therefore the integration of entitle capnography significantly enhances the monitoring capabilities in healthcare settings where CNS depressants are administered myum a benzo dipene also known as versed demonstrates a relatively fast onset of action typically ranging from 1 to 5 minutes when administered intervenous frequently employed during RSI it serves as an adjunct to other selective hypnotic agents notably myum possesses potent amnesic properties impairing a patient's ability to recall the procedure its popularity during Critical Care transport is attributed to its stability at room temperature allowing for prolonged storage utilized for Sedation in CCT patients and to terminate status epileptic seizures myum offers a versatility in administration routes including oral IV IO by Bolis or continuous infusion intramuscular and off Lael intranasal or bual routes dosing is titrated to effect varying based on the indication with initial intramuscular doses for Sedation in patient typically starting at 5 milligrams diazapam another benzo dipene with a moderately long duration of action shares similar indications with mosum however its use for procedural sedation in adults has diminished due to its longer Half-Life dipam also known as vum comes in various dosage forms including a rectal gel designed for the treatment of status epileptic as seizures its rectal gel dosing is age dependent ranging from 0.2 mg per kg for adults to 0.5 mg per kg for children aged 2 to 5 years lorazapam or Adavan is a benzo diazine preferred for emergency treatment of status epilepticus and finds applications in various contexts including accute alcohol withdrawal and as an adjunct anti medic for chemotherapy induced uced naan vomiting PHA barbital a long acting barbituate plays a role in critical care for the treatment of status epilepticus seizures and alcohol withdrawal Dex metat a selective Alpha 2 adrenic receptor Agonist with analgesic and exitic properties is employed in mechanically ventilated patients for procedural sedation and to reduce opioid doses following surgery or trauma propol a general anesthetic serves the induction and maintenance of anesthesia in the operating room as well as sedation in mechanically ventilated patients automode an ultra short acting general anesthetic is popular for procedural sedation induction of general anesthesia and intubation with think lower incidence of hypotension compared to other induction agents ketamine a new favorite of EMS providers exhibits a rapid onset of action and is increasingly used off Lael for procedural sedation and analgesia particularly in patients with excited delirium syndrome halap Idol classified as an anticho finds off Lael use in the critical care setting for the treatment of delirium and severe agitation IV Administration is the preferred route with doses ranging from 0.5 to 10 milligram the dosage is titrated by doubling the initial dose every 15 to 30 minutes until the patient attains a calm state maintenance involves administering 25% of the last bolus every 6 hours intramuscular is a viable alternative when IV access is unavailable though caution is warranted due to the potential for hypotension banine is employed to address delirium and severe agitation the orally disintegrating tablet is preferred for administration and critical care transport with the usual intramuscular adult dose ranging from 5 to 10 milligram additional doses may be administered at 2H hour intervals if needed within a maximum daily adult dose of 30 milligrams cupine another atypical anticho used off label addresses delirium confusion and insomnia in ICU patients initial ual oral dosing starts at 25 to 50 mg adjusted upward daily to a maximum of 400 mg a day many intensivists consider cupine an effective agent for managing ICU delirium fentel a synthetic opiate analgesic is significantly more potent than morphine employed for procedural sedation in in ated patients it is often administered intranasally the typical adult dosing involves Ivy administration of 50 to 100 micrograms over 1 to 3 minutes followed by an infusion starting at 25 micrograms an hour fentel has minimal cardiovascular effects although rare instances of rigid chest wall Syndrome have been associated with rapid Administration sufentanil a medication that is similar to fentanyl offers significant analgesic effects with minimal cardiovascular impact approximately 10 times more potent than fenel so fenel has a shorter Half-Life making it suitable for postoperative ICU settings bolus and infusion doses are tailored based on anticipated surgery duration ranging from 1 to 8 microgram per kg prior to surgery and maintenance doses up to 1.5 micrograms per kg an hour keep in mind caution is advised in patients with respiratory compromise morphine an opioid receptor Agonist provides analgesia in the critical care environment dosing varies widely among patients with IV doses being two to three times more potent than equivalent oral doses diluted Bolis doses administered over 3 to 5 minutes help mitigate side effects including nausea vomiting hypotension and respiratory depression morphine induced histamine release May cause itching which is managed with antihistamines Hydromorphone another opioid analgesic addresses moderate to severe pain not responsive to Morphine or fentanyl IV doses are two to four times more potent than equivalent oral Doses and 1 milligram of hydromorphone is equivalent to 7 milligrams of morphine usual adult dosing ranges from 0.4 4 to 0.8 mg administered IV over 3 to 5 minutes nuan an opioid Agonist antagonist is typically administered at a dose of 10 milligrams every 3 to 6 hours while not commonly used for analgesia in critical care its Agonist antagonist properties make it useful for relieving opioid induced partis IV all flal use is dosed at 2.5 to 5 milligrams and repeated as needed keep in mind the use of nuan severely limits the ability to use other opioid based medications acetaminophen an analgesic and antipyretic is available in oral and rectal forms IV acetominophen approved by the FDA in 2010 is used cautiously and its maximum daily doses should not exceed 4 grams in healthy adults curac is an insid used for pain management and is predominantly administered intravenously the usual IV dose for adults is 15 to 30 milligrams every 6 hours caution is exercised in critically ill patients those over 65 years of age and those with renal insufficiency with the drug typically not used for more than 5 days due to the increased risk of GI bleeding surgical bleeding thrombotic cardiovascular events and compromised renal function it is also contraindicated in patients who were in labor leviter acetam an anti-convulsant emerges as a therapeutic option in the management of status epilepticus following immediate treatment with a short acting benzo dipene administered intravenously the recommended adult dose ranges from 1,000 to 4500 milligram infused at a rate of 2 to 5 mg per kg per per minute while pediatric dosing is 20 to 60 mg per kg Beyond accute seizure control leviter acetam may be employed to prevent seizures following significant brain injury with dosing for seizure prophylaxis in adults at 1,000 milligrams every 12 hours and for children at 15 to 25 milligram per kg every 12 hours photoin another anti-convulsant is employed in critical care for status epilepticus treatment following short acting benzo aspenes the initial IV dosing is 20 milligrams per kg with an additional dose of 5 to 10 milligrams per kg if required photoin use is contraindicated in patients with cardiac arrhythmias and it should be administered only through a central line as it precipitates when mixed with dextrose or other IV Solutions oral photoin loading is considered safer for stable conscious and low-risk patients phosphinine a precursor to photoin serves as a prodrug transformed into photoin in the body IV dosing for status epilepticus is 20 milligrams per kg with a possible second dose of 5 milligrams per kg after 10 minutes phosphino toine is versatile compatible with saline dextrose and lactated ringer Solutions and can even be administered intramuscularly theic acid an anti-convulsant is utilized in the treatment of benzoa aspine resistant status epilepticus adult IV dosing ranges from 20 to 40 migs per kg administered at a rate of 3 to 6 millgram per kg per minute followed by a potential continuous infusion monitoring liver enzymes and serum ammonia levels is critical due to valporic acid's potential for hepatotoxicity and its use may also prolong bleeding times while already discussed earlier phenobarbitol finds application in inducing a barbituate coma in severely brain injured patients with elevated intracranial pressure and in treating refractory status epilepticus patients should be intubated before Administration and the loading dose is 5 to 15 mg per kg at ad ministered intravenously at a control rate quick cessation is cautioned against to prevent withdrawal symptoms restlessness insomnia hallucinations and even death neuromuscular blocking agents or nmbas primarily block the transmission of neuromuscular signals leading to skeletal muscle paralysis this pharmacological effect is particularly viable in medical scenarios where temporary paralysis is beneficial in the critical care setting one of the most prevalent applications is the facilitation of endot tral intubation by inducing skeletal muscle paralysis nmbas enhance the conditions for successful and controlled intubation allowing healthc Care Professionals to secure the airway swiftly and effectively the precise and temporary nature of neuromuscular blockade ensures that the patient remains immobilized only for the necessary duration of the procedure minimizing the risk of complications associated with prolonged muscle paralysis when employing the use of neuromuscular blocking agents it's imperative for critical care transport providers to utilize continuous waveform capnography throughout the administration of the drug beyond the immediate monitoring considerations there is a profound awareness of the potential consequences associated with the long-term chemical paralysis of patients a scenario that healthc care providers must carefully navigate prolonged exposure to paralytic medications can lead to persistent muscle weakness and neuropathies even after the discontinuation of the nmba these lingering conditions pose significant challenges as they have the potential to impede the weaning process from mechanical ventilation prolong intensive care Admissions and compromise overall patient recovery to mitigate these risks the provider must administer paralytics judiciously ensuring the shortest possible duration and the lowest effective dose this approach aligns with the principles of patient safety in Optimal Care and critical care scenarios assessment of the appropriate level of paralysis is required for op patient care providers utilize specialized techniques to evaluate neuromuscular function appropriately three common methods employed for this purpose are the train of four measurement post tianic count and double burst stimulation the train of four measurement involves s stimulating the motor nerve at four successive pulses assessing the resultant muscle response to gauge the degree of neuromuscular blockade post tianic count involves delivering a Titanic stimulus and then counting the number of Twitches during the subsequent period providing insights into the depth of paralysis double burst stimulation evaluates the response to pair bursts of stimuli offering additional information on neuromuscular function given the technical nature of these assessments special instructions are imperative to ensure that Critical Care transport providers possess the requisite skills to perform and interpret these tests accurately sual choline the sole depolarizing neuromuscular blocking agent widely employed in medical practice acts as an Agonist at nicotinic receptors closely mimicking the actions of acetycholine its administration at a dose of 1 to 1.5 milligrams per kg induces rapid muscle relaxation within a approximately 30 seconds resulting in total paralysis in about 45 seconds this Swift onset coupled with a duration of action lasting 4 to Six Minutes positions sual choline as an ideal paralytic agent for medication assisted Airway management however its use requires caution due to potential adverse effects such as bra cardia particularly in pediatric patients and with an inclination to Elevate serum potassium levels posing risks in conditions associated with hyperemia sual choline is contraindicated in patients with a personal or family history of malignant hypothermia Alternatives should be considered for Crush injuries spinal cord injuries and chronic conditions like renal failure in contrast non depolarizing neuromuscular blocking agents include pancuronium vecuronium rocuronium atriuum and CIS atriuum pancuronium is administered as an IV Bolis of 0.06 to 0.1 migrs per kg followed by a continuous infusion of 0.8 to 1.7 microgr per kg per minute it exhibits a rapid onset within 3 to 5 minutes with a duration of around 60 Minutes vecuronium has an initial IV dose of 0.08 to 0.1 milligrams per kg for intubation followed by continuous infusion of 0.8 to 1.7 micrograms per kg per minute rocuronium with the fastest onset time among non-depolarizing agents is generally administered at 0.6 to 1.2 millgram per kg offering a duration of up to 45 minutes atriuum and CIS atriuum are recommended for intubation at 0.4 to 0.5 mg per kg with continuous infusions of 4 to 20 microgram per kg per minute and 1 to 3 microgram per kg to 1 minute while atriuum remains stable at room temperature for 21 days vecuronium and CIS atriuum fals must be refrigerated emphasizing the importance of appropriate storage for these medications the unique pharmacological profiles of these agents necessitate careful consideration and monitoring in critical care settings stress ulcer prophylaxis is a vital intervention in critically ill patients with specific risk factors persisting from more than 48 hours warranting the use of histamine antagonist and proton pump inhibitors or ppis these risk factors include coagulopathy severe sepsis and mechanical ventilation coagulopathy characterized by impaired blood clotting mechanisms increases the susceptibility of critically ill patients to GI bleeding severe sepsis a life-threatening condition resulting from a disregulated host response to infection poses additional stress on the body potentially leading to the development of stress ulcers mechanical ventilation a common intervention in critical care settings is associated with an increased risk of stress ulcers due to factors such as compromised mucosal blood flow and systemic infl inflammation in light of these risk factors histamine antagonists which inhibit gastric acid secretion by blocking histamine receptors and ppis which suppress gastric acid production by inhibiting the proton pump enzyme are administered as prophylactic measures to mitigate the potential development of stress ulcers in critically ill patients the choice between between these agents is often Guided by factors such as patient tolerance contraindications and institutional protocol it's imperative to discontinue stress ulcer prophylaxis once the aforementioned risk factors are resolved the medications that diminish acid production achieve this effect by antagonizing the h H2 receptors notably these medications exhibit High selectivity for the H2 receptors sparing histamine 1 or H1 receptors and do not exert anti-cholinergic effects additionally H2 blockers have a synergistic effect with H1 an ayamy medications commonly used to manage allergic reactions this additive effect proves beneficial in the treatment of severe allergic reactions including anaphylaxis on the other hand ppis act by suppressing gastric acid secretion through the inhibition of the hydrogen pottassium adinis triop phosphate system commonly known as the gastric proton pump this dual approach of H2 antagonists and ppis contributes to effective acid reduction safeguarding the gastrointestinal mucosa from potential damage ppis have gained widespread use globally due to their Superior efficacy compared to H2 blockers positioning them among the most extensively sold drugs worldwide fotene a preferred H2 antagonist distinguishes Itself by lacking significant hemodynamic effects and avoiding alterations in hepatic drug metabolism its safety profile potent inhibitory effect on gastric acid secretion and convenient dosing schedule contribute to its popularity on the other hand citadine another H2 antagonist has seen diminishing use over time as newer H2 antagonists with safer profiles and fewer drug interactions have become more favored in clinical practice among the ppis as meol stands out offering effective acid suppression with a well tolerated profile despite occasional side effects such as headache dizziness and GI symptoms like flatulence abdominal pain diarrhea and nausea this drug is generally well received in critical care settings pentool another ppi is frequently employed to prevent rebleeding in patients with peptic ulcer bleeds like other ppis this drug may lead to side effects such as headache and GI symptoms anti-ed medications designed to alleviate nausea and vomiting Encompass various specific classifications among them are antihistamines and anticholinergics which Target the medulla where nausea and vomiting are typically triggered as well as the vestibular system certain antihistamines such as mecline inhibit histamine activity in the vestibular system thereby suppressing medullary stimulus additionally anticholinergics like Scopolamine block acetylcholine receptors achieving a comparable suppressive effect both drug classes however share potential adverse reactions including sedation visual Acuity changes and a heightened risk of exacerbating narrow angle glaucoma another class dopamine antagonists effectively mitigates nausea and vomiting but comes with notable side effects such as substantial sedation orthostatic hypotension and extra peridial effects anderon classified as a selective 5 ht3 receptor antagonist exerts its antiemetic effects by selectively blocking serotonin acting both peripherally on fagal nerve Terminals and centrally on the chemo receptor trigger Zone its popularity stems from a notably low adverse effect profile with common side effects including headache fatigue and general Mala a tritide a synthetic peptide with actions akin to somata Statin boasts a longer and more clinically useful duration of action common side effects include sinus picardia chest pain itching ngi distressed droperidol functioning as a dopamine blocking agent in critical care serves as an anti-ed for both the treatment and prevention of nausea and vomiting in adults administered intravenously at doses ranging from 0.625 Mig to 1.25 mg every 6 hours it should be given slowly over 2 to 5 minutes notably this drug has QT prolonging effects rendering it contraindicated impatients with prolonged QTC intervals the pulmonary medications discussed in this section are primarily systemic drugs employed in the management of critical and life-saving Pulmonary conditions these medications address conditions such as pulmonary arterial hypertension refractory hypoxemia and ductal issues in neonates the systemic nature of these drugs implies that their effects extend far beyond the local pulmonary environment influencing various physiological processes throughout the body epoprostenol a vasodilator belonging to the protocy and prostag glanding classes serves as an inhibitor of platelet aggregation it finds application in the treatment of pulmonary arterial hypertension severe hypoxemia and acute right heart dysfunction Ty typically administered through intravenous infusion in adults and alternatively through nebulization in pediatric patients this drug has demonstrated comparable or Superior efficacy to inhal nitric oxide in adults adverse effects including nausea vomiting headache jaw pain hypotension and skin flushing may occur alprostadil a prostag Landon inv vasodilator plays a role in maintaining the pon ductus arteriosis in neonates with ductal dependent congenital heart disease it is also utilized in postoperative heart transplant patients to facilitate weaning from cardiopulmonary bypass the neonatal infusion initiates at 0.05 micrograms per kg titrated incrementally until a therapeutic response is achieved adverse effects such as apnea fever flushing hypotension and brto cardia are dose dependent and may occur in varying percentages among infants with congenital heart defects aerosolized epinephrine or rmic epinephrine functions as an alpha and betal Agonist and is employed for alleviating respiratory distress associated with conditions like Strider bronchitis lingula and upper Airway obstruction it is also effective in managing post exavation edema and cout administered via a small volume nebulizer the recommended concentration is 0.5 MLS of a 2.25% solution in 3 MLS of normal saline with effects expected within 1 minute anti-arrhythmic medications constitute a diverse group categorized by the Von Williams classification scheme which organizes them into classes 1 through four based on their impact on heart rhythms class one sodium channel blockers are further subdivided into 1 a 1 B and 1 c 1 a medications exemplified by procainamide increase the effective refractory period and often entail significant adverse reactions class 1B represented by lidocaine decreases the effective refractory period and action potential duration class 1 C suppresses phase zero repolarization particularly useful in managing life-threatening ventricular arrhythmias though these drugs are not routinely employed in critical care transport class two anti- rythmics or beta adrenic blocking agents antagonize beta receptors to inhibit stimulation with drugs like Lial law mopal La and esmolol serving various purposes in the treatment of arrhythmias hypertension and heart failure class three anti rythmics potassium channel blockers such as amiodarone are effective against re-entry tacac cardias and arhythmia resulting from excessive citability amone the most common in this class possesses both Pro rythmic and anti- rythmic properties properties necessitating careful dosing for different indications finally class 4 anti rythmics calcium channel blockers like Verapamil and deltm induce vasod dilation and negatively impact inotropy chronotropy and dmat tropy making them suitable for treating atrial tacki arhythmia in the critical care setting encounters often necessitate interventions related to blood clot management involving both thrombolytics and anti-coagulants thrombolytics are employed for the dissolution of blood clots a process crucial in addressing acute conditions such as stroke or myocardial infarction these agents work by activating plasminogen and plasmin leading to fibron Isis and clot breakdown on the other hand anti-coagulants are utilized to prevent the formation of blood clots a preventative strategy against thrombosis and thromboembolic events common anti-coagulants encountered in the critical care transport setting include heprin and werin anti-coagulant medications address various thrombotic conditions Hein a standard anti-coagulant functions by preventing the growth of existing thrombi without directly dissolving them administered through subcutaneous injection Central Venus or dialysis catheter installation or simply continuous infusion hein's dosing varies based on the specific indication with bleeding being a notable adverse event alop place a thrombotic agent is employed for conditions like acute esemicolonr infarction while the overall bleeding risk is low any serious Hemorrhage necessitates discontinuation of the drug and other anti-coagulants to nectop place another thrombolytic is a single dose weight-based intervention primarily used for stemi accompanied by potential adverse effects like reperfusion arrhythmias and bleeding glycoprotein Inhibitors act as antiplatelet agents during and after percutaneous coronary interventions and in the management of acute coronary syndrome bleeding is the most significant adverse event associated with these Inhibitors requiring careful consideration and consultation with medical control when discontinuation is contemplated for a risk benefit analysis these anti-coagulant medication and thrombolytics collectively contribute to the effective management of thrombotic conditions and critical care scenarios insulin is a vital medication employed for managing hypoglycemia especially in conditions like dka interventions to control hypoglycemia are typically initiated when blood glucose levels reach or exceed 180 milligrams per deciliter with the goal of maintaining it within the range of 140 to 80 mg per deciliter monitoring Protocols are designed to prevent hypoglycemia which has been linked to increased mortality feros amide a loop diuretic is employed to treat edema associated with conditions like heart failure hepatic or renal disease and act as an adjunct treatment for oliguria in severe renal impairment by inhibiting the reabsorption of sodium and chloride ions fermod promotes the excretion of sodium pottassium and excess water in the urine however high doses of feride can Elevate the risk of autotoxicity a concern that is exacerbated by two rapid Bolis injection bumetanide another potent Loop diuretic is often utilized when patients fail to respond to feros amide this drug can be administered as a continuous infusion just like feros amide typically at a rate of 0.5 to 2 milligrams an hour providing an alternative approach to address diuretic resistance in critical care scenarios" + }, + { + "Introduction": "Pain and suffering are not confined within hospital boundaries. Pain is a common complaint of patients cared for by EMS providers. It is estimated that 20% of the approximately 15 million patients transported by EMS annually in the United States experience moderate-to-severe pain. Although prehospital personnel are usually focused on the ABCs, the treatment of pain should be considered an important priority in the care of ill and injured patients. Most studies of EMS analgesia practices show that many patients with moderate-to-severe pain do not receive analgesia in the prehospital phase of their care. NAEMSP currently recommends that EMS systems have a policy to address prehospital pain management. The initial statement in NAEMSP position paper is, \u201cNAEMSP believes that the relief of pain and suffering of our patients must be a priority for every EMS system. Adequate analgesia is an important step for achieving this goal. NAEMSP believes that every EMS system should have a clinical care protocol to address prehospital pain management. Adequate training and education of prehospital personnel and EMS physicians should support the pain management protocol.\u201d Prehospital pain protocols should address the following issues. 1 Mandate for pain assessment 2 Tools for pain measurement 3 Indications and contraindications for prehospital pain management 4 Non-pharmacological interventions for pain management 5 Pharmacological interventions for pain management 6 Patient monitoring and documentation before and after analgesia 7 Transferring information to the receiving medical facility The challenge of treating pain in the prehospital setting is to use agents and techniques that are not only effective but safe and do not lead to physiological compromise or a delay in diagnosis upon arrival in the ED. Because of inordinate fears of and the desire to prevent side-effects, many EMS systems have opted for little or no use of pharmacological analgesics. Providing analgesia has been largely ignored in prehospital care education. Few EMS texts devote significant attention to this topic. Many systems do not have protocols to treat pain and suffering, other than that from ischemic chest pain. Many prehospital providers are frustrated by being unable to offer patients more than the \u201cbite the bullet\u201d approach to providing relief from acute pain. For those systems with reasonable analgesia protocols, the majority of patients are still untreated or undertreated. Many paramedic attitudes have been suggested as reasons for this inadequate treatment of pain. Prehospital pain management is a fertile area for study. Current research topics include barriers to prehospital analgesia, interventions to address barriers, non-opioid alternative analgesics (e.g. ketamine, IV acetaminophen), and alternative routes for pain relief, such as intranasal and transmucosal routes that can be used by basic providers as well as field-based ultrasound-guided nerve blocks that can be useful in wilderness settings or in prolonged extrications.", + "Literature review": "Several studies have shown that oligoanalgesia is more the rule than the exception in prehospital care. One of the most dramatic studies was performed by White et al. in the city of Akron in the late 1990s. At that time, the EMS system had standing orders for either the administration of morphine sulfate, 2\u20135 mg IV push, or nitrous oxide, 50% self-administered. During the study period, 1,073 patients with suspected extremity fractures were identified. Of this large number of patients, only 18 received analgesia: 16 patients received nitrous oxide and two received morphine. McEachin reported on several different EMS agencies transporting patients to a single hospital in Michigan. Of 124 patients suspected of having lower extremity fractures, only 22 (18.3%) received parenteral analgesia. Many of these patients (38.4%) were triaged from an ALS response to a BLS transport. Hennes et al. reported results from prehospital analgesia practice in Milwaukee where a review of 5,383 patients with acute pain showed that morphine was administered in only 258 patients (4.8%). Of those patients with extremity fractures, 37 of 351 (10.5%) received morphine, and morphine was given to only seven of 258 children (3.0%). In patients with burn injury, 16 of 130 (12.3%) received morphine; only one of 12 children received it. Similar findings showing lack of analgesic administration or oligoanalgesia have been replicated in other studies. The benefits of prehospital analgesia are not only physiological. It improves the perception of quality of care provided by EMS. One study showed that 80% of patients reported the overall quality of EMS care to be excellent when they rated their pain management as excellent. Prehospital analgesia also dramatically decreases the time-to-analgesic administration, ranging from 60 to 120 minutes earlier, when compared to analgesic administration being deferred to the emergency department. Evans made the poignant statement, \u201cTo allow a patient to suffer unnecessary pain does harm to the patient \u2013 a violation of the first ethical principle of medicine.\u201d In a 1999 editorial, the late Peter Baskett states, \u201cThe blame for \u2018oligoanalgesia\u2019 must be laid at the door of physicians in authority who have, through ignorance, underplayed the physiologic and psychological benefits of analgesia and overplayed the potential of deleterious side effects of agents that are commonly available.\u201d", + "Opioids": "Opioids are the best class of pharmacological agents to treat acute pain in all areas of medicine, including the prehospital environment. (See Box 67.1 for a list of desirable characteristics, most but not all of which are found in the opioids.) Osler referred to opioids as God\u2019s own medicine. The properties that make opioids desirable in the field include rapid onset, high potency, titrateability, relative safety, and reversibility. Morphine sulfate has been used for ischemic chest pain in the field for the past three decades. Over the past several years, fentanyl has gained increased usage. In many EMS systems, it is now the most commonly used opioid for non-cardiac pain. In emergency departments and in the field, it is increasingly replacing morphine for myocardial ischemia and chest pain. For many types of pain, opioids can be titrated by the IV route to produce safe and effective analgesia and can be administered by the intramuscular and intranasal routes as well. One of the major benefits of opioids is that most side effects can be rapidly reversed with an opioid antagonist, such as naloxone, which is carried by most EMS systems for use in opioid overdoses. With all opioids, EMS systems must adhere to Food and Drug Administration guidelines for monitoring and documenting possession and use. Specialized critical care transport teams seem to provide analgesia and achieve significant pain relief more frequently than described in routine ground-based EMS systems.", + "Fentanyl": "Fentanyl has several properties that make it well suited for prehospital use. It is one of the only opioids that does not cause a release of histamine, thereby preventing potential exacerbation of reactive airway disease, and reducing the chance of inducing significant hemodynamic changes. Fentanyl is very lipid soluble, and it crosses the blood\u2013brain barrier quickly, reaching its peak effect within a few minutes. Its half-life is shorter than most other opioids with a duration of action less than 1 hour. Fentanyl does not cause any decrease in cardiac contractility. Like all opioids, however, it can decrease sympathetic tone and if a patient\u2019s blood pressure is dependent on the sympathetic nervous system, fentanyl can cause some hypotension, but this is relatively uncommon. Kanowitz reported on the use of fentanyl in 2,129 prehospital patients with an average titrated dose of 118 \u03bcg, with a range of 5 to 400 \u03bcg. Only 12 patients had any vital sign abnormalities during the drug\u2019s duration of action, and most of these were relatively minor, with only one patient receiving naloxone reversal. This one patient was an 83-year-old woman with a hip fracture who received two doses of 100 \u03bcg fentanyl and had some respiratory depression while in the ED that was immediately reversed with 0.4 mg of naloxone without any adverse effects. There were no significant complications or deaths as a result of prehospital use of fentanyl. The authors concluded that fentanyl effectively decreased pain scores without causing significant vital sign changes, thereby allowing it to be used safely and effectively for prehospital pain management. Several studies have also been reported showing the safe and effective use of fentanyl in ground and air transport of adult and pediatric patients. Fentanyl has a short half-life and duration of action of 60 minutes or less. Opioid-induced hypotension is rare with fentanyl, but in patients who are only able to maintain normal systemic pressure due to extreme sympathetic drive, fentanyl can blunt the sympathetic response and theoretically lower blood pressure. Should this occur, fluid administration is typically all that is needed, but alpha-adrenergic agents can be used to help to restore blood pressure. The safe and effective use of oral transmucosal use of fentanyl has been described in the battlefield setting. Fentanyl also has been used via the intranasal route through an atomizer device. In some systems, fentanyl is replacing morphine as the opioid of choice for ischemic cardiac chest pain.", + "Morphine": "Morphine has been widely used in EMS systems for the past three decades. Initially it was largely restricted to the treatment of ischemic cardiac pain, but its indications have expanded to a wide variety of pain states. Despite the potential for a multitude of side-effects related to the prehospital use of morphine, the literature does not suggest that these have been a major clinical issue. Morphine has the advantage of having a wide margin of safety when it is used in careful IV titrated fashion. It is safe in patients with liver disease and for acute pain and can be used safely in renal disease. Morphine does not decrease cardiac contractility but does decrease preload and afterload and therefore should be used with caution in any patient who has borderline or frank hemodynamic instability. It is important to titrate the dose to the analgesia accomplished.", + "Opioid agonist-antagonists": "Some characteristics of the opioid agonist-antagonist class of analgesics make them ideally suited for prehospital use. Drugs in this group include nalbuphine and butorphanol. The primary benefits of this class are the ceiling on respiratory depression, minimal euphoria and limited abuse potential, lack of biliary spasm, and minimal hemodynamic effects. Stene et al. described the prehospital use of nalbuphine in 46 patients with moderate-to-severe pain due to multiple trauma, burns, fractures, and intraabdominal conditions. The agent was partially to completely effective in 89% of patients and was without any major untoward effects. Nalbuphine also causes very minimal, if any, hemodynamic changes. Since that early study, others have confirmed the value of IV nalbuphine in the field. Another advantage of this drug is that it is not a controlled substance, easing some of the paperwork required when using morphine. Butorphanol is now available as a nasal spray. This agent and route of administration have many theoretical benefits in the prehospital environment, but studies have yet to be reported on the field use of nasal butorphanol. The use of the agonist-antagonist class of analgesics in the field may result in patients in the ED requiring somewhat higher doses of pure opiate agonists to achieve adequate analgesia.", + "Nitrous oxide": "Nitrous oxide-oxygen mixtures fulfill many of the properties desired for a prehospital analgesic. Several field studies have demonstrated the safety and efficacy of self-administered 50% nitrous oxide in prehospital care. All studies have confirmed that the majority of patients with moderate-to-severe pain from a variety of sources will achieve significant pain relief. In unpublished data from use in the city of Pittsburgh in the past two decades, over 4,000 patients have been treated without any significant major adverse effects. Significant analgesia is achieved in approximately 80% of patients. In a rural EMS system, a nitrous oxide-oxygen mixture led to pain relief in 85% of patients for which it was used. One of the major advantages of the use of nitrous oxide is that it is relatively devoid of serious side-effects. Its major side-effect has been nausea, noted in four patients in a study by Ducasse et al., which also found that numerical rating scores decreased significantly with use of a nitrous oxide-oxygen mixture. In 1994, an alert entitled \u201cControlling exposure of nitrous oxide during anesthetic administration\u201d provided guidelines to prevent environmental levels from exceeding their recommended standards. In a moving vehicle, or one with a fan, short-term administration should be safe for the providers, although well-designed protocols must be written and followed when using this gas mixture. A prototype of a nitrous oxide protocol is shown in Box 67.2; it includes the absolute and relative contraindications to nitrous oxide administration. Recently, Australian authors conducted a systematic review of the safety literature related to the use of 50% nitrous oxide. They identified 12 randomized clinical trials investigating the use of 50% nitrous oxide compared with placebo. They conclude, \u201cNitrous oxide at a concentration of 50% is an effective and safe form of analgesia. The side effect profile of this agent suggests that it could be used by adequately trained laypersons in the prehospital setting. The question of nitrous oxide use by basic EMTs or by even lesser trained individuals such as rescue teams or ski patrol is a legitimate question, particularly in parts of the world where there is a dearth of prehospital advanced life support personnel.", + "Ketamine": "Ketamine is a dissociative anesthetic that is structurally related to phencyclidine, and it has some unique properties. The dissociative state produced by ketamine is characterized by analgesia and amnesia, while preserving airway protective reflexes. Because ketamine is a bronchodilator, it can be used to treat severe asthma. It can be used as a field anesthetic for unusual situations, such as field amputations, dislocation reductions, or prolonged or complicated extrications. It has also been described as a useful agent for field surgical procedures during disasters, especially among children.\n\nAlthough this agent has had little indication for routine prehospital use, recently, at subdissociative dosages, it has been studied as a primary analgesic agent. The intranasal administration of S-ketamine has been described in Scandinavia. It has also been studied as an adjunct agent to decrease the dose of opioid needed to achieve pain relief in the emergency department. Polomano and others describe the use of low-dose IV ketamine in patients with pain from complex combat injuries, showing it to be safe and effective.", + "Non-steroidal antiinflammatory agents": "Currently, few EMS systems routinely use aspirin or other nonsteroidal antiinflammatory (NSAID) drugs. Aspirin is now the standard of care as an antiplatelet drug in the treatment of acute coronary syndrome by field personnel, but rarely is aspirin used for pain management. NSAIDs are particularly well suited for treatment of ureteral and biliary colic. These drugs may also potentiate the analgesic action of opiates.\n\nAlthough these agents do not work as quickly as opiates, if given at the scene they will frequently have beneficial effects before the patient arrives at the hospital and definitely before the time that analgesic agents will be administered in the hospital. These agents should not be considered as a substitute for opiates and nitrous oxide but as another helpful adjunct with selected indications. The major side-effects to consider with a single-dose use in the field would be allergic reactions and platelet inhibition. They should therefore be withheld in the field if the patient has known allergies to NSAIDs or if the anti-platelet effect may exacerbate an underlying problem.", + "Acetaminophen": "Acetaminophen is rarely carried on ambulances or used in the prehospital setting. Acetaminophen, like the NSAIDs, is an effective analgesic, especially in combination with opioids. One potential side-effect, although not likely after a single dose in the field, is the exacerbation of asthma. It is also well known to precipitate acute hepatic failure in patients with underlying liver disease or as a cumulative dose. A single dose in the field is unlikely to lead to acute hepatic failure, but caution would still be advised in these patients. Intravenous acetaminophen is increasingly being used in the hospital and has been studied in the postoperative setting.", + "Communication techniques": "The most ignored aspect of providing prehospital relief to those with pain and suffering is the powerful effects that can result from therapeutic communication techniques. These techniques can be mastered by all providers and can bring a significant degree of comfort to patients without use of pharmacological agents. Jacobs points out that many patient responses to an injury or illness are occurring at an unconscious level and that every word, phrase, sentence, pause, voice inflection, and gesture can initiate automatic psychophysiologic effect. An example of a suggested dialogue for a patient with burns is as follows. I'll bet you can imagine some place you'd rather be than here. As a matter of fact, go ahead and do that now while we get you bandaged up. Think of your favorite place. When you are there in your mind's eye, look around and notice all the things there are to notice. Listen to the sounds. Feel the good feelings. There might even be a special aroma you can smell. When you are really experiencing that place, let me know by raising your index finger. Good. Although many prehospital providers may feel uncomfortable with guided imagery techniques such as this, they all should recognize the powerful implications of their verbal and non-verbal communication. Providers should be capable of engaging patients in a way that distracts them from their injury or illness. Distraction can also be very helpful while prehospital providers are performing potentially painful interventions, such as starting an IV line or splinting a fracture. Music has been shown to be effective in decreasing the pain of laceration repair in EDs and could be adapted for use on an ambulance. Words should be chosen carefully when communicating; mild discomfort is more useful than terms such as bee sting, prick, or shot.", + "Assessment of pain": "Objective assessment of pain can be difficult because it is a subjective symptom. The degree of pain cannot be gauged simply by observing vital signs or facial expressions. The pain literature repeatedly documents the unreliability of both vital signs and facial expression in assessing the severity of pain. For pediatric patients, EMS providers often underestimate pain. However, easy-to-use tools are available for adult and pediatric patients that are based upon patient self-report. According to NAEMSP position statement \u201cPrehospital pain management,\u201d self-report scales are \u201cthe most reliable indicator of pain.\u201d These scales allow not just the quantification of pain at one point in time, but also for monitoring the change in the level of pain over time and after analgesic administration. A helpful technique is to use a 1\u201310 (\u201cno pain\u201d to \u201cunbearable pain\u201d) numerical rating scale (NRS), which is a completely verbal scale. This scale is very easy to use for patients who can speak and are fluent in the same language as the prehospital provider. Alternative scales include the verbal rating scale (VRS) and visual analog scale (VAS). These scales require printed diagrams so are more cumbersome. However, they can be useful for patients who are unable to speak or who are fluent in languages other than that of the prehospital provider. The instructions and diagrams for these two scales can be preprinted in any language. The VRS has five listed pain levels and the patient is asked to pick the one that describes his or her pain. The VAS has a line that is 100 mm long, with \u201cno pain\u201d listed on the left and \u201cmaximal pain\u201d written on the right. The patient is asked to indicate where along the line his or her own pain level lies. According to \u201cPrehospital pain management,\u201d one-dimensional pain scales that can be used for pediatric patients include the Color Analogue Scale (in which colors indicate the intensity of pain) and the Faces Pain Scale (in which cartoon facial expressions indicate the intensity of pain). The Faces Pain Scale also may be useful for non-English-speaking patients or those with limited English comprehension skills.", + "Pitfalls": "The major pitfall regarding analgesia is the attitude that it should not be provided in the field but should wait for hospital evaluation. Safe and effective prehospital pharmacological analgesia should be delivered as soon as possible and non-pharmacological techniques are appropriate for the majority of patients with pain. These techniques will not \u201cmask\u201d the diagnosis or worsen the patient\u2019s condition. Pain is subjective and should be measured by the patient\u2019s words and not expectations of how much a patient should be suffering for a given condition. Another pitfall is to believe that there is a \u201cuniform\u201d dose of analgesic that will bring elimination of pain when using pharmacological therapy. Particularly with the use of opioids, there is tremendous interpatient variability. The best way to approach pain control is to titrate the medication, monitoring for side-effects and efficacy, until the desired result is reached. A particularly common pitfall is the belief that the degree of pain can be gauged by vital signs or facial expressions. The pain literature repeatedly documents the unreliability of either vital signs or facial expression in assessing the severity of pain. The only scale that should be used is verbal expression. A helpful technique to use is a 1\u201310 verbal analog scale, with 10 representing the worst pain the patient has ever experienced. For pediatric patients, using other methods, EMS providers underestimate pain. Another pitfall is to fail to distract the patient while performing painful procedures. Just the opposite usually occurs, with the provider calling attention to every step of the procedure, using terms that are intended to soften the insult but usually actually magnify it. Studies have identified many barriers to prehospital analgesia. These include lack of \u201csignificant objective signs,\u201d concern for malingering, aiming simply to \u201ctake the edge off,\u201d and concern about administering dosages of morphine greater than 5 mg. Specifically in pediatric patients, unfamiliarity with pediatric patients and protocols, insufficient education in pediatrics, difficulty in medication administration in uncooperative pediatric patients and inability to assess pain in children have been reported as barriers to analgesia. Protocol changes have been attempted as a means to improve prehospital analgesia rates by removing protocolized barriers, such as the need for a medical oversight order or restrictive assessment categories (e.g. only allowing analgesics for extremity injury or cardiac chest pain). Removing the need for medical oversight order has been found to increase time to analgesic administration. Neither of these protocol changes has been shown to increase the number of patients receiving analgesia to any clinically important amount. The lack of efficacy of these changes is not surprising considering that they do not address the identified barriers to prehospital analgesia. However, educating prehospital providers about pain management may be a more efficacious route to improving prehospital analgesia because such interventions can address the barriers to analgesia. This has been proven to be the case in multiple studies, showing improved understanding of pain management principles and a significant improvement in prehospital pain treatment after educational interventions.", + "Conclusion": "Treating acute pain and relieving suffering should be a primary mission of all health care providers. Unfortunately, EMS personnel have not been given the tools or training to satisfactorily accomplish this worthy goal. Although patient \u201csafety\u201d and \u201cdoing no harm\u201d must always be considered, these should not be used as excuses for \u201cdoing no good\u201d for patients with acute pain treated in the field." + }, + { + "Entonox Mnemonics": "The cheat sheet outlines contraindications and cautions for administering Entonox. Contraindications include inability to comply, decompression sickness, altered level of consciousness, pneumothorax, air embolism, inhalation injury, and nitroglycerin administration within the last five minutes. Cautions involve shock, abdominal distension, depressant drugs, COPD, and facial injuries. The mnemonic C-D-C-P-A-I-N helps remember the contraindications, while S-A-D-C-F reminds of the cautions. Precautions require monitoring to ensure Entonox does not exacerbate existing conditions. Two precautions indicate contraindicated use.", + "Entonox Administration": "Entonox is indicated for significant pain. Before administration, contraindications must be ruled out using the mnemonic C-D-C-P-A-I-N. Precautions such as shock, abdominal distension, depressant drugs, COPD, and facial injuries need to be noted. Proper storage includes not leaving the bottle unused over long periods, not storing below -6 Celsius, and storing horizontally. Instructions to patients include self-administration using a mask/bite valve, inhaling through the bite valve, and stopping at any time if adverse effects are felt. After discontinuing Entonox, supplemental oxygen with a non-rebreather mask at 15 lpm is provided. For cardiac chest pain, Entonox can be considered if nitroglycerin is contraindicated and has not been administered in the past five minutes." + }, + { + "Salbutamol (Ventolin) Administration \u2013 Nebulizing Mask": "This section provides detailed instructions for administering Salbutamol (Ventolin) via nebulizing mask. It outlines the indications for use, which include shortness of breath associated with bronchospasm, such as asthma, bronchitis, emphysema, and COPD. Contraindications include known hypersensitivity to salbutamol and hemodynamically significant tachycardia. The dose varies based on age: 5 mg in 5 ml of solution for those over 1 year old, repeated every 10 minutes when each dose is finished; 2.5 mg in 2.5 ml of solution for those under 1 year old, also repeated every 10 minutes when each dose is finished. Confirmation steps include ensuring indications are met, ruling out contraindications, documenting vital signs, and auscultating the chest. Preparation involves ensuring the salbutamol ampules are not expired, twisting off the top of the ampule, squirting the appropriate amount into the nebulizer well, attaching oxygen tubing, and turning up the O2 flow meter until medication begins to mist out of the mask (usually at 6-10 lpm). Administration requires placing the nebulizer over the patient's mouth and nose and instructing them to breathe as slowly and deeply as possible. After the medication is finished or after 10 minutes, reassess the patient and repeat the dose as appropriate. Documentation includes recording the medication name, dose, time, route, and effects. Notes emphasize that patients in respiratory distress require urgent transport, and transport may be deferred long enough to administer the first dose of Salbutamol on scene as a critical intervention, but significant delays should be avoided." + }, + { + "Ibuprofen Administration": "This cheat sheet provides guidelines for administering ibuprofen, a nonsteroidal anti-inflammatory drug (NSAID), for mild to moderate pain relief. It outlines the indications for use, which include pain management, and lists contraindications such as hypersensitivity to ibuprofen or other NSAIDs, active gastrointestinal hemorrhage or ulcers, and pregnancy during any trimester. The dosage varies by age group; adults aged 11 years or older can take 300-400 mg orally every 4-6 hours, with a maximum daily dose of 1200 mg. Pediatric patients up to 10 years old should receive 10 mg/kg orally, repeating once after 6 hours, with a maximum daily dose of 40 mg/kg/day. Before administration, it's crucial to confirm that the indications are met and contraindications are ruled out, document vital signs, ensure the medication is not expired, and confirm the correct dosage. The medication should be swallowed, with a small sip of water if necessary, and responders may need extra assistance for pediatric patients. Documentation should include the medication name, dose, time, route, and effects. It's noted that mild to moderate pain is subjective and that ibuprofen can be used concurrently with acetaminophen for analgesia." + }, + { + "Epinephrine Administration \u2013 Intramuscular Injection (IM)": "This section provides guidelines for administering epinephrine intramuscularly. Indications include anaphylaxis, signs of anaphylaxis, history of allergic response, exposure to allergen, and unstable conditions such as DLOC or systolic blood pressure less than 90 mmHg or respiratory distress. There are no absolute contraindications to epinephrine use in life-threatening situations like anaphylaxis. The dose varies by age: adults (11 years or older) receive 0.5 mg in 0.5 ml of 1:1000 solution, up to 3 doses total as needed; pediatric patients (up to 10 years old) receive 0.01 mg per kg of body weight in 1:1000 solution, with a maximum of 0.5 mg per dose, also up to 3 doses total as needed. Confirmation involves ensuring indications are met, ruling out contraindications, documenting vital signs, and auscultating the chest for at least six points. Preparation includes exposing the injection site (deltoid or thigh), cleaning the area with an alcohol swab, ensuring the 1:1000 epinephrine hydrochloride is not expired, calculating the desired dose, removing the top/cover from the ampule/bottle, holding the ampule/bottle upright, inserting the needle, drawing the solution into the syringe, removing the needle from the bottle, and tapping the syringe to expel air. Administration involves stretching the injection site skin using the Z-track technique, inserting the needle at a 90-degree angle to the skin, and injecting the medication into the muscle. Documentation requires recording the medication name, dose, time, route, and effects. Notes emphasize that patients with decreased responsiveness require urgent transport, and transport may be deferred long enough to administer the first dose of epinephrine on scene as a critical intervention, but significant delays in transport should be avoided." + }, + { + "Naloxone (Narcan) Administration": "This cheat sheet provides detailed instructions on administering Naloxone (Narcan) for suspected opioid overdose or poisoning. Indications include decreased level of responsiveness, inadequate or absent respirations, and pinpoint pupils. Contraindications include confirmed medical allergy to Naloxone. The adult dosage is administered in four doses: 0.4 mg, 0.4 mg, 0.8 mg, and 2.0 mg. Pediatric dosages are calculated based on body weight, with a maximum of 2.0 mg per dose and a maximum of four doses. Prior to administering the first dose, priority is given to other life-saving measures such as assisted ventilations and CPR. It is important to collect SAMPLE information and take a full set of vital signs. Preparation involves cleaning the injection site with an alcohol swab, checking the ampoule for clarity, expiration date, dose, and type of medication, breaking the ampoule open at the neck, and drawing the entire contents into a syringe. During the injection, the needle should be inserted at a 90-degree angle into the muscle and all medication should be injected. After the injection, the needle should be retracted and covered, and the syringe and ampoule disposed of in a sharps container. The administration schedule is every three minutes as needed to reverse respiratory depression, with a maximum of four doses. Transport should be initiated after the first dose if appropriate." + }, + { + "Epinephrine Administration \u2013 Auto-Injector (Epi-Pen)": "This section provides guidelines for administering epinephrine using an auto-injector (Epi-Pen) in emergency situations. Indications include anaphylaxis, signs of anaphylaxis, history of allergic response, exposure to allergens, and unstable conditions such as respiratory distress or systolic blood pressure less than 90 mmHg. There are no absolute contraindications to epinephrine use in life-threatening situations like anaphylaxis, but neither Epi-Pen nor Epi-Pen Jr. are appropriate for patients under 14 kg. Dose recommendations vary based on the patient's weight: for those over 30 kg, use an adult Epi-Pen (0.3 mg), with up to 3 doses total as needed; for those between 14 and 30 kg, use an Epi-Pen Jr. (0.15 mg), also with up to 3 doses total as needed. Confirmation involves ensuring indications are met, ruling out contraindications, documenting vital signs, and auscultating the chest. Preparation includes checking the auto-injector for expiration, examining the fluid inside, and explaining the procedure to the patient. Administration involves removing the safety cap, firmly pushing the tip against the middle third of the patient\u2019s outer thigh, holding the auto-injector in place for up to 10 seconds, and rubbing the injection site for up to 30 seconds to promote absorption. Documentation requires recording the medication name, dose, time, route, and effects. Notes emphasize the urgency of transporting patients in respiratory distress and the importance of timely transport, even if the first dose of epinephrine is administered on scene." + }, + { + "Acetaminophen Administration": "This section provides guidelines for administering acetaminophen, a medication used for mild to moderate pain relief. It outlines the indications for use, which include pain management, and lists contraindications such as hypersensitivity to the drug or its components, severe alcoholic hepatitis, liver dysfunction with active alcohol consumption, acute liver injury, and acetaminophen-induced liver disease. The dose varies based on age and weight. For adults aged 11 years or older, the dose is 15 mg/kg PO (parenteral), up to a maximum of 1000 mg, typically available in 500 mg or 1000 mg tablets. Doses can be repeated once after 4 hours, with a 24-hour maximum of 3000 mg. In patients with suspected or known liver dysfunction, the 24-hour maximum is lowered to 1000-2000 mg. For pediatric patients under 10 years old, dosing is 15 mg/kg PO using liquid preparation for those under 30 kg, 500 mg PO for those between 30 kg and 50 kg, and 500-1000 mg PO for those over 50 kg. Dosing may be repeated once after 4 hours, with a 24-hour maximum of 75 mg/kg or 1000 mg. For patients under 12 years old, no more than 5 doses should be given within 24 hours. The instructions for administration include ensuring the medication is not expired, confirming dosage, and documenting the medication name, dose, time, route, and effects. Notes indicate that mild to moderate pain is subjective and that acetaminophen can be used concurrently with ibuprofen for analgesia." + }, + { + "Salbutamol (Ventolin) Administration \u2013 Metered Dose Inhaler (MDI)": "This section provides detailed instructions on administering Salbutamol (Ventolin) using a Metered Dose Inhaler (MDI) for patients experiencing shortness of breath associated with bronchospasm, such as asthma, bronchitis, emphysema, and COPD. The indications include conditions like asthma, bronchitis, emphysema, and COPD. Contraindications include hypersensitivity to salbutamol, hemodynamically significant tachycardia, and patients under 10 kg. One MDI spray contains 100 micrograms (mcg), which can also be expressed as 0.1 milligrams (mg). For adults aged 11 years or older, the dose is 4 x 100 mcg per course, with repeat doses as needed. For pediatric patients up to 10 years old weighing less than 10 kg, the dose is not applicable (n/a). For those between 10-20 kg, the dose is 5 x 100 mcg per course, with repeat doses up to 3 times as needed. For patients over 20 kg, the dose is 10 x 100 mcg per course, with repeat doses up to 3 times as needed. Confirmation involves ensuring the indications are met and contraindications are ruled out, documenting vital signs, and auscultating the chest (minimum of 6 points). Preparation includes ensuring the MDI is not expired, shaking the inhaler, removing the cap, placing the mouthpiece into a spacer, and removing the cap from the spacer. Administration involves having the patient tilt their head back slightly, breathe out slowly and completely, place the mouthpiece into their mouth, press down on the inhaler to spray medication into the spacer, and instruct the patient to start breathing in and out slowly. The process is repeated to the appropriate dose, removing the inhaler after each spray to shake it and reinserting it for the next spray/breath. Documentation requires recording the medication name, dose, time, route, and effects. Notes emphasize that patients in respiratory distress require urgent transport, and transport may be deferred long enough to administer the first dose of Salbutamol on scene as a critical intervention, but significant delays in transport should be avoided." + }, + { + "Glucogel Administration - Parenteral": "The Glucogel protocol is engaged when there is suspected Hypoglycemia with a decreased level of responsiveness and the patient appears capable of maintaining their own airway. Indications include CapBgl < 4mmol and the patient being capable of following instructions and maintaining their own airway. There are no contraindications listed. The dose is 12-15 g glucogel (half of a 30 g tube), administered every 5 minutes up to 4 doses. Consultation with medical supervision is required before exceeding 4 doses. Confirmation involves ensuring indications are met and contraindications are ruled out, documenting vital signs including CapBgl. Administration includes self-administration by the patient of 15 g Glucogel, with other sugars/juice/oral carbohydrates potentially being appropriate. Documentation requires recording the medication name, dose, time, route, and effects. Transport is urgent for patients with a decreased level of responsiveness, though transport may be deferred long enough to administer the first dose on scene as a critical intervention. Additional doses involve remeasuring CapBgl every 5 minutes, applying another 15 g of Glucogel if still below 4 mmol/L, and repeating up to 4 doses (2 tubes) before consulting Medical Supervision." + }, + { + "Common Units of Measurement": "This section lists common units of measurement used in healthcare, including Millimeters of Mercury (mmHg) for blood pressure, Millimoles per Litre (mmol/L) for blood glucose levels, Milligrams (mg) for medications like ASA and Nitro, Litres per minute (lpm) for oxygen flow rates, Drips per millilitre (gtts/ml) for dripset size, and Drips per minute (gtts/minute) for the number of droplets through the dripset in one minute.", + "Assisted Ventilations": "This section outlines assisted ventilation rates for adults and children/infants based on specific respiratory issues. For adults, the ventilation rate is 1 breath every 5-6 seconds when respirations are absent but a pulse is present, greater than 30 breaths per minute, less than 10 breaths per minute, or signs of hypoxia or respiratory distress. For children/infants, the rate is 1 breath every 3-5 seconds under similar conditions. Ventilations are timed between or with the patient's own breaths, and OPA/NPA can be used after the first two successful ventilations.", + "Weight Estimation for Pediatric Patients": "This section provides an age-based weight estimation formula for pediatric patients up to 10 years old: 2 times the age in years plus 8 equals the estimated weight in kilograms. It notes that parent or caregiver estimations are generally more accurate than age-based calculations.", + "A-T-M-I-S-T A-M-B-O": "This section details the verbal handover process using the mnemonic ATMIST and AMBO. ATMIST includes Age, Time, Mechanism, Injuries, Signs, and Treatment, which are the details to mention during the verbal handover. AMBO covers Allergies, Medication, Background, and Other Information, also to be included in the verbal handover." + }, + { + "Glucagon Administration \u2013 Intranasal (IN)": "This section outlines the protocol for administering Glucagon intranasally when there is suspected Hypoglycemia or Unresponsive Newborns/Infants (NYD) who are incapable of maintaining their own airway. Indications include a CapBgl less than 4mmol/L, being over 4 years old, and being incapable of following instructions or maintaining their own airway. Contraindications include known hypersensitivity to glucagon and pheochromocytoma (a tumor on the adrenal gland). The dose for the intranasal spray is 3 mg, which must be administered only once and requires the patient to be over 4 years old. Confirmation involves ensuring the indications are met and contraindications are ruled out, documenting vital signs including CapBgl. Preparation includes checking the glucagon package for compromise or expiration, removing the packaging, opening the lid, and removing the device. Administration involves holding the device between fingers and thumb, placing the nozzle tip into the nostril approximately 3/4\" into the nose, firmly depressing the plunger until the green line disappears, and then removing the device. Documentation should include the medication name, dose, time, route, and effects. Transport notes emphasize the urgency of transporting patients with decreased responsiveness, deferring transport long enough to administer Glucagon on scene as a critical intervention but avoiding significant delays. Responders must ensure indications are met, contraindications are ruled out, and vital signs including CapBgl are documented prior to the first dose. Effects of Glucagon include initiating the release of glycogen stored in the liver into the bloodstream, taking 8-10 minutes for effects to become evident, and potentially minimal effects if the patient does not have sufficient glycogen stores. It is advised not to delay transport to see if the patient responds positively." + }, + { + "Administration of Medications vs Assisting with Medications": "BC EMALB licensed responders administer specific medications such as Entonox, Oxygen, Nitroglycerin, Acetylsalicylic Acid/ASA, Glucagon, Glucogel, Naloxone/Narcan, Salbutamol/Ventolin, Epinephrine by Auto-Injector, Epinephrine by IM Injection, Acetaminophen, and Ibuprofen, adhering to specific administration protocols. If a patient requires any other medications, responders may assist the patient while following the six rights of medication: Person, Medication, Time, Dose, Route, and Documentation.", + "RTC Critical Interventions Requiring History and/or Vital Signs": "Some patients may be RTC (Rapid Transport Candidate), but critical interventions require secondary information before transport. For ASA for cardiac chest pains, the required information includes indications/contraindications (SAMPLE-OPQRST) and a full set of vital signs. For Naloxone by intramuscular injection for opioid overdose, the required information includes indications/contraindications (SAMPLE-OPQRST) and a full set of vital signs. For Glucagon by intramuscular injection to correct hypoglycemia, the required information includes indications/contraindications (SAMPLE-OPQRST) and a full set of vital signs. For Glucagon by intranasal injection to correct hypoglycemia, the required information includes indications/contraindications (SAMPLE-OPQRST), patient age, and a full set of vital signs. For Epinephrine by auto-injector for anaphylaxis, the required information includes indications/contraindications (SAMPLE-OPQRST), patient age/estimated weight, and a full set of vital signs including chest auscultation. For Epinephrine by weight-based intramuscular injection for anaphylaxis, the required information includes indications/contraindications (SAMPLE-OPQRST), estimated patient weight, and a full set of vital signs including chest auscultation. For Salbutamol for bronchospasm, the required information includes indications/contraindications (SAMPLE-OPQRST), estimated patient weight, and a full set of vital signs including chest auscultation. For Nitroglycerin for cardiac chest pains, the required information includes indications/contraindications (SAMPLE-OPQRST) and a full set of vital signs including chest auscultation." + }, + { + "Glucagon Administration \u2013 Intramuscular (IM)": "This section outlines the protocol for administering glucagon intramuscularly when there is suspected hypoglycemia or unresponsive non-yet diagnosed diabetic (NYD) condition, and the patient is incapable of maintaining their own airway. Indications include a capillary blood glucose level less than 4 mmol/L and the patient being incapable of following instructions or maintaining their own airway. Contraindications include known hypersensitivity to glucagon and pheochromocytoma (a tumor on the adrenal gland). The dose varies based on the patient's weight: 0.5 mg for patients under 25 kg and 1.0 mg for those 25 kg or more. The confirmation step involves ensuring the indications are met and contraindications are ruled out, documenting vital signs including capillary blood glucose levels. Preparation includes exposing the injection site (deltoid or thigh), cleaning the area with an alcohol swab, ensuring the glucagon is not expired or non-viable, removing the flip-off seal, and injecting the entire contents of the syringe into the glucagon bottle without removing the plastic clip. The solution should be swirled gently until dissolved completely, ensuring it is clear and has a water-like consistency. Using a syringe, the bottle is held upside down, and the needle tip remains in the solution while all the solution (1 mL mark on the syringe) is withdrawn. The needle is then removed, bubbles are expelled, and the syringe is flicked/tapped to ensure only medication is left. Administration involves stretching the injection site skin using the Z-track technique, inserting the needle at a 90-degree angle to the skin, and injecting the medication into the muscle. Documentation requires recording the medication name, dose, time, route, and effects. Transport notes emphasize the urgency for patients with decreased responsiveness, allowing transport to be deferred long enough to administer glucagon on scene as a critical intervention but avoiding significant delays. Effects of glucagon include initiating the release of glycogen stored in the liver into the bloodstream, which may take 8-10 minutes to become evident. Effects can be minimal if the patient does not have sufficient glycogen stores in their liver, and transport should not be delayed to see if the patient responds positively." + }, + { + "National EMS Education Standard Competencies": "Pharmacology\nApplies fundamental knowledge of the medications that the EMT may assist/administer to a patient during an emergency. Principles of Pharmacology\nMedication safety\nKinds of medications used during an emergency Medication Administration\nSelf-administer medication\nPeer-administer medication\nAssist/administer medication to a patient Emergency Medications\nNames\nEffects\nActions\nIndications\nContraindications Emergency Medications (cont\u2019d)\nComplications\nRoutes of administration\nSide effects\nInteractions\nDosages for the medications administered", + "Introduction Medications are an important intervention.": "Medications may alleviate pain and improve the patient\u2019s condition.\nFailure to administer medications safely and competently can lead to serious consequences for the patient, including death.", + "How Medications Work": "Pharmacology is the science of drugs.\nA medication is a substance used to:\nPrevent or treat disease\nRelieve pain\nPharmacodynamics is a process by which medication works on the body. Agonist: causes stimulation of receptors\nAntagonist: binds to a receptor and blocks other medications or chemicals\nDose: amount of medication given\nAction: the therapeutic effect that a medication is expected to have on the body Pharmacokinetics: actions of the body upon the medication or chemical\nOnset of action\nDuration\nElimination \nPeak Factors affecting how a medication works:\nRoute of administration\nShock states Indications: reasons or conditions\nContraindications: harmful effects\nAbsolute\nRelative\nAdverse effects\nUnintended effects\nUntoward effects", + "Medication Names": "Generic name: a simple, clear, nonproprietary name\nExample: ibuprofen\nTrade name: manufacturer\u2019s brand name\nOne drug may have more than one trade name.\nExample: Tylenol Prescription medications\nOver-the-counter (OTC) medications\nRecreational drugs\nHerbal remedies\nEnhancement drugs\nVitamin supplements\nAlternative medicines", + "Enteral medications enter the body through the digestive system.": "Parenteral medications enter the body by some other means. Absorption is the process by which medications travel through body tissues to the bloodstream.\nCommon routes of administration:\nPer rectum (PR): by rectum\nOral or per os (PO): by mouth Common routes of administration (cont\u2019d):\nIntravenous (IV): into the vein\nIntraosseous (IO): into the bone\nSubcutaneous (SC): beneath the skin\nIntramuscular (IM): into the muscle Common routes of administration (cont\u2019d):\nInhalation: inhaled into the lungs\nSublingual (SL): under the tongue\nTranscutaneous (transdermal): through the skin\nIntranasal (IN): into the nostril via a mucosal atomizer device", + "Medication Forms The form of medication usually dictates the route of administration.": "The manufacturer chooses the form to ensure:\nProper route of administration\nTiming of the medication\u2019s release into the bloodstream\nEffects on the target organs or body systems", + "Tablets and Capsules Capsules are gelatin shells filled with powdered or liquid medication.": "Tablets often contain other materials that are mixed with the medication and compressed.", + "Solutions and Suspensions A solution is a liquid mixture of substances.": "Will not separate by filtering or letting it stand\nCan be given as an IV, IM, or SC injection\nA suspension is substance that does not dissolve well in liquids.\nWill separate if it stands or is filtered.", + "Metered-Dose Inhalers Liquids or solids broken into small enough droplets or particles may be inhaled.": "A metered-dose inhaler (MDI) directs such substances through mouth into lungs.\nDelivers the same amount each time FIGURE 12-2 Some medications are inhaled into the lungs with a metered-dose inhaler so that they can be absorbed into the bloodstream near the site of desired action more quickly. \u00a9 Jones & Bartlett Learning.", + "Topical Medications Include lotions, creams, and ointments": "Applied to skin surface and affect only that area\nExamples\n\tLotion: calamine lotion\n\tCream: hydrocortisone cream\n\tOintment: Neosporin ointment", + "Transcutaneous Medications Designed to be absorbed through the skin": "Also referred to as transdermal\nMay have systemic effects\nIf you touch the medication with your skin, you will absorb it just like the patient.", + "Gels Semiliquid": "Administered in capsules or through plastic tubes\nExample: oral glucose for patient with diabetes FIGURE 12-4 Oral glucose, used in diabetic emergencies, is available in gel and tablet forms. \u00a9 Jones & Bartlett Learning.", + "Gases for Inhalation Usually delivered through a nonrebreathing mask or nasal cannula": "Outside the operating room, most commonly used is oxygen", + "General Steps in Administering Medication": "Medications should be administered only under the authorization of medical control.\nFollow the \u201crights\u201d of medication administration.\nMedication errors almost always result from failure to follow these \u201crights.\u201d", + "Medication Administration and the EMT Circumstances in which medications may be administered:": "Peer-assisted administration\nPatient-assisted administration\nEMT-administered medications\nDetermined by:\nState and local protocols\nMedical control", + "Oral Medications": "Confirm that the patient has a patent airway and is able to swallow, and then instruct the patient to swallow or chew the medication. FIGURE 12-6 Instruct the patient to chew (eg, baby aspirin) or swallow the medication. \u00a9 Jones & Bartlett Learning. Oral glucose\nA sugar that cells use for energy\nTreats hypoglycemia\nEMTs give it only by mouth.\nDo not give to an unconscious patient or one who cannot protect the airway. Aspirin\nReduces fever, pain, and inflammation\nInhibits platelet aggregation \nUseful during heart attack\nContraindications\nHypersensitivity to aspirin\nLiver damage, bleeding disorder, asthma\nShould not be given to children", + "Sublingual Medications": "Advantages\nEasy to advise patients\nQuick absorption\nDisadvantages\nConstant evaluation of the airway\nPossible choking \nNot for uncooperative or unconscious patients Nitroglycerin\nRelieves angina pain (cardiac patients)\nIncreases blood flow\nRelaxes veins FIGURE 12-7 Nitroglycerin, which is prescribed for chest pain, can be given sublingually as a spray (A) or tablet (B). A: Courtesy of Shionogi Pharma, Inc.; B: \u00a9 Jones & Bartlett Learning. Nitroglycerin (cont\u2019d)\nBefore administering:\nCheck blood pressure.\nObtain order to administer.\nPossibility of MI, if no relief\nShould not be used with erectile dysfunction medications\nMay cause mild headache Nitroglycerin (cont\u2019d)\nAdministration by tablet \nSublingually under the tongue\nSlight tingling or burning\nStorage is important.\nAdministration by metered-dose spray\nOn or under tongue\nOne spray = one tablet Administration considerations (for both tablet and spray):\nWait 5 minutes before repeating dose.\nMonitor vital signs.\nWear gloves.\nKnow local protocols.", + "Intramuscular Medications": "Advantages\nQuick, easy access without using vein\nStable blood flow to muscles\nDisadvantages\nUse of a needle (and subsequent pain)\nPatients may fear pain or injury. Epinephrine\nControls fight-or-flight response\nPrimary medication for delivery IM\nAlso called adrenaline, released inside the body under stress\nSympathomimetic Epinephrine (cont\u2019d)\nIncreases heart rate and constricts blood vessels\nDo not give to patients with hypertension, hypothermia, MI, or wheezing.\nMay be delivered with an auto-injector to treat life-threatening anaphylaxis", + "Naloxone": "Used to reverse the effects of an opioid overdose\nImportant considerations:\nConsult medical direction.\nEffects may not last as long as opioids; repeated doses may be necessary\nCan cause severe withdrawal symptoms\nConsider your safety.\n\nThe most common technique for naloxone administration is via the intranasal route. Intranasal Medications FIGURE 12-9 Some EMTs may administer naloxone\nintranasally to treat an opioid overdose. \u00a9 Jones & Bartlett Learning.", + "Oxygen": "All cells need it to survive.\nGenerally administered via:\nNonrebreathing mask \nNasal cannula", + "MDIs and nebulizers": "Liquid turned into mist or spray\nMedication breathed in and delivered to alveoli\nFast absorption rate \nEasy route to access\nPortable FIGURE 12-10 Metered-dose inhalers and small-volume nebulizers (shown here) convert liquid medications into a fine mist. \u00a9 Charles Brutlag/Shutterstock.", + "Use a spacer to avoid spray misdirection": "Fits over the inhaler like a sleeve \nPatient sprays the prescribed dose into the chamber and then breathes in and out of the mouthpiece. \nEspecially useful with young children FIGURE 12-11 Some inhalers have spacer devices to better direct the medication spray. \u00a9 Jones & Bartlett Learning.", + "Inhalation Medications": "Small-volume nebulizers \nEasier to use than MDIs\nTake longer to deliver medication\nRequire an external air or oxygen source\nMore effective in patients with moderate to severe respiratory distress\nCan be used while a patient is on CPAP and during bag-mask ventilation FIGURE 12-12 With a small-volume nebulizer, liquid medication is atomized by the flow of oxygen. The patient then breathes in the medication. \u00a9 Jones & Bartlett Learning.", + "Patient Medications": "Patient assessment includes finding out which medications the patient is taking.\nProvides vital clues to the patient\u2019s condition\nGuides treatment\nWill be useful to the emergency department", + "Do not underestimate the importance of obtaining a thorough medication history.": "Medications are often not taken as prescribed.\nMedications may alter the clinical presentation.", + "Medication Errors": "Inappropriate use of a medication that could lead to patient harm\nMay be possible to minimize errors if circumstances are understood\nEnsure the environment does not contribute to errors. If a medication error occurs:\nProvide appropriate patient care.\nNotify medical control.\nFollow protocols.\nDocument thoroughly, accurately, and honestly.\nTalk with your partner, supervisor, or medical director." + }, + { + "drug class": "nitrate", + "mechanism of action": "causes vasodilation which reduces preload, cardiac output, and myocardial oxygen demand. dilates coronary arteries which results in improved perfusion to ischemic myocardium. relief of ischemia alleviates chest pain.", + "pharmacokinetics": "onset: 1-3 min isl, 30 min td\npeak: 5-10 min sl\nduration: 20-30 min sl, 3-6 hours td", + "indications": "cardiac chest pain, acute pulmonary edema, htn crisis", + "contraindications": "sbp<100, ed medication use in last 24 hours, right sided ami", + "precautions": "check vs after each administration. preferable to have an iv in place prior to administration. right-sided ami can result in severe hypotension.", + "side effects": "n/v if administered rapidly", + "dosing": "adult: .4 mg sl q 5 min (emt-b)\n5 mcg/min iv titrated to effect (paramedic)" + }, + { + "\u0101": "before", + "\u0101 \u0101": "of each", + "ac": "before meals", + "ad lib.": "freely, as desired", + "admov": "apply", + "am": "before noon", + "atc": "around the clock", + "bib": "drink", + "bid": "twice a day", + "d": "day", + "dc, d/c": "discontinue", + "h": "hour", + "hs": "at bedtime", + "npo": "nothing by mouth", + "od": "every day, daily", + "p": "after", + "qd": "every day", + "qh": "every hour", + "qid": "four times a day", + "ql": "as much as desired", + "qm": "every morning", + "qn": "every night", + "qod": "every other day", + "qon": "every other night", + "qp": "as much as desired", + "qpm, qn": "every night/evening", + "qs": "quantity sufficient", + "semih": "half an hour", + "sos": "if necessary", + "tid": "three times a day", + "tin": "three times a night", + "ut dict": "as directed" + }, + { + "acd": "anticonvulsant drug", + "adr": "adverse drug reactions", + "asa": "acetylsalicylic acid (aspirin)", + "cd": "curative dose", + "d, dose": "dose, dosage", + "daw": "dispense as written", + "dawn": "drug abuse warning network", + "dig": "digitalis", + "dsb": "drug-seeking behavior", + "ind": "investigational new drug", + "inh": "isoniazid (tb drug)", + "ld": "lethal dose", + "maoi": "monoamine oxidase inhibitor", + "moa": "mechanism of action", + "mar": "medication administration record", + "meds": "medications", + "nsaid": "non-steroidal anti-inflammatory drug", + "od": "(drug) overdose", + "otc": "over the counter", + "pca": "patient-controlled analgesia", + "pcn": "penicillin", + "rx": "prescription, drug, medication", + "sig": "label", + "tdm": "therapeutic drug monitoring" + }, + { + "drug class": "sympathomimetic", + "mechanism of action": "stimulates both alpha and beta adrenergic receptors.\nalpha: increases inotropic, chronotropic, and dromotropic responses\nbeta1: causes bronchodilation, inhibits mucous secretion\nbeta2: inhibits mast cell degranulation", + "pharmacokinetics": "onset: <2 min iv, 3-10 min sq\npeak: 5 min iv, 20 min sq\nduration: 5-10 min iv, 20-30 min sq", + "indications": "allergic reactions, anaphylaxis, bronchospasm, bronchoconstriction, bradycardia, pulseless arrest, croup", + "contraindications": "tachydysrhythmias, coronary artery disease", + "side effects": "increased myocardial oxygen demand, ischemia, tachydysrhythmias, tissue necrosis in presence of extravasation", + "precautions": "maoi\u2019s potentiate its effects", + "interactions": "sodium bicarbonate can deactivate catecholamines", + "dosing": "emt-basic:\nanaphylaxis: .3-.5 mg sq q 5-15 min (1:1,000)\nparamedic:\npulseless arrest: 1 mg q 3-5 min iv (1:10,000)\nbradycardia: 2-10 mcg/min drip\n .3-.5 mg iv q 3-5 min slow push (1:10,000)\ncroup: .05 ml/kg via nebulizer (2.25% racemic epi in 3ml ns)" + }, + { + "hypo (route)": "hypodermic", + "ic, icav": "intracavitary", + "id": "intradermal", + "im": "intramuscular", + "inhal": "inhalation", + "it": "intrathecal", + "iv": "intravenous", + "ivp": "intravenous push", + "ivpb": "intravenous piggyback", + "mdi": "metered-dose inhaler", + "parent, p": "parenteral", + "po": "orally", + "pr": "through rectum, per rectum", + "sl, subl": "sublingual", + "sc, sq": "subcutaneous", + "tdd": "transdermal drug delivery", + "top": "topically", + "ndc": "national drug code", + "nf": "national formulary", + "pdr": "physician's desk reference", + "dea": "drug enforcement agency", + "fda": "food and drug administration", + "usp": "united sates pharmacopeia" + }, + { + "drug class": "opiate antagonist", + "mechanism of action": "a competitive antagonist that displaces analgesics from their receptor sites, which reverses their effects (respiratory depression, sedation, papillary miosis, and euphoria).", + "pharmacokinetics": "onset: 1-2 min iv, 2-5 min im/in\nduration: 60-100 min\nhalf life: 60-90 min", + "indications": "opiate od, clonidine od", + "contraindications": "neonates with narcotic-addicted mothers", + "precautions": "can precipitate severe withdrawal symptoms in individuals who are physically dependent on opioids. use repeated small doses for patients taking chronic narcotics. consider physical restraints prior to administration. may precipitate seizures in neonates.", + "side effects": "n/v if administered rapidly", + "dosing": "adult: .1-2 mg (iv, im, sq, ett) may be repeated to max of 8 mg" + }, + { + "aer": "aerosol", + "aq": "water, aqueous", + "bol, pil": "pill", + "cap": "capsule", + "comp": "compound", + "dil": "dilute", + "elix": "elixer", + "ext": "extract", + "fld": "fluid", + "garg": "a gargle", + "gtt, gt": "drops", + "linim": "liniment", + "liq": "liquid", + "lot": "lotion", + "m": "mixture", + "pulv": "powder (pulvule)", + "sol, soln": "solution", + "solv": "dissolve", + "spt": "spirit", + "supp": "suppository", + "susp": "suspension", + "syr": "syrup", + "tab": "tablet", + "tinct": "tincture", + "ung": "ointment" + }, + { + "drug class": "antihistamine/anticholinergic", + "mechanism of action": "blocks h1 receptors and thus reduces histamine effects: sneezing, nasal secretions, itching, uticaria, watery eyes. also has central antimuscarinic effects (aka antiparkinson action)", + "pharmacokinetics": "onset: 15 min iv\npeak: 1-4 hours\nhalf-life: 2-10 hours", + "indications": "allergic and anaphylactic reactions. overdose resulting in dystonic or extrapyramidal reactions (phenothiazines, thioxanthines, and butyrophenones)", + "contraindications": "none", + "side effects": "anticholinergic effects, most commonly constipation, decrease in sweating, difficulty urinating, visual disturbances, photophobia, and dry mouth.", + "precautions": "altered mental status, asthma, and nursing mothers", + "interactions": "sedation when mixed with other cns depressants", + "dosing": "adult: 25-50 mg iv, im, or po\npediatric: 1 mg/kg up to adult dose" + }, + { + "drug class": "carbohydrate", + "mechanism of action": "increases glucose levels in the blood", + "pharmacokinetics": "rapid absorption in the bloodstream", + "indications": "hypoglycemia, hyperkalemia (if given concurrently with insulin)", + "contraindications": "none", + "side effects": "tissue necrosis if iv extravasates. n/v if given too rapidly.", + "precautions": "use a large bore iv if available. if the patient is suspected to be malnourished (i.e., alcohol, homeless, elderly), give thiamine before administration of d-50.", + "dosing": "adult: 25g initial dose, slow bolus.\na second dose of 25g may be given if needed." + }, + { + "drug class": "hormone/antihypoglycemic", + "mechanism of action": "causes a breakdown of glycogen stores in the liver to raise circulating blood glucose levels. helpful in presence of beta-blocker od due to its positive inotropic/chronotropic effects on the heart independent of beta-adrenergic receptors.", + "pharmacokinetics": "onset: 5-20 min\npeak: 30 min\nduration: 1-1.5 hours\nhalf-life: 30 min", + "indications": "hypoglycemia, beta-blocker od, ca2+ channel blocker od, esophageal obstruction", + "contraindications": "none", + "precautions": "patients who have already reduced their glycogen stores", + "side effects": "n/v, ha if given too rapidly", + "dosing": "hypoglycemia: 1 mg im\nbeta-blocker od: 3-10 mg iv" + }, + { + "drug class": "inhalational anesthetic", + "mechanism of action": "cns depressant with analgesic properties", + "pharmacokinetics": "onset: immediate\nduration: 2-5 min", + "indications": "pain secondary to trauma/burns, renal calculi", + "contraindications": "ams, etoh/drug od, head injury, copd, suspected pneumothorax, suspected bowel obstruction, hypoxia", + "precautions": "ventilate the ambulance well. store tank at appropriate temperature per manufacturer guidelines. have oxygen readily available. no must be mixed with oxygen to prevent hypoxia.", + "side effects": "delirium", + "dosing": "adult: self-administered through a ppdv mask at a concentration of 50% o2 / 50% no" + }, + { + "drug class": "antiemetic", + "mechanism of action": "selective inhibitor of type 3 serotonin (5-ht3) receptors", + "indications": "uncontrollable n/v", + "contraindications": "none", + "precautions": "use with caution in patients with diagnosed or suspected bowel obstruction", + "side effects": "generally tolerated well", + "dosing": "generally tolerated well" + }, + { + "drug class": "antidysrhythmic/electrolyte", + "mechanism of action": "increases magnesium levels, thus correcting cardiac dysrhythmias which are associated with hypomagnesemia. interferes with neuromuscular transmission, reducing muscle contractions in seizures and bronchoconstriction.", + "pharmacokinetics": "onset: immediate\nduration: 30 min", + "indications": "torsades, refractory v-fib, preeclampsia, eclampsia, refractory bronchoconstriction, tca od (if qrs is wide).", + "contraindications": "shock, heart block, renal disease", + "precautions": "if respiratory depression ensues give calcium chloride, use with caution in renal failure patients", + "side effects": "hypotension, respiratory depression, flushing, loss of deep-tendon reflexes, flushing, sweating", + "interactions": "may block the effects of digitalis", + "dosing": "cardiac arrest: 1-2 g iv\ncardiac (w/ pulse): 1-2 g over 5-60 min\neclampsia: 2-4 g over 5-60 min\nbronchoconstriction: 2 g iv over 5-60 min" + }, + { + "drug class": "hormone", + "mechanism of action": "directly stimulates contraction of uterine smooth muscle by increasing the sodium permeability of uterine myofibrils. produces intense uterine contractions.", + "pharmacokinetics": "onset: immediate\nduration: 1 hour", + "indications": "postpartum bleeding after expulsion of the placenta", + "contraindications": "sbp<100, ed medication use in last 24 hours, right sided ami", + "precautions": "od can cause uterine rupture. the absence of additional fetuses must be established, placenta must be delivered before administration", + "side effects": "cardiac dysrhythmias, htn", + "dosing": "adult: 10-40 units in 1,000 ml titrated to uterine response 10 units im" + }, + { + "drug class": "antidote/vitamin", + "mechanism of action": "a natural derivative of vitamin b-12, it binds with circulating cellular cn molecules to form cyanocobalamin which gets excreted in the urine.", + "pharmacokinetics": "unknown", + "indications": "suspected cn poisoning", + "contraindications": "unknown", + "side effects": "allergic reactions, htn, chromaturia, and rash", + "dosing": "adult: 5 g iv over 15 minutes\npediatric: 70 mg/kg" + }, + { + "drug class": "general anesthetic", + "mechanism of action": "decreases activity of the reticular formation in the brainstem with minimal cardiac or respiratory effects.", + "pharmacokinetics": "onset: 10-20 sec\npeak: 1-2 min\nduration: 4-12 min", + "indications": "induction of general anesthesia for intubation", + "contraindications": "none", + "side effects": "myoclonus", + "dosing": "adult: .3 mg/kg may repeat once if necessary" + }, + { + "drug class": "calcium channel blocker", + "mechanism of action": "causes vascular dilation and slows conduction through the av node. it slows the rapid ventricular rate associated with a-fib, a-flutter, and svt.", + "pharmacokinetics": "onset: 5-15 min", + "indications": "used to convert supra ventricular tachydysrhymias refractory to adenosine and slow a-fib/flutter with rvr", + "contraindications": "hypotension, cardiogenic shock, v-tach, a-flutter/a-fib with wpw", + "precautions": "monitor bp constantly, calcium can be used to prevent the hypotensive effects", + "side effects": "dizziness, ha, bradycardia, heart block, hypotension, and asystole", + "dosing": "adult: .25 mg/kg over 2 min, may repeat at .35mg/kg if no response in 15 min.\nmax single dose: 20-25 mg\nmaintenance infusion: 5-15 mg/hr" + }, + { + "drug class": "benzodiazapine/anticonvulsant/sedative/hypnotic", + "mechanism of action": "enhances the effect of gaba, an inhibitory neurotransmitter in the brain. by enhancing the gaba effect the brain typically will slow transmission of seizure activity. also is a potent skeletal muscle relaxant.", + "pharmacokinetics": "onset: 3-5 min\npeak: 20-60 min\nduration: <2 hours\nhalf life: 1- hours", + "indications": "major motor seizures, cardioversion, tcp, sedation w/ rsi, muscle spasms, anxiety, agitation (cocaine, amphetamine od)", + "contraindications": "hypotension, narrow-angle glaucoma", + "side effects": "hypotension, respiratory depression", + "interactions": "effects are additive with other cns depressants or etoh", + "dosing": "adult: seizure/sedation: 2.5-10 mg iv/im in 2.5mg increments\nrsi: .1mg/kg to a max of 10 mg\npediatric: .05-.2 mg/kg to a max of 5 mg" + }, + { + "drug class": "salicylate/platelet inhibitor/analgesic/antipyretic/nsaid", + "mechanism of action": "inhibits prostaglandin formation associated with pain, fever, and inflammation. asa inhibits platelet aggregation for the life of the platelet (7-10 days)", + "pharmacokinetics": "onset: 5 - 30 minutes\npeak: 15 minutes - 2 hours\nduration: 1 - 4 hours", + "indications": "acute chest pain of suspected cardiac origin", + "contraindications": "allergy, ulcer, gi bleeding, anticoagulants", + "side effects": "n/v/d, heartburn, gi bleeding", + "dosing": "adult: 324 mg po" + }, + { + "drug class": "anti-pyretic & non-narcotic analgesic", + "mechanism of action": "cox 3 variant within the cns\nprostaglandin synthesis inhibition\ncentral action in the hypothalamus", + "pharmacokinetics": "peak: 1-2 hours\nduration: 3-4 hours\nhalf-life: 1-3 hours", + "indications": "fever\nfebrile seizures", + "contraindications": "allergy to apap\nrecent consumption of apap containing medications", + "side effects": "none", + "dosing": "adult: 650-1000 mg po\npediatric: 10-20 mg/kg" + }, + { + "drug class": "antidote", + "mechanism of action": "acts as a sulfur donor which is used to change cn into thiocyanate, which is then excreted in the urine", + "pharmacokinetics": "half-life: 15-20 min", + "indications": "cn or cyanogenic compound poisoning", + "contraindications": "absolute: none\nrelative: unprotected airway", + "side effects": "n/v, localized pain at injection site. may cause hypovolemia through diuresis", + "dosing": "adult: 1 ampule iv over 10-20 min\npediatric: 1.6 ml/kg over 10-20 min" + }, + { + "drug class": "nonsteroidal anti-inflammatory agent", + "mechanism of action": "inhibits cyclooxygenase and prevents the synthesis of prostaglandins and thromboxane. this reduces inflammation and ultimately provides pain relief.", + "indications": "mild to moderate pain", + "contraindications": "allergy to nsaid\u2019s", + "precautions": "use extreme caution when patient has a history of renal or hepatic disease", + "side effects": "increased risk of bleeding when given with other nsaid\u2019s", + "interactions": "when given concurrently with d50 insulin will stimulate the cellular uptake of potassium.", + "dosing": "adult: 60 mg im, 30 mg iv\n(decrease dose by half if patient is younger than 65-years-old)" + }, + { + "drug class": "parasympatholytic/bronchodilator", + "mechanism of action": "acts directly on the smooth muscle of the respiratory tract and decreases secretions. reduces vagally mediated reflex bronchospasm caused by inhaled irritants.", + "indications": "asthma, bronchospasm associated with copd and anaphylaxis", + "contraindications": "none", + "precautions": "delayed onset of action. not to be used as sole bronchodilator in the emergency setting.", + "side effects": "palpations, anxiety, dizziness, dry mouth, ha, cough", + "interactions": "when given concurrently with d50 insulin will stimulate the cellular uptake of potassium.", + "dosing": "0.5 mg in 2.5 ml saline" + }, + { + "drug class": "beta-blocker", + "mechanism of action": "beta-adrenergic blocking agent with beta-1 predominance. causes a reduction in heart rate, systolic blood pressure, and cardiac output. it is thought to be protective of the heart and is used to reduce potential complications in select patients who\u2019ve suffered ami\u2019s.", + "pharmacokinetics": "onset: immediate\npeak: 20 min\nduration: 13-19 hours\nhalf life: 3-4 hours", + "indications": "suspected or hemodynamically stable ami", + "contraindications": "hr<45 bpm, sbp<100mmhg, moderate to severe chf, high degree heart blocks (2 and 3), late signs of shock", + "precautions": "chf, bradycardia, shock, heart block, bronchospasm", + "side effects": "bradycardia, hypotension, dyspnea, and wheezing", + "dosing": "adult: 5 mg slow ivp q 5 min x 3 total doses if vs remain stable" + }, + { + "drug class": "calcium channel blocker", + "mechanism of action": "causes vascular dilation and slows conduction through the av node. it slows the rapid ventricular rate associated with a-fib, a-flutter, and svt.", + "pharmacokinetics": "onset: 5-15 min", + "indications": "used to convert supraventricular tachydysrhymias refractory to adenosine, and slow a-fib/flutter with rvr", + "contraindications": "hypotension, cardiogenic shock, v-tach, a-flutter/a-fib with wpw", + "precautions": "monitor bp constantly, calcium can be used to prevent the hypotensive effects", + "side effects": "dizziness, ha, bradycardia, heart block, hypotension, and asystole", + "dosing": "adult: 2.5-5mg/2 min iv, may repeat in 15-30 min at 5-10 mg/2min to a maximum dose of 20 mg" + }, + { + "drug class": "antidote", + "mechanism of action": "organophosphates inhibit cholinesterase by phosphorylation of the enzyme. pralidoxime reactivates cholinesterase by kicking out the phosphoryl group bound to the ester group. during this reaction, both the pralidoxime and the organophosphates are mutually inactivated. together, these products are rapidly metabolized, leading to the removal of the organophosphate.", + "pharmacokinetics": "less effective after the nerve agent has aged", + "indications": "toxic exposure \u2013 organophosphate/nerve agent poisoning", + "contraindications": "absolute: inability to perform eti relative: myasthenia gravis, renal failure", + "side effects": "blurred vision, dysphasia, tachypnea, dizziness, tachycardia, pain at injection site, muscle weakness, ha, nausea", + "dosing": "adult: 1-2 g iv over 5-10 minutes repeated once 1 hour later if weakness or fasciculation have not resolved. 500 mg/hr continuous iv infusion for 24 hours after initial bolus.\npediatric: 20-40 mg/kg iv over 10 min. 5-10 mg/kg/hr continuous iv infusion for 24 hours after initial bolus." + }, + { + "drug class": "antidiuretic hormone", + "mechanism of action": "in high doses, vasopressin acts as a non-adrenergic peripheral vasoconstrictor. when given during cpr, it increases coronary perfusion pressure, blood flow to vital organs, and decreases the defibrillation threshold.", + "pharmacokinetics": "onset: <2 min\nduration: 10-20 min", + "indications": "v-fib, pulseless v-tach, pea, and asystole", + "contraindications": "none", + "precautions": "patients with perfusing rhythms", + "side effects": "none", + "dosing": "adult: single 40 unit bolus iv" + }, + { + "drug class": "nondepolarizing neuromuscular blocker", + "mechanism of action": "competitively binds to cholinergic receptors. reversible in the presence of acetylcholinesterase inhibitors, such as neostigmine.", + "pharmacokinetics": "onset: rapid to intermediate\nduration: intermediate", + "indications": "rsi, maintenance of desired paralysis", + "contraindications": "none", + "side effects": "bronchospasm, tachycardia, htn", + "interactions": "intensity and duration of paralysis may be prolonged by use of succinylcholine, general anesthesia, lidocaine, quinidine, procainamide, beta-adrenergic-blocking agents, potassium-losing diuretics, or magnesium", + "dosing": "adult: .6 mg/kg" + }, + { + "drug class": "nitrite", + "mechanism of action": "induces low levels of methemoglobinemia, which in turn binds cyanide", + "pharmacokinetics": "onset: immediate", + "indications": "cyanide, cyanogenic, and sulfide poisoning", + "contraindications": "hypotension, carbon monoxide poisoning", + "side effects": "headache, hypotension", + "dosing": "adult: 1 ampule inhaled 30 seconds each minute.\nchange ampule every 3 minutes." + }, + { + "drug class": "hormone", + "mechanism of action": "promotes the storage of glucose as glycogen. increases fat and protein synthesis. it inhibits the breakdown of glycogen, protein, and fat. stimulates the cellular uptake of potassium. all types of insulin have the same effect on the body. the difference lies in onset, duration, concentration, source, and purity.", + "indications": "hyperkalemia, hyperglycemia", + "contraindications": "hypoglycemia", + "precautions": "repeat cbg measurements often", + "side effects": "hypoglycemia", + "interactions": "when given concurrently with d50 insulin will stimulate the cellular uptake of potassium.", + "dosing": "hyperkalemia: 5-10 units iv given with 25 g d50\nhyperglycemia: depends on prescribed amount" + }, + { + "drug class": "narcotic analgesic", + "mechanism of action": "natural opium alkaloid that acts on opiate receptors in the brain. peripheral vasodilation of veins and arteries resulting in enhanced cardiac function.", + "pharmacokinetics": "onset: immediate\npeak: 20 min\nduration: 2-7 hours", + "indications": "pain, cardiac chest pain, burns, and acute pulmonary edema", + "contraindications": "head injury, hypotension, hypovolemia, traumatic abdominal pain", + "precautions": "may cause n/v if given too rapidly", + "side effects": "respiratory depression, hypotension, decreased mental status, and histamine release", + "dosing": "adult: 2-5 mg slow ivp or im titrated to effect. max dose 20 mg prior to contacting olmc." + }, + { + "drug class": "non-depolarizing paralytic agent", + "mechanism of action": "competes with acetylcholine for cholinergic receptor sites on the post junctional membrane, resulting in paralysis", + "pharmacokinetics": "onset: 1 min\npeak: 3 min\nduration: 25-30 min", + "indications": "paralysis to obtain eti, maintenance of desired paralysis", + "contraindications": "none", + "side effects": "none", + "dosing": "adult: .1 mg/kg" + }, + { + "drug class": "electrolyte", + "mechanism of action": "antagonizes hyperkalemia toxicity by stabilizing the cardiac cell membrane against depolarization", + "pharmacokinetics": "onset: immediate\npeak: immediate", + "indications": "ca2+ channel blocker od, beta-blocker od, hf acid burns, hyperkalemic arrest", + "contraindications": "digitalis, cardiac glycoside medications, renal/cardiac insufficiency", + "side effects": "tissue necrosis, hypotension, syncope, cardiac arrest", + "dosing": "adult: \ncalcium chloride: 5-10 ml slow iv push\n10 ml of 10% solution = 13.6 meq ca2+ \ncalcium gluconate: 10-30 ml slow iv push\n10 ml of 10% solution = 4.6 meq ca2+" + }, + { + "drug class": "nitrate", + "mechanism of action": "induces low levels of methemoglobinemia which combines with cyanide to form nontoxic cyanomethemoblobin.", + "pharmacokinetics": "peak effect: 30-70 minutes", + "indications": "cyanide, cyanogenic compound, sulfide poisoning", + "contraindications": "absolute: allergy\nrelative: significant hypotension, methemoglobinemia > 40%, and co poisoning", + "precautions": "frequent bp monitoring during administration. give over 5 minutes, dilute in 50-100 ml ns.", + "side effects": "ha, hypotension, tachycardia, hypoperfusion (shock), excessive methemoglobinemia", + "dosing": "adult: 1 ampule over no less than 5 minutes\npediatric: .12 - .33 ml/kg, up to 10 ml over at least 5" + }, + { + "drug class": "benzodiazapine/anticonvulsant/sedative/hypnotic", + "mechanism of action": "enhances the effect of gaba, an inhibitory neurotransmitter in the brain. by enhancing the gaba effect the brain typically will slow transmission of seizure activity. also is a potent skeletal muscle relaxant.", + "indications": "major motor seizures, cardioversion, tcp, sedation w/ rsi, muscle spasms, anxiety, agitation (cocaine, amphetamine od)", + "contraindications": "hypotension, acute narrow angle glaucoma", + "side effects": "hypotension, respiratory depression", + "interactions": "effects are additive with other cns depressants or etoh", + "dosing": "adult: .05 mg/kg iv, max 4 mg" + }, + { + "drug class": "sedative/neuroleptic", + "mechanism of action": "blocks dopamine receptors in the brain", + "pharmacokinetics": "onset: 15-30 min", + "indications": "chemical restraint requiring rapid tranquilization", + "contraindications": "hypotension, prolonged qt-interval, lithium", + "precautions": "monitor bp and respiratory status. restrain the patient in a way that allow them to breathe normally. cardiac monitoring required.", + "side effects": "extrapyramidal or dystonic reactions, have diphenhydramine ready", + "dosing": "adult: 2-5 mg im, may be combined with midazolam" + }, + { + "drug class": "antidysrhythmic/anesthetic", + "mechanism of action": "antidysrhythmic: suppresses the automaticity, excitability, and spontaneous depolarization of the ventricles. \nanesthetic: produces local anesthesia by inhibiting transport of ions across neuronal membranes, preventing initiation and conduction of normal nerve impulses.", + "pharmacokinetics": "onset: 3 min\npeak: 5-7 min\nduration: 10-20 min\nhalf-life: 1.5-2 hours", + "indications": "ventricular dysrhythmias, non-perfusing pvc\u2019s, pre-medication for rsi, local anesthesia for iv\u2019s and suturing. the viscous form is commonly used as a local anesthetic prior to nasal intubation or ng tube placement", + "contraindications": "high degree heart blocks, ventricular ectopy in conjunction with hypoxia or bradycardia. hr<50, bp <90, chf, shock.", + "precautions": "use caution in patients with hepatic failure and >70-years-old", + "side effects": "seizures, slurred speech, ams, tinnitus, perioral twitching", + "interactions": "typically should not be given with other antidysrhythmics, except in v-fib and pulseless v-tach", + "dosing": "pulseless v-tach/v-fib: 1.5 mg/kg iv q 3-5 min, max 3 mg/kg\nv-tach with a pulse: 1-1.5 mg/kg slow ivp, repeat at half dose\npost-conversion: 1-4 mg/min\nio placement: 20-40 mg io" + }, + { + "drug class": "benzodiazapine/anticonvulsant/sedative/hypnotic", + "mechanism of action": "enhances the effect of gaba, an inhibitory neurotransmitter in the brain. by enhancing the gaba effect the brain typically will slow transmission of seizure activity. also is a potent skeletal muscle relaxant.", + "pharmacokinetics": "onset: 1-5 min iv, 15-30 min im\npeak: 15 min iv, 30 min im\nhalf-life: 20-50 min", + "indications": "major motor seizures, cardioversion, tcp, sedation w/ rsi, muscle spasms, anxiety, agitation (cocaine, amphetamine od)", + "contraindications": "hypotension", + "side effects": "hypotension, respiratory depression, confusion, amnesia", + "precautions": "use large vein if possible and monitor respiratory status", + "interactions": "effects are potentiated when used w/ cns depressants or etoh", + "dosing": "adult: 5-15 mg iv\npediatric: .5 mg/kg rectally" + }, + { + "drug class": "antiemetic/antihistamine", + "mechanism of action": "a phenothiazine derivative with potent antihistamine and anticholinergic properties. it also possesses sedative and antiemetic properties. it competitively blocks h1 receptors.", + "pharmacokinetics": "onset: 5 min iv, 20 min im\nduration: 2-8 hours", + "indications": "n/v, sedation, motion sickness", + "contraindications": "coma, nursing mothers, newborn infant", + "side effects": "drowsiness, sedation, blurred vision, tachycardia, bradycardia, and dizziness.", + "interactions": "depressant effects on the cns from narcotics, sedatives, or hypnotics, and alcohol is potentiated.", + "dosing": "adult: 12.5-25 mg iv or deep im\npediatric: .25 mg/kg up to 6.25 mg" + }, + { + "drug class": "narcotic analgesic", + "mechanism of action": "stimulates the mu receptors to achieve analgesic and sedative therapeutic values.", + "pharmacokinetics": "onset: immediate\npeak: 3-5 min\nduration: 30-60 min", + "indications": "moderate to severe pain, adjunct in rsi", + "contraindications": "severe hemorrhage, shock, maoi\u2019s within the last 14 days", + "side effects": "drowsiness, hypotension, bradycardia, respiratory depression, n/v, weakness, and dizziness", + "dosing": "adult: 1- 2 mcg/kg iv or im, up to 100 mcg" + }, + { + "drug class": "sympathomimetic/beta-2 agonist/bronchodilator", + "mechanism of action": "a smooth muscle relaxant with minimal beta-1 effects. reduces mucous secretions and edema. stimulates the cellular uptake of potassium.", + "pharmacokinetics": "onset: 5-15 minutes\npeak: 1-1.5 hours\nduration: 3-6 hours\nhalf-life: 3 hours", + "indications": "asthma, copd, cardiac asthma, hyperkalemia, sob associated with pneumonia or anaphylaxis", + "contraindications": "none", + "side effects": "hypertension, tachycardia, anxiety, palpations", + "interactions": "side effects are potentiated with other sympathomimetics. beta-blockers may blunt desired effects.", + "dosing": "adult: 2.5mg in 3ml saline nebulized" + }, + { + "drug class": "depolarizing neuromuscular blocking agent", + "mechanism of action": "combines with cholinergic receptors in motor nerves to cause depolarization. neuromuscular transmission is inhibited, causing temporary paralysis, until succinylcholine is metabolized and cells become repolarized.", + "pharmacokinetics": "onset: 1-2 min\nduration: 5-10 min", + "indications": "temporary paralysis for eti when muscle tone impedes successful intubation.", + "contraindications": "hyperkalemia, hx of malignant hyperthermia, penetrating eye injury, ms, paralysis > 1 day, crush injuries > 3 days, severe burns > 3 days", + "precautions": "make sure all intubation equipment is ready prior to administering succinlycholine. bradycardia is a strong possibility during rsi, especially those patients with chf", + "side effects": "arrhythmias, bradycardia, increased iop, increased icp, hyperkalemia", + "dosing": "dosing \"adult: 1-2 mg/kg iv or im\npediatric: 2 mg/kg iv or im\"" + }, + { + "drug class": "vitamin", + "mechanism of action": "restores body\u2019s supply of vitamin b1 in malnourished patients. this prevents development of wernicke\u2019s syndrome and korsakoff\u2019s psychosis. thiamine is an essential coenzyme of carbohydrate metabolism.", + "pharmacokinetics": "onset: immediate", + "indications": "coma of unknown origin, especially if alcohol is involved, delirium tremens", + "contraindications": "none", + "precautions": "none", + "side effects": "none", + "interactions": "none", + "dosing": "adult: 100 mg iv or im" + }, + { + "drug class": "parasympatholytic/anticholinergic/antimuscarinic/vagolytic", + "mechanism of action": "a competitive antagonist that selectively blocks all muscarinic responses to acetylcholine (ach). by blocking vagal impulses it thereby increases sa node firing, enhances av conduction, and cardiac output. actions of the drug can be dose-dependent: \nlow doses: decrease sweating, salivation, and respiratory secretions and cause bronchodilation. \nmedium doses: pupil dilation, loss of visual acuity, increases hr, conduction, velocity, and inotropy. \nlarge doses: decrease gi secretions and motility of the gi and gu tracts.", + "pharmacokinetics": "onset: immediate\npeak: 2-4 min\nhalf life: 2-3 hours", + "indications": "symptomatic bradycardia, aystole, pea (hr<60), organophosphate poisoning, nerve agent poisoning", + "contraindications": "none", + "side effects": "acute psychosis, mydriasis, vasodilation, dehydration, elevated temperature", + "interactions": "additive anticholinergic effects with antihistamines and tca\u2019s", + "dosing": "adult: bradycardia: .5-1 mg q 3-5 min\nasystole: 1 mg q 3-5 min\npoisoning: 1-2 mg, repeated q 5-60 min prn" + }, + { + "drug class": "glucocorticosteroid/anti-inflammatory", + "mechanism of action": "alters the body\u2019s immune response. reduces swelling because it prevents white blood cells from traveling to the area.", + "pharmacokinetics": "peak: 6-8 hours\nhalf life: 2.5-3.5 hours", + "indications": "allergic reactions/anaphylaxis, asthma, copd exacerbation, sci", + "contraindications": "none", + "side effects": "peptic ulcers, hyperglycemia, hypokalemia", + "dosing": "adult: 60-125 mg iv or im over 1 min\npediatric: 2 mg/kg up to 125 mg iv over 1 min" + }, + { + "drug class": "sympathomimetic/vasopressor", + "mechanism of action": "stimulates alpha, beta-1, and dopaminergic receptors. indirectly causes the release of norepinephrine from sympathetic nerve-ending storage sites. the effects of the drug are ultimately dose-related: \nlow doses (2-5mcg/kg/min): increases perfusion of the mesenteric arteries and the kidneys.\nmedium doses: (5-10mcg/kg/min): increases force of contraction, heart rate, and conduction.\nhigh doses: (10-20mcg/kg/min): peripheral alpha receptors are stimulated, causing an increase in vascular constriction (pvr).", + "pharmacokinetics": "onset: <5 min\nduration: <10 min\nhalf-life: 2 min", + "indications": "non-traumatic hypotension/hypoperfusion, shock, bradycardia refractory to atropine and pacing.", + "contraindications": "hypovolemic shock, pheochromocytoma (adrenal tumors), htn, tachydysrhythmias", + "side effects": "tachydysrhythmias, n/v, headache, tissue necrosis, increase in myocardial oxygen demand, ischemia", + "precautions": "maoi\u2019s (marplan, eutonyl, parinate, nardil) potentiate the effects", + "interactions": "sodium bicarb can deactivate catecholamines", + "dosing": "adult: 5-20 mcg/kg/min, dose depends on desired effect" + }, + { + "drug class": "sedative hypnotic", + "mechanism of action": "unknown, dose dependent cns depressant", + "pharmacokinetics": "onset: 40 sec, 1-3 min for anesthesia", + "indications": "rsi, general anesthesia, maintenance of general anesthesia", + "contraindications": "hypotension, allergy to soy, egg, or lecithin", + "precautions": "may need a smaller dose if cns depressants or narcotics have been taken.\nrequires specialized training and permission to administer. \nnot administered in the pre-hospital setting.", + "side effects": "pain during administration, bradycardia, arrhythmia, hypotension, rash", + "dosing": "adult: 1 mg/kg initial bolus over 10 sec, may repeat 25-50 mg as necessary to maintain desired level of sedation." + }, + { + "drug class": "antidysrhythmic", + "mechanism of action": "sodium, potassium and calcium channel blocker. prolongs action potential duration and refractory period of all cardiac fibers. it\u2019s also a weak, non-competitive, alpha and beta blocking agent.", + "pharmacokinetics": "onset: rapid\nduration: long, maintenance drip not usually required", + "indications": "v-fib, pulseless v-tach, svt, and v-tach with pulses", + "contraindications": "cardiogenic shock, bradycardia, second/third degree block", + "side effects": "hypertension, bradycardia, av block, increased qt interval", + "dosing": "adult only!\nwith pulses: 150mg over 10 min may repeat once\npulses: 300mg iv bolus may repeat 150mg dose once\nmaintenance infusion: 1mg/minute" + }, + { + "drug class": "endogenous nucleoside/antidysrhythmic", + "mechanism of action": "decreases sa node impulse formation, slows av node conduction, and depresses left ventricular function. interrupts reentry pathways and accessory bypass tracts that cause svt.", + "pharmacokinetics": "onset: immediate\npeak: 20-30 seconds\nhalf-life: 2-10 seconds", + "indications": "svt, wpw, lgl", + "contraindications": "a-fib or a-flutter with a history of wpw, sick sinus syndrome, second or third-degree av blocks, and known hypersensitivity", + "side effects": "apprehension, flushing, chest pain, headache, n/v, hypotension. periods of asystole, bradycardia, and ventricular ectopy", + "interactions": "effects are decreased by theophylline and caffeine thus higher starting doses may be necessary. effects are potentiated by carbamazepine and dipyridamole thus use of adenosine is cautioned.", + "dosing": "adult: 6mg iv bolus with rapid 20cc flush, if no response repeat in 1-2 minutes with 12mg iv bolus followed by rapid 20cc flush. this dose may be repeated one more time." + }, + { + "drug class": "platelet aggregation inhibitor", + "mechanism of action": "prevents the formation of clots by inhibiting platelets from sticking together", + "pharmacokinetics": "peak: 1 hour\nhalf life: 8 hours", + "indications": "acute coronary syndrome", + "contraindications": "active pathological bleeding (gi, intracranial)", + "side effects": "bleeding, including both gi and intracranial", + "dosing": "adult: 300 mg" + }, + { + "drug class": "loop diuretic", + "mechanism of action": "blocks the reabsorption of sodium and chloride ions in the kidneys through the ascending loop of henle. causes increased diuresis and venodilation.", + "pharmacokinetics": "onset: 5-10 min\npeak: 20-60 min\nduration: 6 hours\nhalf-life: 30 min", + "indications": "chf, pulmonary edema, htn crisis, hyperkalemia", + "precautions": "patients with pneumonia, hypersensitivity to sulfa drugs", + "contraindications": "hypovolemia, anuria, pregnancy, hypokalemia", + "side effects": "hypokalemia, hypotension, dehydration, urination, muscle cramps", + "dosing": "adult: 20-80 mg iv / im" + }, + { + "drug class": "alkalinizing agent/electrolyte/antidysrhythmic", + "mechanism of action": "once disassociated, bicarbonate binds with hydrogen ions to decrease metabolic acidosis. when given for tca od, it acts as an antidysrhythmic. reduces the effects of hyperkalemia by shifting potassium into the cells.", + "pharmacokinetics": "onset: immediate\nduration: 1-2 hours", + "indications": "hyperkalemia, tca od, late management of cardiac arrest", + "contraindications": "none", + "precautions": "patient must be breathing spontaneously or adequately ventilated prior to receiving the drug", + "side effects": "metabolic acidosis, hypokalemia, fluid overload", + "interactions": "deactivates catecholamines, precipitates with calcium chloride, and always flush the iv line between drugs to prevent interactions.", + "dosing": "adult: 1 meq/kg iv push", + "mass action effect": "mass action effect = h2o + co2 h2co3 h+ + hco3-" + }, + { + "introduction": "medication safety in ems, medication administration is one of our primary methods of managing a patients complaints, safety, and wellbeing. if used therapeutically, medications can improve, correct, or reduce the symptoms or even underlying sources of a patients complaint. on the opposite side of that coin, medications administered incorrectly, whether to treat the wrong ailment, through the wrong route or the wrong dosage, can cause severe or life-threatening consequences in of themselves. because of this, comprehensive knowledge of medications in your scope is a critical aspect of becoming a quality first responder.", + "principles of pharmacology": "pharmacology refers to the branch of medicine that studies the uses, effects, and modes of action of drugs. medications are essentially a substance, or collection of chemicals, used to treat an illness or complaint. drugs are any substance that can cause a physiological effect when its been absorbed and circulated by the body.", + "kinds of medications used in an emergency": "medications used in the emergency setting are unique in that they are often designed to treat acute symptoms. there are only a small number of medications utilized in the emergency setting that is keyed towards the long-term improvement of a patients symptoms, as first responders are uniquely trained to respond to assess and treat the patient with an acute complaint. because of this, many ems medications can be expected to have a rapid onset of action, with trackable effects on the patients chief complaint, vital signs, and other objective markers.", + "forms of medication": "medications can be procured or fabricated from a vast swath of potential sources, and the practice of utilizing the environment to create solutions to medical complaints is as ancient as written human history. medications can be sourced from organic materials, like plants and animals, or inorganic materials, like gas and minerals. medications can be administered in any number of forms, including solids, liquids, and gasses; the shape the medication takes will determine the pharmacokinetics of the drug, which is to say, how the medication is absorbed by the body.", + "solid medications": "capsules are powdered or solid medications sealed in a water-soluble gelatin shell. after it is ingested, the fluids in the digestive tract will dissolve the shell and allow the chemicals inside to be absorbed by the lining of the stomach and circulated through the body. examples include tylenol, ibuprofen, and benadryl. tablets are solid particles bound into a digestible shape that is then swallowed and then broken down in the digestive tract. it operates very similarly to capsules, except it is not sealed in a gelatin shell. examples include aspirin and tums. powder comes in the form of minuscule particles that are stored in a dry form before they are dissolved into a solution in preparation for administration. usually water or saline; after its mixed, it can be administered. examples include glucagon, vecuronium, and solu-medrol.", + "liquid medications": "enteral liquid medications are administered within the digestive tract. they are swallowed and enter the digestive tract and, like tablets or capsules, are absorbed by the digestive tract. examples include cough syrup and infant acetaminophen. parenteral liquid medications are administered outside of the digestive tract. this almost exclusively refers to medications administered via injection - intravenously, subcutaneously, intramuscularly, or absorbed ointment. examples include fentanyl and adenosine.", + "gaseous medications": "inhalers and spray medications come in the form of a gas or fine mist that are inhaled and are then absorbed usually across the alveolocapillary membrane in the lungs. examples include albuterol and atrovent.", + "basic medication terminology": "within the us, every medication comes with three different names: the chemical name, generic or nonproprietary name, and brand or proprietary name. the chemical name is usually made in the development and reflects the chemical components of the medication, though rarely used in clinical practice (with some exceptions, such as sodium bicarbonate or calcium gluconate.) the generic name may be proposed by the manufacturer but must be approved by the united states adopted names council and the world health organization (who); this name is usually used internationally. many of these names include a stem that connects them to other medications in the same class. finally, the brand name of a medication is created by the manufacturer and approved by the fda. this name does not have the same functional requirements as the generic name but still must meet fda criteria. these names are often selected for marketing purposes or for attaching the medication to a specific condition that it treats.", + "example of medication names": "chemical name: ondansetron hydrochloride, generic name: ondansetron, brand name: zofran", + "drug profile": "pharmacodynamics is the study of how a drug affects the body, producing a reaction - desirable or otherwise. a drug works by being absorbed and distributed through the body. from there, it can attach to receptor sites and affect its change, causing consequences and physiologic changes through the body. this can be affected, for good or ill, by other factors, such as age, weight, genetic factors, and more.", + "indication, intended effects, side effects, and contraindications": "an indication is a complaint or set of signs and symptoms that suggest a medication be used to treat the patient. for example, a complaint of pain indicating the use of analgesics, or a low blood sugar indicating the use of glucose. intended effects refers to the change in symptoms or complaints that are desired after the use of the medication. for example, a patients pain improving after use of analgesics, or a patients mentation and cbg improving after use of glucose. side effects are secondary symptoms that appear after the administration of a medication. these are not intended, but are sometimes predictable and even deemed acceptable if the changes these cause are outweighed by the benefits of the medication being administered. contraindications are a collection of signs or symptoms that indicate a medication should not be used to treat a complaint, even if that medication might improve other symptoms, the possible consequences are worse than the complaint.", + "untoward effects and dose": "untoward effects are secondary, undesired or even unexpected symptoms that appear after the administration of a medication. some of these are mild and/or expected, such as a headache after the use of nitroglycerin, and some of these are severe and/or unexpected, such as an extreme allergic reaction to an iv medication. dose refers to the amount of medication administered. a certain amount of medication must be administered before it can have an effect on the body. this is called the therapeutic threshold and it must be reached before any changes are seen.", + "route of administration": "route is a part of the pharmacokinetics of a medication. if pharmacodynamics is the study of how a drug affects the body, pharmacokinetics is the study of how the body absorbs and breaks down a medication. the medications form will determine by which route the body is exposed to it and it can do this through one of four different methods: ingestion, inhalation, absorption, and injection.", + "prescription and administration": "some medications require a doctors prescription in order to be obtained, where others can be purchased over the counter without a medical consult. the medications found in the first responders toolkit fall under the auspices of medical direction. as always, when preparing to administer a medication, consult your protocols or olmc.", + "medication legislation": "medication legislation refers to the legal history and laws in place surrounding medication use in the united states. as it stands, there is a comprehensive system of medication and drug regulation. regulation first began in the us around 1906, with the passage of the pure food and drug act, which was the first piece of legislation that prohibited altering or mislabeling medications. from there, we moved on to more rigorous legislation, such as the federal food, drog and cosmetic act, 1938, which gave the federal drug administration (fda) enforcement authority to ensure new drugs were safe for public use. to this day, the fda remains the power responsible for approving new medications in the us, as well as removing unsafe medications from use. getting approval for a new medication often takes several years, though occasional breakthrough medications for severe conditions or vaccines for rampant epidemics might receive expedited consideration. only a small amount of medications submitted to the fda are approved and of those, many medications are used off-label, which is a term that means a drug used for a method not approved by the fda, or at dose or via different routes that haven't been approved. off-label use is quite common in health care, such as using benadryl as a sedative which is a common protocol in several agencies, though a physician medical director or paramedic may have a larger risk of legal liability if there's a bad patient outcome second to off-label drug use.", + "controlled substances": "in 1970, the controlled substances act was put through legislation, and it classified certain medications with the potential of abuse into five categories, otherwise known as schedules, with associated security, dispensing, and record-keeping requirements.", + "schedules of controlled substances": "schedule i medications cannot be prescribed, dispensed, used, or administered for medical use. it includes drugs such as heroin, lsd, and marijuana. although marijuana is legally used both medically and recreationally in many states today, at the federal level it is still considered a schedule i controlled substance.\nschedule ii medications have as high a potential for abuse as schedule i medications, however, they have been federally recognized as having a medical use. these include drugs such as fentanyl (sublimaze), methylphenidate (ritalin), and cocaine.\nschedule iii drugs have a lower potential for abuse than schedule ii drugs. examples include vicodin, ketamine, and acetaminophen with codeine.\nschedule iv drugs have a lower potential for abuse than schedule iii drugs. examples include diazepam and lorazepam.\nschedule v drugs have a lower potential for abuse than schedule iv drugs. examples include narcotic cough medicines.", + "medication storage and security": "almost important as medication administration protocols are protocols for drug storage and security. there are several factors affecting drug potency in storage and failure to take these into account may reduce the effectiveness of medications you're attempting to administer.", + "phases of medication activity": "the reason for medication administration is to produce a desired effect in the patient, usually in the treatment of symptoms or underlying condition, or prevent a serious decline in the patient's status.", + "terminology": "antagonism: an interaction between two or more drugs that have opposite effects on the body. drug antagonism may block or reduce the effectiveness of one or more of the drugs.\nbolus: a single dose of a drug or other substance given over a short period of time.\ncontraindications: a condition that serves as a reason to not take a specific medical treatment due to harm that could potentially cause a patient.\ncumulative action: condition in which repeated administration of a drug produces a more pronounced effect than that which was produced on the initial dose.\ndepressant: a drug that reduces functional or nervous activity.\nhabituation: the process of developing a resistance to a drug or medication through habitual or regular use.\nhypersensitivity: an immune-mediated reaction to a drug that might produce an allergic response or other symptoms.\nidiosyncrasy: unexpected and undesired reaction to a drug that occurs in a small percentage of patients and has no obvious relationship to dose or duration of therapy.\nindication: a condition that serves as a reason to take a specific medication or undergo treatment that specifically treats a malady or condition.\npotentiation: an interaction between two or more medications that causes an increase in the potency of the treatment and the medications involved.\nrefractory: a disease or condition that causes a resistance or immunity to treatment or medication.\nside effects: symptoms or conditions that appear when treatment goes beyond or in addition to desired effect.\nstimulant: a drug that increases functional or nervous activity.\nsynergism: the interaction of two or more drugs that have a greater effect when combined than the sum of effects when given individually.\ntherapeutic action: is the results of medical treatment of any kind, whether for good or ill.\ntolerance: a diminished response to treatment or medication built up after frequent exposure.\nuntoward effect: a harmful, abnormal, or adverse effect in response to a medication's administration.", + "pharmacokinetics": "pharmacokinetics refers to the body's effect on a medication and can be broken down into some key principles: absorption, distribution, biotransformation, metabolism & excretion.", + "pharmacodynamics": "pharmacodynamics are, as discussed earlier, how we measure the drug's changes to the human body and physiology, as opposed to pharmacokinetics, which is a measure of how a drug is absorbed and how the body's physiology affects an absorbed drug.", + "medication response relationship": "medication response relationship, also known as the dose response relationship, is used to define the total response of an organism to a medication dose.", + "factors that alter a drug's response": "age is a major factor to how medications are metabolized.\nsex can have a more potent affect on the outcomes of a pharmacological intervention.\nweight has a distinct impact on many medication doses, which are often calculated based on a patient's weight.\nthe environment can also play into how a drug is metabolized by the body.\nthe pathologic state can affect how efficiently a patient can utilize and metabolize a drug.\ngenetic factors play into pharmacology the same way pre existing conditions and comorbidities play into.\ntime of administration sometimes known as chronotherapy determines what time of day or in which order a medication should be administered.\ntolerance refers to an observable phenomenon in pharmacology in which repeated exposure to a medication leads to diminished effects.", + "schedule i": "schedule i medications cannot be prescribed, dispensed, used, or administered for medical use. it includes drugs such as heroin, lsd, and marijuana. although marijuana is legally used both medically and recreationally in many states today, at the federal level it is still considered a schedule i controlled substance.", + "schedule ii": "schedule ii medications have as high a potential for abuse as schedule i medications, however, they have been federally recognized as having a medical use. these include drugs such as fentanyl (sublimaze), methylphenidate (ritalin), and cocaine.", + "schedule iii": "schedule iii drugs have a lower potential for abuse than schedule ii drugs. examples include vicodin, ketamine, and acetaminophen with codeine.", + "schedule iv": "schedule iv drugs have a lower potential for abuse than schedule iii drugs. examples include diazepam and lorazepam.", + "schedule v": "schedule v drugs have a lower potential for abuse than schedule iv drugs. examples include narcotic cough medicines.", + "medication administration in special populations": "when determining dosage, some considerations have to be made for special populations, as they have different ways of tolerating and metabolizing different meds. for example, geriatric populations usually have a less-efficient liver and ability to process medications, so some meds - such as toradol - need to be altered after a certain patient age, to prevent long term damage to a patient's organ systems.", + "pregnancy risk categories": "category a: controlled studies in women fail to demonstrate a risk to the fetus in the first trimester and possibility of fetal harm appears remote. category b: either animal-reproduction studies have not demonstrated fetal risk but there are no controlled studies in pregnant women, or animal-reproduction studies have shown an adverse effect that was not confirmed in controlled studies in women in their first trimester.", + "medication naming": "within the us, every medication comes with three different names: the chemical name, generic or nonproprietary name, and brand or proprietary name.", + "medication classifications": "while there are thousands of medications in the world, each one is usually designed for a specific purpose and treatment focus. this focus is what classifies a drug and it is determined by the body system affected and the mechanism of action.", + "sources of drugs": "medications are derived or constructed from a wide range of sources. since ancient times, treatments have been harnessed from the world around them; organic (plants, alkaloids, and animals) and inorganic (minerals) both providing isolatable compounds for use in the treatment of maladies and illness.", + "absorption": "absorption refers to the route by which the body is exposed to the medication or substance.", + "distribution": "distribution through the body is determined by the chemical and physical properties of the medication administered.", + "biotransformation": "some medications change their chemical structure after entering the body. this process is known as biotransformation.", + "excretion": "excretion occurs after a medication has served its purpose and is then processed through the body before being eliminated.", + "mechanism of action": "mechanism of action refers to the means by which a chemical affects the body, producing an intended response.", + "drug receptor interactions": "drug receptor interactions are the basis of most chemical interactions in the body." + }, + { + "Anaphylactic Precautions": "GENERAL INFORMATION \n \n \nAll medications in this manual listed as IV may also be administered IO. \n \nA known hypersensitivity is a contraindication to that medication. \n \nFor all medications, follow dosages specified in the current Delaware Paramedic Standing Orders document. \n \n \n \nANAPHYLACTIC PRECAUTIONS \n \n \nAnaphylaxis: \n \nA generalized reaction occurring with dramatic suddenness (usually within a few minutes) after \nexposure to some foreign material. \n \nCause: \n \nAny drug has the potential to precipitate anaphylaxis. Generally medications administered \nintravenously or parenterally are more likely to result in life-threatening or fatal anaphylaxis than \nmedications ingested or applied to the skin or mucous membranes. \n \nClinical features: \n \nThe patient with anaphylaxis may develop laryngeal edema and bronchospasm which cause \nrespiratory distress and anoxia. The sooner the symptoms develop after the initiating stimulus the \nmore intense the reaction. The symptoms include the following: generalized flush, urticaria, pruritus, \nanxiety, dyspnea, wheezing, choking, orthopnea, vomiting, cyanosis, paresthesia, shock, and loss of \nconsciousness. Anoxia, shock, and death may occur within 5-10 minutes. \n \nPrevention: \nA. \nKnow the patient's allergy history by asking the patient or family before giving a new \nmedication. \n \nB. \nKnow the precautions listed for each drug. \n \nTreatment: \nA. \nStop the infusion of the medication but keep the IV line open. \n \nB. \nMaintain the airway. \n \nC. \nBe prepared to treat anaphylactic shock according to The Statewide Standard Treatment \nProtocol \n \nD. \nCall the medical command physician. \n \nE. \nAfter the emergency episode is over, calm the patient. Be certain that the patient has been \ninformed of the allergy and that the allergy is documented on the report form. Verbally report \nthe episode on arrival to hospital personnel and complete a variance report.", + "Infiltration Precautions": "INFILTRATION PRECAUTIONS \n \nBefore administering any IV medication or solution, the paramedic must check the IV site for patency and \nsigns of infiltration and/or phlebitis. If infiltration occurs, stop the drug but do not remove the IV device. \nContact the medical control physician immediately for orders. \n \nFACTORS THAT INCREASE THE RISK OF INFILTRATION \n \nA. \nSclerotic vascular disease \nB. \nVenous obstruction in the arm (check for edema) \nC. \nRadiation treatment near the site of injection \nD. \nHigh drug concentration \nE. \nLimited choice for vein selection \nF. \nMultiple venipunctures \nG. \nElderly or debilitated \nH. \nSuperior vena cava syndrome \nI. \nSpecific characteristics of the drug \nJ. \nUncooperative/irrational individual \n \nSYMPTOMS OF AN INFILTRATION \n \nIf pain, burning or stinging occurs at the injection site, evaluate the site for swelling, redness, and \ninflammation. The presence of a blood return or absence of edema does not negate the possibility of \nan infusate being outside the vein in surrounding tissue. Drug leakage may occur at the site of a \nprevious vessel injury while the needle/catheter is still in the vein. \n \nIRRITANTS (DEXTROSE, DIAZEPAM) \n \n \nA. \nDefinition: An irritant is a medication that induces a local inflammatory reaction within the \nvein at the IV site. \n \n \nB. \nGuidelines for reducing irritation: Reduce local irritation by decreasing the infusion rate or \nby decreasing the drug concentration (increasing the diluent and/or increasing the \nintravenous solution flow rate while injecting the drug). \n \nVESICANTS \n \n(i.e. DOPAMINE) \n \nA. \nDefinition: A vesicant is a medication that induces blistering of tissues and may \n \n lead to tissue necrosis if the medication extravasates (infiltrates) \n \n from the vein into the surrounding tissue. \n \n \nB. \nGuidelines to reduce the danger of infiltration \nBecause the consequences may be severe to the patient, implement every effort to \nprevent infiltration. Observe the IV site frequently so that an infiltration can be \nidentified early and further damage prevented. \n \n \nC. \nTreatment Guidelines for Vesicant Infiltration \n \n1) \nSTOP INJECTION IMMEDIATELY: If possible, leave the IV device in place. \nIt may be possible to aspirate the drug or administer an antidote through the \ndevice. \n \n2) \nCALL MEDICAL CONTROL PHYSICIAN FOR INSTRUCTIONS \n \n3) \nReport the reaction on arrival to the hospital and note infiltration on report \nform. \n \n4) \nApply cold compress if possible.", + "Acetaminophen": "ACETAMINOPHEN (Tylenol\u00ae) \n \nClass \u2013 analgesic and antipyretic \nPharmacologic Action \u2013 exact mechanism of action not fully determined, may inhibit nitric oxide pathway \nmediated by neurotransmitters like NMDA to elevate pain threshold. Antipyretic action through inhibition of \nprostaglandin synthesis and release in CNS with effects in the heat-regulating center of hypothalamus. Little \neffect on platelet function and not known to cause gastrointestinal bleeding. Not an NSAID \u2013 has no anti-\ninflammatory properties \nOnset: 30 - 45 minutes \n \nPeak Effect: 1 hour \n \n \nDuration: 4-6 hours \nIndications: \n\u2022 \nPain of musculoskeletal injury origin \nContraindications: \n\u2022 \nAllergy \n\u2022 \nLiver disease or injury \n\u2022 \nReduced hepatic function \n\u2022 \nHeavy alcohol abuse \nWarnings: \n \n\u2022 \nUse with caution in pregnancy and thrombocytopenia \n \n \nDrug Interactions: \n\u2022 \nLeeflunomide, levoketoconazole, lomitapide, mipomersen, pexidartinib, teriflunomide \u2013 may all \nincrease risk of liver damage \n \n \nAdverse Reactions: \n \n \nNausea/vomiting and abdominal pain \n \n \n \n \nProtocols Containing Acetaminophen: \n \nPediatric and Adult Pain Management", + "Adenosine": "ADENOSINE (Adenocard\u00ae) \n \nClass \u2013 Antidysrhythmic (Class V) \nPharmacologic Action - Slows conduction through AV node and interrupts AV reentry pathways, which \nrestore normal sinus symptoms. \nOnset: 20-30 seconds \nPeak Effect: 20-30 seconds \n \nDuration: 30 seconds \nIndications: \n\u2022 \nConversion of regular, narrow complex tachycardia \u2013 stable supraventricular tachycardia (SVT) or \nregular, monomorphic wide complex tachycardia (WCT). \nContraindications: \n\u2022 \nSecond- or third-degree AV Block (except those on pacemakers). \n\u2022 \nSick sinus syndrome. \n\u2022 \nAtrial flutter or fibrillation. \n\u2022 \nVentricular tachycardia / Torsades. \n\u2022 \nAsthma. \nWarnings: \n \n\u2022 \nMay produce a short period of first-, second-, or third-degree AV block as well as transient or prolonged \nasystole. \n\u2022 \nUse with caution in patients taking digoxin and/or verapamil as cases of ventricular fibrillation have \nbeen reported. \n\u2022 \nMay produce new arrhythmias during conversion. \n\u2022 \nMay cause bronchoconstriction and/or respiratory compromise in asthma or COPD patients. \n \nDrug Interactions: \n \n\u2022 \nDigoxin or verapamil - potential for additive or synergistic effects. \n\u2022 \nMethylxanthines (caffeine, aminophylline and theophylline) - antagonize action of adenosine (may \nrequire higher doses). \n\u2022 \nDipyridamole (Persantine\u00ae, Aggrenox\u00ae) - potentiates the effect of adenosine (reduce adenosine \ndoses). \n\u2022 \nCarbamazepine (Tegretol\u00ae) - may increase degree of heart block following adenosine administration. \n \nAdverse Reactions: \n \n \nMay result in facial flushing, diaphoresis, headache, chest pain, palpitations, hypotension, and shortness \nof breath, lightheadedness, paresthesia, or nausea. \n \nProtocols Containing Adenosine: \n \nAdult Stable Tachycardia \nAdult Unstable Tachycardia \nPediatric Tachycardia", + "Albuterol Sulfate": "ALBUTEROL SULFATE (Proventil\u00ae, Ventolin\u00ae) \n \nClass \u2013 Beta-2 sympathetic agonist \nPharmacologic Action \u2013 Sympathomimetic selective for beta-2 receptors. Relaxes bronchial smooth \nmuscle with little effect on heart rate. \nOnset: 5-15 minutes \nPeak Effect: 1 \u2013 1.5 hours \n \nDuration: 3-6 hours \n \nIndications: \n\u2022 \nBronchospastic lung disease. \nContraindications: \n\u2022 \nTachycardic dysrhythmias (rate greater than 150 bpm). \n \nWarnings \n \n\u2022 \nMay not adequately control asthma when used alone; consider corticosteroids. \n\u2022 \nMay cause a significant cardiovascular effect (increased pulse rate or blood pressure, ECG changes) \nas well as pronounced hypokalemia \u2013 caution with use in elderly or those with cardiac history. \n\u2022 \nImmediate hypersensitivity reactions may occur, such as urticaria, angioedema, and anaphylaxis. \n\u2022 \nLarge doses of albuterol have been reported to worsen preexisting diabetes and ketoacidosis. \n \nDrug Interactions \n \n\u2022 \nSympathetic agonists \u2013 increase potential for side effects. \n\u2022 \nBeta-blockers \u2013 may blunt effects of albuterol. \n \nAdverse Reactions \n \n \nTremors, dizziness, headache, nausea, nasal congestion, tachycardia, arrhythmias, hypertension, \nbronchospasm, and cough. \n \nProtocols Containing Albuterol: \n \nAdult Acute Respiratory Distress \nPediatric Acute Respiratory Distress", + "Amiodarone": "AMIODARONE (Cordarone\u00ae) \n \nClass \u2013 Antidysrhythmic (Class III) \nPharmacologic Action - Inhibits adrenergic stimulation; affects sodium, potassium, and calcium channels; \nmarkedly prolongs action potential and repolarization; decreases AV conduction and sinus node function. \nAlso has some alpha- and beta-adrenergic blocking properties. \nOnset: 1-2 minutes \n \nPeak Effect: 10 minutes \n \nDuration: \nIndications \n\u2022 \nRegular wide complex tachycardia in stable patients. \n\u2022 \nIrregular wide complex tachycardia in stable patients. \n\u2022 \nAntidysrhythmic for the management of ventricular fibrillation (VF) and pulseless ventricular \ntachycardia (VT). \nContraindications \n \n\u2022 \nCardiogenic shock marked sinus bradycardia, and second- or third-degree AV block (unless a \npacemaker is available). \n \nWarnings: \n \n\u2022 \nDrug-related bradycardia or worsening of existing arrhythmias may also occur. \n\u2022 \nUse in pregnancy should only occur if the potential benefit to the mother justifies the risk to the fetus. \n\u2022 \nCaution with use in heart failure. \n \nDrug Interactions: \n \n\u2022 \nWarfarin, digoxin, quinidine, procainamide, disopyramide (Norpace\u00ae), fentanyl, lidocaine, and \ncyclosporine \u2013 amiodarone may increase their effects. \n\u2022 \nCholestyramine and phenytoin (Dilantin\u00ae) - may decrease levels of amiodarone in the body. \n\u2022 \nCimetidine may increase amiodarone levels. \n\u2022 \nBeta- or calcium channel blockers - may worsen hypotension or result in bradycardia. \n \nAdverse Reactions: \n \n \nHypotension is the most common adverse effect. Other adverse effects include cardiac arrest, \nasystole, PEA, cardiogenic shock, CHF, bradycardia, V-Tach, and AV block. Angioedema and anaphylaxis \nmay also occur. \n \nProtocols Containing Amiodarone: \n \n \nAcute Coronary Syndrome \n \nST Elevation Myocardial Infarction (STEMI) \n \nAdult Stable Tachycardia \n \nAdult Unstable Tachycardia \n \nAdult Ventricular Fibrillation (VF) and/or Pulseless Ventricular Tachycardia (VT) \nPediatric Ventricular Fibrillation (VF) and/or Pulseless Ventricular Tachycardia (VT)", + "Amyl Nitrate": "AMYL NITRATE \n \nClass \u2013 Nitrate, Cyanide antidote \nPharmacologic Action - Oxidizes hemoglobin to form methemoglobin. Methemoglobin is incapable of \noxygen transport but has a high affinity for cyanide. Cyanide preferentially binds to methemoglobin instead of \ncytochrome a3 in the mitochondria. This forms cyanomethemoglobin that carries the cyanide to the liver for \ndetoxification and elimination. \nOnset: 10 \u2013 30 seconds \n \nPeak Effect: 30 seconds \n \nDuration: 3 \u2013 5 minutes \nIndications \n\u2022 \nAcute cyanide toxicity. \nContraindications \n\u2022 \nNone in the case of suspected pure cyanide toxicity. \n\u2022 \nDo not use in cases of known or suspected carbon monoxide poisoning. \nWarnings: \n \n\u2022 \nThere is a risk of worsening hypoxia due to methemoglobin formation. \n\u2022 \nAmyl Nitrate vapors are extremely flammable, do not use near open flame or intense heat. \n\u2022 \nUse in children has not been studied. \n \nDrug Interactions: \n \n\u2022 \nAntihypertensive medications, nitrates, beta-blockers, antiemetics (phenothiazines) \u2013 potentiate \nhypotensive effects and may result in severe hypotension. \n \nAdverse Reactions: \n \n \nHeadache, dizziness, weakness, orthostatic hypotension, tachycardia, and nausea/vomiting. \n \nProtocols Containing Amyl Nitrate: \n \n \nCyanide Exposure (ToxMedic) \n \nSulfide Exposure (Toxmedic)", + "Aspirin": "ASPIRIN \n \n \nClass \u2013 Antiplatelet agent, non-steroidal anti-inflammatory drug (NSAID). \nPharmacologic Action - Inhibits synthesis of prostaglandin by cyclooxygenase inhibiting platelet \naggregation. Aspirin also has antipyretic and analgesic activity. \nOnset: 5-30 minutes \n \nPeak Effect: 15-120 minutes \n \nDuration: 1-4 hours \nIndications \n\u2022 \nAcute coronary syndrome. \nContraindications \n\u2022 \nHypersensitivity to aspirin or NSAIDs (aspirin-associated hypersensitivity reactions include aspirin-\ninduced urticarial or aspirin-intolerant asthma). \n\u2022 \nBleeding disorders \u2013 ulcers, hemophilia, hemorrhagic diathesis, hemorrhoids, thrombocytopenia, and \nulcerative colitis. \n\u2022 \nHemolytic anemia from pyruvate kinase (PK) and glucose-6-phosphate dehydrogenase (G6PD) \ndeficiency. \n\u2022 \nLactating mother. \nWarnings: \n \n\u2022 \nIncreases bleeding by inhibiting platelet function in patients with bleeding disorders. \n\u2022 \nPatients with peptic ulcer disease should avoid aspirin, as it may result in irritation and bleeding. \n \nDrug Interactions: \n \n\u2022 \nACE inhibitors \u2013 ASA diminishes their effects by affecting the renin-angiotensin conversion pathway. \n\u2022 \nWarfarin, Heparin, Coumadin - prolongs prothrombin and bleeding times. \n\u2022 \nPhenytoin \u2013 decreases concentration of phenytoin. \n\u2022 \nValproic acid \u2013 increases concentration of valproic acid. \n\u2022 \nBeta blockers and diuretics - may be less effective due to decreased renal blood flow and retention of \nsalt and fluid. \n\u2022 \nMethotrexate \u2013 inhibits clearance which may result in toxicity. \n\u2022 \nOral hypoglycemics \u2013 may increase their effectiveness resulting in hypoglycemia. \n\u2022 \nAntacids \u2013 reduce absorption of aspirin. \n \nAdverse Reactions: \n \n \n Anaphylaxis, bronchospasm/wheezing, dysrhythmias, hypotension, tachycardia, agitation, cerebral \nedema, intracranial hemorrhage, dehydration, hyperkalemia, heartburn, and renal failure. \n \nProtocols Containing Aspirin: \n \nAcute Coronary Syndromes (ACS) \nST Elevation Myocardial Infarction (STEMI)", + "Atropine Sulfate": "ATROPINE SULFATE \n \nClass \u2013 Anticholinergic \nPharmacologic Action \u2013 Parasympatholytic, blocks acetylcholinesterase receptors and inhibits \nparasympathetic stimulation. Positive chronotropic properties with little or no inotropic effects. \nOnset: Immediate \n \nPeak Effect: 2-4 minutes \n \nDuration: 4 hours \nIndications: \n\u2022 \nSymptomatic bradycardia (primary or related to toxin ingestion). \n\u2022 \nNerve agent/organophosphate and carbamate insecticide toxicity. \nContraindications: \n\u2022 \nNone in emergency situations (ACLS/nerve agent/organophosphate scenarios). \n\u2022 \nRelative contraindications: \no \nNarrow-angle glaucoma. \no \nGI obstruction / toxic megacolon. \no \nSevere ulcerative colitis. \no \nBladder outlet obstruction. \no \nMyasthenia gravis. \no \nHemorrhage with cardiovascular instability. \no \nThyrotoxicosis (excess production of thyroid hormones accelerating metabolic processes, \nmore common in women). \nWarnings: \n \n\u2022 \nV Fib and V Tach have occurred following IV administration. \n\u2022 \nMay induce tachycardia harmful to patients suffering AMI or infarction due to increased myocardial \noxygen demand. \n\u2022 \nDoses less than 0.5 mg in an adult can induce paradoxical bradycardia and ventricular arrhythmias. \n\u2022 \nIneffective in hypothermic bradycardias. \n \nDrug Interactions: \n \n\u2022 \nWith other anticholinergics - may increase effects of vagal blockade. \n\u2022 \nAntihistamines, procainamide, quinidine, and psychotropic medications \u2013 may enhance atropine\u2019s \neffects. \n \nAdverse Reactions: \n \n \nExcessive doses of atropine can cause delirium, tachycardia, coma, flushed and hot skin, ataxia and \nblurred vision. Paradoxical bradycardia may result from doses less than 0.5 mg. Side effects may include \npalpitations, dysrhythmias, headache, dizziness, nausea and vomiting. \n \nProtocols Containing Atropine: \n \n \nAdult Hemodynamically Compromising Bradycardia \n \nPediatric Bradycardia \nPatient Restraint \nCholinesterase Inhibitor Exposure (Tox Medic)", + "Buprenorphine": "BUPRENORPHINE \n \nClass \u2013 Narcotic analgesic \nPharmacologic Action \u2013 Opioid partial agonist-antagonist used to prevent withdrawal symptoms in treating \nopioid dependence. \nOnset: 30-60 minutes \n \nPeak Effect: 3-4 hours \n \nDuration: 24-72 hours \nIndications: \n\u2022 \nAdult patients who received naloxone to reverse opioid overdose. \nContraindications: \n\u2022 \nPatient unwilling to participate in program \u2013 does not provide name and date of birth \n\u2022 \nPregnancy \n\u2022 \nMethadone use less than 45 minutes prior to buprenorphine \n\u2022 \nAltered mental status \n\u2022 \nUnable to give consent \nWarnings: \n \n\u2022 \nMay precipitate withdrawal symptoms in patients who are addicted to opioids. \n\u2022 \nCaution in patients with respiratory depression and gastrointestinal obstruction. \n \nDrug Interactions: \n \n\u2022 \nCaution in patients receiving other opioids/narcotics. \n \n \nAdverse Reactions: \n \n \nNausea, vomiting, drowsiness, dizziness, headache, memory loss, sweating, dry mouth, miosis, \northostatic hypotension, urinary retention, abdominal pain, constipation, blurred vision \n \n \nProtocols Containing Buprenorphine: \n \n \nAdult Altered Mental Status \n \nBuprenorphine", + "Calcium Chloride": "CALCIUM CHLORIDE \n \nClass \u2013 Calcium salt \nPharmacologic Action - Bone mineral component; cofactor in enzymatic reactions, essential for myocardial \ncontraction, neurotransmission, muscle contraction, and many signal transduction pathways. Provides free \ncalcium (Ca2+ ). \nOnset: Immediate \n \nPeak Effect: Unknown \n \n \nDuration: Varies \nIndications: \n\u2022 \nCalcium channel blocker overdose. \n\u2022 \nHyperkalemia/hypocalcemia (chronic renal failure/dialysis). \n\u2022 \nAntidote for magnesium sulfate overdose. \n\u2022 \nTopical burns caused by hydrofluoric acid. \nContraindications: \n\u2022 \nHypercalcemia. \n\u2022 \nSevere hypokalemia. \nWarnings: \n \n\u2022 \nUse of Calcium Chloride limited to medical control consult only. \n\u2022 \nRisk for digitalis toxicity. \n\u2022 \nCaution with peripheral IV use as significant tissue necrosis at injection site may occur. \n\u2022 \nRapid injection may result in bradycardia. \n\u2022 \nMay produce coronary and cerebral artery spasm. \n \nDrug Interactions: \n \n\u2022 \nDigoxin - may increase ventricular irritability and precipitate digitalis toxicity. \n\u2022 \nSodium Bicarbonate - calcium salts will precipitate from solution \u2013 flush line between meds. \n\u2022 \nVerapamil - may antagonize vasodilatory action of verapamil. \n \nAdverse Reactions: \n \n \nMay cause bradycardia, asystole, and hypotension. \n \nProtocols Containing Calcium Chloride: \n \n \nAdult Altered Mental Status \n \nAdult Hemodynamically Compromising Bradycardia \n \nAdult Stable Tachycardia \n \nAdult Unstable tachycardia \n \nAdult Ventricular Fibrillation (VF) and/or Pulseless Ventricular Tachycardia (VT) \n \nAdult Asystole / Pulseless Electrical Activity", + "Calcium Gluconate": "CALCIUM GLUCONATE \n \nClass \u2013 Calcium salt \nPharmacologic Action \u2013 In cases of hydrofluoric acid (HF) exposure, HF will seek out calcium stores in the \nbody. Primary sources are the bones and the cardiac conduction system. Calcium gluconate will supply \nelemental calcium to the HF in order to substitute for the body\u2019s natural calcium stores. \nOnset: 1 \u2013 3 minutes (IV) \n \nPeak Effect: Variable \n \nDuration: 30 \u2013 60 minutes \nIndications: \n\u2022 \nTopical burns caused by hydrofluoric acid. \n\u2022 \nCalcium channel blocker overdose. \nContraindications: \n\u2022 \nHypercalcemia. \n\u2022 \nSarcoidosis. \n\u2022 \nSuspected severe hypokalemia (life-threatening cardiac arrhythmias may occur). \nWarnings: \n \n\u2022 \nRisk of digitalis toxicity. \n\u2022 \nSQ or IM administration can cause severe tissue necrosis and tissue sloughing. \n\u2022 \nCan induce serious cardiac dysrhythmias. \n \nDrug Interactions: \n \n\u2022 \nNone known. \n \nAdverse Reactions: \n \n \nUsually adverse reactions are seen in calcium over-dosage. Clinical manifestation includes \nconstipation, mouth drying, headache, anxiety, thirst, appetite loss, depression, metal taste, fatigue, and \nweakness. In fast parenteral injection nausea, vomiting, diarrhea, bradycardia, hypotension and, rarely, \ncollapse may appear. \n \nProtocols Containing Calcium Gluconate: \n \n \n Hydrofluoric Acid Exposure (Tox Medic)", + "Dextrose": "DEXTROSE \n \nClass \u2013 Carbohydrate \nPharmacologic Action \u2013 Rapidly increases blood glucose. Oxidizes to carbon dioxide and water. Provides \n3.4 kilocalories/gram of d-glucose (this is the primary form of sugar used by the body). \nOnset: < 1 minute \n \nPeak Effect: Variable \nDuration: Variable \n \nIndications: \n\u2022 \nHypoglycemia \nContraindications: \n\u2022 \nHyperglycemia. \n\u2022 \nAnuria. \n\u2022 \nDiabetic coma. \n\u2022 \nIntracranial or intraspinal hemorrhage. \n\u2022 \nIncreased intracranial pressure. \n\u2022 \nDehydration with delirium. \n\u2022 \nGlucose-galactose malabsorption syndrome. \nWarnings: \n \n\u2022 \nExtravasation may result in tissue necrosis - use large vein for access. \n\u2022 \nMay induce acute thiamine deficiency (Wernicke-Korsakoff syndrome) in malnourished patients and \nchronic alcoholics. \n \nDrug Interactions: \n \n\u2022 \nNone known \n \nAdverse Reactions: \n \nWarmth, pain, burning, or phlebitis secondary to injection. \n \nProtocols Containing Dextrose: \n \n \nAdult Altered Mental Status \n \nSuspected Stroke \n \nAdult Seizures (Active) \n \nPediatric Altered Mental Status \n \nPediatric Seizures (Active)", + "Diazepam": "DIAZEPAM (Valium\u00ae) \n \nClass \u2013 Benzodiazepine \nPharmacologic Action \u2013 Binds to sites on gamma-aminobutyric acid (GABA). Has no direct effect on \nGABA receptors but potentiates the effects of GABA within the brain (GABA is the main inhibitory \nneurotransmitter in the CNS \u2013 by potentiating the effects of GABA, Diazepam promotes sedation). In \nseizures, does not atop abnormal discharge focus but does stop the spread of seizure activity though the \nmotor cortex. Skeletal muscle relaxant (ortho injuries) and induces amnesia. Modulates postsynaptic effects \nof GABA-A transmission, resulting in an increase in presynaptic inhibition. Appears to act on part of the \nlimbic system, as well as on the thalamus and hypothalamus, to induce a calming effect. \nOnset: 1 \u2013 5 minutes (IV) \n \nPeak Effect: 15 minutes (IV) \n \nDuration: 15 \u2013 60 minutes \n \nOnset: 15 \u2013 30 minutes (IM) \n \nPeak Effect: 30 \u2013 45 minutes (IM) \nDuration: 15 \u2013 60 minutes \n \nIndications: \n\u2022 \nActive seizures (Under DE protocol \u2013 diazepam is only used IM for seizures caused by \ncholinesterase inhibitor exposure). \nContraindications: \n\u2022 \nSevere respiratory depression. \nWarnings: \n \n\u2022 \nMay cause respiratory depression. \n\u2022 \nNo effect on pain. \n \nDrug Interactions: \n \n\u2022 \nOther CNS depressants \u2013 may result in significant CNS depression. \n\u2022 \nOther IV meds - may precipitate, flush line between meds. \n \nAdverse Reactions: \n \n \nHypotension, tachycardia, respiratory depression, confusion, nausea, and impairment. \n \nProtocols Containing Diazepam: \n \n \nCholinesterase Inhibitor Exposure (Tox Medic).", + "Diltiazem Hydrochloride": "DILTIAZEM HYDROCHLORIDE (Cardizem\u00ae) \n \nClass \u2013 Antidysrhythmic (Class IV), calcium channel blocker \nPharmacologic Action - Inhibits extracellular calcium ion influx across membranes of myocardial cells and \nvascular smooth muscle cells, resulting in inhibition of contraction and thereby dilating main coronary and \nsystemic arteries. No effect on serum calcium concentrations. Substantial inhibitory effects on cardiac \nconduction system, acting principally at AV node, slowing the ventricular rate associated with Atrial \nFibrillation and Atrial Flutter. \nOnset: 3 minutes \n \nPeak Effect: 7 minutes \nDuration: 1-3 hours \nIndications: \n\u2022 \nNarrow complex tachycardias \u2013 Atrial Fibrillation/Atrial Flutter. \n\u2022 \nSVT not responding to adenosine. \nContraindications: \n\u2022 \nCongestive Heart Failure. \n\u2022 \nWolff-Parkinson-White syndrome. \n\u2022 \nLown-Ganong-Levine syndrome. \n\u2022 \nSymptomatic severe hypotension (systolic BP < 90 mm Hg) \n\u2022 \nSick sinus syndrome (if no pacemaker). \n\u2022 \nSecond and third degree heart block (if no pacemaker present) and complete heart block. \n\u2022 \nConcomitant beta-blocker therapy. \n\u2022 \nCardiogenic shock. \n\u2022 \nVentricular tachycardia (must determine whether origin is supraventricular or ventricular). \nWarnings: \n \n\u2022 \nProlongation of AV node conduction may result in second- or third-degree AV block. \n\u2022 \nShould not be administered to compromised myocardium (severe CHF, AMI, or cardiomyopathy). \n\u2022 \nUse caution when giving to hypotensive patients. \n\u2022 \nMay result in hepatic injury. \n\u2022 \nCalcium chloride is an antidote for cases of hypotension due to overdose of Diltiazem. \n \n \n \nDrug Interactions: \n \n\u2022 \nBeta blockers \u2013 do not administered together or within a few hours. \n\u2022 \nAnesthetics - may potentiate the effects on cardiac contractility, conductivity, and automaticity. \n\u2022 \nCarbamazepine (Tegretol\u00ae) \u2013 may elevate levels of Tegretol (toxicity). \n\u2022 \nDigoxin - use with caution. \n \nAdverse Reactions: \n \n \nHypotension, asystole, AV block, bradycardia, chest pain, CHF, ventricular arrhythmias, flushing, \ninjection site reactions, nausea, vomiting, and dizziness. \n \nProtocols Containing Diltiazem: \n \n \nAdult Stable Tachycardia", + "Diphenhydramine Hydrochloride": "DIPHENHYDRAMINE HYDROCHLORIDE (Benadryl\u00ae) \n \nClass - Antihistamine \nPharmacologic Action - Histamine H1-receptor antagonist of effector cells in respiratory tract, blood \nvessels, and GI smooth muscle. Blocks histamine response. Also has anticholinergic actions. \nOnset: 10 \u2013 15 minutes (IV) \n \nPeak Effect: 1 hour \n \nDuration: 6 \u2013 8 hours \n \nIndications: \n\u2022 \nUrticarial and/or pruritus from allergic reactions. \n\u2022 \nDystonia/akathisia (extrapyramidal symptoms). \nContraindications: \n\u2022 \nPremature infants and neonates. \nWarnings: \n \n\u2022 \nUse with caution in patients with severe vomiting, asthma, narrow-angle glaucoma, benign prostatic \nhypertrophy, and alcohol intoxication. \n \n \nDrug Interactions: \n \n\u2022 \nMAO inhibitors - may prolong and potentiate diphenhydramine. \n\u2022 \nFurosemide \n \nAdverse Reactions: \n \n \nDrowsiness, thickening of bronchial secretions, hypotension, tachycardia, bradycardia, and dry mouth. \n \nProtocols Containing Diphenhydramine: \n \n \nAdult Allergic/Adverse Reactions/Dystonic Reaction (Severe and Moderate/Dystonic) \n \nPediatric Allergic Reactions (Severe and Moderate) \n \nPatient Restraint", + "Droperidol": "Droperidol \n \nClass- Antipsychotic; Antiemetic \n \nPharmacologic Action- Dopamine antagonist, predominantly blocks dopamine-2 receptors in the brain, also \nalpha-adrenergic blockade \n \nOnset: 3-10 minutes \n \nPeak Effect: ~30 minutes \n \nDuration: 2-4 hours \n \nIndications: \n \n\u2022 \nAcute psychosis or agitated/violent behavior refractory to non-pharmacologic interventions. \n\u2022 \nNausea and vomiting refractory to Zofran(Ondansetron) \n \nContraindications: \n \n\u2022 \nSevere CNS depression \n\u2022 \nProlonged QT interval or history of long QT syndrome (QTc >440 msec for males or >450 msec for \nfemales) \n\u2022 \nNeuroleptic malignant syndrome \n\u2022 \nParkinson\u2019s disease \n \nWarnings: \n \n\u2022 \nRisk of QT prolongation and/or torsades de pointes \n\u2022 \nUse caution in patients with cardiac disease or bradycardia (HR<50/minute) \n \nDrug Interactions: \n \n\u2022 \nMay increase the effects of other sedating medications. \n\u2022 \nAntihypertensive medications\u2014may increase the possibility of orthostatic hypotension. \n\u2022 \nAnti-Parkinson agents (such as carbidopa/levodopa)\u2014may diminish effects of Anti-Parkinson \nmedications through dopamine blockade. \n\u2022 \nAntiarrhythmics (such as flecainide, amiodarone, or sotalol) which may prolong the QT interval. \n \nAdverse Reactions: \n \n\u2022 \nCNS depression, orthostatic hypotension, respiratory depression. \n\u2022 \nExtrapyramidal reactions, such as akathisia or dystonic reactions (have diphenhydramine available) \n\u2022 \nNeuroleptic malignant syndrome, rarely. \n\u2022 \nRisk of QT prolongation, although more recent studies have suggested risk is less than previously \nstated. \n \nProtocols Containing Droperidol: \n \nPatient restraint \n \nGeneral Patient Care", + "Epinephrine": "EPINEPHRINE \n \nClass \u2013 Sympathetic (Alpha/beta adrenergic) agonist \nPharmacologic Action \u2013 Epinephrine has both alpha- and beta-adrenergic effects. Epi\u2019s beta-adrenergic \neffects are much stronger than it\u2019s alpha effects. Alpha stimulation increases peripheral vascular resistance \nthrough vasoconstriction and helps to increase the force of cardiac contractions. The stronger beta effects \nincrease the heart rate, contractility, and automaticity. Strong beta-1- and moderate beta-2-adrenergic effects \nresult in bronchial smooth muscle relaxation. There are also secondary relaxation effects on smooth muscle \nof stomach, intestine, uterus, and urinary bladder. \nOnset: < 2 minutes (IV) \n Peak Effect: < 5 minutes (IV) \nDuration: 5-10 minutes (IV) \n \nOnset: 3-10 minutes (IM) \n Peak Effect: 20 minutes (IM) \nDuration: 20-30 minutes (IM) \n \nIndications: \n\u2022 \nAnaphylaxis. \n\u2022 \nShock. \n\u2022 \nCardiac arrest. \n\u2022 \nBradycardia. \n\u2022 \nExacerbation of some COPD, croup/bronchiolitis and refractory acute asthma. \nContraindications: \n\u2022 \nCardiac dilatation and coronary insufficiency. \nWarnings: \n \n\u2022 \nCauses a dramatic increase in myocardial oxygen demand). \n \nDrug Interactions: \n \n\u2022 \nSodium bicarbonate - inactivates epinephrine. \n\u2022 \nMAO inhibitors, antidepressants, and bretylium - may potentiate epinephrine. \n\u2022 \nBeta antagonists - may negatively affect epinephrine. \n\u2022 \nSympathomimetics and phosphodiesterase inhibitors - may act as proarrhythmics in conjunction with \nepinephrine. \n \nAdverse Reactions: \n \n \nHeadache, nausea, restlessness, palpitations, weakness, dysrhythmias, hypertension, and angina. \n \nProtocols Containing Epinephrine: \n \nAdult Acute Respiratory Distress \n \nAdult Allergic/Adverse Reactions/Dystonic Reaction (Severe) \n \nAdult Hemodynamically Compromising Bradycardia \n \nAdult Ventricular Fibrillation (VF) and/or Pulseless Ventricular Tachycardia (VT) \n \nAdult Asystole/Pulseless Electrical Activity (PEA) \n \nPediatric Acute Respiratory Distress \n \nPediatric Allergic Reaction (Severe) \n \nPediatric Bradycardia \n \n \nPediatric Ventricular Fibrillation (VF) and/or Pulseless Ventricular Tachycardia (VT) \n \nPediatric Asystole / Pulseless Electrical Activity (PEA)", + "Esmolol Hydrochloride": "ESMOLOL HYDROCHLORIDE (Brevibloc\u00ae) \n \nClass \u2013 Beta-blocker (Antiarrhythmic Class II) \nPharmacologic Action \u2013 Competitively blocks beta 1 receptors in cardiac muscle. This reduces both \ncontractility and heart rate. \nOnset: < 5 minutes \n \nPeak Effect: 10-20 minutes \n \nDuration: 10-30 minutes \n \nIndications: \n\u2022 \nPersistent or recurrent Ventricular Fibrillation or Ventricular Tachycardia after the administration of a \ntotal of 5 mg of Epinephrine. \nContraindications: \n\u2022 \nBradycardia. \n\u2022 \nSecond- and third-degree AV blocks. \n\u2022 \nCardiogenic shock. \n\u2022 \nCongestive heart failure. \nWarnings: \n \n\u2022 \nWorsens heart failure. \n\u2022 \nHypotension can occur (usually dose related) \u2013 reduce dose. \n \nDrug Interactions: \n \n\u2022 \nCalcium channel blockers and antihypertensive medications. \n\u2022 \nMorphine \u2013 increases blood levels of Esmolol. \n \nAdverse Reactions: \n \n \nBradycardia, dizziness, hypotension, lethargy, CHF, dyspnea, wheezing, weakness. \n \nProtocols Containing Esmolol: \n \n \nAdult Ventricular Fibrillation (VF) and/or Pulseless Ventricular Tachycardia (VT)", + "Etomidate": "ETOMIDATE (Amidate\u00ae) \n \nClass \u2013 Sedative and hypnotic \n \n \nPharmacologic Action - Appears to act similar to GABA by depressing the activity of the brain stem reticular \nactivating system. No analgesic properties. Minimal respiratory and cardiovascular effects. Does not cause \na histamine release (like many other sedative/hypnotics do). \n \nOnset: 10 \u2013 20 seconds \n \nPeak Effect: < 1 minute \n \nDuration: 3 \u2013 5 minutes \n \n \nIndications: \n \n\u2022 \nInduction of general anesthesia and sedation of critically ill patients prior to cardioversion or intubation. \n \nContraindications: \n \n\u2022 \nKnown hypersensitivity. \n \nWarnings: \n \n \n\u2022 \nNot intended for prolonged infusion due to suppression of cortisol and aldosterone production. \n \nDrug Interactions: \n \n\u2022 \nMany prescription medications (alpha blockers, beta blockers, and antipsychotic) \u2013 increase risk for \nhypotension. \n\u2022 \nVerapamil - may result in increased hypotension as well as AV delay. \n \nAdverse Reactions: \n \n \nMyoclonic skeletal muscle movements, post-operative nausea and vomiting, pain at the injection \nsite, apnea, hypoventilation or hyperventilation, laryngospasm, hypertension or hypotension, and tachycardia \nor bradycardia. \n \nProtocols Containing Etomidate: \n \n \nAdult Unstable Tachycardia \n \nPediatric Tachycardia \n \nCyanide Exposure (Tox Medic) \n \nCholinesterase Inhibitor Exposure (Tox Medic) \n \nHydrofluoric Acid Exposure (Tox Medic)", + "Fentanyl Citrate": "FENTANYL CITRATE (Sublimaze\u00ae) \n \nClass \u2013 Synthetic opioid, analgesic (Schedule II) \nPharmacologic Action - Narcotic agonist-analgesic of opiate receptors; inhibits ascending pain pathways, \nthus altering response to pain; increases pain threshold; produces analgesia, respiratory depression, and \nsedation. 50-100 times more potent than morphine but with a shorter duration of action. Respiratory effects \ntend to last longer than the analgesic effects. Less emetic activity than other narcotics. \nOnset: Immediate \n \nPeak Effect: 3 \u2013 5 minutes (IV) \nDuration: 30 \u2013 60 minutes \n \nIndications: \n\u2022 \nManagement of acute pain. \nContraindications: \n\u2022 \nHypoventilation. \n\u2022 \nSevere hemorrhage. \nWarnings: \n \n\u2022 \nCaution using in elderly, patients with hypotension, bradycardia, suspected gastrointestinal \nobstruction, head injury, and patients taking CNS depressants. \n\u2022 \nMay result in respiratory depression. \n\u2022 \nHas been rarely linked to muscle rigidity, particularly involving the muscles of respiration (in extended \npostoperative period usually following high dose administration). \n\u2022 \nUse with caution in presence of liver or kidney disease (affect drug elimination). \n \nDrug Interactions: \n \n\u2022 \nCNS depressants \u2013 potentiate effects (lessen dose) \n\u2022 \nMAO inhibitors (within the last 14 days) \u2013 cause paradoxical excitation. \n \nAdverse Reactions: \n \n \nBradycardia, restlessness, circulatory depression, respiratory depression, muscle rigidity and \neuphoria. \n \nProtocols Containing Fentanyl: \n \n \nAcute Coronary Syndromes (ACS) \n \nST Elevation Myocardial Infarction (STEMI) \n \nAdult Hemodynamically Compromising Bradycardia \n \nPediatric and Adult Airway Management \n \nPediatric and Adult Pain Management \n \n \n.", + "Glucagon": "GLUCAGON \n \nClass \u2013 Hormone, antihypoglycemic \nPharmacologic Action - Stimulates cyclic adenosine monophosphate (cAMP) synthesis to accelerate \nhepatic glycogenolysis and gluconeogenesis (breaks down stored glycogen to form glucose and prevents the \nreverse process). These processes increase the amount of glucose in the blood stream. Glucagon is only \neffective if there are sufficient stores of glycogen in the liver. Also relaxes smooth muscles of GI tract. \nPositive inotrope (cardiac) and decreases renal vascular resistance. \nOnset: 5 \u2013 20 minutes \nPeak Effect: 30 minutes \n \nDuration: 1 \u2013 2 hours \n \nIndications: \n\u2022 \nHypoglycemia. \n\u2022 \nAntidote for symptomatic bradycardia caused by beta-blocker or calcium channel blocker overdoses. \nContraindications: \n\u2022 \nPheochromocytoma (adrenal gland tumor). \n\u2022 \nInsulinoma (pancreatic tumor). \nWarning: \n\u2022 \nNausea and vomiting occur commonly after administration \u2013 protect airway. \n\u2022 \nOnset is much slower than when using D50 \u2013 usually 5-20 minutes. \n\u2022 \nCaution in cardiovascular or renal disease. \n \nDrug Interactions: \n \n\u2022 \nNone known \n \nAdverse Reactions: \n \n \nNausea and vomiting, hypotension, dizziness, headache. \n \nProtocols Containing Glucagon: \n \n \nAdult Altered Mental Status \n \nSuspected Stroke \n \nAdult Seizures (Active) \n \nPediatric Altered Mental Status \n \nPediatric Seizures (Active)", + "Glucose, Oral": "GLUCOSE, ORAL \n \nClass \u2013 Carbohydrate gel \nPharmacologic Action \u2013 Provides source of carbohydrates for cellular metabolism. \nOnset: \n \n \nPeak Effect: \n \nDuration: \n \nIndications: \n\u2022 \nAltered mental status due to hypoglycemia in patient with ability to swallow. \nContraindications: \n\u2022 \nUnresponsive patient. \n\u2022 \nInability to swallow or follow commands. \nWarning: \n\u2022 \nPatient must be able to maintain the patency of their own airway to prevent oral glucose gel from \nbecoming a potential airway obstruction or aspiration risk. \n\u2022 \nIncrease in blood glucose level may be transient. Patient will need to consume a more robust source \nof carbohydrates in order to maintain adequate glucose levels. \n \nDrug Interactions: \n \n\u2022 \nNone known \n \nAdverse Reactions: \n \n \nNone \n \n \n \n \nProtocols Containing Oral Glucose: \n \n \nAdult Altered Mental Status", + "Haloperidol": "HALOPERIDOL (Haldol\u00ae) \n \nClass \u2013 Antipsychotic, neuroleptic \nPharmacologic Action - Antagonizes dopamine-1 and dopamine-2 receptors in brain (this blocks the \ndopamine receptors associated with mood and behavior); depresses reticular activating system and inhibits \nrelease of hypothalamic and hypophyseal (associated with body growth) hormones, \nOnset: 30 \u2013 45 minutes \n \nPeak Effect: 10 \u2013 20 minutes \nDuration: Variable \n \nIndications: \n\u2022 \nAcute psychosis or agitated/violent behavior refractory to non-pharmacologic interventions. \nContraindications: \n\u2022 \nSevere CNS depression (including coma). \n\u2022 \nNeuroleptic malignant syndrome. \n\u2022 \nPoorly controlled seizure disorder. \n\u2022 \nParkinson\u2019s disease. \n\u2022 \nPatients taking pentazocine (Talwin\u00ae). \nWarnings: \n\u2022 \nRisk of sudden death, torsades de pointes, and prolonged QT interval from off-label IV administration \nof higher than recommended dose. \n\u2022 \nContinuous cardiac monitoring is required if administering IV. \n\u2022 \nMental and physical impairment. \n\u2022 \nOrthostatic hypotension. \n\u2022 \nDystonic reaction possible. \n \nDrug Interactions: \n \n\u2022 \nTalwin\u00ae \u2013 results in addictive depression, sedation, and anesthesia. \n\u2022 \nAntihypertensive medications - additive effect (increasing the possibility of orthostatic hypotension). \n\u2022 \nLithium \u2013 use caution, may cause brain damage (encephalopathic syndrome). \n\u2022 \nAnticoagulants \n \nAdverse Reactions: \n \n \nPhysical and mental impairment, dystonic reactions (have Benadryl\u00ae ready), akathisia, dry mouth, \nblurred vision, and orthostatic hypotension. \n \nProtocols Containing Haldol: \n \n \nPatient Restraint", + "Hydroxocobalamin": "HYDROXOCOBALAMIN (Cyanokit\u00ae) \n \nClass \u2013 Cyanide antidote \nPharmacologic Action \u2013 Precursor to Vitamin B12. In the mitochondria, converts cyanide on cytochrome \noxidase to cyanocobalamin (Vitamin B12) which is then excreted safely in the urine. \nOnset: 2 \u2013 15 minutes \nPeak Effect: Variable \nDuration: Variable \nIndications: \n\u2022 \nCyanide toxicity. \nContraindications: \n\u2022 \nDocumented hypersensitivity. \nWarnings: \n\u2022 \nCauses discoloration of the skin and urine. \n\u2022 \nDiscoloration can interfere with pulse oximetry and certain diagnostic blood tests. It is suggested to \ndraw prehospital lab work prior to the administration of hydroxocobalamin. \n\u2022 \nCan cause allergic reactions. \n \nDrug Interactions: \n \n\u2022 \nDiazepam, dopamine, and fentanyl \u2013 may cause particle formation if given via same IV line. \n\u2022 \nSodium thiosulfate, sodium nitrite and ascorbic acid \u2013 chemically incompatible. \n \n \nAdverse Reactions: \n \n \nRed colored urine, redness at the infusion site and erythema were frequently reported. Other adverse \nreactions include: hypertension, rash, nausea, headache, dizziness. \n \nProtocols Containing Hydroxocobalamin: \n \nPediatric and Adult Smoke Inhalation \nCyanide Exposure (Tox Medic)", + "Ipratropium Bromide": "IPRATROPIUM BROMIDE (Atrovent\u00ae) \n \n \nClass \u2013 Anticholinergic \nPharmacologic Action - Anticholinergic (parasympatholytic) agent; inhibits vagally mediated reflexes by \nblocking acetylcholine receptors; prevents increase in intracellular calcium concentration that is caused by \ninteraction of acetylcholine with muscarinic receptors on bronchial smooth muscle. Also dries secretions. \nOnset: Variable \n \nPeak Effect: 1.5 \u2013 2 hours \n \nDuration: 4 \u2013 6 hours \n \nIndications: \n\u2022 \nBronchoconstriction - asthma and COPD. \nContraindications: \n\u2022 \nDocumented hypersensitivity to ipratropium, atropine, or derivatives. \nWarnings: \n \n\u2022 \nUse with caution in patients with hepatic and renal insufficiency due to lack of research. \n\u2022 \nUse with caution in patients with narrow-angle glaucoma, prostatic hypertrophy, and bladder \nobstruction. \n \nDrug Interactions: \n \n\u2022 \nNone known \n \nAdverse Reactions: \n \n \nPalpitations, dizziness, anxiety, headache, eye pain, urinary retention, and nervousness. \n \nProtocols Containing Ipratropium Bromide: \n \n \nAdult Acute Respiratory Distress \n \nPediatric Acute Respiratory Distress", + "Ketamine": "KETAMINE (Ketalar\u00ae) \n \n \nClass \u2013 Anesthetic, analgesic \nPharmacologic Action \u2013 Ketamine is thought to cause a dissociation between the cortical and limbic \nsystems. This results in what appears to be an awake patient who is unaware of their environment. Ketamine \nalso has analgesic and sedative properties. \nOnset: < 1 minute \n \nPeak Effect: Variable \nDuration: 10 \u2013 15 minutes \n \nIndications: \n\u2022 \nExcited delirium. \n\u2022 \nAlternate induction agent (reactive airways disease, adrenal insufficiency (sepsis), or in children). \nContraindications: \n\u2022 \nConditions in which elevated blood pressure is hazardous. \n\u2022 \nKnown or suspected schizophrenia. \n\u2022 \nInfants < 3 months of age. \nWarnings: \n \n\u2022 \nCan cause severe hallucinations following waking (more frequently in adults than in children). Keep \nthe environment quiet when the patient emerges from the anesthesia. \n\u2022 \nMonitor vital signs closely. \n \nDrug Interactions: \n \n\u2022 \nNarcotics and barbiturates \u2013 prolong recovery time. \n \nAdverse Reactions: \n \n \nHallucinations, increased skeletal muscle tone, increased bronchial secretions, nausea, and \nvomiting. Protective airway reflexes may be enhanced. \n \nProtocols Containing Ketamine: \n \n \nAcute Respiratory Distress \n \nGeneral Adult Cardiac Arrest Bundle of Care \nPatient Restraint \n \nPediatric and Adult Airway Management \n \nPediatric and Adult Pain Management", + "Ketorolac": "KETOROLAC (Toradol\u00ae) \n \n \nClass \u2013 non-steroidal, anti-inflammatory \nPharmacologic Action \u2013 An anti-inflammatory drug that also exhibits peripherally acting non-narcotic \nanalgesic activity by inhibiting prostaglandin synthesis. \nOnset: 30 minutes \n \n \nPeak Effect: 2-3 hours \nDuration: 4-6 hours \n \nIndications: \n\u2022 \nModerate to severe pain \nContraindications: \n\u2022 \nPatient taking anticoagulants or blood thinners \n\u2022 \nActive or suspected bleeding \n\u2022 \nBleeding or clotting disorders \n\u2022 \nSuspected closed head injury or intracranial bleeding \n\u2022 \nMultisystem trauma \n\u2022 \nAnticipated surgical candidate with open fracture or fracture deformities \n\u2022 \nAllergy to ASA or NSAIDS \n\u2022 \nSevere renal disease or kidney transplant \n\u2022 \nPatient breastfeeding \nWarnings: \n \n\u2022 \nRisk of GI bleeding and ulcers \n\u2022 \nRisk of renal papillary necrosis and other renal injury \n \nDrug Interactions: \n \n\u2022 \nAliskiren, ACE inhibitors, angiotensin II blockers, methotrexate, and corticosteroids \n\u2022 \nMay increase risk of bleeding when given with anti-platelet drugs \n \n \nAdverse Reactions: \n \nNausea, vomiting, bloating, gas, loss of appetite, sweating, dizziness, drowsiness, blurred vision, dry \nmouth, irritation at the injection site, and abnormal tastes may occur \n \n \n \nProtocols Containing Ketorolac: \n \n \nPediatric and Adult Pain Management", + "Labetalol": "LABETALOL (Trandate\u00ae) \n \nClass - Beta adrenergic antagonist (Antidysrhythmic Class II) \n \nPharmacologic Action \u2013 Labetolol is different from other beta-blockers because it also blocks alpha 1 \nreceptors. By blocking the alpha 1 receptors, it inhibits peripheral vasoconstriction and causes vasodilation. \nThis lowers blood pressure in hypertensive emergencies. Beta blockade decreases the strength of the \nheart\u2019s contractions and decreases the heart rate. The resulting decrease in cardiac output lowers the blood \npressure as well. In addition, myocardial oxygen demand decreases. \n \nOnset: 2-5 minutes \n \nPeak Effect: 5-15 minutes \n \nDuration: 2-4 hours \n \nIndications: \n \n\u2022 \nSevere hypertension (with nausea/vomiting, headache, altered mental status, chest pain, renal \nfailure). \n \nContraindications: \n \n\u2022 \nHypotension. \n\u2022 \nCardiogenic shock. \n\u2022 \nAcute pulmonary edema. \n\u2022 \nHeart failure. \n\u2022 \nSevere bradycardia. \n\u2022 \nSick sinus syndrome \n\u2022 \nSecond- or third-degree heart block. \n\u2022 \nAsthma or acute bronchospasm. \n\u2022 \nCocaine-induced ACS. \n \nWarnings: \n \n\u2022 \nUse of Labetalol is limited to medical control consult only. \n\u2022 \nUse caution in Pheochromocytoma (adrenal tumor), cerebrovascular disease or stroke, poorly \ncontrolled diabetes, with hepatic disease. \n\u2022 \nUse with caution at lowest effective dose in chronic lung disease. \n\u2022 \nObserve for congestive heart failure, hypotension, CNS depression, bradycardia, shock, heart blocks, \nand bronchospasm \u2013 stop medication if any occur. \nDrug Interactions: \n\u2022 \nCalcium Channel Blockers and anit-hypertensive medications \n \nAdverse Effects: \n \nUsually mild and transient; hypotensive symptoms, nausea/vomiting, bronchospasm, arrhythmia, \nbradycardia, AV block. \n \n \nProtocols Containing Labetalol: \n \n \nHypertensive Crisis", + "Lidocaine": "LIDOCAINE (Xylocaine\u00ae) \n \nClass \u2013 Antidysrhythmic (Class Ib) \nPharmacologic Action - Combines with fast sodium channels and inhibits recovery after repolarization \n(depresses depolarization and automaticity in the ventricles while having very little effect in the atria). Also \nprovides local anesthesia to ease discomfort caused by infusion of fluids or medications through an \nIntraosseous (IO) site. \nOnset: < 3 minutes \n \nPeak Effect: 5-7 minutes \n \nDuration: 10-20 minutes \nIndications: \n\u2022 \nPain control prior to IO flush \n \nContraindications: \n\u2022 \nHypersensitivity to lidocaine or amide-type local anesthetic. \n\u2022 \nAdam-Stokes syndrome (periodic syncope due to intermittent heart blockage). \n\u2022 \nSA/AV/intraventricular heart block in the absence of artificial pacemaker. \n\u2022 \nCHF. \n\u2022 \nCardiogenic shock. \n\u2022 \nSecond- and third-degree heart block (if no pacemaker is present). \n\u2022 \nWolff-Parkinson-White Syndrome. \n \nWarnings: \n \n\u2022 \nLidocaine toxicity - begins with numbness of the tongue, lightheadedness, and visual disturbances and \nprogresses to muscle twitching, unconsciousness, and seizures, then coma, respiratory arrest, and \ncardiovascular depression. \n\u2022 \nIncreased risk of toxicity: 1) Liver dysfunction (lidocaine is metabolized by the liver), 2) low protein \n(lidocaine is protein bound), and 3) Acidosis (increases the potential of lidocaine to dissociate from \nplasma proteins). \n \nDrug Interactions: \n \n\u2022 \nBeta blockers - decrease metabolism of lidocaine \n\u2022 \nPhenytoin (Dilantin\u00ae) - cardiac depression may occur \n\u2022 \nProcainamide - may result in additive neurologic effect. \n \nAdverse Reactions \n \n \nLightheadedness, drowsiness, slurred speech, seizures, heart blocks, AMS, hypotension, and \nbradycardia. \n \nProtocols Containing Lidocaine: \n \n \nAdult General Patient Care \n \nPediatric General Patient Care", + "Maalox": "MAALOX \n \n \nClass \u2013 Antacid \nPharmacologic Action - Combines with stomach acid to neutralize it. Aluminum Hydroxide, Magnesium \nHydroxide is available without a prescription. \nIndications: \n\u2022 \nTreat the symptoms of gas such as uncomfortable or painful pressure, fullness, and bloating. \n\u2022 \nUnder DE protocol - used to provide a liquid to facilitate administration of PO prednisone. \n \nContraindications: \n\u2022 \nAllergy or sensitivity \n \nWarnings: \n \n\u2022 \nUse with in patients with renal insufficiency (magnesium) or gastric outlet obstruction. \n \n \nDrug Interactions: \n \n\u2022 \nBenzodiazepines, chloroquine, digoxin, naproxen, mycophenolate, phenytoin, quinolones (e.g. \nciproflaxin), tetracyclines and Iron - interferes with their absorption. \n \nAdverse Reactions \n \n \nNone common. May cause constipation, decreased bowel motility, encephalopathy, and phosphorus \ndepletion. \n \nProtocols Containing Maalox: \n \n \nAdult Acute Respiratory Distress \n \nAdult Allergic/Adverse Reactions/Dystonic Reaction (Moderate) \n \nPediatric Acute Respiratory Distress", + "Magnesium Sulfate": "MAGNESIUM SULFATE \n \nClass \u2013 Antidysrhythmic (Class V), electrolyte \nPharmacologic Action - Depresses CNS, blocks peripheral neuromuscular transmission, produces \nanticonvulsant effects; decreases amount of acetylcholine released at end-plate by motor nerve impulse. \nSlows rate of sino-atrial (SA) node impulse formation in myocardium and prolongs conduction time. \nPromotes movement of calcium, potassium, and sodium in and out of cells and stabilizes excitable \nmembranes. Smooth muscle relaxant (reverses vasospasm in pre-eclampsia/eclampsia) \u2013 aids in \nmaintaining placental perfusion. \nOnset: Immediate \n \nPeak Effect: Variable \nDuration: 1 hour \nIndications: \n\u2022 \nTorsades de pointes. \n\u2022 \nSevere bronchoconstriction with impending respiratory failure. \n\u2022 \nSeizure during the third trimester of pregnancy or in the postpartum patient. \n \nContraindications: \n\u2022 \nMyocardial damage. \n \n \n \n\u2022 \nDiabetic coma. \n\u2022 \nHeart blocks. \n\u2022 \nHypermagnesemia. \n\u2022 \nHypocalcemia. \n\u2022 \nShock. \n\u2022 \nDialysis. \n\u2022 \nPersistent severe hypertension. \nWarnings: \n \n\u2022 \nRespiratory depression may occur with rapid intravenous administration \u2013 administer slowly. \n\u2022 \nCheck reflexes. \n\u2022 \nCaution with use in presence of renal insufficiency. \n\u2022 \nCalcium is the antidote for side effects due to overdosing. \n \nDrug Interactions: \n \n\u2022 \nCNS depressants - may have additive CNS effects \n\u2022 \nDigitalis \u2013 may cause cardiac conduction problems \n \nAdverse Reactions: \n \n \nFlushing, loss of tendon reflexes, impairment of mental and psychomotor function, confusion, and \napnea with high doses. \n \nProtocols Containing Magnesium Sulfate: \n \nAdult Acute Respiratory Distress \n \nAdult Seizures (Active) \n \n \nAdult Ventricular Fibrillation (VF) and/or Pulseless Ventricular Tachycardia (VT) \n \nHypertensive Crisis \n \nPediatric Acute Respiratory Distress \n \nPediatric Ventricular Fibrillation (VF) and/or Pulseless Ventricular Tachycardia (VT)", + "Methylprednisolone Sodium Succinate": "METHYLPREDNISOLONE SODIUM SUCCINATE (Solu-Medrol\u00ae) \n \nClass \u2013 Corticosteroid, anti-inflammatory \nPharmacologic Action - Potent synthetic steroid that inhibits many substances that cause inflammatory \nresponse (cytokines, interleukin, interferon). It also controls or prevents inflammation by controlling rate of \nprotein synthesis, suppressing migration of polymorphonuclear leukocytes (PMNs) and fibroblasts, reversing \ncapillary permeability, and stabilizing lysosomes at cellular level. \nOnset: Variable \n \nPeak Effect: 4 \u2013 8 days (IM) \n \nDuration: 1 \u2013 5 weeks (IM) \n \nIndications: \n\u2022 \nAcute bronchospastic disease (asthma, COPD), allergies). \n \nContraindications: \n\u2022 \nUntreated serious infections. \n\u2022 \nTraumatic brain injury (high doses). \n\u2022 \nIM route contraindicated in idiopathic thrombocytopenic purpura. \n\u2022 \n \nWarnings: \n \n \n\u2022 \nUse with caution in pregnant patients and patients with GI bleeding. \n\u2022 \nUse with caution in patients with diabetes mellitus (hypoglycemic responses to insulin and oral \nhypoglycemic agents may be blunted). \n\u2022 \nHold steroids for suspected pneumonia, CHF or \u201cmetabolic hyperventilation\u201d (DKA, sepsis, etc.). \n\u2022 \nLong-term use may cause GI bleeding, prolonged healing, and suppression of adrenocortical steroids. \n \nDrug Interactions: \n \n\u2022 \nPotassium-depleting agents - may potentiate hypokalemia. \n \n \nAdverse Reactions: \n \n \nHeadache, hypertension, sodium and water retention, CHF, hypokalemia, alkalosis, gastritis, vertigo, \nmalaise, and steroid-induced psychosis. \n \nProtocols Containing Methylprednisolone: \n \n \nAdult Acute Respiratory Distress \n \nAdult Allergic/Adverse Reactions/Dystonic Reaction (Severe) \n \nPediatric Acute Respiratory Distress \nPediatric Allergic Reaction (Severe)", + "Metoprolol Tartrate": "METOPROLOL TARTRATE (Lopressor\u00ae) \n \nClass \u2013 Beta-blocker (Antidysrhythmic Class II) \nPharmacologic Action \u2013 Selective inhibitor of Beta 1 adrenergic receptors with little or no effect on beta 2 \nreceptors (at doses less than 100 mg). Reduces heart rate, systolic blood pressure, and cardiac output. \nOnset: Immediate \n \nPeak Effect: 20 minutes \n \nDuration: 5-8 hours \nIndications: \n\u2022 \nAtrial Fibrillation / Atrial Flutter \n \nContraindications: \n\u2022 \nOther beta-blocker use. \n\u2022 \nHeart blocks. \n\u2022 \nBradycardia. \n\u2022 \nSystolic blood pressure < 100 mmHg. \n\u2022 \nBronchospastic disease. \n\u2022 \nCongestive heart failure. \n \nWarnings \n \n\u2022 \nMay have profound effects on blood pressure, heart rate, and EKG. \n\u2022 \nObserve for signs of CHF, hypotension, CNS depression, bradycardia, shock, heart blocks, and \nbronchospasm \u2013 stop if any of these occur. \n\u2022 \nCaution in patients with sick sinus syndrome and diabetes (may potentiate hypoglycemia). \n \nDrug Interactions \n \n\u2022 \nAcetylcholinesterase inhibitors, amiodarone, and cardiac glycosides \u2013 enhance bradycardia. \n\u2022 \nCalcium channel blockers \u2013 enhance hypotensive effects. \n\u2022 \nAntihypertensive agents \n \nAdverse Reactions \n \n \nHypotension, bradycardia, first-degree AV block, CHF, dizziness, fatigue, vertigo, wheezing, and \ndyspnea. \n \nProtocols Containing Metoprolol: \n \n \nAdult Stable Tachycardia", + "Midazolam": "MIDAZOLAM (Versed\u00ae) \n \nClass \u2013 Benzodiazepine, Anticonvulsant \nPharmacologic Action - Binds to sites on gamma-aminobutyric acid (GABA). Has no direct effect on GABA \nreceptors but potentiates the effects of GABA within the brain (GABA is the main inhibitory neurotransmitter \nin the CNS \u2013 by potentiating the effects of GABA, Diazepam promotes sedation). In seizures, does not stop \nabnormal discharge focus but does stop spread of seizure activity though the motor cortex. Skeletal muscle \nrelaxant (ortho injuries) and induces amnesia. Modulates postsynaptic effects of GABA-A transmission, \nresulting in an increase in presynaptic inhibition. Appears to act on part of the limbic system, as well as on \nthe thalamus and hypothalamus, to induce a calming effect. Three to four times more potent than Diazepam. \nOnset: 3 \u2013 5 minutes (IV) \n \nPeak Effect: 20 \u2013 60 minutes (IV) \nDuration: < 2 hours (IV) \n \nOnset: 15 minutes (IM) \n \nPeak Effect: \n \n \nDuration: 1 \u2013 6 hours (IM) \n \nIndications: \n\u2022 \nActive seizures. \n\u2022 \nPatient sedation during advanced airway management. \n\u2022 \nUncontrolled shivering in hypothermia. \n\u2022 \nAgitated or violent patients suffering behavioral emergencies. \n \nContraindications: \n\u2022 \nSevere respiratory depression \n\u2022 \nSleep apnea. \n\u2022 \nNarrow angle glaucoma. \n\u2022 \nShock. \n\u2022 \nUnresponsive alcohol overdose. \n \nWarnings: \n \n\u2022 \nUse with caution with patients with altered mental status - respiratory depression may occur. \n\u2022 \nNo effect on pain. \n \nDrug Interactions: \n \n\u2022 \nCNS depressants (alcohol, narcotics, and barbiturates) \u2013 potentiate CNS depression. \n \nAdverse Reactions: \n \n \nLightheadedness, laryngospasm, bronchospasm, respiratory depression, respiratory arrest, motor \nimpairment, ataxia, impairment of mental and psychomotor function, confusion, slurred speech, and amnesia. \n \nProtocols Containing Midazolam: \n \n \nAdult Seizures (Active) \n \nPediatric Seizures (Active) \n \nPatient Restraint", + "Naloxone": "NALOXONE (Narcan\u00ae) \n \nClass \u2013 Opioid antagonist \nPharmacologic Action \u2013 Because it is chemically similar to opioids, naloxone competes for opiate receptors \nin the brain. Displaces opioid molecules from these receptors and reverses their effects. \nOnset: < 2 minutes (IV/IO) \n Peak Effect: <2 minutes (IV/IO) \n Duration: 20 \u2013 120 minutes \nOnset: 2 \u2013 10 minutes (IM) \n Peak Effect: 2 \u2013 10 minutes (IM) \n Duration: 20 \u2013 120 minutes \nIndications: \n\u2022 \nAcute opioid toxicity. \n \nContraindications: \n\u2022 \nHypersensitivity \n \nWarnings: \n\u2022 \nAdminister with caution to those patients with suspected physical addiction to opioids. Can result in \nthe sudden onset of opiate withdrawal (agitation, tachycardia, pulmonary edema, nausea, vomiting, \nand seizures(neonates)). \n\u2022 \nWorks on: morphine, meperidine (Demerol\u00ae), heroin, paregoric, hydromorphone (Dilaudid\u00ae), codeine, \noxycodone (Percodan\u00ae, Percocet\u00ae), fentanyl, methadone, and synthetic agents (nalbuphine (Nubain\u00ae), \npentazocine (Talwin\u00ae), and butorphanol (Stadol\u00ae)). \n \nDrug Interactions: \n \n\u2022 \nBisulfite and alkaline solutions \u2013 incompatible. \n \n \nAdverse Reactions: \n \n \nTachycardia, hypertension, dysrhythmias, nausea, vomiting, and diaphoresis. \n \nProtocols Containing Naloxone: \n \n \nAdult Altered Mental Status \n \nPediatric Altered Mental Status", + "Nitroglycerin": "NITROGLYCERIN \n \nClass \u2013 Nitrate, anti-anginal \nPharmacologic Action \u2013 Potent smooth muscle relaxant. Nitrate enters vascular smooth muscle and is \nconverted to nitric oxide (NO) which leads to the activation of cyclic guanosine monophosphate (cGMP) and \nvasodilation. Relaxes smooth muscle via dose-dependent dilation of arterial and venous beds to reduce both \npreload and afterload, and reduces myocardial oxygen demand. Also improves coronary collateral \ncirculation. Lowers blood pressure, increases heart rate, and occasional may result in a paradoxical \nbradycardia. \nOnset: 1-3 minutes (SL) \n Peak Effect: 5-10 minutes (SL) \nDuration: 20-30 minutes (SL) \nOnset: 30 minutes (TD) \n Peak Effect: Varies (TD) \n \nDuration: 3-6 hours (TD) \nIndications \n\u2022 \nAcute coronary syndromes (management of chest pain). \n\u2022 \nAcute pulmonary edema (reduce preload). \n \nContraindications: \n\u2022 \nHypotension (systolic BP < 90 mmHg or > 30 mm below patient\u2019s baseline). \n\u2022 \nRecent use of erectile dysfunction medications (see drug interactions below). \n\u2022 \nExtreme bradycardia (heart rate < 50 bpm). \n\u2022 \nTachycardia in the absence of heart failure (> 100 bpm). \n\u2022 \nRight ventricular infarction. \n\u2022 \nIncreased intracranial pressure. \n\u2022 \nSevere anemia. \n\u2022 \nNarrow angle glaucoma (controversial). \n \nWarnings \n \n\u2022 \nMay cause hypotension, especially if given in conjunction with other vasodilators. \n\u2022 \nFrequent nitroglycerine users may build up a tolerance and require higher doses. \n \nDrug Interactions: \n\u2022 \nErectile dysfunction medications (sildenafil (Viagra\u00ae) \u2013 within last 24 hours or tadalafil \n(Cialis\u00ae)/vardenafil (Levitra\u00ae) \u2013 within the last 48 hours)), or other phosphodiesterase-5 inhibitors) \u2013 \nmay cause profound hypotension \u2013 withhold nitrates. \n\u2022 \nBeta-blockers \u2013 may cause orthostatic hypotension. \n\u2022 \nAlcohol (recent) \u2013 may cause hypotension. \n \nAdverse Reactions \n \n \nDose-related but may include headache, hypotension, nausea, vomiting, and dizziness. \n \nProtocols Containing Nitroglycerine: \n \n \nPulmonary Edema due to Congestive Heart Failure \n \nAcute Coronary Syndrome \n \nST Elevation Myocardial Infarction (STEMI)", + "Norepinephrine": "NOREPINEPHRINE (LEVOPHED\u00ae) \n \nClass \u2013 Sympathetic agonist \nPharmacologic Action \u2013 Norepinephrine is a naturally occurring catecholamine that acts on both alpha- and \nbeta-adrenergic receptors. The action on alpha-receptors is stronger and results in peripheral \nvasoconstriction. This increases the blood pressure in hypotensive states such as cardiogenic shock and \nsepsis \nOnset: Immediate \n \nPeak Effect: < 1 minute \n \nDuration: 1-2 minutes \n \nIndications: \n\u2022 \nHypotension not related to hypovolemia. \n\u2022 \nNeurogenic shock. \n \nContraindications: \n\u2022 \nHypotension caused by hypovolemia. \n \nWarnings: \n \n\u2022 \nMonitor blood pressure closely. \n\u2022 \nEnsure adequate fluid replacement before starting norepinephrine. \n\u2022 \nAdminister through largest vein possible to reduce risk of tissue necrosis if it extravasates. \n\u2022 \nUse caution in cases of cardiac ischemia as norepinephrine increases myocardial oxygen demand. \n \nDrug Interactions: \n\u2022 \nSodium Bicarbonate \u2013 deactivates norepinephrine \n\u2022 \nBeta-blockers \u2013 drastically elevate blood pressure \n \n \n \nAdverse Reactions: \n \n \nUsually dose-related but may include tremors, headache, myocardial ischemia, nausea, vomiting, and \ndizziness. May also cause bradycardia (usually because of increased peripheral vasoconstriction). \n \nProtocols Containing Norepinephrine: \n \n \nAdult Non-traumatic Hypotension \n \nSepsis \n \nAdult Asystole/Pulseless Electrical Activity (PEA) \n \nAdult Post Resuscitation Care with Targeted Temperature Management", + "Ondansetron": "ONDANSETRON (Zofran\u00ae) \n \nClass \u2013 Antiemetic \nPharmacologic Action - Mechanism not fully characterized; selective 5-HT3 receptor antagonist; binds to \nserotonin receptors in the chemoreceptor trigger zone (located in the medulla). The primary effects occur in \nGI tract (stomach and small intestine). Has no effect on dopamine receptors and therefore does not cause \nextrapyramidal symptoms. \nOnset: 10 \u2013 30 minutes \n \nPeak Effect: 1.5 hours \nDuration: 8 hours \n \nIndications: \n\u2022 \nNausea or vomiting. \n \nContraindications: \n\u2022 \nCo-administration with apomorphine (used in treatment of Parkinson\u2019s disease). \n \nWarnings: \n\u2022 \nMay cause dose-dependent QT prolongation, avoid in patients with congenital long QT syndrome. \n\u2022 \nEKG monitoring is recommended in patients who have electrolyte abnormalities, CHF, or \nbradyarrhythmias or who are also receiving other medications that cause QT prolongation. \n \nDrug Interactions: \n \n\u2022 \nApomorphine (Apokyn\u00ae, Ixense\u00ae, Spontane\u00ae, Uprima\u00ae) \u2013 profound hypotension and loss of \nconsciousness may occur \n\u2022 \nSerotonin blockers \n \nAdverse Reactions: \n \n \nHeadache, lightheadedness, dizziness, constipation, and fever. Rarely seen are angina chest pain, \nseizures, akathisia and acute dystonic reactions. \n \nProtocols Containing Ondansetron: \n \n \n \nAdult General Patient Care \n \nPediatric General Patient Care \n \nBuprenorphine", + "Oxygen": "OXYGEN \n \nDescription - Naturally occurring gas. \n \n \nPharmacologic Action - Oxygen is present in room air at a concentration of approximately 21%. Providing \nsupplemental oxygen elevates oxygen tension and increases oxygen content in the blood, thus improving \ntissue oxygenation, promoting aerobic metabolism, and reversing hypoxemia. \n \nOnset: Immediate \n \nPeak Effect: < 1 minute \n \nDuration: < 2 minutes \n \nIndications: \n \n\u2022 \nSuspected hypoxemia of any etiology \n \nContraindications: \n \n\u2022 \nNon-hypoxic patients. \n \nWarnings: \n \n\u2022 \nCaution when administered to patients with COPD and chronic carbon dioxide retention \u2013 monitor \npulse oximetry and capnography closely. \n\u2022 \nTitrate oxygen to avoid hypoxia. \n\u2022 \nNever withhold oxygen from those in obvious need. \n\u2022 \nMay increase toxicity of certain ingested herbicides (paraquat and diaquat). \n \nDrug Interactions: \n \n\u2022 \nNone known \n \nAdverse Reactions: \n \n \nDecreased levels of consciousness and respiratory depression may result from administering high \nlevels of oxygen to patients with COPD and chronic carbon dioxide retention. \n \nProtocols Containing Oxygen: \n \nAdult General Patient Care, Opioid Overdose, Suspected Stroke, ACS, STEMI, Pediatric \nGeneral Patient Care, Pediatric and Adult Airway, and Suspected EID Management.", + "Pralidoxime": "PRALIDOXIME (2-PAM) \n \nClass \u2013 Cholinergic \nPharmacologic Action - Binds to organophosphates and breaks alkyl phosphate-cholinesterase bond \n(removes phosphate group from cholinesterase) to restore activity of acetylcholinesterase. Detoxifies some \norganophosphates by direct chemical reaction. Reverses respiratory depression and skeletal muscle \nparalysis. Must be administered before the alkyl phosphate-cholinesterase bond becomes permanent (this is \nreferred to as aging). \nOnset: Variable \n \nPeak Effect: 10 \u2013 20 minutes (IM) \nDuration: Variable \n \nIndications: \n\u2022 \nPoisoning by organophosphate insecticides and related nerve gases (e.g. tabun, sarin, soman). \n \nContraindications: \n\u2022 \nNot required for carbamate poisoning. \n \nWarnings: \n \n\u2022 \nRapid injection may cause laryngospasm, tachycardia, and muscle rigidity - intubation may be \nrequired. \n\u2022 \nSpeeds the effect of atropine when used together. \n\u2022 \nExcitement and manic behavior can occur immediately after recovery from unconsciousness. \n \nDrug Interactions: \n \n\u2022 \nRespiratory depressants (narcotics, phenothiazines, antihistamines, alcohol) \u2013 may potentiate the \neffect of the organophosphate. \n \nAdverse Reactions: \n \nRare: dizziness, headache, blurred visions, nausea and diplopia (although these signs and \nsymptoms may be related to the underlying poisoning as well). \n \nProtocols Containing Pralidoxime: \n \n \nCholinesterase Inhibitor Exposure (Tox Medic)", + "Prednisolone": "PREDNISOLONE (Prednisone\u00ae) \n \n \nDescription - Corticosteroid. \n \n \n \nPharmacologic Action - Prednisolone suppresses acute and chronic inflammation, potentiates vascular \nsmooth muscle relaxation, and may alter airway hyperactivity. \n \nOnset: Variable \n \nPeak Effect: 1 \u2013 2 hours (PO) \nDuration: 1 \u2013 1.5 days \n \n \nIndications: \n \n\u2022 \nBronchoconstriction (COPD, asthma) \n\u2022 \nAnaphylaxis. \n \nContraindications: \n \n\u2022 \nKnown hypersensitivity to prednisolone. \n \nWarnings: \n \n\u2022 \nCaution in patients with diabetes mellitus - the hypoglycemic responses to insulin and oral \nhypoglycemic agents may be blunted. \n\u2022 \nUse with caution in pregnant patients and patient with GI bleeding. \n\u2022 \nHold steroids for suspected pneumonia, CHF or \u201cmetabolic hyperventilation\u201d (DKA, sepsis, etc.). \n \nDrug Interactions: \n \n\u2022 \nAnticoagulants \u2013 their actions could be enhanced or inhibited. \n\u2022 \nPotassium-depleting agents - may potentiate hypokalemia \n \nAdverse Reactions \n \n \nHeadache, hypertension, sodium and water retention, hypokalemia, alkalosis, and gastritis. \n \nProtocols Containing Prednisolone: \n \n \nAdult Acute Respiratory Distress \n \nAdult Allergic/Adverse Reactions/Dystonic Reaction (Moderate) \n \n \nPediatric Acute Respiratory Distress", + "Rocuronium Bromide": "ROCURONIUM BROMIDE (Zemuron\u00ae) \n \n \nDescription \u2013 Non-depolarizing neuromuscular blocker \n \n \nPharmacologic Action \u2013 Binds to nicotinic cholinergic receptor sites at the motor end plate. Antagonizes \nacetylcholine binding at these sites to result in neuromuscular blockade. The effects are reversible by using \nan acetylcholinesterase inhibitor (neostigmine, edrophonium). \n \nOnset: 30 \u2013 60 seconds \n \nPeak Effect: 1 \u2013 3 minutes \n \nDuration: 30 \u2013 60 minutes \n \n \nIndications: \n \n\u2022 \nInduction of paralysis to facilitate endotracheal intubation in cases where succinylcholine is \ncontraindicated. \n\u2022 \nAfter successful advanced airway placement to facilitate muscle relaxation during mechanical \nventilation. \n \nContraindications: \n \n\u2022 \nKnown hypersensitivity. \n \nWarnings: \n \n\u2022 \nUse of Rocuronium limited to medical control consult only. \n\u2022 \nUse ideal body weight for dosing. \n\u2022 \nSlightly elevates heart rate and blood pressure. \n\u2022 \nTachycardia may occur in children. \n \nDrug Interactions: \n \n\u2022 \nSuccinylcholine, general anesthesia, lidocaine, quinidine, procainamide, beta-blockers, potassium \ndepleting diuretics, magnesium sulfate \u2013 prolong paralysis. \n \nAdverse Reactions \n \n \nBronchospasm (rare). \n \nProtocols Containing Rocuronium: \n \n \nPediatric and Adult Airway Management", + "Sodium Bicarbonate": "SODIUM BICARBONATE \n \nClass \u2013 Alkalinizing agent \n \n \nPharmacologic Action - Sodium bicarbonate reacts with hydrogen ions, forming water and carbon dioxide, \ncorrecting metabolic acidosis and increasing blood pH (this speeds excretion of some medications from the \nbody). \n \nOnset: Immediate \n \nPeak Effect: <15 minutes \n \nDuration: 1-2 hours \nIndications: \n \n\u2022 \nKnown acidotic states. \n\u2022 \nAspirin overdose. \n\u2022 \nTricyclic antidepressant (TCA) overdose. \n \nContraindications: \n \n\u2022 \nHypocalcemia. \n\u2022 \nHypokalemia. \n\u2022 \nAlkalosis. \n\u2022 \nElectrolyte loss due to vomiting and diarrhea. \n \nWarnings: \n \n\u2022 \nUse of Sodium Bicarbonate limited to medical control consult only. \n\u2022 \nMay worsen hyperosmolality, hypernatremia, metabolic alkalosis, and acute hypokalemia. \n \nDrug Interactions: \n \n\u2022 \nCalcium - may precipitate \n\u2022 \nVasopressors and catecholamines \u2013 may be deactivated by sodium bicarbonate \n \nAdverse Reactions \n \n \nMetabolic alkalosis, hypoxia, electrolyte imbalance, and seizures. \n \nProtocols Containing Sodium Bicarbonate: \n \n \nAdult Altered Mental Status \n \nAdult Hemodynamically Compromising Bradycardia \n \nAdult Stable Tachycardia \n \nAdult Unstable Tachycardia \n \nAdult Ventricular Fibrillation (VF) and/or Pulseless Ventricular Tachycardia (VT) \n \nAdult Asystole/Pulseless Electrical Activity (PEA)", + "Sodium Nitrite": "SODIUM NITRITE \n \nClass \u2013 Nitrate \nPharmacologic Action - Oxidizes hemoglobin to form methemoglobin. Methemoglobin is incapable of \noxygen transport but has a high affinity for cyanide. Cyanide preferentially binds to methemoglobin instead of \ncytochrome a3 in the mitochondria. This forms cyanomethemoglobin that carries the cyanide to the liver for \ndetoxification and elimination. \nOnset: 2 \u2013 5 minutes \nPeak Effect: 30 \u2013 70 minutes \nDuration: Variable \nIndications: \n\u2022 \nCyanide toxicity \n \nContraindications: \n\u2022 \nAsymptomatic patients. \n\u2022 \nDo not administer to patients experiencing isolated carbon monoxide poisoning. \n \nWarnings: \n\u2022 \nRisk of worsening hypoxia due to methemoglobin formation. If hypotension is severe, consider \nskipping the sodium nitrite and proceeding directly to sodium thiosulfate. \n\u2022 \nCan cause serious adverse reactions and death from hypotension and methemoglobin formation. \n\u2022 \nMonitor closely to ensure adequate perfusion and oxygenation. \n\u2022 \nCaution with use in pregnancy \u2013 crosses the placenta and can induce fetal methemoglobinemia. \n\u2022 \nSigns of excessive methemoglobinemia: persistent cyanosis unresponsive to oxygen, chocolate-\nbrown color to blood. \n\u2022 \nMay precipitate an acute hemolytic reaction in patients with glucose-6-phosphodehydrogenase \n(G6PD) deficiency. \n\u2022 \nDo not administer to isolated carbon monoxide poisoning. \n \n \nDrug Interactions: \n \n\u2022 \nAmyl nitrite - may potentiate methemoglobin formation. \n \nAdverse Reactions: \n \n \nSyncope, hypotension and potential for excessive methemoglobinemia with decreased O2 saturations. \n \nProtocols Containing Sodium Nitrite: \n \n \nCyanide Exposure (Tox Medic)", + "Sodium Thiosulfate": "SODIUM THIOSULFATE \n \nClass \u2013 Cyanide antidote \nPharmacologic Action \u2013 In the treatment of cyanide poisoning, nitrate administration creates a state of \nmethemoglobinemia that aids to remove cyanide from the cellular mitochondria and attach it to the \nmethemoglobin molecule. This facilitates the removal of cyanide from the cell and transports it to the liver to \nfor detoxification. At the liver, rhodanese (an enzyme) uses sulfur to detoxify the cyanide. Normally there is \nsufficient rhodanese for this process. The limiting factor most times is the element sulfur. Thiosulfate is a \nsulfur donor and supplies the needed sulfur for detoxification to occur. The result is the production of \nthiocyanate that is less toxic than cyanide and eliminated through the kidneys. \nOnset: 2 \u2013 5 minutes \nPeak Effect: Variable \nDuration: Variable \nIndications: \n\u2022 \nCyanide toxicity \n \nContraindications: \n\u2022 \nDocumented hypersensitivity. \n \nWarnings: \n \n\u2022 \nMay cause nausea and vomiting \u2013 be sure to maintain a patent airway. \n \nDrug Interactions: \n \n\u2022 \nNone reported. \n \nAdverse Reactions: \n \n \nHypotension, nausea, vomiting, and joint aches. \n \nProtocols Containing Sodium Thiosulfate: \n \n \nCyanide Exposure (Tox Medic)", + "Tranexamic Acid": "TRANEXAMIC ACID (TXA) \n \nClass \u2013 Antifibrinolytic agent \n \n \nPharmacologic Action \u2013 Binds reversibly to lysine receptor sites on plasminogen or plasmin. Prevents \nplasmin from binding to and degrading fibrin. Slows the breakdown of blood clots. \n \nOnset: Variable \n \nPeak Effect: 2.5 hours \nDuration: 10 hours \n \nIndications: \n \n\u2022 \nAdult patients in hemorrhagic shock as a result of trauma < 3 hours old with suspected need for \nmassive blood transfusion, AND a sustained heart rate > 110, AND sustained hypotension with a \nsystolic blood pressure < 90 mmHg. \n \nContraindications: \n \n\u2022 \nArterial or venous thromboembolism. \n\u2022 \nRenal impairment. \n \nWarnings: \n \n\u2022 \nTo avoid hypotension, do not inject faster than 100 mg/min.. \n \nDrug Interactions \n \n\u2022 \nAnticoagulants \n \nAdverse Reactions \n \n \nGI upset (nausea/vomiting, diarrhea), allergic dermatitis, hypotension (from rapid administration). \n \nProtocols Containing Tranexamic Acid: \n \n \nAdult Allergic/Adverse Reactions/Dystonic Reaction (Angioedema) \n \nPediatric and Adult Trauma \n \nPenetrating Trauma \n \nAdult Blood Administration", + "Dose / Protocol Quick Reference Charts": "Delaware Protocol Medication Dose Reference \n(For pediatric dosing refer to Handtevy) \n \nMedication \nAdult Protocol and Dose \nAcetaminophen \n\u2022 \nContraindicated in liver disease \nPediatric and Adult Pain \nManagement: \n\u2022 \n975-1000 mg PO \n\u2022 \nPediatric: 15 mg/kg \nAdenosine \n\u2022 Contraindicated in WPW \n\u2022 Use half dose with \npatients taking \nPersantine\u00ae \n \nStable Tachycardia: \nUnstable Tachycardia: \n\u2022 6 mg rapid IV. \n\u2022 Repeat at 12 mg rapid IV if no \nresponse. \n\u2022 Max of 3 total doses. \nAlbuterol \n \nAcute Respiratory Distress: \n\u2022 Up to 5 mg nebulized. \n \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nAmiodarone \n\u2022 Caution with use in heart \nfailure/cardiogenic \nshock. \nAcute Coronary \nSyndromes: \nST Elevation Myocardial \nInfarction: \n\u2022 150 mg IV over 10 minutes for \npersistent ventricular ectopy (hold if \nheart rate < 50 bpm). \n \nStable Tachycardia: \nUnstable Tachycardia: \n\u2022 150 mg over 10 minutes (for wide \ncomplex tachycardia rate > 150 bpm). \n \nVentricular Fibrillation \nand/or Pulseless \nVentricular Tachycardia: \n\u2022 300 mg IV. \n\u2022 Repeat dose of 150 mg IV after 10 \nminutes. \n\u2022 150 mg IV infused over 10 minutes with \nROSC (if patient received <1 dose \nduring resuscitation). \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nAmyl Nitrate \n\u2022 Monitor BP and watch \nfor hypotension. \n\u2022 Not for CO poisoning. \nCyanide Exposure (Tox \nMedic): \n\u2022 Inhale ampule 30 seconds of each \nminute. \n\u2022 Change ampule after 3 minutes. \nAspirin \nAcute Coronary \nSyndromes: \nST Elevation Myocardial \nInfarction: \n\u2022 324 mg PO. \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nAtropine \n\u2022 Doses < 0.5 mg in adults \ncan induce paradoxical \nbradycardia \nHemodynamically \nCompromising \nBradycardia: \n\u2022 1 mg IV. \n\u2022 Repeat 1 mg IV every 3 \u2013 5 minutes to a \nmax of 3 mg or a heart rate > 50 bpm \n \nPatient Restraint (for \nhypersecretion/salivation): \n\u2022 0.5 mg IV or, \n\u2022 0.5 mg IM. \n \nCholinesterase Inhibitor \nExposure (Tox Medic): \n\u2022 2 mg IV every 5 minutes until \nbronchorrhea, bronchospasm, and \nbradycardia resolve. \n\u2022 May be given via autoinjector. \nBuprenorphine \n\u2022 Adult patient consenting \nto participate \n\u2022 Contraindicated in \npregnancy and \nmethadone use < 72 \nhours prior. \n \nBuprenorphine: \n* If COWS score > 5 OR opioid-free for 72 \nhours, administer 16 mg SL \nIf symptoms worsen or persist after 10 \nminutes, contact medical control to \nadminister additional 8 mg SL. \nMax dose 24 mg. \n \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nCalcium Chloride \n\u2022 Contraindicated in \nhypercalcemia and \nsevere hypokalemia. \n\u2022 Precipitates when given \nin same line as bicarb. \nAltered Mental Status: \n*Contact Medical Control for dose in \nsuspected calcium channel blocker OD* \nHemodynamically \nCompromising \nBradycardia: \nStable Tachycardia: \nUnstable Tachycardia: \n*Contact Medical Control for order in \npatients with chronic renal failure and \neither hemodialysis or peritoneal dialysis* \nVentricular Fibrillation \nand/or Pulseless \nVentricular Tachycardia: \nAsystole/Pulseless \nElectrical Activity: \nHistory of chronic renal failure or \nsuspected hyperkalemia: \n\u2022 1 gm IV \nAdult Blood Administration \n\u2022 1 g IV/IO over 3 minutes \nCalcium \nGluconate \nCholinesterase Inhibitor \nExposure (Tox Medic): \n\u2022 0.5 mL per cm2 SQ titrate to pain relief. \n\u2022 10 \u2013 30 mLs IV titrated to cardiac \ndysrhythmias. \n \n \n \nMedication \nAdult Protocol and Dose \nDextrose \nAltered Mental Status: \nSuspected Stroke: \nSeizures (Active): \n\u2022 Up to 25 g IV (FSBS < 60 mg/dl) OR in \n50 mL boluses 1 minute apart. \nDiazepam \n\u2022 Monitor for respiratory \ndepression. \nCholinesterase Inhibitor \nExposure (Tox Medic): \n\u2022 10 mg autoinjector. \nDiltiazem \n\u2022 Contraindicated in CHF, \nhypotension, heart \nblocks. \nStable Tachycardia: \n\u2022 0.25 mg/kg (25 mg) IV over 2 minutes. \n*Contact Medical Control (after 15 minutes \nif no response to initial dose) for 0.35 \nmg/kg (max dose 35 mg) IV over 2 \nminutes. \nDiphenhydramine Dystonic Reaction: \nModerate Allergic Reaction: \n\u2022 50 mg IV/IM. \nSevere Allergic Reaction: \n\u2022 50 mg IV or IM. \nDroperidol \nAdult General Patient Care \n\u2022 1.25 mg slow IVP for nausea and \nvomiting refractory to Zofran. \nPatient Restraint \nModerate Agitation: \n\u2022 2.5-5 mg IV, IM **Lower dose for elderly \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nEpinephrine \n\u2022 Increases myocardial \noxygen demand. \n\u2022 Effects may be blunted \nin patients on beta-\nblockers. \nAcute Respiratory Distress: \n\u2022 0.5 mg (1 mg/mL) IM \u2013 (< 60 y/o in \npending respiratory failure). \n \nSevere Allergic Reaction: \n\u2022 0.5 mg (1 mg/mL) IM \u2013 may repeat \nevery 5 minutes times three as needed. \n\u2022 0.25 mg (0.1 mg/mL) IV over one \nminute (may mix 0.25 mg (0.1 mg/mL) \nepinephrine with 100 mL NSS and run \nwide open). \n \nHemodynamically \nCompromising \nBradycardia: \n\u2022 2 \u2013 10 mcg/min infusion if pacing and \natropine ineffective. Titrate to sBP > 90 \nmmHg. \n \nVentricular Fibrillation \nand/or Pulseless \nVentricular Tachycardia: \nAsystole/Pulseless \nElectrical Activity: \n\u2022 1 mg (0.1 mg/mL) every 3-5 minutes. \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nEsmolol \nVentricular Fibrillation \nand/or Pulseless \nVentricular Tachycardia: \n\u2022 0.5 mg/kg IV/IO (after 5 mg of \nEpinephrine). \n\u2022 May repeat once after 5 minutes if \nneeded. \nEtomidate \nUnstable Tachycardia: \n\u2022 0.1 mg/kg (max 10 mg) IV prior to \ncardioversion of an alert patient (if IV \nestablished). \n \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nFentanyl \n\u2022 Monitor ventilation \n(etCO2) closely. \nAcute Coronary Syndromes: \nST Elevation Myocardial \nInfarction: \n\u2022 Up to 200 mcg in 100 mcg increments \nevery 5 minutes IV (for continued pain \nafter 3 NTG and sBP > 90 mmHg). \nIn cases of STEMI, may be administered \nas soon as IV is established. \nHemodynamically \nCompromising Bradycardia: \n\u2022 Up to 200 mcg in 50 mcg increments \nevery 5 minutes IV (for discomfort from \npacing and sBP > 90 mmHg). \nPediatric and Adult Airway \nManagement: \n\u2022 100 mcg IV after intubation or rescue \nairway. \n\u2022 100 mcg every 10 min if needed (max \ndose 400 mcg before contacting \nMedical Control \nPediatric and Adult Pain \nManagement: \n\u2022 50 \u2013 100 mcg IV/IM/IN. \n\u2022 Repeat after 5 minutes for continued \nmoderate to severe pain. \n*Contact Medical Control for additional \ndoses* \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nGlucagon \n\u2022 May take 5 \u2013 20 minutes \nto work. \n\u2022 Requires adequate \nglycogen stores in \npatient. \nAltered Mental Status: \nSuspected Stroke: \nSeizures (Active): \n\u2022 1 mg IM/IN (FSBS < 60 mg/dl and no \nIV). \nGlucose, Oral \nAltered Mental Status: \n\u2022 15-24 grams PO \n\u2022 Must be able to follow command, \nmaintain patent airway \nHydroxocobalamin \n\u2022 Draw blood before \nadministration if possible \nPediatric and Adult Smoke \nInhalation: \nCyanide Exposure (Tox \nMedic): \n\u2022 5 g IV over 15 minutes. \n\u2022 Under the Tox Medic protocol, a \nsecond 5 g dose may be administered \nif the initial response is incomplete. \nIpratroprium \nAcute Respiratory \nDistress: \n\u2022 0.5 mg nebulized with albuterol. \n \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nKetamine \n\u2022 Contact medical control \nfor Ketamine dosing in \npatients < 8 yrs. \n\u2022 Can cause severe \nhallucinations (more \nfrequently in adults). \nAcute Respiratory \nDistress: \n\u2022 25 mg IV (may repeat in 5 minutes) or \n50 mg IM \u2013 to allow for CPAP \ntolerance. \nHemodynamically \nCompromising \nBradycardia \n\u2022 0.25 mg/kg IV/IO for pacing \nPatient Restraint: \n\u2022 5 mg/kg IM. \nPediatric and Adult Airway \nManagement: \n\u2022 2 mg/kg IV (pre-induction). \n2 mg/kg IV (post-intubation/rescue \nairway established) - may repeat in 20 \nminutes. \nPediatric and Adult Pain \nManagement: \n\u2022 0.25 mg/kg IV over 5 minutes (max \ndose 25 mg) \u2013 for severe pain from \nextrication/burns/ortho injuries. \nKetorolac \n\u2022 May cause local irritation \nPediatric and Adult Pain \nManagement: \n\u2022 15 mg IV/IM \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nLabetolol \n\u2022 Contraindicated in \nbradycardias, heart \nblocks, CHF, patients on \nbeta- and calcium \nchannel blockers. \nHypertensive Crisis: \n*Contact Medical Control for \nadministration of 10 mg IV slow over 2 \nminutes. * \n*Contact Medical Control for repeat dose \nof 10 \u2013 20 mg IV if dBP remains > 120 \nmmHg* \nLidocaine \n\u2022 Monitor for toxicity. \nGeneral Patient Care: \n\u2022 20 \u2013 40 mg over 1 minute before \ninfusing fluid or meds via an IO in \nconscious patients. \nMaalox \nAcute Respiratory \nDistress: \nModerate Allergic \nReaction: \n\u2022 50 mg PO (to facilitate prednisone \nadministration). \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nMagnesium Sulfate Acute Respiratory \nDistress: \n\u2022 2 g IV over 10 minutes (for pending \nrespiratory failure secondary to \nasthma). \nHypertensive Crisis \n\u2022 5g IV over 20 minutes \nSeizures (Active): \n\u2022 5 g IV over 20 minutes (for seizures \nsecondary to eclampsia). \nVentricular Fibrillation \nand/or Pulseless \nVentricular Tachycardia: \n\u2022 2 g IV over 1-2 minutes (for \nTorsades). \nMethylprednisolone \n\u2022 Hold steroids for \npneumonia, CHF, DKA, \nsepsis. \nAcute Respiratory \nDistress (secondary to \nasthma/COPD): \nSevere Allergic Reaction: \n\u2022 125 mg IV or IM. \nMetoprolol \n\u2022 Caution with heart blocks, \nbradycardia, CHF, and \nbeta- or calcium channel \nblocker use. \nStable Tachycardia: \n\u2022 5 mg IV given over 1 \u2013 2 minutes. \n\u2022 May repeat every 5 minutes if needed \nfor a total of 3 doses (15 mg). \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nMidazolam \n\u2022 Monitor for respiratory \ndepression. \nSeizures (Active): \n\u2022 10 mg IM (if no IV). \n\u2022 5 mg IV slowly \u2013 may repeat up to 5 \nmg IV/IM in 5 minutes \nPatient Restraint: \n\u2022 Up to 2.5 \u2013 5 mg IV / IM (use lower \ndose in elderly). \nNaloxone \n\u2022 Ensure ventilation and \noxygenation before \nadministering. \n\u2022 Monitor for withdrawal \nsymptoms. \nAltered Mental Status: \n\u2022 Up to 2 mg IV, IN, or IM. \n\u2022 Additional dose of up to 2 mg if \nrequired to maintain respirations. \n*Contact Medical Control for additional \ndoses. * \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nNitroglycerin \n\u2022 IV before NTG for patients \nwith sBP < 150 mmHg or \npatients not prescribed and \ntaking NTG \n \n\u2022 Withhold NTG if patient \nused: \n \no Sildenafil (Viagra\u00ae / \nRevatio\u00ae) or \nvardenafil (Levitra\u00ae) \nwithin last 24 hours \no Tadalafil (Cialis\u00ae, \nAdcirca\u00ae) of any \nother prescription ED \ndrugs within last 48 \nhours. \nPulmonary Edema Due to \nCongestive Heart Failure: \n\u2022 0.8 mg SL. \n\u2022 Repeat at 0.8 mg every 3 \u2013 5 minutes \n(as long as BP remains > 120 mmHg) \n\u2022 Apply 1\u201d paste TD (if sBP > 120 \nmmHg). \n \nAcute Coronary \nSyndromes: \nST Elevation Myocardial \nInfarction: \n\u2022 0.4 mg SL. \n\u2022 Repeat 0.4 mg every 3 \u2013 5 minutes \n(as long as BP remains > 90 mmHg) \nuntil chest pain or signs of \nischemia/injury resolve. \n\u2022 If sBP < 90 mmHg, hold NTG until \nsBP > 100 mmHg. \n\u2022 Apply 1\u201d paste TD (if sBP > 90 \nmmHg) even if pain free. \n \n \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nNorepinephrine \n\u2022 After 2000 mL NSS \n\u2022 30 mL/kg in sepsis \n \n \nNon-traumatic \nHypotension: \nSepsis: \n\u2022 10 - 50 mcg/min infusion (titrate to \nmaintain MAP > 65 mmHg). \nAsystole/Pulseless \nElectrical Activity: \nAdult Post Resuscitation \nCare with Targeted \nTemperature \nManagement: \n\u2022 10 - 50 mcg/min infusion (titrate to \nmaintain MAP 80-90 mmHg). \nOndansetron \nGeneral Patient Care: \nBuprenorphine: \n\u2022 4 - 8 mg ODT, IV, or IM. \nPralidoxime \nCholinesterase Inhibitor \nExposure (Tox Medic): \n\u2022 600 mg IM via autoinjector \nPrednisone \n\u2022 Hold steroids for \npneumonia, CHF, DKA, \nsepsis. \nAcute Respiratory Distress \n(Mild): \nModerate Allergic Reaction: \n\u2022 60 mg PO \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nRocuronium \n\u2022 Used for induction in cases \nwhere succinylcholine is \ncontraindicated. \n\u2022 Use ideal weight for \ndosing. \nPediatric and Adult \nAirway Management: \n\u2022 1 mg/kg IV. \n \nSodium \nBicarbonate \n\u2022 Can precipitate when given \nwith calcium. \n\u2022 Can deactivate some \nvasopressors and \ncatecholamines. \nAltered Mental Status: \n*Contact Medical Control for dose in \nsuspected tricyclic antidepressant OD* \nHemodynamically \nCompromising \nBradycardia: \nStable Tachycardia: \nUnstable Tachycardia: \n*Contact Medical Control for order in \npatients with chronic renal failure and \neither hemodialysis or peritoneal \ndialysis* \n \nVentricular Fibrillation \nand/or Pulseless \nVentricular Tachycardia: \nAsystole/Pulseless \nElectrical Activity: \n50 mEq IV \u2013 history of chronic renal \nfailure or suspected underlying \nhyperkalemia. \n \n \n \n \n \n \nMedication \nAdult Protocol and Dose \nSodium Nitrite \n\u2022 Monitor for hypotension. \nCyanide Exposure (Tox \nMedic): \n\u2022 1 amp (300 mg) IV over no less than \n5 minutes (may dilute in 50 \u2013 100 mL \nof NSS and titrated to avoid \nhypotension). \nSodium Thiosulfate Cyanide Exposure (Tox \nMedic): \n\u2022 1 amp (12.5 g) IV over 10 - 20 \nminutes (may dilute in 50 \u2013 100 mL of \nNSS and titrated to avoid \nhypotension). \nTranexamic Acid \n\u2022 Do not inject faster than \n100 mg/minute. \nAllergic/Adverse \nReactions/Dystonic \nReaction (Angioedema): \n\u2022 Consider 1 g infusion \n \nAdult Blood \nAdministration \n\u2022 2 g IV/IO \n \nPediatric and Adult \nTrauma: \n\u2022 2 g IV / IO over 10 minutes \n(Hemorrhagic shock < 3 hours old \u2013 \nanticipated need for blood transfusion). \n \n \n \n \n \nPharmacology References \n \n \nBledsoe, Bryan E., & Clayden, Dwayne E. (2012). Prehospital emergency pharmacology \u2013 \nseventh edition. New York, NY: Pearson. \nConnectiveRx. Prescriber\u2019s Digital Reference, https://www.pdr.net/. \nU.S. National Library of Medicine, PubChem, PubChem (nih.gov) \nU.S. National Library of Medicine, MedlinePlus, MedlinePlus - Health Information from the National \nLibrary of Medicine" + }, + { + "Acetaminophen": "Acetaminophen (Tylenol, APAP) \n \n \n \n \n \n \n \nClassification: \nAnalgesic, antipyretic \n \nGeneral: \n \nAcetaminophen has analgesic and antipyretic properties with effects equivalent to those of \naspirin. Its analgesic and antipyretics effects are likely the result from the inhibition of \nprostaglandin E2 (PGE2). It does not fall into the non-steroidal anti-inflammatory class of \nmedications as it has no anti-inflammatory effects. Acetaminophen acts on a variant of \ncycloxygenase (COX3) that is only expressed in the central nervous system. Unlike aspirin, it has \nno effect on COX1 or COX2 and therefore, it has no effect on platelets. Acetaminophen elevates \nthe pain threshold and readjusts the hypothalamic temperature regulatory center. \n \nProtocol Indication(s): \n \n1. \nMild to moderate pain \n2. \nFever \n \nContraindications: \n \n1. \nKnown hypersensitivity \n2. \nEnvironmental hyperthermia \n \nPrecautions: \n \n1. \nAcetaminophen should be used with caution in patients with liver disease/failure. \n2. \nThe maximum adult daily dose of acetaminophen is 4,000 mg. \n \nSignificant adverse/side effects: \n \n1. \nNausea/vomiting \n2. \nStevens-Johnson Syndrome (rare) \n3. \nToxic epidermal necrolysis (rare) \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.07 \nPatient Comfort - Pediatric \n \n \n \n \n2.15 \nFever - Adult \n \n \n \n \n2.15 \nFever - Adult", + "Activated charcoal": "Activated Charcoal \n \n \n \n \n \n \n \n \nClassification: \nGastric decontaminant \n \nGeneral: \n \nActivated charcoal (AC) is charcoal which has been treated with oxygen, which results in the \nopening up of millions of pores between the charcoal\u2019s carbon atoms. These pores directly \nabsorb (bind) the molecules of a multitude of substances. In the EMS setting, AC is utilized as a \nsingle dose gastrointestinal decontaminant following the oral ingestion of a toxin (in the hospital, \nmultiple doses are sometimes administered to enhance elimination of a toxin). There are a \nnumber of substances that are not chemically attracted to AC and are absorbed poorly if at all by \nAC. These include electrolytes, iron, lithium, heavy metals, acids or bases, alcohols, cyanide, most \ncommon solvents, and most water insoluble compounds such as hydrocarbons (petroleum \ndistillates). \n \nProtocol Indication(s): \n1. \nOral toxic ingestion within 1 hour of EMS contact \n \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nPatient with altered mental status without a protected airway (i.e. not intubated) \n3. \nDue to the increased risk of aspiration without out benefit, AC should not be administered \nfollowing the ingestion of a substance known not to be absorbed by AC \n4. \nCorrosive ingestion (AC obscures endoscopy, which is performed in such ingestions) \nunless there are life threatening co-ingestants which are adsorbed by AC \n \nPrecautions: \n1. \nAdministration of AC increases the risk for aspiration. \n \nSignificant adverse/side effects: \n \n1. \nNausea/vomiting \n2. \nIntestinal obstruction (associated with the administration of multiple doses) \n \nDosage per protocol(s): \n4.18 \nToxicological Emergencies - Adult \n \n \n \n \n4.18 \nToxicological Emergencies - Pediatric", + "Adenosine": "Adenosine (Adenocard) \n \n \n \n \n \n \n \nClassification: \nAntiarrhythmic \nGeneral: \nAdenosine is a naturally occurring nucleoside found in all cells of the body. Adenosine is \nbyproduct of the breakdown of adenosine triphosphate (ATP). Adenosine specific receptors are \nlocated in the lungs and cardiomyocytes. Stimulation of these receptors results in decreased \nelectrical conduction. As a result, SA node automaticity is decreased and conduction velocity is \nslowed and AV nodal refractoriness is increased. Adenosine terminates reentrant pathways that \ninclude the AV node as part of the circuit resulting in restoration of sinus rhythm in \nsupraventricular tachycardia. In atrial fibrillation and flutter, adenosine may transiently increase \nAV block and unmask fibrillation or flutter waves. Adenosine does not convert atrial fibrillation, \natrial flutter, or most forms of ventricular tachycardia and is not indicated in irregular \ntachycardias. The administration of adenosine to a patient with atrial fibrillation and Wolff-\nParkinson-White (WPW) Syndrome may result in ventricular fibrillation. Following IV \nadministration, adenosine is rapidly taken up by erythrocytes and the vascular endothelium. Due \nto its rapid uptake, adenosine has a half-life of <2 seconds. The side effects of adenosine can be \ndramatic (sinus pause, asystole), but due to the very short half-life of the drug, they are usually \ntransient in nature. The uptake of adenosine may be inhibited by some medications, such as \ndipyridamole (Persantine). If a patient is on dipyridamole, the dose of adenosine should be \nreduced. Some medications, such as theophylline and related methylxanthines (caffeine) act as \nantagonist at adenosine receptors. The dose of adenosine may need to be increased if a patient \nis on one of these medications. Patients that are status post cardiac transplant may demonstrate \nincreased sensitivity to adenosine. \n \nProtocol Indication(s): \n \n1. \nNarrow complex tachycardia \n2. \nWide complex tachycardia (regular, monomorphic) \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nAtrial fibrillation associated with WPW Syndrome \n \nPrecautions: \n \n1. \nThe administration of adenosine to a patient with atrial fibrillation and Wolff-Parkinson-\nWhite (WPW) Syndrome may result in ventricular fibrillation. \n \n2. \nAdenosine may induce airway hyperresponsiveness and should be used with caution in \npatients with a history of reactive airway disease (asthma). \nPrecautions: \n \n3. \nPatients that are status post cardiac transplant may demonstrate increased sensitivity to \nadenosine. \n4. \nPatients who receive adenosine via central line should receive half the normal dose. \n \nSignificant adverse/side effects: \n1. \nHeadache \n2. \nChest pain \n3. \nFlushing \n4. \nDyspnea/bronchoconstriction \n5. \nBradycardia \n6. \nAV block \n7. \nSinus pause/asystole \n \nDosage per protocol(s): \n3.06 \nNarrow Complex Tachycardia - Adult \n \n \n \n \n3.06 Narrow Complex Tachycardia - Pediatric \n \n \n \n \n3.07 \nWide Complex Tachycardia - Adult", + "Albuterol": "Albuterol (Ventolin, Proventil) \n \n \n \n \n \n \n \n \nClassification: \nBeta adrenergic agonist (\u03b22 selective) \n \nGeneral: \n \nAlbuterol is a short acting \u03b22 selective adrenergic receptor agonist used in the management of \nbronchospasm. Albuterol stimulates \u03b22 receptors resulting in an increase in cyclic adenosine \nmonophosphate (cAMP), which leads to the activation of protein kinase A inhibiting \nphosphorylation of myosin and lowering intracellular ionic calcium concentrations, resulting in \nrelaxation of bronchial smooth muscle (bronchodilation) and relaxation of uterine and vascular \nsmooth muscle. Increasing cAMP concentrations also inhibits the release of mediators from \nmast cells in the airway. Because it relaxes vascular smooth muscle, some peripheral \nvasodilation may also occur, which may be reflected by a decrease in the diastolic blood pressure. \nAs a result of sympathomimetic stimulation, an intracellular shift of potassium may occur. This \nmay result in a small (approximately 0.5 mEq/L) decrease in the serum potassium concentration. \nThis is generally not of clinical concern, unless large doses of beta agonist are being administered. \nHowever, this effect may be useful in the management of hyperkalemia. Due to its effect on \nuterine smooth muscle, it may be used to arrest premature labor. When administered via \ninhalation, significant bronchodilation occurs within 15 minutes, and this effect is demonstrated \nfor 3-4 hours. \n \nProtocol Indication(s): \n1. \nBronchospasm (asthma/reactive airway) \n2. \nPremature labor \n3. \nHyperkalemia \n \nContraindications: \n1. \nKnown hypersensitivity \n \nPrecautions: \n1. \nUse with caution in patients with myocardial ischemia. \n2. \nParadoxical bronchospasm may occur in a small percentage of patients who receive \nalbuterol. A proposed etiology is attributed to other compounds in the albuterol \npreparation. If paradoxical bronchospasm (evidenced by significantly increased and \nsevere bronchospasm following administration) is suspected, discontinue use (avoid \nlevalbuterol as well). \n \n \n \nSignificant adverse/side effects: \n \n1. \nTachycardia \n2. \nPalpitations/cardiac ectopy \n3. \nTremor \n4. \nHeadache \n5. \nNausea/vomiting \n \nDosage per protocol(s): \n2.04 \nAllergic Reaction - Anaphylaxis - Adult \n \n \n \n \n2.05 \nAllergic Reaction - Anaphylaxis - Pediatric \n \n \n \n \n2.18 \nObstetrical Complications \n \n \n \n \n4.09 \nCrush Injury", + "Amiodarone": "Amiodarone (Cordarone, Nexterone) \n \n \n \n \n \n \nClassification: \nAntiarrhythmic \nGeneral: \nAmiodarone is primarily a class III antiarrhythmic, but it also demonstrates electrophysiological \neffects of class I, II, and IV antiarrythmics. As a class III antiarrhythmic, it binds to and blocks the \npotassium channels that are responsible for phase 3 repolarization. By blocking potassium \nchannels, it delays repolarization, which leads to an increase in action potential duration and an \nincrease in the effective refractory period (ERP) of all cardiac fibers. This prolongs the period of \ntime that the cell is unexcitable (refractory) and therefore makes the cell less excitable. \nAmiodarone depresses the slope of phase 0 by inhibiting the transmembrane influx of \nextracellular sodium ions (class 1 effect), antagonizes beta receptors (class II effect) and displays \nweak calcium channel blocking effects (class IV). Amiodarone also has \u03b1 adrenergic blocking \nproperties, which in combination with its beta antagonistic properties, are likely to be partly \nresponsible for its hypotensive effects. Amiodarone decreases the rate of SA node firing, \nsuppresses automaticity, and interrupts reentrant pathways. On the ECG, it prolongs the PR, \nQRS and QT intervals. Amiodarone is useful in the management of atrial (atrial fibrillation) and \nventricular tachyarrhythmias, particularly those resulting from a reentrant mechanism. In \nventricular fibrillation or ventricular fibrillation, evidence demonstrating the superiority of \namiodarone over lidocaine is lacking. \n \nProtocol Indication(s): \n \n1. \nVentricular tachycardia \n2. \nVentricular fibrillation \n3. \nWide complex tachycardia \n4. \nPediatric narrow complex tachycardia \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nIodine hypersensitivity \n3. \nBradycardia \n4. \nAV block >1 degree in the absence of a pacemaker \n5. \nHypotension (SBP <100 mmHg) \n \nPrecautions: \n \n1. \nDue to its vasodilatory properties, the administration of amiodarone in cardiac arrest \nshould be preceded by the administration of a vasopressor (i.e. epinephrine). \n \nPrecautions: \n \n2. \nAmiodarone should not be used in individuals with polymorphic VT associated with a \nprolonged QT interval. \n3. \nAmiodarone for infusion should only be diluted with D5W and given with an in-line filter. \n4. \nUse with beta or calcium blocking agents may increase risk of hypotension and \nbradycardia. \n \nSignificant adverse/side effects: \n1. \nHypotension \n2. \nBradycardia \n3. \nAV block \n4. \nTorsades de pointes \n5. \nCongestive heart failure \n6. \nPhlebitis \n \nDosage per protocol(s): \n3.03 \nCardiac Arrest - Adult \n \n \n \n \n3.03 \nCardiac Arrest - Pediatric \n \n \n \n \n3.06 \nNarrow Complex Tachycardia - Pediatric \n \n \n \n \n3.07 \nWide Complex Tachycardia - Adult \n \n \n \n \n3.07 \nWide Complex Tachycardia - Pediatric \n \nNotes: \n1. \nThe conventional IV preparation of IV amiodarone contains polysorbate 80 and benzyl alcohol. \nThese preservatives are believed to be partly responsible for bradycardia and hypotension \nassociated with the administration of amiodarone. A newer formulation (Nexterone) that \ndoes not contain polysorbate 80 or benzyl alcohol is available. \n2. \nInfusions of amiodarone should be mixed in D5W. In cardiac arrest, the bolus dose may \nbe diluted in 20-50 ml normal saline or D5W. \n3. \nThe total maximum cumulative 24 hour dose of amiodarone is 2.2 gm.", + "Aspirin": "Aspirin (acetylsalicylic acid, ASA) \n \n \n \n \n \n \n \n \nClassification: \nNon-steroidal Anti-inflammatory (NSAID) \n \nGeneral: \n \nAspirin (ASA) has analgesic, antipyretic, anti-inflammatory and antithrombotic effects. ASA is \nmetabolized to salicylic acid, which is the active agent. Salicylic acid irreversibly inhibits the \ncycloxygenase (COX) enzyme and results in the decreased production of COX enzyme mediated \nend products such as thromboxane A2 (TXA2) and prostaglandin E2 (PGE2). TXA2 stimulates the \nactivation of new platelets and also increases platelet aggregation (clumping). By decreasing \nlevels of TXA2, ASA decreases platelet activation and aggregation. Antiplatelet activity is present \nwithin 30-60 minutes of oral ASA administration and lasts the lifetime of the platelet (7-10 days) \nsince the effects of ASA are irreversible. PGE2 production. PGE2 is thought to act as a mediator \nof inflammation and to sensitize nerve endings to chemical mediators that are released locally \nby the inflammatory response. By decreasing levels of PGE2, ASA decreases pain and \ninflammation. ASA also reduces fever, which occurs when the set point of the anterior \nhypothalamic thermoregulatory center is elevated. Elevation of the hypothalamic \nthermoregulatory center can be caused by increased PGE2 synthesis, stimulated by pyrogens \nreleased from white blood cells that are activated by infection, hypersensitivity, malignancy, or \ninflammation. ASA decreases the body temperature in febrile patients by impeding the synthesis \nand release of PGE2. \n \nProtocol Indication(s): \n \n1. \nChest pain/discomfort believed to be of cardiac etiology \n2. \nAcute coronary syndrome/STEMI \n3. \nAcute decompensated heart failure/pulmonary edema \n \n4. \nMild to moderate pain in an adult patient \n \nContraindications: \n \n1. \nKnown hypersensitivity \n2. \nEnvironmental hyperthermia \n3. \nPeptic ulcer disease (relative for cardiac indications) \n4. \nPediatric or adolescent patient \n \n \n \n \nPrecautions: \n \n1. \nASA is contraindicated in pediatric or adolescents due to concern for Reye\u2019s syndrome \n(Reye\u2019s syndrome is characterized by CNS damage, liver injury, and hypoglycemia). \n \nSignificant adverse/side effects: \n \n1. \nGastritis \n2. \nNausea \n3. \nVomiting \n4. \nUpper GI bleeding \n5. \nIncreased bleeding \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n3.01 \nAcute Decompensated Heart Failure - Pulmonary Edema \n \n \n \n \n \n3.02 \nChest Pain - Acute Coronary Syndrome - STEMI", + "Atropine sulfate": "Atropine Sulfate \n \n \n \n \n \n \n \n \n \nClassification: \nAnticholinergic (more specifically, antimuscarinic) \n \nGeneral: \n \nAtropine sulfate competitively antagonizes acetylcholine (Ach) at muscarinic cholinergic \nreceptors found predominantly in the heart, lungs, GI tract, GU tract, and glands. Atropine \nsulfate does not antagonize Ach at nicotinic cholinergic receptors (nicotinic receptors are \ncholinergic receptors found at the neuromuscular junction). Ach is constantly released from \nparasympathetic nerve endings and stimulates muscarinic receptors. In the heart (SA/AV nodes) \nstimulation of muscarinic receptors by Ach decreases heart rate and conduction velocity. \nAtropine sulfate increases heart rate and conduction velocity by removing the influence of Ach. \nAs noted above, muscarinic receptors are located in other areas of the body and are affected by \nthe antagonism of Ach. In the respiratory tract, antagonism of Ach results in decreased airway \nsecretions and bronchodilation (this is the mechanism of action of ipratropium bromide). This \nincludes the effect of decreased salivation (antisialagogue effect) and this is why atropine is \nsometimes administered to manage increased salivation associated with ketamine \nadministration. In the GI tract it decreases secretions and motility. Ocular effects include \nmydriasis (pupillary dilation), unresponsiveness to light, and cycloplegia (inability to focus for \nnear vision). In the genitourinary tract, it results in decreased bladder motility and urinary \nretention. While not an actual antidote for organophosphate toxicity, atropine is used in its \nmanagement by antagonizing the action of acetylcholine at muscarinic receptors. \nOrganophosphates inhibit acetylcholinesterase (the enzyme responsible for the breakdown of \nAch) resulting in increased levels of Ach at the muscarinic receptor sites. \n \nProtocol Indication(s): \n1. \nBradycardia associated with inadequate perfusion \n2. \nOrganophosphate/nerve agent toxicity \n3. \nHypersalivation associated with ketamine administration \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nGlaucoma (relative contraindication to atropine administration in the setting of life \nthreatening bradycardia) \n \nPrecautions: \n1. \nAtropine should be used cautiously in the presence of myocardial ischemia and hypoxia \nsince it increases oxygen demand of heart and can worsen ischemia. \nPrecautions: \n \n2. \nAtropine administration should not delay implementation of external pacing for patients \nwith poor perfusion. \n3. \nAtropine sulfate may not be effective for infranodal (type II) AV block and new third-\ndegree block with wide QRS complexes where the location of block is likely to be in non-\nnodal tissue (bundle of His or more distal conduction system). \n4. \nTransplanted (donor) hearts are denervated and are not responsive to atropine. \n \nSignificant adverse/side effects: \n \n1. \nTachycardia (may worsen myocardial ischemia) \n2. \nBlurred vision (high doses) \n3. \nUrinary retention \n4. \nDry skin \n5. \nConfusion (high doses) \n6. \nAcute angle closure glaucoma \n \nDosage per protocol(s): \n2.25 \nExcited Delirium \n3.05 \nBradycardia - Adult \n3.05 \nBradycardia - Pediatric \n4.10 \nOrganophosphate or Nerve Agent Toxicity", + "Calcium chloride": "Calcium Chloride \nClassification: \nElectrolyte \nGeneral: \nCalcium is a positively charged ion involved in multiple physiologic functions. Calcium is required \nfor muscle contraction, nerve impulse transmission, hormone secretion, blood coagulation, cell \ndivision, cell motility and wound healing. In vascular smooth muscle, calcium is involved in the \nmaintenance of vascular tone. Calcium is also required for cardiac muscle contraction. The \nentry of calcium into cardiac cells during depolarization triggers additional intracellular calcium \nrelease from the sarcoplasmic reticulum, leading to myocardial contraction. The cardiac \npacemaker cells of the SA and AV nodes depend on an inward calcium current for depolarization. \nCalcium antagonizes the effects of both potassium and magnesium at the cell membrane. \nCalcium chloride contains three times more elemental calcium than calcium gluconate (1 gm of \ncalcium chloride is equivalent to 3 gm of calcium gluconate). \nProtocol Indication(s): \n1. \nHyperkalemia \n2. \nHydrofluoric acid (HF) exposure \n3. \nCalcium channel blocker toxicity \n4. \nBeta blocker toxicity \n5. \nMuscle spasm following marine envenomation \n6. \nPretreatment prior to the administration of a calcium channel blockers in a patient with \na tenuous blood pressure \n \nContraindications: \n \n1. \nKnown hypersensitivity \n2. \nDigitalis toxicity \n \nPrecautions: \n1. \nAdminister slowly if not in cardiac arrest. \n \nSignificant adverse/side effects: \n1. \nBradycardia \n2. \nVentricular fibrillation \n3. \nExtravasation necrosis \n4. \nAbdominal pain \n5. \nNausea/vomiting \n \nDosage per protocol(s): \n3.06 \nNarrow Complex Tachycardia \n \n \n \n \n4.18 \nToxicological Emergencies - Adult \n \n \n \n \n \n4.18 \nToxicological Emergencies - Pediatric \n4.09 \nCrush Injury \n \n \n \n \n2.11 Dialysis Emergencies and Renal Failure \n \n \n \n \n4.08 \nChemical and Electrical Burn Injury \n \n \n \n \n4.16 Marine Envenomation \nNotes: \n\uf0b7 Calcium was routinely administered in cardiac arrest (asystole, PEA). It is now known that \ncalcium is a prime mediator in ischemic neuronal damage and should be reserved for cardiac \narrest related to hyperkalemia, calcium channel or beta blocker overdose. \n\uf0b7 \nFluoride ions bind calcium and magnesium and may result in hypocalcemia following exposure to HF. \n\uf0b7 In hyperkalemia, calcium antagonizes cardiac membrane excitability. It has no effect on the \nserum potassium level. The effect of cardiac membrane stabilization is temporary (20-40 \nmin) and some patients may require a repeat dose. \n\uf0b7 Calcium chloride and calcium gluconate are two commonly used parenteral formations of \ncalcium. In the EMS setting, the two preparation may be used interchangeably, but it should \nbe noted that calcium chloride contains three time more elemental calcium than does \ncalcium gluconate (1 gm of calcium chloride is equivalent to 3 gm of calcium gluconate). \n\uf0b7 Calcium chloride has greater bioavailability, but is more likely to cause tissue damage if \nextravasation occurs. \n\uf0b7 Sodium bicarbonate and calcium preparations are not compatible and should be given \nthrough separate IV lines if possible. If they must be administered via the same IV line, the \nline should be flushed in between the administration of each. \n\uf0b7 Calcium channel blockers of the dihydropyridine class [nifedipine, nicardipine] reduce \nvascular tone by blocking calcium entry through voltage gated channels.", + "Calcium gluconate": "Calcium Gluconate \nClassification: \nElectrolyte \nGeneral: \nCalcium is a positively charged ion involved in multiple physiologic functions. Calcium is required \nfor muscle contraction, nerve impulse transmission, hormone secretion, blood coagulation, cell \ndivision, cell motility and wound healing. In vascular smooth muscle, calcium is involved in the \nmaintenance of vascular tone. Calcium is also required for cardiac muscle contraction. The \nentry of calcium into cardiac cells during depolarization triggers additional intracellular calcium \nrelease from the sarcoplasmic reticulum, leading to myocardial contraction. The cardiac \npacemaker cells of the SA and AV nodes depend on an inward calcium current for depolarization. \nCalcium antagonizes the effects of both potassium and magnesium at the cell membrane. \nCalcium chloride contains three times more elemental calcium than calcium gluconate (1 gm of \ncalcium chloride is equivalent to 3 gm of calcium gluconate). \nProtocol Indication(s): \n1. \nHyperkalemia \n2. \nHydrofluoric acid (HF) exposure \n3. \nCalcium channel blocker toxicity \n4. \nBeta blocker toxicity \n5. \nMuscle spasm following marine envenomation. \n6. \nPretreatment prior to the administration of a calcium channel blockers in a patient with \na tenuous blood pressure \n \nContraindications: \n \n1. \nKnown hypersensitivity \n2. \nDigitalis toxicity \n \nPrecautions: \n1. \nAdminister slowly if not in cardiac arrest. \n \nSignificant adverse/side effects: \n1. \nBradycardia \n2. \nVentricular fibrillation \n3. \nExtravasation necrosis \n4. \nAbdominal pain \n5. \nNausea/vomiting \n \nDosage per protocol(s): \n3.06 \nNarrow Complex Tachycardia \n \n \n \n \n4.18 \nToxicological Emergencies - Adult \n \n \n \n \n \n4.18 \nToxicological Emergencies - Pediatric \n4.09 \nCrush Injury \n \n \n \n \n2.11 Dialysis Emergencies and Renal Failure \n \n \n \n \n4.08 \nChemical and Electrical Burn Injury \n \n \n \n \n4.16 Marine Envenomation \nNotes: \n\uf0b7 Calcium was routinely administered in cardiac arrest (asystole, PEA). It is now known that \ncalcium is a prime mediator in ischemic neuronal damage and should be reserved for cardiac \narrest related to hyperkalemia, calcium channel or beta blocker overdose. \n\uf0b7 \nFluoride ions bind calcium and magnesium and may result in hypocalcemia following exposure to HF. \n\uf0b7 In hyperkalemia, calcium antagonizes cardiac membrane excitability. It has no effect on the \nserum potassium level. The effect of cardiac membrane stabilization is temporary (20-40 \nmin), some patients may require a repeat dose. \n\uf0b7 Calcium chloride and calcium gluconate are two commonly used parenteral formations of \ncalcium. In the EMS setting, the two preparation may be used interchangeably, but it should \nbe noted that calcium chloride contains three time more elemental calcium than does \ncalcium gluconate (1gm of calcium chloride is equivalent to 3gm of calcium gluconate). \n\uf0b7 Sodium bicarbonate and calcium preparations are not compatible and should be given \nthrough separate IV lines if possible. If they must be administered via the same IV line, the \nline should be flushed in between the administration of each. \n\uf0b7 Calcium channel blockers of the dihydropyridine class [nifedipine, nicardipine] reduce \nvascular tone by blocking calcium entry through voltage gated channels.", + "Cefazolin": "Cefazolin (Ancef) \n \n \n \n \n \n \n \nClassification: \nCephalosporin antibiotic \n \nGeneral: \nCefazolin is a first generation cephalosporin antibiotic. It inhibits cell wall synthesis. First \ngeneration cephalosporins are most active against aerobic gram-positive cocci and are often used \nfor skin infections caused by S. aureus and Streptococcus. Cephalosporins also have activity \nagainst E. coli and some activity against H. influezae and Klebsiella species, but because of limited \ngram negative coverage, they are not first line agents for infections that are likely to be caused \nby gram negative bacteria. \n \nProtocol Indication(s): \n \n1. \nOpen fractures \n2. \nAmputations \n3. \nGrossly contaminated soft tissue wounds \n \nContraindications: \n1. \nHistory of allergy to any cephalosporin class antibiotic \n2. \nPenicillin allergy \n \nPrecautions: \n \n1. \nThere is believed to be some cross-allergy between penicillin and cephalosporin \nantibiotics. Providers should inquire to determine if there is a history of allergy to \npenicillin or cephalosporin antibiotics prior to administering cefazolin, however the \ninability to determine such should not preclude the administration of cefazolin. \n \nSignificant adverse/side effects: \n1. \nPain, swelling, rash at the injection site \n \nDosage per protocol(s): \n4.05 \nExtremity Trauma and Musculoskeletal Trauma", + "Dexamethasone": "Dexamethasone \n \n \n \n \n \n \n \nClassification: \nSteroid (glucocorticoid) \n \nGeneral: \nDexamethasone is a glucocorticoid steroid. Glucocorticoid receptors are found in virtually every \ncell in the body and exert a powerful physiologic effect on every body system. Glucocorticoids \nstimulate the formation of glucose (gluconeogenesis) and cause the breakdown of protein into \namino acids (catabolism). Because dexamethasone inhibits the inflammatory and immunologic \nresponse, it is useful in the management of allergic and anaphylactic reactions and in the \nmanagement of disease processes that involve airway inflammation or edema (i.e. reactive \nairway disease, asthma). In reversing asthmatic obstruction, glucocorticoids probably have \nmultiple actions including the reduction of inflammatory mucosal edema, bronchial smooth \nmuscle reaction, bronchial vasoconstriction, and decreasing capillary permeability. They may \nalso restore the responsiveness of asthmatic patients to beta agonist. Dexamethasone tends to \nbe the preferred agent for reducing cerebral edema associated with tumors and is used in the \nmanagement of high altitude cerebral edema (HACE). Dexamethasone has an elimination half-\nlife of 3.5-5 hours and a duration of action of 36-54 hours. Dexamethasone may also be used \nfor replacement therapy in patients with adrenal insufficiency. \n \nProtocol Indication(s): \n \n1. \nAdrenal insufficiency \n2. \nLaryngotracheal bronchitis (croup) \n \nContraindications: \n1. \nKnown hypersensitivity to any steroid \n2. \nSystemic fungal infections \n \nPrecautions: \n \nNone \n \nSignificant adverse/side effects: \n1. \nHyperglycemia \n2. \nImmunosuppression \n3. \nNausea/vomiting \n4. \nEdema \n \n \nDosage per protocol(s): \n2.03 \nAdrenal Insufficiency \n \n \n \n \n2.08 \nRespiratory Distress (Asthma/RAD/Croup) - Pediatric", + "Dextrose (5%, 10%, 25%, 50%)": "Dextrose (D5W, D10%, D25%, D50%) \n \nClassification: \nCarbohydrate \nGeneral: \nFor the purposes of this discussion, the terms glucose and dextrose are interchangeable. Glucose \nis the primary carbohydrate used by cells for the production of adenosine triphosphate (ATP), \nthe main source of energy in the body. Glucose is taken into cells by glucose-transporter \nproteins. These proteins are activated or stimulated by insulin, which is released by pancreatic \nbeta cells. While insulin stimulates the rapid uptake of glucose by all tissues, it is not required \nfor uptake by the brain and some other tissues. Once in the cell, through the process of glycolysis, \nglucose is converted to pyruvate, giving off a small amount of chemical energy (ATP). Pyruvate \nis then converted to Acetyl CoA. Through the citric acid cycle (Krebs cycle), Acetyl CoA is \nprocessed in the mitochondria to produce energy precursors. Then through oxidative \nphosphorylation of ADP, ATP is produced. In states of low blood glucose or when glucose is \nunable to enter the cell, ATP production is decreased, leading to enzymatic and organ \ndysfunction. Glucose is rapidly absorbed after IV administration, with a clinical response \nobservable within minutes. Distribution is widespread, and it reaches the CNS very quickly. The \nbrain is one of the organs most sensitive to hypoglycemia, but it is unable to store glucose, \nmaking it susceptible to hypoglycemia. Dextrose is administered to treat known or suspected \nhypoglycemia from a variety of causes. Dextrose 5% and water (D5W) is sometimes used as a \ndiluent for IV admixtures and is sometimes used as a primary IV fluid for \u201ckeep vein open\u201d \npurposes. Dextrose is also combined with sodium chloride (D5NS, D5\u00bdNS) or Lactated Ringers \nSolution (D5LR) to alter the osmolality of the solution or to add nutrient value. In some cases \n(e.g. TPN, insulin therapy for hyperkalemia or calcium-channel blocker toxicity) dextrose may be \nadministered to prevent development of hypoglycemia. Due to the dangers of hyperglycemia \nin patients with acute cerebral pathology (traumatic brain injury, stroke, and post cardiac arrest), \nconfirmation of hypoglycemia is preferred before the administration of dextrose. However, in \nthe event that the ability to measure the plasma glucose is not available and there is a high index \nof suspicion for hypoglycemia, dextrose should be administered. \nProtocol Indication(s): \n \n1. \nHypoglycemia \n \nContraindications: \n1. \nD5W should be avoided in the setting of increased ICP. \n \n \n \n \nPrecautions: \n \n1. \nIV dextrose preparations for the management of hypoglycemia include D10%, D25%, and \nD50%. Because higher concentration solutions are hypertonic and their extravasation my \nlead to tissue injury, D10% is the preferred preparation for the management of \nhypoglycemia in the field. \n2. \nThe patency and function of the IV line should be verified prior to administration. D50% \nshould be administered slow IV push. \n3. \nThe blood glucose should be checked following the administration of glucose for the \nmanagement of hypoglycemia. \n4. \nWhen glucose is administered to patients with a known or suspected history of alcohol \nabuse or malnutrition, thiamine should also be administered (see thiamine for more \ninformation). \n5. \nOnly D10% should be utilized in neonates. \n \nSignificant adverse/side effects: \n1. \nLocal skin irritation \n2. \nThrombophlebitis \n3. \nExtravasation with subsequent tissue necrosis \n4. \nHyperglycemia \n5. \nOsmotic diuresis \n \nDosage per protocol(s): \n2.10 \nDiabetic Emergencies - Adult \n \n \n \n \n2.10 \nDiabetic Emergencies - Pediatric \n \n \nNotes: \n1. \nOne study found that the administration of 25 gm (50 ml of D50%) raised the blood \nglucose by an average of 166 mg/dl, but the response was variable among patients from \nan increase of 37 mg/dl to 370 mg/dl. \n2. \nAnother study comparing the administration of D10% or D50% to patients with \nhypoglycemia and altered mental status, both groups had a median recovery time of 8 \nminutes. Patients who were treated with D10% received 15 gm less glucose and where \nless likely to have high glucose levels after treatment. Patients who were treated with \nD50% group were more likely to have hyperglycemia and difficulty in bringing their blood \nglucose levels back into a normal range.", + "Diazepam": "Diazepam (Valium) \n \n \n \n \n \n \n \n \nClassification: \nBenzodiazepine \n \nGeneral: \n \nDiazepam binds to the gamma-aminobutryic acid receptor complex A (GABA-A), increasing the \naffinity of the receptor for GABA, enhancing the effects of GABA. GABA is the primary inhibitory \nneurotransmitter in the CNS which counterbalances the action of the excitatory neurotransmitter \nglutamate. Enhancing the effects of GABA results in anxiolysis, sedation, amnesia, increased \nseizure threshold and muscle relaxation. Like other benzodiazepines, the effects of diazepam \nare dose dependent (e.g. anxiolysis occurs at doses that do not result in sedation). Diazepam \ncan be administered via the oral, IV/IO and rectal routes (the IV preparation may be used \u201cas is\u201d \nfor rectal administration). Due to slow and erratic abortion following IM administration, \ndiazepam should not be administered via the IM route if possible. Following IV administration, \nthe onset of action is 1-5 minutes with a duration of action of 30-60 minutes. Compared to other \nbenzodiazepines, diazepam has the strongest muscle relaxant effects. \n \nProtocol Indication(s): \n1. \nSeizures \n2. \nSedation \n \nContraindications: \n \n1. \nKnown hypersensitivity \n2. \nHypotension (SBP <100 mmHg) \n3. \nAcute angle glaucoma (relative) \n4. \nPregnancy (relative for active seizures, all benzodiazepines are pregnancy safety category \nD) \n \nPrecautions: \n1. \nDiazepam can cause respiratory depression, particularly when it is administered with \nopioids or to patients at extremes of age or those with respiratory conditions. Dosing \nshould be reduced in these patients. \n2. \nWhen administered to a non-intubated patient, close monitoring of the airway and \nventilation is necessary (the use of waveform capnography is highly recommended). \n \n \n \n \nPrecautions: \n3. \nHypotension is less of a concern than respiratory depression, but may occur if it is \nadministered quickly, to volume depleted patients, or to patients with hemodynamic \ninstability. \n \n4. \nDiazepam tends to precipitate when mixed and should be given undiluted \n5. \nDiazepam should be administered into as large a vein as available (in order to reduce risks \nof thrombosis). \n6. \nDo not administer diazepam emulsified injection through filters with pore size <5 microns.\n \n \nSignificant adverse/side effects: \n \n1. \nRespiratory depression \n2. \nHypotension \n3. \nConfusion \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.19 \nSeizures - Adult \n \n \n \n \n2.19 \nSeizures - Pediatric \n \n \n \n \n \n3.06 \nNarrow Complex Tachycardia - Adult \n \n \n \n \n \n \n3.07 \nWide Complex Tachycardia - Adult", + "Diltiazem": "Diltiazem (Cardizem) \n \n \n \n \n \n \nClassification: \nCalcium channel blocker (non-dihydropyridine) \nGeneral: \nDiltiazem antagonizes the influx of calcium through L-type voltage gated calcium channels in \ncardiac and vascular smooth muscle cells. In cardiac pacemaker cells, it also delays the recovery \nof calcium channels to their preactivated state. Diltiazem decreases myocardial contractility, \nreduces the rate of SA node firing, and decreases AV conduction. Diltiazem is used for the control \nof rapid, narrow-complex ventricular response rate in the presence of atrial tachyarrhythmias \n(e.g. atrial fibrillation, atrial flutter). In the setting of PSVT, diltiazem administration may be \nassociated with reversion to normal sinus rhythm. Non-acutely (i.e. not in the EMS or ED setting), \ndiltiazem may be used in the management of angina (especially when due to coronary \nvasospasm) and hypertension. It is metabolized by the liver primarily and excreted by the \nkidneys. The onset of action is 2-5 minutes. \n \nProtocol Indication(s): \n \n1. \nNarrow complex tachycardia \n2. \nAtrial fibrillation with rapid ventricular response \n \nContraindications: \n1. \nKnow hypersensitivity \n2. \nPregnancy \n3. \nAV block >1 degree in the absence of a pacemaker \n3. \nSick sinus syndrome in the absence of a pacemaker \n4. \nHypotension (SBP <100 mmHg) \n5. \nEvidence of heart failure/pulmonary edema/cardiogenic shock \n6. \nWolff-Parkinson-White syndrome or short PR syndrome \n7. \nVentricular tachycardia \n \nPrecautions: \n \n1. \nAdministration in combination with other nodal agents (e.g. beta antagonist) may result \nin increased effect and unintended consequences (e.g. increased block). \n2. \nSustained hypotension after administration may be treated with IV fluid (unless there is \nevidence of heart failure/pulmonary edema) and some patients may respond to the \nadministration of calcium. \n3. \nDiltiazem is incompatible with furosemide, flush IV tubing well before administering \ndiltiazem in the same IV line. \n \nSignificant adverse/side effects: \n1. \nHypotension \n2. \nBradycardia \n3. \nAV block \n4. \nPeripheral edema \n5. \nItching/burning at injection site \n \nDosage per protocol(s): \n3.06 \nNarrow Complex Tachycardia - Adult", + "Diphenhydramine": "Diphenhydramine (Benadryl) \n \n \n \n \n \n \n \n \n \nClassification: \nAntihistamine (H1) \n \nGeneral: \n \n \n \nDiphenhydramine is a histamine 1 (H1) receptor antagonist used in the management of allergic \nreactions and anaphylaxis. Histamine is a chemical messenger that modulates a multitude of \ncellular responses, including allergic and inflammatory reactions, gastric acid secretion, and \npossibly neurotransmission in parts of the brain. Histamine is located in most tissues in the \nhuman body, with high amounts found in the lung, skin, and gastrointestinal tract. Histamine is \nfound in high concentrations in mast cells and basophils. During allergic reactions, histamine is \nreleased and exerts its effects by binding to histamine receptors (H1 and H2) located on cellular \nsurfaces (H3 receptors are found in the nervous system and not relevant to discussion related to \nallergic and anaphylactic reactions). Histamine receptors exert their effects by distinctly \ndifferent second messenger pathways. Some of the effects of histamine are mediated by \nstimulation of one or both receptors. H1 receptors mediate increased mucous production, \nbronchoconstriction, constriction of intestinal smooth muscle (cramping, diarrhea), and pruritus. \nH1 and H2 receptors mediate vasodilation resulting in decreased peripheral vascular resistance \nand hypotension. Both also mediate increased capillary permeability and dilation resulting in \nurticaria \n(hives). \nDiphenhydramine \nreverses \nhistamine \ninduced \nbronchoconstriction, \nvasodilation, and capillary permeability. Diphenhydramine has antiemetic properties and is \nalso useful in the prevention of motion sickness. It is also effective in preventing or diminishing \nnausea and vomiting mediated by the vestibular pathway (vertigo). Diphenhydramine exerts \nsome anticholinergic properties and may be used for the management of dystonic reactions. \nDiphenhydramine has sodium channel blocking properties and is sometimes used as local \nanesthetic. \n \nProtocol Indication(s): \n \n1. \nAllergic or anaphylactic reaction \n2. \nDystonic reaction \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nNarrow angle glaucoma \n3. \nProstatic hypertrophy or bladder neck obstruction (relative) \n \nPrecautions: \n1. \nThe drug of choice for anaphylaxis is epinephrine, not diphenhydramine. \nSignificant adverse/side effects: \n \n1. \nSedation \n2. \nHypotension (rare) \n3. \nMay cause paradoxical excitation in young children \n \nDosage per protocol(s): \n2.04 \nAllergic Reaction - Anaphylaxis - Adult \n \n \n \n \n2.04 \nAllergic Reaction - Anaphylaxis - Pediatric \n \n \n \n \n4.18 \nToxicological Emergencies - Adult \n \n \n \n \n4.18 \nToxicological Emergencies - Pediatric", + "Dopamine HCL": "Dopamine Hydrochloride \n \nClassification: \nMixed adrenergic receptor agonist (\u03b11, \u03b21, \u03b22, D1) \n \nGeneral: \n \nDopamine is the immediate precursor of norepinephrine. It demonstrates mixed adrenergic \nreceptor agonistic effects with a dose dependent receptor response. At low doses (<5 \nmcg/kg/min), dopamine stimulates dopamine D1 receptors resulting in increased splanchnic \nblood flow and renal vasodilation. At intermediate doses (5-10 mcg/kg/min), dopamine \nstimulates \u03b21 receptors resulting in increased heart rate and contractility. In this dosage range \nit also has very minimal stimulating effects on vascular \u03b22 receptors, but hypotension secondary \nto vasodilation is uncommon. At high doses (>15 mcg/kg/min), dopamine stimulates \u03b11 \nreceptors resulting in vasoconstriction. At doses above 20 mcg/kg/min, the \u03b11 response \npredominates. Dopamine is used primarily for its effect on \u03b21 and \u03b11 receptors. Dopamine \nincreases blood pressure through increases in both myocardial contractility (\u03b21 effect) and \nvasoconstriction (\u03b11 effect). Because at low \u201cdopaminergic\u201d doses, dopamine may facilitate \nurine output and natriuresis, it was used in the management of acute kidney injury (AKI). \nHowever, the overall benefit of this effect in renal protection is not established and this practice \nis not recommended. Dopamine was considered the first line vasoactive drug in the \nmanagement of septic shock, however it has been replaced by norepinephrine for this purpose. \n \nProtocol Indication(s): \n \n1. \nCardiogenic shock \n2. \nBradycardia \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nSulfite allergy \n3. \nPheochromocytoma \n \nPrecautions: \n \n1. \nThe dosage should be reduced in patients taking monoamine oxidase inhibitors (MOAIs). \n2. \nThe cardiac effects of dopamine are antagonized by beta blocking agents. \n3. \nDopamine is inactivated by alkaline solutions. \n4. \nVasopressors are only to be utilized in hemorrhagic shock as a bridge to blood products \nand/or surgical intervention and only after fluid resuscitation as appropriate for the \netiology. \n \nSignificant adverse/side effects: \n \n1. \nTachycardia \n2. \nArrhythmias \n3. \nTissue necrosis secondary to extravasation \n4. \nMesenteric or peripheral ischemia at high doses \n \nDosage per protocol(s): \n2.20 \nGeneral Shock and Hypotension - Adult \n \n \n \n \n \n2.20 \nGeneral Shock and Hypotension - Pediatric \n \n \n \n \n2.22 \nSeptic Shock - Adult \n \n \n \n \n3.05 \nBradycardia - Adult \n \n \n \n \n3.05 \nBradycardia - Pediatric \n \n \n \n \n4.18 \nToxicological Emergencies - Adult \n \n \n \n \n4.18 \nToxicological Emergencies - Pediatric", + "Droperidol": "Droperidol (Inapsine) \n \n \n \n \n \n \nClassification: \nAntipsychotic \nGeneral: \nHaloperidol is a typical antipsychotic agent which blocks dopamine (D2), muscarinic cholinergic, \nalpha adrenergic, and histamine (H1) receptors. Haloperidol\u2019s antipsychotic effects are thought \nto be a result of its selective blockade of postsynaptic dopamine receptors. Haloperidol reduces \nthe hallucinations and agitation associated with schizophrenia. Droperidol can cause \nextrapyramidal side effects, including dystonia (continuous spasms and contraction of muscle \ngroups, often of the neck) Parkinsonism (rigidity, tremor, and shuffling gait), akathisia (motor \nrestlessness), and tardive dyskinesia (stereotyped involuntary movements, such as lip smacking, \njaw movements, darting of the tongue, or purposeless movement of the limbs). Dystonic \nreactions may be managed with diphenhydramine. A rare, potentially life threatening neurologic \nside effect associated with antipsychotics is neuroleptic malignant syndrome (NMS). NMS \nresembles a very severe form of Parkinsonism, with catatonia, fever, autonomic instability, and \naltered mental status. NMS is has occurred with all antipsychotics and is more commonly seen \nwhen higher doses of the more potent agents are used. Droperidol also has a central antiemetic \naction and is utilized as an antiemetic in adults using doses as low as 0.625 mg. In the ED, \ndroperidol is also used in the management headache and as an adjunct to analgesia. In 2001 \nthe US Food and Drug Administration issued a black box warning for droperidol over concerns of \nQT prolongation and the potential for torsades de pointes. The FDA recommended continuous \nECG monitoring for patients receiving droperidol and withholding droperidol if the QTI was \nprolonged (>440 ms in males, >450 ms in females). In 2013 the American Academy of Emergency \nPhysicians (AAEM) conducted a review of the safety of droperidol and issued a clinical practice \nstatement. The AAEM concluded that the black box warning was not supported by the literature \nfor doses <2.5 mg and recommends against ECG monitoring for doses <2.5 mg and that IM doses \nup to 10 mg appear to be safe and effective as other medications used for sedation of agitated \npatients. \n \nProtocol Indication(s): \n \n1. \nAggressive or agitated behavior with suspected substance abuse (alcohol). \n2. \nAlternative to haloperidol or ketamine for the management of excited delirium \n \nsyndrome. \n \nContraindications: \n1. \nDepressed mental status \n2. \nParkinson\u2019s disease \n3. \nProlonged QTI (>440 ms in males, >450 ms in females) \n \nPrecautions: \n \n1. \nElderly patients with dementia related psychosis. \n2. \nUtilize caution if combined with other medications that may prolong the QTI \n \n(ondansetron). \n \nSignificant adverse/side effects: \n1. \nExtrapyramidal symptoms (dystonia) \n2. \nQT prolongation \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.09 \nBehavioral Emergencies \n \n \n \n \n2.13 Excited Delirium \n \n \nRecommended reading: \nAmerican Academy of Emergency Physicians, Clinical Practice Statement, Safety of Droperidol \nUse in the Emergency Department, 09/07/2013.", + "Enalaprilat": "Enalalprilat (Vasotec) \n \n \n \n \n \n \n \n \n \nClassification: \nAngiotensin enzyme inhibitor (ACE-I) \n \nGeneral: \nEnalalprilat inhibits angiotensin, an enzyme that converts angiotensin I to angiotensin II. \nAngiotensin II is a potent vasoconstrictor and stimulator of aldosterone secretion. Inhibition of \nangiotensin II synthesis results in decreased blood circulating levels of this potent vasoconstrictor \nand decreased secretion of aldosterone, which results in a net water loss (aldosterone promotes \nwater and sodium retention and potassium secretion). The net result is a reduction in afterload, \nmaking enalalprilat a useful drug in the management of acute decompensated heart failure with \nhypertension. \nProtocol Indication(s): \n1. \nAcute decompensated heart failure (cardiogenic pulmonary edema) with hypertension \n \n(SBP>140mmHg) refractory to nitrates \nContraindications: \n1. \nKnown hypersensitivity \n2. \nHypotension (SBP <100 mmHg) \n3. \nPregnancy \n4. \nHistory of ACE-E induced angioedema \n5. \nHereditary angioedema \n \nPrecautions: \n 1. \nExcretion may be prolonged in patients with impaired renal function. \nSignificant adverse/side effects: \n1. \nHypotension \nDosage per protocol(s): \n3.01 \nAcute Decompensated Heart Failure - Pulmonary Edema", + "Epinephrine": "Epinephrine (Adrenaline) \n \n \n \n \n \n \n \nClassification: \nEndogenous Catecholamine \nGeneral: \nEpinephrine is the synthetic formulation of the endogenous hormone adrenaline. Adrenaline \nis synthesized in the adrenal medulla and released, with small quantities of norepinephrine, into \nthe systemic circulation. It is a potent stimulator of both \u03b1 and \u03b2 receptors and it affects \nmultiple organs. Its effects are dose dependent and its net effect depends on the dose \nadministered. At low doses, peripheral \u03b22 effects predominate, resulting in vascular smooth \nmuscle relaxation (vasodilation). Stimulation of cardiac \u03b21 receptors results in increased \ncontractility, heart rate, and conduction velocity. As a result, cardiac output and myocardial \noxygen demand are increased. Stimulation of bronchial \u03b22 receptors results in bronchial smooth \nmuscle relaxation, reversal of bronchospasm and decreased release of histamine, tryptase, and \nother mediators of inflammation from mast cells and basophils. Stimulation of \u03b11 receptors \nresults in vasoconstriction and increased afterload. At higher doses, as used in cardiac arrest, \u03b1 \neffects (vasoconstriction) predominate. Aerosolized epinephrine may act on subglottic mucosal \n\u03b1 receptors to reverse edema in some situations (croup). \n \nProtocol Indication(s): \n \n1. \nCardiac arrest \n2. \nBradycardia \n3. \nAnaphylaxis (drug of choice) \n4. \nAsthma \n5. \nLaryngotracheobronchitis (croup) \n6. \nShock (pediatric) \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nAge \u226550 years of age (asthma) \n3. \nPheochromocytoma \n \nPrecautions: \n \n1. \nThe use of an auto-injector is strongly recommended for the administration of IM \nepinephrine at all provider levels if available. \n \n \n \n \nPrecautions: \n \n2. \nIn the setting of allergic reaction/anaphylaxis, patients \u226550 years of age, with a history of \ncardiac disease, or a heart rate >150 are at risk for cardiac ischemia following the \nadministration of epinephrine (these patients should have ongoing cardiac monitoring \nand a multi-lead ECG following the administration of epinephrine). \n3. \nIn the setting of asthma and allergic reactions of mild or moderate severity and no \nrespiratory symptoms (wheezing, dyspnea, hypoxia), epinephrine administration should \nbe avoided in patients \u226550 years of age due to the risk for adverse cardiovascular events. \nEpinephrine should never be withheld in cases of allergic reaction/anaphylaxis with \nsevere symptoms. \n4. \nUse of nebulized epinephrine for croup should be limited to those patients with significant \nrespiratory distress or stridor at rest. \n5. \nIn shock situations, assessment of volume status and volume administration should \nprecede epinephrine administration. \n \nSignificant adverse/side effects: \n1. \nTachycardia and arrhythmias \n2. \nMyocardial ischemia/infarction \n3. \nHypertension \n4. \nTremor \n5. \nAnxiety \n6. \nHeadache \n7. \nNausea/vomiting \n \nDosage per protocol(s): \n2.04 \nAllergic Reaction - Anaphylaxis - Adult \n \n \n \n \n2.04 \nAllergic Reaction - Anaphylaxis - Pediatric \n \n \n \n \n2.08 \nRespiratory Distress (Asthma-RAD-COPD) - Adult \n \n \n \n \n \n2.08 \nRespiratory Distress (Asthma-RAD-Croup) - Pediatric \n \n \n \n \n2.20 \nGeneral Shock and Hypotension - Pediatric \n \n \n \n \n3.03 \nCardiac Arrest - Adult \n \n \n \n \n3.03 \nCardiac Arrest - Pediatric \n \n \n \n \n3.05 \nBradycardia - Adult \n \n \n \n \n3.05 \nBradycardia - Pediatric \nNotes: \n1. \n1:1000 preparation contains 1mg epinephrine per mL of solution (10 mg in 10 mL). \n2. \n1:10000 preparation contains 0.1mg (100 mcg) epinephrine per mL of solution (1 mg in \n10 mL). \n3. \n1:100000 preparation contains 0.01mg (10 mcg) epinephrine per mL of solution (0.1 mg \nin 10 mL).", + "Etomidate (restricted use)": "Etomidate (Amidate) \n \n \nRESTRICTED USE MEDICATION \n \n \nClassification: \nSedative-hypnotic \n \nGeneral: \n \nEtomidate is a sedative-hypnotic agent frequently used in rapid sequence intubation \n(RSI)/medication assisted intubation (MAI). The exact mechanism of action is unknown, but it is \nbelieved that etomidate enhances the effect of gamma-aminobutryic acid (GABA) at the GABA \nreceptor complex. GABA is the primary inhibitory neurotransmitter in the CNS which \ncounterbalances the action of the excitatory neurotransmitter glutamate. Enhancing the effects \nof GABA results sedation. It has an onset of action of 15-45 seconds and a duration of action of \n3-12 minutes. When used within the recommended dosage range, etomidate has minimal effect \non hemodynamics. It decreases intracranial pressure by decreasing cerebral blood flow and \ncerebral metabolic demand (CMRO2). Etomidate has no analgesic properties. The \nadministration of etomidate may result in adrenal suppression. While this is only likely to be of \nsignificance when it is administered by infusion over a period of time, this effect is seen following \nsingle bolus of the drug. There has been considerable discussion in the medical literature \nregarding etomidate related adrenal suppression and the safety of etomidate in the setting of \nsepsis. To date there have been no randomized controlled studies examining outcomes \nfollowing the administration of etomidate as a single bolus for RSI/MAI in the setting of sepsis. \nDue to its rapid onset of action and hemodynamic profile, etomidate has become the induction \nagent of choice for most situations requiring RSI/MAI. \n \nProtocol Indication(s): \n1. \nInduction agent for RSI/MAI \n \nContraindications: \nNone \n \nPrecautions: \n1. \nUse of etomidate is restricted to paramedics participating in a CEMS approved medication \nassisted intubation program. \n2. \nDose should be adjusted in patients with hemodynamic instability. \n \nSignificant adverse/side effects: \n \n1. \nPain on injection (secondary to propylene glycol diluent, may be reduced by administering \nthrough a rapidly flowing IV placed in a large vein). \nSignificant adverse/side effects: \n \n2. \nMyoclonus (not of clinical significance), can be reduced or mitigated by the co-\nadministration of an opioid or benzodiazepine. \n \n \nDosage per protocol(s): \n5.04 \nRapid Sequence Intubation/Medication Assisted \n Intubation", + "Famotidine": "Famotidine (Pepcid) \n \nClassification: \nAntihistamine (H2) \n \n \nGeneral: \n \nFamotidine is a H2 antagonist useful in the management of allergic and anaphylactic reactions. \nHistamine is a chemical messenger that modulates a multitude of cellular responses, including \nallergic and inflammatory reactions, gastric acid secretion, and possibly neurotransmission in \nparts of the brain. Histamine is located in most tissues in the human body, with high amounts \nfound in the lung, skin, and gastrointestinal tract. Histamine is found in high concentrations in \nmast cells and basophils. During allergic reactions, histamine is released and exerts its effects by \nbinding to H1 and H2 receptors located on cellular surfaces (H3 receptors are found in the nervous \nsystem and not relevant to discussion related to allergic and anaphylactic reactions). Histamine \nreceptors exert their effects by distinctly different second messenger pathways. Some of the \neffects of histamine are mediated by stimulation of one or both receptors. H1 receptors mediate \nincreased mucous production, bronchoconstriction, constriction of intestinal smooth muscle \n(cramping, diarrhea), and pruritus. H1 and H2 receptors mediate vasodilation resulting in \ndecreased peripheral vascular resistance and hypotension. Both mediate increased capillary \npermeability and dilation resulting in urticaria (hives). H2 receptors mediate gastric acid \nsecretion (hence the use of H2 antagonist in gastroesophageal reflux disease). Famotidine \nreverses some of effects that are secondary to stimulation of the H2 receptors. Additionally, it \nis believed that famotidine may enhance the effects of H1 antagonist (diphenhydramine). \n \nProtocol Indication(s): \n \n1. \nAllergic or anaphylactic reaction \n \nContraindications: \n1. \nKnown hypersensitivity \n \nPrecautions: \n1. \nThe dosage should be adjusted in the setting of decreased renal function, but this is not \nan issue when used acutely for allergic or anaphylactic reactions. \n \nSignificant adverse/side effects: \n \nNone \n \n \nDosage per protocol(s): \n2.04 \nAllergic Reaction - Anaphylaxis - Adult \n \n \n \n \n2.04 \nAllergic Reaction - Anaphylaxis - Pediatric", + "Fentanyl": "Fentanyl (Sublimaze) \n \n \n \n \n \n \n \n \n \nClassification: \nSynthetic opioid \nGeneral: \nFentanyl is a synthetic opioid with a potency 100 times greater than that of morphine sulfate. \nFentanyl provides analgesia by primarily stimulating mu (\u00b5) receptors in the central nervous \nsystem (CNS). In addition to analgesia, stimulation of \u00b5 receptors may also result in respiratory \ndepression, sedation (as a secondary effect), euphoria, decreased gastrointestinal motility and \nbradycardia. Respiratory depression associated with fentanyl is enhanced when it is co-\nadministered with benzodiazepines or administered to patients who have consumed alcohol. \nFentanyl\u2019s onset of action is almost immediate and it\u2019s analgesic effects last 30-60 minutes. Its \nultra-short onset of action and short duration of action make fentanyl an ideal agent for us by \nEMS as an analgesic. Unlike morphine sulfate, fentanyl does not result in a significant histamine \nrelease and therefore is associated with a lesser risk of bronchoconstriction, tachycardia, or \nhypotension. \nProtocol Indication(s): \n1. \nModerate to severe pain \nContraindications: \n1. \nKnown hypersensitivity \n2. \nHypotension (SBP <100 mmHg) \n \nPrecautions: \n1. \nFentanyl should be administered slowly. \n \n2. \nCareful monitoring (including the use of waveform capnography) is warranted when co-\nadministering with benzodiazepines or to patients who have consumed alcohol as these \npatients are at risk for ventilatory depression. \n \n \nSignificant adverse/side effects: \n \n1. \nRespiratory depression \n2. \nHypotension \n3. \nChest rigidity (this is an extremely rare adverse effect associated with the rapid \nadministration of high doses (>5 mcg/kg) \n \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.07 \nPatient Comfort - Pediatric \nNotes: \n\uf0b7 Fentanyl and morphine sulfate belong two different drug classes (phenylpiperidine and \nphenanthrene classes respectively). There is no cross reaction between these two classes \nso fentanyl can be administered to patients with an allergy to morphine sulfate.", + "Furosemide": "Furosemide (Lasix) \n \n \n \n \n \n \n \nClassification: \nDiuretic \nGeneral: \nAs a loop diuretic, furosemide decreases the reabsorption of sodium, chloride and potassium in \nthe loop of Henle causing the excretion of these electrolytes in the urine. In an effort to maintain \nosmolarity, water follows sodium and diuresis occurs. \n \nProtocol Indication(s): \n \n1. \nAcute decompensated heart failure \n \nContraindications: \n1. \nHypotension (SBP <100 mmHg) \n \nPrecautions: \n \n1. \nThere\u2019s minimal or no role for the administration of furosemide early in the management \nof acute decompensated heart failure (ADHF). The majority of patients with ADHF aren\u2019t \nvolume overloaded. Use only \n2. \nThe immediate management of the patient with ADHF should focus on the application of \nCPAP and the administration of nitroglycerin. \n3. \nThe administration of furosemide may lead to a decrease in cardiac output in patients \nwith left ventricular failure. This is a result of decreased venous return and increased \nsystemic afterload. Increased systemic afterload may occur due to stimulation of the \nrenin angiotensin system (RAS) resulting in the release of renin, raising circulating levels \nof angiotensin, a powerful vasoconstrictor. \n \nSignificant adverse/side effects: \n1. \nHypotension \n2. \nHypovolemia \n3. \nHypokalemia \n4. \nHyponatremia \n5. \nHypochloremia \n6. \nHypomagasemia \n7. \nOtotoxicity/hearing loss (usually associated with rapid administration or administration \nwith aminoglycoside antibiotics). \n \nDosage per protocol(s): \n3.01 \nAcute Decompensated Heart Failure", + "Glucagon": "Glucagon \n \n \n \n \n \n \nClassification: \n Hormone \nGeneral: \nGlucagon is a polypeptide hormone that is produced by the alpha islet cells of the pancreas. \nIt enhances gluconeogenesis (generation of glucose from certain non-carbohydrate carbon \nsubstrates) and glycogenolysis (breakdown of glycogen to glucose). The net effect is a transient \n(short term) increase in the blood glucose level. This effect is dependent on adequate glycogen \nstores and may be inadequate if glycogen stores are depleted. Because its effect on blood \nglucose is transient, hypoglycemic patients treated with glucagon must be administered glucose \nor be feed to prevent recurrent hypoglycemia. Glucagon also relaxes gastrointestinal smooth \nmuscle and is sometimes used in the management of esophageal obstruction and to facilitate \nradiological examination of the gastrointestinal tract. Glucagon is also used in beta blocker \ntoxicity because it activates adenyl cyclase and exerts inotropic and chronotropic effects via an \nalternate pathway that bypasses blocked beta receptors. It is also sometimes used in calcium \nblocker toxicity for its inotropic and chronotropic properties. It should be noted that the use of \nglucagon in the setting of beta blocker and calcium channel blocker toxicity is based primarily on \ntheoretic evidence and its efficacy for this use has been recently questioned. \n \nProtocol Indication(s): \n \n1. \nHypoglycemia \n2. \nAnaphylaxis in patients on beta-blockers \n3. \nBeta blocker toxicity \n \nContraindications: \n1. \nKnown hypersensitivity \n \nPrecautions: \n \nNone \n \nSignificant adverse/side effects: \n1. \nNausea and vomiting \n2. \nHypokalemia \n3. \nHyperglycemia \n \n \n \n \nDosage per protocol(s): \n2.08 \nAllergic Reaction - Anaphylaxis - Adult \n \n \n \n \n2.08 \nAllergic Reaction - Anaphylaxis - Pediatric \n \n \n \n \n2.10 \nDiabetic Emergencies - Adult \n \n \n \n \n2.10 \nDiabetic Emergencies - Pediatric \n \n \n \n \n4.18 \nToxicological Emergencies - Adult \n \n \n \n \n4.18 \nToxicological Emergencies - Pediatric", + "Glucose (oral)": "Glucose (oral) \n \nClassification: \nCarbohydrate \nGeneral: \nGlucose is the primary carbohydrate used by cells for the production of adenosine triphosphate \n(ATP), the main source of energy in the body. Glucose is taken into cells by glucose-transporter \nproteins. These proteins are activated or stimulated by insulin, which is released by pancreatic \nbeta cells. While insulin stimulates the rapid uptake of glucose by all tissues, it is not required \nfor uptake by the brain and some other tissues. Once in the cell, through the process of \nglycolysis, glucose is converted to pyruvate, giving off a small amount of chemical energy (ATP). \nPyruvate is then converted to Acetyl CoA. Through the citric acid cycle (Krebs cycle), Acetyl CoA \nis processed in the mitochondria to produce energy precursors. Then through oxidative \nphosphorylation of ADP, ATP is produced. In states of low blood glucose or when glucose is \nunable to enter the cell, ATP production is decreased, leading to enzymatic and organ \ndysfunction. The brain is one of the organs most sensitive to hypoglycemia, but it is unable to \nstore glucose, making it susceptible to hypoglycemia. Due to the dangers of hyperglycemia in \npatients with acute cerebral pathology (traumatic brain injury, stroke, and post cardiac arrest), \nconfirmation of hypoglycemia is preferred before the administration of glucose. However, in \nthe event that the ability to measure the plasma glucose is not available and there is a high index \nof suspicion for hypoglycemia, glucose should be administered. Oral glucose should only be \nadministered to patients with intact airway protective reflexes (ability to swallow and cough). \nFor patients with a decreased level of consciousness or who are at risk for aspiration, the \nadministration of IV glucose or IM glucagon is indicated. \nProtocol Indication(s): \n \n1. \nHypoglycemia \n2. \nBeta antagonist toxicity \n \nContraindications: \n1. \nLoss of airway protective reflexes or other risk for aspiration. \n2. \nPatient <2 years of age. \n \nPrecautions: \n \n1. \nThe blood glucose should be checked following the administration of glucose for the \nmanagement of hypoglycemia. \n \n \nSignificant adverse/side effects: \n1. \nAspiration \n2. \nVomiting \n \nDosage per protocol(s): \n2.10 \nDiabetic Emergencies - Adult \n \n \n \n \n2.10 \nDiabetic Emergencies - Pediatric", + "Haloperidol": "Haloperidol (Haldol) \n \n \n \n \n \n \n \nClassification: \nAntipsychotic \n \nGeneral: \n \nHaloperidol is a typical antipsychotic agent which blocks dopamine (D2), muscarinic cholinergic, \nalpha adrenergic, and histamine (H1) receptors. Haloperidol\u2019s antipsychotic effects are thought \nto be a result of its selective blockade of postsynaptic dopamine receptors. Haloperidol reduces \nthe hallucinations and agitation associated with schizophrenia. Haloperidol can cause \nextrapyramidal side effects, including dystonia (continuous spasms and contraction of muscle \ngroups, often of the neck) Parkinsonism (rigidity, tremor, and shuffling gait), akathisia (motor \nrestlessness), and tardive dyskinesia (stereotyped involuntary movements, such as lip smacking, \njaw movements, darting of the tongue, or purposeless movement of the limbs). Dystonic \nreactions may be managed with diphenhydramine. An elevated risk of acute dystonia is \nobserved in males and younger age groups. A rare, potentially life threatening neurologic side \neffect associated with antipsychotics is neuroleptic malignant syndrome (NMS). NMS resembles \na very severe form of Parkinsonism, with catatonia, fever, autonomic instability, and altered \nmental status. NMS is has occurred with all antipsychotics and is more commonly seen when \nhigher doses of the more potent agents are used. Haloperidol also has antiemetic properties, \nbut is not commonly used as an antiemetic agent. Haloperidol is used to manage aggressive or \nagitated behavior and is an alternative to ketamine for the management of excited delirium \nsyndrome (ExDS). \n \n Protocol Indication(s): \n \n1. \nAggressive or agitated behavior with suspected substance abuse (alcohol) \n2. \nAlternative to ketamine for the management of excited delirium syndrome \n \nContraindications: \n \n1. \nDepressed mental status \n2. \nParkinson\u2019s disease \n3. \nProlonged QTI (>440 ms in males, >450 ms in females) \n \nPrecautions: \n \n1. \nElderly patients with dementia related psychosis. \n \n \n \nSignificant adverse/side effects: \n \n1. \nExtrapyramidal symptoms (dystonia) \n2. \nQT prolongation \n \nDosage per protocol(s): \n2.09 \nBehavioral Emergencies \n \n \n \n \n2.13 Excited Delirium", + "Hydrocortisone": "Hydrocortisone (Solu-Cortef) \n \n \n \n \n \n \nClassification: \nSteroid (synthetic glucocorticoid) \nGeneral: \nHydrocortisone is synthetically produced cortisol, the primary glucocorticoid in humans. \nHydrocortisone exerts its effects in a similar fashion to cortisol. Glucocorticoid receptors are \nfound in virtually every cell in the body and exert a powerful physiologic effect on every body \nsystem. Glucocorticoids stimulate the formation of glucose (gluconeogenesis) and cause the \nbreakdown of protein into amino acids (catabolism). Because hydrocortisone inhibits the \ninflammatory and immunologic response, it is useful in the management of allergic and \nanaphylactic reactions and in the management of disease processes that involve airway \ninflammation or edema (i.e. reactive airway disease, asthma). In reversing asthmatic \nobstruction, glucocorticoids probably have multiple actions including the reduction of \ninflammatory mucosal edema, bronchial smooth muscle reaction, bronchial vasoconstriction, \nand decreasing capillary permeability. They may also restore the responsiveness of asthmatic \npatients to beta agonist. Hydrocortisone may be used for replacement therapy in patients with \nadrenal insufficiency. \n \nProtocol Indication(s): \n \n1. \nAdrenal insufficiency \n2. \nAsthma \n3. \nCOPD exacerbation \n4. \nAllergic and anaphylactic reactions \n \nContraindications: \n1. \nKnown hypersensitivity to any steroid \n2. \nSystemic fungal infections \n \nPrecautions: \n \nNone \n \nSignificant adverse/side effects: \n1. \nHyperglycemia \n2. \nImmunosuppression \n3. \nNausea/vomiting \n4. \nEdema \n \nDosage per protocol(s): \n2.03 \nAdrenal Insufficiency \n \n \n \n \n2.04 \nAllergic Reaction - Anaphylaxis - Adult \n \n \n \n \n2.04 \nAllergic Reaction - Anaphylaxis - Pediatric \n \n \n \n \n \n \n2.08 \nRespiratory Distress (Asthma/RAD/COPD) - Adult \n2.08 \nRespiratory Distress (Asthma/RAD/Croup) - Pediatric", + "Hydroxocobalamin": "Hydroxocobalamin (vitamin B12a) \n \n \n \n \n \n \n \n \nClassification: \nAntidote \n \n \nGeneral: \n \nHydroxcobalamin is a natural precursor for cyanocobalamin (vitamin B12). Hydroxocobalamin is \nutilized as an antidote for cyanide toxicity. Cyanide is a cellular asphyxiant which disrupts \nmetabolism dependent on metal-containing enzymes. In particular, it binds to ferric iron present \nin the cytochrome oxidase system disrupting oxidative phosphorylation (oxidative \nphosphorylation is the final metabolic pathway of cellular respiration). Cells then shift to \nanaerobic metabolism which results in the production of lactic acid, which is manifested clinically \nas metabolic acidosis. Each hydroxocobalamin molecule deactivates one cyanide ion when its \nhydroxo portion is replaced by the cyanide ion creating cyanocobalamin. Cyanocobalamin is \nexcreted in the urine. \n \nProtocol Indication(s): \n \n1. \nKnown or suspected cyanide toxicity \n \nContraindications: \n \n1. \nKnown anaphylactic reaction to hydroxocobalamin or cyanocobalamin \n \nPrecautions: \n \n1. \nIf other cyanide antidotes are to be administered, they should not be administered \nconcurrently in the same intravenous line. \n \nSignificant adverse/side effects: \n1. \nHypertension \n2. \nChromaturia (abnormal coloration of the urine) \n3. \nNausea \n4. \nHeadache \n5. \nErythema \n6. \nRash \n \nDosage per protocol(s): \n4.18 \nToxicological Emergencies - Adult \n \n \n \n \n4.18 \nToxicological Emergencies - Pediatric", + "Ibuprofen": "Ibuprofen (Advil, Motrin) \n \n \n \n \n \n \n \nClassification: \nNon-steroidal anti-inflammatory \nGeneral: \nIbuprofen is a non-steroidal anti-inflammatory agent (NSAID) with analgesic effects, anti-\ninflammatory, and antipyretic effects. NSAIDs are thought to exert their effects by inhibiting \nprostaglandin synthesis by inhibiting the cyclooxygenase (COX) enzyme, which catalyzes the \nconversion of arachidonic acid to prostaglandin and endoperoxide. Prostaglandins are a \nmodulator of inflammation and are also involved in thermoregulation, pain transmission, and \nplatelet aggregation. Ibuprofen should be avoided in patients with chronic kidney disease due \nto the risk of renal injury. NSAID related renal injury occurs secondary to changes in renal \nhemodynamics (renal blood flow), which is mediated by prostaglandins, particularly in the \npresence of circulating vasoconstrictors (angiotensin II). Prostaglandins modulate vasodilation \nof the afferent arterioles which supply blood to the glomerulus maintaining glomerular perfusion \nand glomerular filtration. Inhibition of prostaglandins results in unopposed constriction of the \nafferent arterioles and decreased renal perfusion. \n \nProtocol Indication(s): \n \n1. \nMild to moderate pain \n2. \nFever \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nAllergy to any NSAID (including aspirin) \n3. \nAsthma \n4. \nRenal insufficiency \n5. \nPeptic ulcer disease or GI bleeding \n6. \nPregnancy \n7. \nHypovolemia \n8. \nTrauma other than isolated extremity trauma \n9. \nAnticipated major surgery (within 7 days) \n \nPrecautions: \n \n1. \nIbuprofen is not indicated for the treatment of abdominal pain. \n \n \n \nSignificant adverse/side effects: \n1. \nGI bleeding \n2. \nNausea/vomiting \n3. \nHeadache \n4. \nDrowsiness \n5. \nAbdominal pain \n6. \nDyspepsia \n7. \nDiarrhea \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.07 \nPatient Comfort - Pediatric \n \n \n \n \n2.15 \nFever - Adult \n \n \n \n \n2.15 \nFever - Adult", + "Intravenous Fat Emulsion 20%": "Intravenous Fat Emulsion (IFE) 20% (Intralipid) \n \n \n \nClassification: \nSoy based long chain fatty acid emulsion \nGeneral: \nIntravenous fat emulsion (IFE) is a soy based long change fatty acid emulsion used as a \ncomponent of total parenteral nutrition as a source of fatty acids and calories. Over the last \ndecade, IFE has emerged as a novel antidote for agents that have an affinity for or a tendency to \nbind with lipids (e.g. lipophilic agents). There are several theories as to the mechanism of action \nfor IFE as an antidote, but the exact mechanism is not completely understood. The most common \ntheory is the known as the \u201clipid sink\u201d theory. The lipid sink theory postulates that administering \nIFE creates a \u201clipid sink\u201d providing an alternative binding site for the lipophilic toxic agent. It is \nlikely that mechanisms other than the \u201clipid sink\u201d may also contribute to IFE role as an antidote. \nThe first reported use of IFE as an antidote was for local anesthetic toxicity. Since this time, there \nhave been multiple case reports involving the use of IFE to reverse cardiotoxicity and cardiac \narrest secondary to multiple lipophilic agents, including beta blockers, calcium channel blockers, \ntricyclic antidepressants, and selective serotonin uptake inhibitors. \n \nProtocol Indication(s): \n1. \nProfound hemodynamic compromise or cardiac arrest associated with a highly lipophilic \nagent \n \nContraindications: \n1. \nKnown hypersensitivity to any component of the formulation, or severe egg or legume \n \n(soybean) allergies \n \nPrecautions: \n \n1. \nDo not use in infants <30 days. \n \nSignificant adverse/side effects: \n1. \nFat embolism \n2. \nFat overload syndrome (not of concern in acute setting) \n3. \nHypertriglyceridemia (longer term use) \n4. \nAcute pancreatitis (longer term use) \n5. \nCholestasis (longer term use) \n6. \nIncreased risk of infection (longer term use) \n \n \n \nDosage per protocol(s): \n4.18 \nToxicological Emergencies - General - Adult \n \n \n \n \n4.18 \nToxicological Emergencies - General - Pediatric \n \n \nNotes: \n\uf0b7 There is currently ongoing research into the use of IFE in the management of refractory \nventricular fibrillation. \n\uf0b7 The IFE bolus dose (1.5 ml/kg) should be drawn up into a syringe and administered IVP over \ntwo minutes. This dose may be repeated twice. An infusion of 15 ml/kg may be started at \nthe time of the first bolus dose and administered over 60 minutes. \n \nSuggested reading: \nBania TC. Antidotes in Depth: Intravenous Fat Emulsions. In: Flomenbaum NE, Goldfrank LR, \nHoffman RS et al, eds: Goldfrank\u2019s Toxicologic Emergencies. New York NY, 2011; 976-981. \n \nMirtallo, JM, et al. State of the Art Review: Intravenous Fat Emulsions: Current Applications, \nSafety Profile, and Clinical Implications. Ann Pharmacother 2010; 44:688- 700. \n \nCave, G, Harvey, M. Intravenous Lipid Emulsion as Antidote Beyond Local Anesth Toxicity: \nA \nSystematic Review. Acad Emerg Med 2009; 16:815-824. \n \nWebsite: www.lipidrescue.org", + "Ipratropium bromide": "Ipratropium Bromide (Atrovent) \n \nClassification: \nAnticholinergic \n \n \nGeneral: \n \nIpratropium bromide is an anticholinergic agent used in the management of bronchospasm. \nIpratropium competes with acetylcholine for binding at the cholinergic muscarinic receptors in \nthe lung (M1, M2, M3). Antagonism of the cholinergic muscarinic receptors results in a decrease \nin the formation of cyclic guanosine monophosphate (cGMP), which leads to decreased \ncontractility of bronchial smooth muscle resulting bronchodilation. When administered via \ninhalation, the effects of ipratropium are almost exclusively limited to the airway. Inhaled \nipratropium has minimal effect on heart rate or intraocular pressure. Ipratropium may be \nadministered by inhalation alone or in combination with albuterol (Combivent). \n \nProtocol Indication(s): \n \n1. \nBronchospasm \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nBenign prostatic hypertrophy (relative) \n3. \nBladder neck obstruction (relative) \n \nPrecautions: \n1. \nDue to the risk of inadvertent topical administration (of the nebulization preparation), \nipratropium should be used with caution in patients with narrow-angle glaucoma. \n2. \nMetered-dose-inhaler ipratropium preparations may include allergens contraindicating \nuse in patients with soy or nut allergies. \n3. \nParadoxical bronchospasm may occur in a small percentage of patients who receive \nipratropium. A proposed etiology is attributed to other compounds in the ipratropium \npreparation. If paradoxical bronchospasm (evidenced by significantly increased and \nsevere bronchospasm following administration) is suspected, discontinue use. \n \nSignificant adverse/side effects: \n \n1. \nCough \n2. \nThroat irritation \n3. \nHeadache \n \nSignificant adverse/side effects: \n \n4. \nDry mouth \n5. \nUrinary retention \n \n \nDosage per protocol(s): \n2.04 \nAllergic Reaction - Anaphylaxis - Adult \n \n \n \n \n2.04 \nAllergic Reaction - Anaphylaxis - Pediatric \n \n \n \n \n2.08 \nRespiratory Distress (Asthma/COPD/RAD) - Adult \n2.08 \nRespiratory Distress (Asthma/RAD/Croup) - Pediatric \n2.18 \nObstetrical Complications \n \n \n \n \n4.09 \nCrush Injury", + "Ketamine": "Ketamine (Ketalar) \n \n \n \n \n \n \n \nClassification: \nDissociative general anesthetic \nGeneral: \nKetamine is a dissociative anesthetic agent, structurally similar to phencyclidine (PCP), which \ninterrupts the connection between the cortex and the limbic system. This results in profound \nsedation in a \u201cdissociative\u201d state of anesthesia. In this state, the patient appears awake, but is \nunaware of their surroundings. The patient\u2019s eyes remain open with corneal and light reflexes \nmaintained and nystagmus may develop. Airway protective reflexes are maintained and unless \nadministered rapidly or in conjunction with opioids, ketamine\u2019s effect on ventilation is minimal. \nKetamine also stimulates opioid receptors and is thus a unique sedative agent in that it also \nprovides analgesia as well. Ketamine stimulates the sympathetic nervous system and releases \ncatecholamines resulting in augmentation of the blood pressure and heart rate and increased \nmean arterial pressure (MAP). Ketamine directly and indirectly stimulates pulmonary \nbronchodilation. The onset of action for IV ketamine is 1-2 minutes and 3-8 minutes for IM \nadministration. As the dose related effect of ketamine transitions from analgesia to anesthesia, \nnystagmus emerges as a side effect. Nystagmus may be used as an endpoint indicator for \nketamine dosing. Ketamine is often the induction agent of choice for rapid sequence intubation \nof patients with reactive airway disease and in certain shock states. \n \nProtocol Indication(s): \n1. \nModerate to severe pain \n2. \nPre-cardioversion sedation when IV access is unavailable \n3. \nExcited delirium \n4. \nCombative behavior unresponsive to other interventions \n \nContraindications: \n1. \nCardiac ischemia/infarction or history of coronary artery disease (relative) \n2. \nPenetrating ocular injury \n3. \nPatient \u2264 3 months of age \n4. \nSchizophrenia \n \nPrecautions: \n \n1. \nIntravenous ketamine should be administered over 60 seconds. \n2. \nWhen not used in conjunction with a neuromuscular blocking agent, the most common \n \nrespiratory side effect associated with ketamine is laryngeal spasm. It is usually transitory \n \nand easily managed with positive pressure ventilation. \n \nPrecautions: \n \n3. \nExcessive salivation may occur in some patients. This can be managed with atropine 0.5 \n \nmg IV/IM. \n4. \nEmergence reactions may occur following the administration of ketamine. These \nreactions occur more commonly in adult patients. Emergence reactions may be treated \nwith low does benzodiazepines. \n \nSignificant adverse/side effects: \n1. \nEmergence reaction \n2. \nTachycardia \n3. \nHypotension/hypertension \n4. \nHypersalivation \n5. \nLaryngospasm \n6. \nIncreased intraocular pressure \n7. \nVomiting \n8. \nTransient apnea (if given rapidly via IV route) \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.07 \nPatient Comfort - Pediatric \n \n \n \n \n2.13 \nExcited Delirium \n \n \n \n \n2.09 \nBehavioral Emergencies \n \n \nNotes: \n\uf0b7 Ketamine is often the induction agent of choice for rapid sequence intubation of patients with \nreactive airway disease and in certain shock states. \n\uf0b7 Ketamine has been used extensively in military tactical combat care and its use in US civilian \nEMS for analgesia, sedation, and rapid sequence intubation. \n\uf0b7 Historically ketamine was avoided in cases of increased intracranial pressure (ICP) due to its \npotential to increase ICP, however it is now believed that any increase in ICP is offset by an in \nincrease in the MAP resulting in an increase in cerebral perfusion pressure.", + "Ketorolac": "Ketorolac tromethamine (Toradol) \n \n \n \n \n \n \n \n \nClassification: \nNon-steroidal anti-inflammatory \nGeneral: \nKetorolac is a non-steroidal anti-inflammatory agent (NSAID) with potent analgesic effects and \nmoderate anti-inflammatory effects. NSAIDs are thought to exert their effects by inhibiting \nprostaglandin synthesis by inhibiting the cyclooxygenase (COX) enzyme, which catalyzes the \nconversion of arachidonic acid to prostaglandin and endoperoxide. Prostaglandins are a \nmodulator of inflammation and are also involved in thermoregulation, pain transmission, and \nplatelet aggregation. Ketorolac also has antipyretic properties, but is not used primarily to treat \nfever. Ketorolac should be avoided in patients with chronic kidney disease due to the risk of \nrenal injury. NSAID related renal injury occurs secondary to changes in renal hemodynamics \n(renal blood flow), which is mediated by prostaglandins, particularly in the presence of circulating \nvasoconstrictors (angiotensin II). Prostaglandins modulate vasodilation of the afferent arterioles \nwhich supply blood to the glomerulus maintaining glomerular perfusion and glomerular filtration. \nInhibition of prostaglandins results in unopposed constriction of the afferent arterioles and \ndecreased renal perfusion. Ketorolac is frequently used in the management of pain associated \nwith renal colic. \n \nProtocol Indication(s): \n \n1. \nMild to moderate pain \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nAllergy to any NSAID (including aspirin) \n3. \nAsthma \n4. \nRenal insufficiency \n5. \nPeptic ulcer disease or GI bleeding \n6. \nPregnancy \n7. \nHypovolemia \n8. \nTrauma other than isolated extremity trauma \n9. \nAnticipated major surgery (within 7 days) \n \nPrecautions: \n \n1. \nKetorolac is not indicated for the treatment of abdominal or chest pain. \n2. \nThe dose of ketorolac should be reduced by 50% in patients >65 yo due to concern for \nage related reduction of renal function. \nSignificant adverse/side effects: \n1. \nGI bleeding \n2. \nNausea/vomiting \n3. \nHeadache \n4. \nDrowsiness \n5. \nAbdominal pain \n6. \nDyspepsia \n7. \nDiarrhea \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.07 \nPatient Comfort - Pediatric", + "Labetalol": "Labetalol (Trandate) \n \n \n \n \n \n \n \n \n \nClassification: \nCombined alpha and beta antagonist \n \nGeneral: \n \nLabetalol is a combined alpha and beta antagonist. Labetalol blocks \u03b11, \u00df1, and \u00df2 receptors. \nLabetalol\u2019s antagonistic effects are greater on beta receptors than on alpha receptors (1:7 for IV \nadministration). It is rapidly absorbed and widely distributed to relevant target tissues after an \nIV dose. The onset of action for a given dose occurs within about 5-10 minutes after \nadministration. The half-life of labetalol is about 8 hours. Labetalol is administered by bolus or \ninfusion. The maximum cumulative dose of labetalol is 300 mg. \n \nProtocol Indication(s): \n1. \nBlood pressure reduction in patients with ischemic stroke who are candidates to receive \n \nor are receiving tPA. \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nHeart rate <60 \n3. \nAV block >1 degree in the absence of a pacemaker \n4. \nHypotension (SBP <100 mmHg) \n \n5. \nAcute decompensated heart failure \n \nPrecautions: \n1. \nPatients receiving labetalol for acute BP reduction should have frequent monitoring of \n \ntheir BP (generally every 5-10 minutes in the EMS/transport setting). \n \nSignificant adverse/side effects: \n \n1. \nHypotension \n2. \nBradycardia \n3. \nDizziness \n \nDosage per protocol(s): \n2.13 \ntPA for Acute Ischemic Stroke", + "Lactated Ringers Solution": "Lactated Ringers Solution \n \n \n \n \n \n \nClassification: \nCrystalloid \nGeneral: \nLactated Ringers (LR) is a balanced resuscitation fluid. Balanced resuscitation fluids have an \nelectrolyte composition similar to human blood plasma. In contrast to sodium chloride 0.9% \n(NaCl 0.9%), LR has less chloride, a small amount of additional electrolytes, and an anion buffer \n(lactate). LR has a strong ion difference (SID) of +28. The SID is the difference between the \nconcentrations of strong cations and strong anions. While a detailed explanation of the SID is \nbeyond the scope of this guide, it is useful to know that the administration of a resuscitation fluid \nwith a SID less than the serum bicarbonate level (normal range 22\u201326\u202fmmol/L) will lead to a more \nacidotic state (\u2193pH) and the administration of a resuscitation fluid with a SID greater than the \nserum bicarbonate level leads to a more alkalotic state (\u2191pH). The table below compares the \nelectrolyte composition and SID of LR and NaCl 0.9% to human blood plasma (concentrations are \nin mEq/L): \n \n \nSodium (Na+) \nChloride (Cl-) \nPotassium (K+) \nCalcium (Ca++) \nLactate \nSID \nPlasma \n1-2 \n+40 \nLR \n+28 \nNaCl 0.9% 154 \n \nCompared to NaCl 0.9%, LR is more physiologically similar to human plasma. There is some \nrecent data that suggests that outcomes may be worse in patients who receive fluid resuscitation \nwith NaCl 0.9% v. those who receive fluid resuscitation with LR or other buffered resuscitation \nfluids. Specifically, resuscitation with NaCl 0.9% was associated with an increase in acute kidney \ninjury, hyperchloremic metabolic acidosis, and increased mortality. For this reason, LR was \nchosen as the fluid of choice for patients requiring large volume fluid resuscitation. \n \nProtocol Indication(s): \n \n1. \nDehydration \n2. \nHypovolemia \n3. \nShock \n4. \nBurns \n5. \nOcular irrigation \n \n \n \n \nContraindications: \n1. \nProfound liver failure (LR may increase the lactate level, but it should be noted that the \nlactate in LR is in the form of sodium lactate, not lactic acid and it will not make the patient \nmore acidotic) \n \nPrecautions: \n \n1. \nFluids should be administered judiciously to patients with evidence of or a history of heart \nfailure. \n2. \nBecause LR is slightly hypotonic, large volumes may increase intracranial pressure. \n3. \nThe calcium in LR can bind to the citrated anticoagulant in blood products and lead to \ninactivation of anticoagulant and promote the formation of clots in donor blood. For this \nreason, LR is contraindicated as a diluent for red blood cell transfusions. \n \nSignificant adverse/side effects: \n1. \nFluid overload \n2. \nMetabolic alkalosis \n3. \nIncreased intracranial pressure (large volumes, primarily of concern in patients with \nalready increased intracranial pressure). \n \nDosage per protocol(s): \n1.01 \nRoutine Patient Care \n2.20 \nGeneral Shock and Hypotension - Adult \n2.20 \nGeneral Shock and Hypotension - Pediatric \n2.21 \nHemorrhagic Shock - Adult \n2.21 \nHemorrhagic Shock - Pediatric \n2.22 \nSeptic Shock - Adult \n2.22 \nSeptic Shock - Pediatric \n3.03 \nCardiac Arrest - Adult \n3.03 \nCardiac Arrest - Pediatric \n4.06 \nTraumatic Cardiac Arrest - Adult \n4.06 \nTraumatic Cardiac Arrest - Pediatric \n4.07 \nThermal Burns - Adult \n4.07 \nThermal Burns - Pediatric \n4.11 \nOcular Trauma and Emergencies \n4.22 \nRadiation Incident \n7.44 \nOcular Irrigation - Morgan Lens\u00a9 \n \n \n \nNotes: \n\uf0b7 Because only 25% of crystalloid fluids remain in the vascular compartment, the infusion of LR \nshould not be expected to have a significant impact on serum lactate levels. \n\uf0b7 Contrary to popular belief, LR is safe to use as a resuscitation fluid in the patient with \nhyperkalemia.", + "Levalbuterol": "Levalbuterol (Xopenex) \n \nClassification: \nBeta adrenergic agonist (\u03b22 selective) \n \n \nGeneral: \n \nLevalbuterol is a \u03b22 selective adrenergic receptor agonist used in the management of \nbronchospasm. Stimulation of \u03b22 receptors results in an increase in cyclic adenosine \nmonophosphate (cAMP), which leads to the activation of protein kinase A inhibiting \nphosphorylation of myosin and lowering intracellular ionic calcium concentrations, resulting in \nrelaxation of bronchial smooth muscle (bronchodilation). Increasing cAMP concentrations is \nalso inhibits the release of mediators from mast cells in the airway. As a result of \nsympathomimetic stimulation, an intracellular shift of potassium may occur. This may result in a \nsmall (approximately 0.5 mEq/L) decrease in the serum potassium concentration. This is \ngenerally not of clinical concern, unless large doses of beta agonist are being administered. \nHowever, this effect may be useful in the management of hyperkalemia. Albuterol is a 50/50 \nracemic mixture of two isomers. The R- isomer which causes bronchodilation and the S-isomer \nis devoid of any clinical utility, but is believed to increase airway reactivity and may contribute to \nparadoxical bronchospasm. Because of its slow metabolism, the S-isomer exists in higher and \nprolonged plasma concentrations. Some clinical trials comparing racemic albuterol and \nlevalbuterol in patients with asthma have demonstrated lower mean heart rates in patients using \nlevalbuterol, while other trials demonstrated no difference in heart rate. Levalbuterol may be \nconsidered in patients with a history of arrhythmias, structural heart disease, or cardiac \nconditions that could worsen with an episode of tachycardia (e.g., decompensated heart failure). \n \nProtocol Indication(s): \n \n1. \nBronchospasm associated with asthma or COPD \n \nContraindications: \n1. \nKnown hypersensitivity to levalbuterol or albuterol \n \nPrecautions: \n1. \nUse with caution in patients with coronary artery disease. \n2. \nAdministered with to patients being treated with monoamine oxidase inhibitors or \ntricyclic antidepressants, or within 2 weeks of discontinuation of such agents, because the \ncardiovascular effects of levalbuterol may be potentiated. \n \n \n \nSignificant adverse/side effects: \n \n1. \nTachycardia \n2. \nPalpitations \n3. \nNervousness, tremor, anxiety \n4. \nHeadache \n5. \nNausea \n6. \nHypokalemia \n \nDosage per protocol(s): \n2.08 \nRespiratory Distress (asthma, COPD, RAD) - Adult", + "Lidocaine": "Lidocaine (Xylocaine) \n \n \n \n \n \n \nClassification: \nAntiarrhythmic \nGeneral: \nLidocaine is a class IB antiarrhythmic that suppresses ventricular arrhythmias. Lidocaine acts \nselectively on diseased or ischemic non-nodal tissue, where it blocks sodium entry into sodium \nfast channels, resulting in a decrease in the rate and magnitude of depolarization. Conduction \nvelocity is decreased and arrhythmias originating from a reentrant mechanism may be \ninterrupted. Lidocaine reduces automaticity by decreasing the slope of phase 4 depolarization. \nIt also decreases the effective refractory period (ERP). It has no direct effect on nodal tissue via \nsodium channel blockade and has no effect on QRS duration at non-toxic levels and has limited \neffects on the action potential duration (APD) and the QT interval. Lidocaine is not useful in the \nmanagement of atrial arrhythmias. Lidocaine may be useful in the management of arrhythmias \nassociated with digitalis toxicity. The plasma half-life (t\u00bd) is short (approximately 20 minutes). \nIt is metabolized by the liver and its t\u00bd may be prolonged when hepatic function or blood flow is \ndecreased (states of decreased cardiac output, congestive heart failure, liver disease). Lidocaine \nalso has local anesthetic properties and for this purpose, it may be administered by topical \nadministration, infiltration, or inhalation. \n \nProtocol Indication(s): \n \n1. \nVentricular tachycardia \n2. \nVentricular fibrillation \n \nContraindications: \n1. \nKnown hypersensitivity or allergy to any local anesthetic in the amide class \n2. \nAV block > 1st degree in the absence of a pacemaker \n3. \nIdioventricular escape rhythm in the absence of a pacemaker \n4. \nStokes-Adams syndrome \n5. \nWolff-Parkinson-White (WPW) syndrome \n \nPrecautions: \n \n1. \nPlasma half-life may be prolonged in the setting of congestive heart failure, advanced age, \nliver disease or any condition resulting in decreased hepatic blood flow. The maintenance \ninfusion should be reduced in patients >70 yo, congestive heart failure, or hepatic failure. \n2. \nLidocaine should not be administered in the setting of an idioventricular escape rhythm \nin the absence of a pacemaker. \n \nSignificant adverse/side effects: \n1. \nDrowsiness \n2. \nParesthesia \n3. \nSlurred speech \n4. \nNystagmus (early sign of toxicity) \n5. \nSeizures (severe toxicity) \n \nDosage per protocol(s): \n3.03 \nCardiac Arrest - Adult \n \n \n \n \n3.03 \nCardiac Arrest - Pediatric \n \n \n \n \n3.04 \nPost Cardiac Arrest Care - Adult \n \n \n \n \n3.07 \nWide Complex Tachycardia - Adult \n \n \n \n \n3.07 \nWide Complex Tachycardia - Pediatric \n \n \n \n \n7.44 \nOcular Irrigation - Morgan Lens\u00a9 \n \n \n \n \n7.45 \nGastric Tube Placement \n \n \n \n \n7.61 \nVascular Access - Intraosseous", + "Lorazepam": "Lorazepam (Ativan) \n \n \n \n \n \n \n \n \nClassification: \nBenzodiazepine \n \nGeneral: \n \nLorazepam binds to the gamma-aminobutryic acid receptor complex A (GABA-A), increasing the \naffinity of the receptor for GABA, enhancing the effects of GABA. GABA is the primary inhibitory \nneurotransmitter in the CNS which counterbalances the action of the excitatory neurotransmitter \nglutamate. Enhancing the effects of GABA results in anxiolysis, sedation, amnesia, increased \nseizure threshold and muscle relaxation. The effects of benzodiazepines are dose dependent \n(e.g. anxiolysis occurs at doses that do not result in sedation). Lorazepam can be administered \nvia the PO, IV/IO, PR and IM routes. Following IV administration, the onset of action is within 5 \nminutes with peak effects occurring at 5-10 minutes. The duration of action may be 4-6 hours. \nDue to its long half-life, lorazepam provides longer seizure protection than midazolam or \ndiazepam. Unlike midazolam and diazepam, there are no active metabolites. \n \nProtocol Indication(s): \n1. \nSeizures \n2. \nSedation \n3. \nSympathetic agent toxicity \n4. \nMuscular spasm associated with a sting or envenomation \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nHypotension (SBP <100 mmHg) \n3. \nAcute angle glaucoma (relative) \n4. \nPregnancy (relative for active seizures, all benzodiazepines are pregnancy safety category \nD) \n \nPrecautions: \n1. \nLorazepam can cause respiratory depression, particularly when it is administered with \nopioids or to patients at extremes of age or those with respiratory conditions. Dosing \nshould be reduced in these patients. \n \n \n \n \nPrecautions: \n2. \nWhen administered to a non-intubated patient, close monitoring of the airway and \nventilation is necessary (the use of waveform capnography is highly recommended). \n3. \nHypotension is less of a concern than respiratory depression, but may occur if it is \nadministered quickly, to volume depleted patients, or to patients with hemodynamic \ninstability. \n \n4. \nDue to the viscosity of the lorazepam drug formulation, the dose is usually diluted with \nand equal amount of saline. \n \nSignificant adverse/side effects: \n \n1. \nRespiratory depression \n2. \nHypotension \n3. \nConfusion \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.07 \nPatient Comfort - Pediatric \n \n \n \n \n2.19 \nSeizures - Adult \n \n \n \n \n2.19 \nSeizures - Pediatric \n \n \n \n \n \n4.18 \nToxicological Emergencies", + "Magnesium Sulfate": "Magnesium Sulfate \n \nClassification: \nElectrolyte \n \n \nGeneral: \n \nMagnesium sulfate is the common formulation of magnesium used for IV administration. \nMagnesium is a positively charged electrolyte (cation). Magnesium is a cofactor in a multitude \nof enzymatic reactions and is required for all biologic activities involving adenosine triphosphate \n(ATP). It is also required for the proper function of the Na+ - K+ exchange pump, which transfers \nNa+ out of the cell in exchange for K+ providing electrical stability of the cellular membrane. \nMagnesium demonstrates antiarrhythmic effects which are possibly mediated by blockade of \nsodium currents. It is useful in the management of torsades de pointes associated with a \nprolonged QTI. These antiarrhythmic effects are demonstrated in the presence of normal serum \nmagnesium levels. Magnesium is also a nonselective calcium antagonist and blocks a number \nof calcium dependent processes. By inhibiting calcium uptake by smooth muscle, administration \nresults in bronchial, vascular, and uterine relaxation (tocolysis), making it useful in the \nmanagement of bronchospasm and premature labor. Magnesium decreases neuronal and \nneuromuscular excitability. Magnesium is the anticonvulsant of choice in eclampsia. Its \nanticonvulsant activity is likely multifactorial and may include antagonism of the excitatory \nneurotransmitter N-methyl-d-aspartate (NMDA). Clinical manifestations of hypomagnesaemia \ninclude cardiovascular abnormalities (QTI prolongation, arrhythmias, vasospasm, and myocardial \nischemia) and neuromuscular abnormalities (weakness, tremor, seizures, tetany, and altered \nmental status). Patients who are malnourished, chronic alcohol users, and those taking diuretics \nare at particular risk for hypomagnesaemia. \n \nProtocol Indication(s): \n \n1. \nPolymorphic ventricular tachycardia associated with a prolonged QTI (Torsade\u2019s de \npointes) \n2. \nCardiac arrest with suspected hypomagnesaemia \n3. \nAsthma \n4. \nPreterm labor \n \nContraindications: \n1. \nKnown hypersensitivity \n \n \n \nPrecautions: \n1. \nHypotension, bradycardia, and conduction disturbances may occur if administered too \nrapidly. Administer with caution in patients with bradycardia. \n2. \nToxicity is associated with CNS and neuromuscular depression. A decrease in deep \ntendon reflexes (DTRs) is an early sign of toxicity and may indicate impending respiratory \ndepression. \n3. \nThe administration of calcium reverses respiratory depression associated with \nmagnesium toxicity. \n4. \nRepeat doses should be administered cautiously in patients with decreased renal \nfunction. \n \nSignificant adverse/side effects: \n \n1. \nHypotension \n2. \nBradycardia/conduction disturbance (administer with caution in patients with \nbradycardia) \n3. \nRespiratory depression \n4. \nFlushing \n \nDosage per protocol(s): \n2.08 Asthma - Reactive Airway Disease - COPD - Adult \n \n \n \n \n \n2.08 Asthma - Reactive Airway Disease - Croup - Pediatric \n \n \n \n \n2.18 \nObstetrical Complications \n \n \n \n \n3.03 Cardiac Arrest - Adult \n \n \n \n \n3.03 Cardiac Arrest - Pediatric \n \n \n \n \n3.07 Wide Complex Tachycardia - Adult \n \n \n \n \n3.07 \nWide Complex Tachycardia - Pediatric", + "Methylprednisolone": "Methylprednisolone ( Solu-Medrol) \n \n \n \n \n \n \nClassification: \nSteroid (synthetic glucocorticoid) \nGeneral: \nMethylprednisolone is a synthetic glucocorticoid. Glucocorticoid receptors are found in virtually \nevery cell in the body and exert a powerful physiologic effect on every body system. \nGlucocorticoids stimulate the formation of glucose (gluconeogenesis) and cause the breakdown \nof protein into amino acids (catabolism). Because methylprednisolone inhibits the inflammatory \nand immunologic response, it is useful in the management of allergic and anaphylactic reactions \nand in the management of disease processes that involve airway inflammation or edema (i.e. \nreactive airway disease, asthma). In reversing asthmatic obstruction, glucocorticoids probably \nhave multiple actions including the reduction of inflammatory mucosal edema, bronchial smooth \nmuscle reaction, bronchial vasoconstriction, and decreasing capillary permeability. They may \nalso restore the responsiveness of asthmatic patients to beta agonist. Methylprednisolone may \nalso be used for replacement therapy in patients with adrenal insufficiency. \n \nProtocol Indication(s): \n \n1. \nAdrenal insufficiency \n2. \nAsthma \n3. \nCOPD exacerbation \n4. \nAllergic and anaphylactic reactions \n \nContraindications: \n1. \nKnown hypersensitivity to any steroid. \n2. \nSystemic fungal infections. \n \nPrecautions: \n \nNone \n \nSignificant adverse/side effects: \n1. \nHyperglycemia \n2. \nImmunosuppression \n3. \nNausea/vomiting \n4. \nEdema \n \n \n \nDosage per protocol(s): \n2.03 \nAdrenal Insufficiency \n \n \n \n \n2.04 \nAllergic Reaction - Anaphylaxis - Adult \n \n \n \n \n2.04 \nAllergic Reaction - Anaphylaxis - Pediatric \n \n \n \n \n \n \n2.08 \nRespiratory Distress (Asthma/RAD/COPD) - Adult \n2.08 \nRespiratory Distress (Asthma/RAD/Croup) - Pediatric", + "Metoprolol": "Metoprolol (Lopressor) \n \n \n \n \n \n \n \n \n \n \nClassification: \nBeta antagonist (\u03b21 selective) \n \nGeneral: \n \nMetoprolol is a \u03b21 (cardiac) selective beta antagonist and thereby reduces sympathetic \nstimulation of the heart resulting in decreases in the heart rate, cardiac output, and AV \nconduction. Metoprolol reduces myocardial oxygen consumption. Metoprolol is classified as \na Class 2 antiarrhythmic agent. Like other cardioselective beta antagonist, metoprolol loses its \ncardioselectivity at higher doses and will inhibit \u03b22 receptors. Metoprolol is used in the chronic \nmanagement of angina, hypertension, tachyarrhythmias, and heart failure. Acutely, metoprolol \nis used for ventricular rate control (supraventricular tachycardia, atrial fibrillation/flutter), \nhypertension and thyrotoxicosis. It may also be used in the management of recurrent and \nrefractory ventricular fibrillation or tachycardia. The onset of action following IV administration \nis within 5 minutes with a peak effect in less than 1 hour and a duration of action of 5 to 8 hours. \n \nProtocol Indication(s): \n1. \nRefractory and recurrent ventricular fibrillation/tachycardia \n2. \nNarrow complex tachycardia \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nHeart rate <60 \n3. \nAV block >1 degree in the absence of a pacemaker \n4. \nHypotension (SBP <100 mmHg) \n \n5. \nAcute decompensated heart failure \n \nPrecautions: \n1. \nMetoprolol should be used cautiously in combination with other nodal agents (diltiazem) \nand this combination should be avoided whenever possible. \n2. \nIn response to hypoglycemia the sympathetic nervous system stimulates an increase in \nblood glucose via \u03b2 receptors. Antagonism of \u03b2 receptors will result in the blood glucose \nremaining low. Antagonism of the \u03b2 receptors will also suppress the sympathetic signs \nassociated with hypoglycemia. \n3. \nThe hypotensive effects of metoprolol may be enhanced in patients receiving amiodarone \nor antihypertensive agents. \n4. \nMetoprolol may enhance the CNS depressive effects of benzodiazepines. \n \nSignificant adverse/side effects: \n \n1. \nHypotension \n2. \nBradycardia \n3. \nAV block \n4. \nDizziness \n5. \nBronchospasm \n6. \nHeart failure \n \nDosage per protocol(s): \n3.03 \nCardiac Arrest - Adult \n \n \n \n \n3.06 \nNarrow Complex Tachycardia - Adult", + "Midazolam": "Midazolam (Versed) \n \n \n \n \n \n \n \nClassification: \nBenzodiazepine \n \nGeneral: \n \nMidazolam binds to the gamma-aminobutryic acid receptor complex A (GABA-A), increasing the \naffinity of the receptor for GABA, enhancing the effects of GABA. GABA is the primary inhibitory \nneurotransmitter in the CNS which counterbalances the action of the excitatory neurotransmitter \nglutamate. Enhancing the effects of GABA results in anxiolysis, sedation, amnesia, increased \nseizure threshold and muscle relaxation. The effects of midazolam are dose dependent (e.g. \nanxiolysis occurs at doses that do not result in sedation). As compared to other benzodiazepines, \nmidazolam has the most profound anterograde amnestic effects and it is therefore the generally \npreferred agent when a benzodiazepine is being used for this effect (e.g. pre cardioversion). \nMidazolam can be administered via the oral, IV/IO, IM, PR and IN routes. Following IV \nadministration, the onset of action is 1-5 minutes with peak effects occurring at 2-3 minutes. The \nduration of action is 20-30 minutes. Midazolam is metabolized in the liver and has an active \nmetabolite. Compared to diazepam, midazolam is 3-4 times more potent and has a more rapid \nonset and recovery. \n \nProtocol Indication(s): \n1. \nSeizures \n2. \nSedation \n3. \nSympathetic agent toxicity \n4. \nMuscle spasm associated with a sting or envenomation \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nHypotension (SBP <100 mmHg) \n3. \nAcute angle glaucoma (relative) \n4. \nPregnancy (relative for active seizures, all benzodiazepines are pregnancy safety category \nD) \n \nPrecautions: \n1. \nMidazolam can cause respiratory depression, particularly when it is administered with \nopioids or to patients at extremes of age or those with respiratory conditions. Dosing \nshould be reduced in these patients. \n \n \nPrecautions: \n \n2. \nWhen administered to a non-intubated patient, close monitoring of the airway and \nventilation is necessary (the use of waveform capnography is highly recommended). \n3. \nHypotension is less of a concern than respiratory depression, but may occur if it is \nadministered quickly, to volume depleted patients, or to patients with hemodynamic \ninstability. \n \n \nSignificant adverse/side effects: \n \n1. \nRespiratory depression \n2. \nHypotension \n3. \nConfusion \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.07 \nPatient Comfort - Pediatric \n \n \n \n \n2.09 \nBehavioral Emergencies \n \n \n \n \n2.19 \nSeizures - Adult \n \n \n \n \n2.19 \nSeizures - Pediatric \n \n \n \n \n \n2.25 \nExcited Delirium \n \n \n \n \n3.01 \nAcute Decompensated Heart Failure - Pulmonary Edema \n \n \n \n \n3.06 \nNarrow Complex Tachycardia - Adult \n \n \n \n \n \n \n3.06 \nNarrow Complex Tachycardia - Pediatric \n \n \n \n \n3.07 \nWide Complex Tachycardia - Adult \n \n \n \n \n \n \n \n3.07 \nWide Complex Tachycardia \u2013 Pediatric \n \n \n \n \n4.17 \nBites - Stings - Envenomation \n \n \n \n \n4.18 \nToxicological Emergencies", + "Naloxone": "Naloxone (Narcan) \n \n \n \n \n \n \n \n \n \nClassification: \nOpioid antagonist \n \nGeneral: \n \n \n \nNaloxone is an opioid antagonist which binds with high affinity to opioid receptors (\u00b5, k, \u03b4) but \ndoes not activate a receptor mediated response. It rapidly displaces bound opioid molecules and \nreverses the effects of opioids. While naloxone it a competitive antagonist at all of the opioid \nreceptors, its effects on the \u00b5 (mu) receptor are ten times greater on other opioid receptors. \nFollowing IV administration, it rapidly (within 30 seconds) reverses opioid related respiratory \ndepression and coma. Naloxone has a \u00bd life of about 20 minutes. Naloxone has a lesser effect \non the analgesic effect of opioids mediated by the k (kappa) receptors. The primary goal of \nnaloxone administration is to reverse respiratory depression associated with opioid use or \ningestion and its administration should be titrated to this effect. Naloxone is not indicated in \ncardiac arrest, even if the etiology of the arrest is opioid related. Naloxone may be administered \nvia the IV/IM/SC/IN routes. Patients that have taken/ingested very high amounts of opioids, \nany doses of propoxyphene, or potent (usually synthetic) agents, may require high doses of \nnaloxone (up to 10 mg) before a clinical response is achieved. \n \nProtocol Indication(s): \n \n1. \nOpioid related respiratory depression. \n \nContraindications: \n1. \nKnown hypersensitivity \n \nPrecautions: \n1. \nAdministration of naloxone to chronic opioid users may precipitate symptoms of \nwithdrawal. \n \n \n2. \nNaloxone\u2019s short serum t \u00bd life should be considered when administered to patients who \nhave taken/received longer duration opioids. Rebound opioid intoxication may occur. \n3. \nPatients that have taken/ingested very high amounts of opioids, any doses of \npropoxyphene, or potent (usually synthetic) agents, may require high doses of naloxone \n(up to 10mg) before a clinical response is achieved. \n \n \n \n \n \nSignificant adverse/side effects: \n \n1. \nAcute withdrawal syndrome \n2. \nVomiting \n3. \nPulmonary edema (rare) \n \nDosage per protocol(s): \n4.18 \nToxicological Emergencies - General - Adult \n \n \n \n \n4.18 \nToxicological Emergencies - Pediatric - Pediatric \n \nNotes: \n\uf0b7 If naloxone is administered to a patient with no opioid on board, miossis (pupillary \nconstriction) may occur.", + "Nicardipine": "Nicardipine (Cardene) \n \n \n \n \n \n \n \n \n \n \nClassification: \nCalcium channel blocker (dihydropyridine class) \n \nGeneral: \n \nNicardipine is a dihydropyridine class calcium channel blocker (CCB). Nicardipine antagonizes \nthe influx of calcium through L-type voltage gated calcium channels in vascular smooth muscle \ncells, resulting in arteriolar dilation and decreased systemic vascular resistance (afterload). \nThe effects of nicardipne are dose dependent and when used within the recommended dosing \nrange, nicardipine has no significant effect on cardiac conduction or contractility. Unlike sodium \nnitroprusside, an older drug used for acute blood pressure reduction, nicardipine does not \nincrease intracranial pressure. The onset of action for nicardipine is 5-10 minutes. Rapid dose-\nrelated increases in nicardipine plasma concentrations are seen during the first two hours after \nadministration by IV infusion. Plasma concentrations increase at a much slower rate after the \nfirst few hours, and approach a steady state at 24-48 hours. On termination of IV infusion, \nnicardipine concentrations rapidly decrease, with at least 50% decrease during the first 2 hours \npost-termination of the infusion. \n \nProtocol Indication(s): \n1. \nBlood pressure reduction in patients with ischemic stroke who are candidates to receive \n \nor are receiving tPA \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nSevere aortic stenosis \n3. \nHypotension (SBP <100 mmHg) \n \nPrecautions: \n1. \nPatients receiving nicardipine for acute reduction of their BP should have frequent \n \nmonitoring of their BP (generally every 5-10 minutes in the EMS/transport setting). \n \nSignificant adverse/side effects: \n \n1. \nHypotension \n2. \nTachycardia \n3. \nHeadache \n \nDosage per protocol(s): \n2.13 \ntPA for Acute Ischemic Stroke", + "Nitroglycerin": "Nitroglycerine (NTG) \n \nClassification: \nOrganic nitrate \n \nGeneral: \nNitroglycerin is an organic nitrate that is metabolized by smooth muscle to its active metabolite, \nnitric oxide (NO). NO relaxes vascular smooth muscle resulting in marked venous and arterial \ndilation. The end result is a reduction in cardiac pre and afterload and a reduction in myocardial \noxygen demand. In the setting of cardiac ischemia, NTG decreases myocardial oxygen demand \nand improves myocardial oxygen supply. The reduction of preload decreases heart size and \nreducing afterload decreases left ventricular (LV) wall tension (the pressure in the wall of the left \nventricle during ejection). The effect of decreasing heart size and LV wall tension is decreased \noxygen demand. The increase in myocardial oxygen supply occurs secondary to two effects. \nDecreasing preload decreases the distending pressure of the heart increasing subendocardial \nblood flow (increased pressure collapses the subendocardial vasculature) and by vasodilating \nepicardial and collateral coronary arteries, blood flow to ischemic myocardium is increased. In \nthe setting of acute decompensated heart failure (cardiogenic pulmonary edema), NTG reduces \npulmonary congestion by reducing venous return (preload), which decreases pulmonary blood \nflow and by reducing afterload, which results in increased left ventricular stroke volume (the \nvolume of blood ejected out of the left ventricle with one contraction). \n \nProtocol Indication(s): \n1. \nAcute decompensated heart failure (ADHF) [cardiogenic pulmonary edema] \n2. \nChest pain/discomfort related to cardiac ischemia \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nHypotension (SBP <100mmHg) \n3. \nRecent use of a phosphodiesterase type 5 inhibitor (sildenafil [Viagra, Revatio] or \n \nvardenafil [Levitra] with 24 hours or tadalafil [Cialis, Adcirca]) within 36 hours. \n4. \nRight ventricular infarction (RVI) \n5. \nTachycardia (HR>100) in the absence of heart failure \n6. \nIncreased intracranial pressure \n \n \n \n \nPrecautions: \n1. \nPatients with right ventricular infarction (RVI) are very preload sensitive and can develop \nsevere hypotension in response to nitrates or other preload-reducing agents. If \nhypotension develops following the administration of NTG, an IV fluid bolus may be \nnecessary. In patients with inferior wall STEMI, also obtain right sided leads to assess for \nevidence of RVI. \n2. \nPatients with aortic stenosis are very preload dependent to maintain cardiac output. \n \nThe use of NTG in patients with known aortic stenosis or a suggestive murmur should \n \nbe judicious and carefully titrated. \nSignificant adverse/side effects: \n1. \nHypotension \n2. \nHeadache \n3. \nTachycardia (reflex) \n4. \nBradycardia \n5. \nMethmemoglobinemia (nitrate ions can oxidize hemoglobin to methmemoglobin [this is \n \na long term effect and unlikely to be seen in the EMS setting). \n \nDosage per protocol(s): \n3.01 \nAcute Decompensated Heart Failure - Pulmonary Edema \n \n \n \n \n3.02 \nChest Pain - Acute Coronary Syndrome - STEMI \nNotes: \n\uf0b7 \nAt lower doses, venodilation is greater than arteriodilation. At higher doses (those used \n \nfor the management of ADHF), widespread arteriodilation occurs. \n\uf0b7 NO activates guanylate cyclase and increases cGMP (cGMP is a second messenger \n involved in the regulation of smooth muscle tone). Increasing cGMP results in the \n dephosphorization of myosin light chains and in the subsequent relaxation of smooth \n muscle. \n \nSuggested reading: \nClaveau D et al. Complications associated with nitrate use in patients presenting with acute \npulmonary edema and concomitant moderate or severe aortic stenosis. Ann Emerg Med 2015 \nOct; 66:355.", + "Nitrous Oxide": "Nitrous Oxide (N2O) \n \n \n \n \n \n \n \n \n \nClassification: \nInorganic gas, inhaled anesthetic \nGeneral: \nN2O is an inorganic gas with analgesic properties useful in the treatment of mild to moderate \npain, or as a bridge to IV analgesia. The exact mechanism of action for N2O is unknown, but its \neffects take place within the pain centers of the brain and spinal cord. It is thought to affect the \nrelease of endogenous neurotransmitters such as opioid peptides and serotonin. The release of \nthese neurotransmitters is thought to activate descending pain pathways that inhibit pain \ntransmission. Additionally, it is thought to have an effect on the gamma aminobutryic acid \n(GABA) receptors increasing inhibition of nerve cells causing drowsiness and sleep. The onset of \naction is 30-60 seconds and the peak effect is seen within 2-5 minutes. N20 is able to diffuse from \nthe blood in to closed gas spaces (i.e. bowel, middle ear, pneumothorax) causing them to expand. \nBecause N20 is self-administered by the patient, the patient must be able to understand and \nfollow directions. N20 is blended with oxygen and in the EMS setting is delivered in a 50/50 \nconcentration. \nProtocol Indication(s): \n1. \nMild to moderate pain \nContraindications: \n1. \nKnown hypersensitivity \n2. \nAltered mental status \n3. \nAcute intoxication or drug use \n4. \nPregnancy (except during delivery) \n5. \nBlunt or penetrating chest trauma/pneumothorax \n6. \nCraniofacial injury/traumatic brain injury/increased intracranial pressure \n7. \nUndifferentiated abdominal pain \n8. \nDiving emergencies (decompression illness) \n9. \nRespiratory distress \n10. \nMaxillofacial abnormalities/facial trauma or burns \n11. \nStatus-post retinal surgery \n \nPrecautions: \n1. \nThe patient must be able to self-administer N20. \n2. \nBeware that the delivered FiO2 is 50%. \n \n \nSignificant adverse/side effects: \n1. \nNausea and vomiting (especially if used with a narcotic analgesic) \n2. \nLightheadedness/dizziness \n3. \nEuphoria \n4. \nRespiratory depression \n \n \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.07 \nPatient Comfort - Pediatric \nSuggested reading: \nProcedure Protocol 7.56 Nitrous Oxide Administration", + "Norepinephrine": "Norepinephrine (Levophed) \n \nClassification: \nAdrenergic receptor agonist (\u03b11, \u03b21, \u03b22) \n \n \nGeneral: \n \nNorepinephrine is an adrenergic agonist with activity on \u03b11, \u03b21, and \u03b22 receptors. \nNorepinephrine\u2019s activity is strongest on the \u03b11 receptor and it has moderate agonistic activity \non the \u03b2 receptors, with greater \u03b21 receptor activity than \u03b22. The vasoconstrictive effects of \nnorepinephrine are greater than its inotropic or chronotropic effects. In septic shock, due to an \nincrease risk for death and arrhythmic events associated with the administration of dopamine, \nnorepinephrine is now the vasopressor of choice in patients with septic shock refractory to fluid \nresuscitation. \n \nProtocol Indication(s): \n \n1. \nShock/hypotension \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nSulfite allergy \nPrecautions: \n1. \nNorepinephrine may not be appropriate as a single agent in some case of cardiogenic \nshock secondary to its effect of increased afterload. \n2. \nDue to concern for oxidation which may occur when norepinephrine is mixed in 0.9% \nsodium chloride, D5W is the preferred diluent for admixtures containing norepinephrine. \nHowever, this is a long term effect and in the EMS setting, it may be mixed in normal \nsaline if D5W is not available. \n3. \nThe dosage should be reduced in patients taking monoamine oxidase inhibitors (MOAIs). \n4. \nNorepinephrine and other vasopressors are only to be utilized in hemorrhagic shock as a \nbridge to blood products and/or surgical intervention and only after fluid resuscitation as \nappropriate for the etiology. \n \nSignificant adverse/side effects: \n \n1. \nHypertension \n2. \nReflex bradycardia \n3. \nMesenteric or peripheral ischemia at high doses \n \nDosage per protocol(s): \n2.20 \nGeneral Shock and Hypotension - Adult \n \n \n \n \n \n2.20 \nGeneral Shock and Hypotension - Pediatric \n \n \n \n \n2.21 \nHemorrhagic Shock - Adult \n2.21 \nHemorrhagic Shock - Pediatric \n \n \n \n \n2.22 \nSepsis and Septic Shock - Adult \n \n \n \n \n2.22 \nSepsis and Septic Shock - Pediatric \n \n \n \n \n4.18 \nToxicological Emergencies - Adult \n4.18 \nToxicological Emergencies - Pediatric \nNotes: \n \n\uf0b7 Norepinephrine is the preferred vasopressor for the management of hypotension associated \nwith tricyclic antidepressant (TCA) toxicity (endogenous norepinephrine stores become \ndepleted with TCA toxicity).", + "Ondansetron": "Ondansetron (Zofran) \n \n \n \n \n \n \n \n \n \nClassification: \nAntiemetic \n \nGeneral: \n \n \n \nOndansetron is a 5-HT3 (serotonin) receptor antagonist which is used as an antiemetic. 5-HT3 \nreceptors are expressed in the enteric (intestinal) nervous system, the nerve endings of the vagus \nnerve, and the central nervous system, particularly in the chemoreceptor trigger zone (CTZ). The \nCTZ is an area of the vomiting center (area postrema) of the brain. Because ondansetron is not \nassociated with many of the risks associated with other antiemetics (e.g. hypotension, \nextrapyramidal reactions), it is often the antiemetic of choice. Ondansetron has not been found \nuseful in the treatment of motion induced nausea and vomiting and it has little effect on nausea \nassociated with vertigo. \n \nProtocol Indication(s): \n1. \nNausea/vomiting \n2. \nPenetrating ocular injury \n \nContraindications: \n \n1. \nKnown hypersensitivity \n2. \nProlonged QT interval (male >440 msec, female >450 msec) \n3. \nPregnancy (1st trimester) \n \nPrecautions: \n1. \nUse with caution if administering with other agents that may cause QTI prolongation. \n \nSignificant adverse/side effects: \n \n1. \nHeadache (particularly in those prone to migraine headaches) \n2. \nQTI prolongation \n3. \nAV conduction disturbance (associated with rapid administration) \n4. \nSedation \n5. \nDiarrhea \n6. \nDry mouth \n7. \nSerotonin syndrome \n \n \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult \n \n \n \n \n2.07 \nPatient Comfort - Pediatric \n \n \n \n \n4.11 \nOcular Trauma and Emergencies", + "Oxygen": "Oxygen (O2) \n \n \n \n \n \n \n \nClassification: \nElemental gas \nGeneral: \nOxygen is an odorless, tasteless, colorless gas that supports combustion. It is present in ambient \nair at a concentration of 21%. Oxygen is required by the body to facilitate the breakdown of \nglucose (aerobic metabolism) into a useable form, without oxygen, the breakdown of glucose is \nineffective and incomplete (anaerobic metabolism). All cells require oxygen to survive and \nfunction. The majority of oxygen in the body is transported to the cells bound to hemoglobin \n(Hb), a protein molecule contained in erythrocytes (red blood cells). A small percentage (2-4%) \nof oxygen is dissolved in blood plasma. The binding of oxygen and Hb is reversible. The \noxyhemoglobin dissociation curve (below) demonstrates the ability of Hb to combine with \noxygen and relates oxygen saturation (SaO2/SpO2) and partial pressure of oxygen in the arterial \nblood (PaO2). Because the affinity of Hb for oxygen is affected by many variables, the position \nof the curve changes. Acidosis (decreased pH), increased CO2, increased body temperature, and \nincreased levels of DPG (a substance which binds reversibly with Hg and facilitates the release of \noxygen) cause the curve to shift to the right. When the curve is shifted to the right, the affinity \nof Hb for oxygen is decreased and the off-loading of oxygen occurs more easily. Conversely, \nconditions that are opposite of those which result in a rightward shift of the curve result in a \nleftward shift of the curve. These conditions include alkalosis (increased pH), decreased CO2, \ndecreased body temperature, and decreased levels of DPG. When the curve is shifted to the \nleft, the affinity of Hg for oxygen is increased and the off-loading of oxygen is more difficult. \n \n \n \n \nNote that the curve contains a steep slope below a PaO2 of 60 mmHg, but beyond a PaO2 of 60 \nmmHg, the curve is almost flat, indicating that small changes in the PaO2 in this range will result \nin little change in saturation above this point. But, at a PaO2 of less than 60 mmHg the curve is \nvery steep, and small changes in the PaO2 greatly increase or reduce the SaO2. The time to \ndesaturate from a 90% to 0% is dramatically less than the time to desaturate from 100% to 90%. \nDuring the preoxygenation phase of rapid sequence intubation, oxygen is administered to create \nan oxygen reservoir in the lungs, blood and tissues. During preoxygenation, oxygen replaces the \npredominantly nitrogenous mixture of room air and oxygen in the functional residual capacity \n(FRC) with 100% oxygen. The establishment of an oxygen reservoir permits several minutes of \napnea to occur prior to arterial oxygen desaturation to less than 90%. \n \nProtocol Indication(s): \n \n1. \nPatient with dyspnea/shortness of breath, chest pain/discomfort presumed to be of \ncardiac etiology and/or with a SpO2 of <94% \n2. \nPediatric patient with asthma, reactive airway disease, bronchiolitis, croup and a \n \nSpO2 of < 92% \n3. \nCardiac arrest \n4. \nPreoxygenation prior to suctioning or intubation \n5. \nSickle cell crisis \n6. \nObstetrical delivery/complications \n7. \nCarbon monoxide exposure \n8. \nDiving emergencies (pulmonary over pressure syndrome, arterial gas embolism, \ndecompression sickness, nitrogen narcosis) \n \nContraindications: \n1. \nParaquat toxicity (may potentiate harmful superoxide formation) \n2. \nBleomycin use (may increase injury associated with pulmonary toxicity) \n \nPrecautions: \n \n1. \nOxygen is a drug and should be administered only when an indication for administration \nis present. The longstanding EMS practice of empiric \u201chigh flow/concentration\u201d oxygen \nin normoxic patients must be abandoned. \n \n \n \n \n \n \nPrecautions: \n \n2. \nThe use of oxygen in patients with chronic obstructive pulmonary disease (COPD) \ncommonly carries a precautionary warning and is the subject of discussion and debate in \nthe pulmonary medicine literature. Most concerns are related to decreased minute \nventilation (depressed ventilation) and increased CO2 levels associated with the \nadministration of supplemental oxygen to patients with COPD, particularly those with \nchronic hypercapnia \u201cCO2 retainers\u201d. In such patients, the central chemoreceptors \nbecome less sensitive to these changes. The stimulus for ventilation then originates from \nperipheral chemoreceptors located in the carotid bodies and the aortic arch. These \nreceptors are stimulated by low arterial oxygen levels, transmitting signals to the \nrespiratory center in the medulla. This leads to an increased minute ventilation, with a \nlow arterial oxygen level, and a reduced minute ventilation with a high arterial oxygen \nlevel. Oxygen administration may also result in increased CO2 levels from changes in \nventilation and perfusion (V/Q) matching and a phenomenon known as the Haldane \neffect (the binding of oxygen to Hb displaces CO2). Both of these topics are beyond the \nscope of this reference guide. Information regarding these two concepts should easily be \nfound in any physiology textbook. The best approach to the administration of oxygen to \npatients with COPD is to tolerate lower SpO2 levels, but never withhold oxygen from a \nseriously ill hypoxic patient due to fear of cause hypercapnic respiratory failure. Should \nventilator depression occur, it should be managed accordingly. \n 3. \nThere is concern regarding possible hyperoxic injury secondary to supranormal arterial \noxygen levels. Hyperoxic injury may affect multiple organ systems (lungs, heart, and \nbrain). Recently published data demonstrated worse outcomes with hyperoxia after \nresuscitation from cardiac arrest. The exact mechanism of injury is unclear, but \nhyperoxic injury may be mediated by reactive oxygen species (ROS), hyperoxia-induced \nvasoconstriction, or amplified reperfusion injury. For this reason, the lowest possible \nconcentration of oxygen should administered. In the post cardiac arrest patient, the \nFiO2 should be titrated to the minimum concentration required to maintain the SpO2 \n\u2265 94%, but less than 100%. Care should be taken when titrating oxygen concentrations \nto avoid hypoxia. \n4. \nIn patients with suspected or proven acute coronary syndromes and the absence of \nhypoxia, the benefit of oxygen therapy is uncertain, and in some cases oxygen therapy \nmay be harmful. \n5. \nThe routine use of supplemental oxygen is not recommended in acute stroke patients \nwho are not hypoxic. \n \nSignificant adverse/side effects: \n1. \nHyperoxic injury \n2. \nRetinopathy of prematurity \nDosage per protocol(s): \n1.01 \nRoutine Patient Care \n \n \n \n \n2.08 \nRespiratory Distress - Adult \n \n \n \n \n2.08 \nRespiratory Distress - Pediatric \n \n \n \n \n2.16 \nNeonatal Resuscitation \n \n \n \n \n2.17 \nObstetrical Delivery \n \n \n \n \n2.18 \nObstetrical Complications \n \n \n \n \n3.03 \nCardiac Arrest - Adult \n \n \n \n \n3.03 \nCardiac Arrest - Pediatric \n \n \n \n \n3.04 \nPost Cardiac Arrest - Adult \n \n \n \n \n3.04 \nPost Cardiac Arrest - Pediatric \n \n \n \n \n3.05 \nBradycardia - Pediatric \n \n \n \n \n4.13 \nHypothermia and Localized Cold Injury - Adult \n \n \n \n \n4.13 \nHypothermia and Localized Cold Injury - Pediatric \n \n \n \n \n4.15 \nDiving Emergencies \n \n \n \n \n4.20 \nCarbon Monoxide Exposure \nNotes: \n \n\uf0b7 An arterial saturation (SpO2) of 90% correlates to a PaO2 of 60 mmHg. \n\uf0b7 An arterial saturation (SpO2) of 100% may correlate to a PaO2 anywhere between \napproximately 80-500 mmHg. \n\uf0b7 Administering oxygen in the setting of paraquat toxicity may potentiate harmful superoxide \nformation. Superoxides are thought to be involved in the pathogenesis of pulmonary \ndamage. Oxygen should only be considered in cases associated with profound hypoxia. \n \nSuggested reading: \nAbdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care. 2012 \nOct 29; 16(5):323. \nAubier M et al. Effects of the administration of O2 on ventilation and blood gases in patients with \nchronic obstructive pulmonary disease during acute respiratory failure. Am Rev Respir Dis.1980; \n122(5):747\u2013754. \nGirardis M et al. Effect of Conservative vs Conventional Oxygen Therapy on Mortality among \nPatients in an Intensive Care Unit: The Oxygen-ICU Randomized Clinical Trial. JAMA 2016; \n316(15): 1583-1589.", + "Oxymetazoline": "Oxymetazoline (Afrin, Zicam) \n \nClassification: \nAdrenergic receptor agonist (\u03b11 and partial \u03b12) \n \n \nGeneral: \n \nOxymetazoline is a \u03b11 adrenergic receptor agonist with partial \u03b12 agonistic properties. It is a \nvasoconstrictor typically administered intranasal as a decongestant or to treat epistaxis. \n \nProtocol Indication(s): \n \n1. \nEpistaxis \n \nContraindications: \n1. \nKnown hypersensitivity \n1. \nHypertension (DBP >100 mmHg) \n2. \nCoronary artery disease \n3. \nPatient taking monoamine oxidase (MAO) inhibitor \n \nPrecautions: \nNone \n \nSignificant adverse/side effects: \n \n1. \nHypertension \n2. \nDizziness \n3. \nHeadache \n4. \nCardiac irregularities (palpitations, tachycardia) \n \nDosage per protocol(s): \n2.14 \nEpistaxis", + "Phenobarbital": "Phenobarbital \n \nClassification: \nBarbiturate \nGeneral: \nPhenobarbital acts on GABAA receptors, increasing synaptic inhibition. This produces sedative \nhypnotic effects and elevates the seizure threshold, reducing the spread of seizure activity from \na seizure focus. Phenobarbital may also inhibit calcium channels, resulting in a decrease in \nexcitatory transmitter release. Phenobarbital is used as a second line agent in the management \nof seizures. Phenobarbital is also used in the management of delirium tremens associated with \nalcohol withdrawal. \nProtocol Indication(s): \n \n1. \nSeizures refractory benzodiazepines \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nHypotension (SBP <100 mmHg) \n \nPrecautions: \n \n1. \nBarbiturates suppress the hypoxic and chemoreceptor response to CO2. Consider the use \nof sidestream waveform capnography in patients receiving phenobarbital. Be aware of \npossible need for airway management. \n2. \nPhenobarbital should be administered at a rate less than 1 mg/kg/min. \n \nSignificant adverse/side effects: \n1. \nRespiratory depression \n2. \nHypotension \n3. \nAdministration may result in hyperactive behavior in pediatric patients \nDosage per protocol(s): \n2.19 \nSeizures - Pediatric", + "Phenylephrine": "Phenylephrine (Neosynephrine) \n \nClassification: \nAdrenergic receptor agonist (\u03b11) \n \n \nGeneral: \n \nPhenylephrine is an adrenergic agonist with activity on the \u03b11 receptor. Phenylephrine\u2019s effect \nis primarily venous and arterial vasoconstriction. The administration of phenylephrine results in \nthe increase of the mean arterial blood pressure (MAP) without any significant effect on heart \nrate or ventricular contractility. However, significant elevation blood pressure may result it reflex \nbradycardia. Phenylephrine may be the vasopressor of choice in the patient with atrial \nfibrillation who is tachycardic with hypotension (unrelated to their heart rate). Phenylephrine \nmay be administered by intravenous infusion or by IV bolus. Administration by IV bolus is \nreserved for the profoundly hypotensive or periarrest patient. Bolus administration is usually a \nbridge to the establishment of an IV infusion of phenylephrine or another vasopressor. \nPhenylephrine is commonly used in patients with neurogenic shock, however secondary to the \nmechanism of neurogenic shock, these patients may experience bradycardia which may be \nexacerbated by the administration of phenylephrine. Phenylephrine may also be applied \ntopically to the mucosa as a vasoconstrictor. \n \nProtocol Indication(s): \n \n1. \nShock/hypotension \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nSulfite allergy \n3. \nBradycardia \n \nPrecautions: \n1. \nPhenylephrine and other vasopressors are only to be utilized in hemorrhagic shock as a \nbridge to blood products and/or surgical intervention and only after fluid resuscitation as \nappropriate for the etiology. \n2. \nAny concern for local extravasation of phenylephrine must be communicate to the \nreceiving facility as it may require treatment with phentolamine (an alpha agonist). \n \n \n \n \n \nSignificant adverse/side effects: \n \n1. \nHypertension \n2. \nReflex bradycardia \n3. \nMesenteric or peripheral ischemia at high doses \n \nDosage per protocol(s): \n2.20 \nGeneral Shock and Hypotension - Adult \n \n \n \n \n \n2.20 \nGeneral Shock and Hypotension - Pediatric \n \n \n \n \n2.21 \nHemorrhagic Shock - Adult \n \n \n \n2.21 \nHemorrhagic Shock - Pediatric \n \n \n \n \n2.22 \nSepsis and Septic Shock - Adult \n \n \n \n \n2.22 \nSepsis and Septic Shock \u2013 Pediatric \n \n \n \n \n7.45 \nGastric Tube Insertion", + "Pitocin": "Pitocin (Oxytocin) \n \n \n \n \n \n \n \n \n \nClassification: \nHormone (synthetic) \n \nGeneral: \n \nPitocin is a synthetic version of oxytocin, a hormone endogenously produced in the posterior \npituitary gland. Binding sites for oxytocin are found on the membranes of uterine smooth \nmuscle. Pitocin lowers the threshold for depolarization in uterine smooth muscle resulting in \nan increase of the frequency and force of uterine contractions (i.e. increases uterine tone). The \nmost common cause of postpartum hemorrhage (PPH) is uterine atony. Pitocin can also initiate \nuterine contractions at any time and is frequently used to induce labor. In the EMS setting, \npitocin is used for the prevention and management of postpartum hemorrhage. \n \nProtocol Indication(s): \n1. \nPostpartum hemorrhage (prevention and management) \n \n \nContraindications: \n \n1. \nKnown hypersensitivity \n2. \nPresence of a second fetus \n \nPrecautions: \n1. \nPitocin should not be administered until after delivery of the placenta. \n2. \nWhen used for the management of active postpartum hemorrhage, pitocin should be \nused in conjunction with fundal massage. \n \nSignificant adverse/side effects: \n \n1. \nHypotension \n2. \nTachycardia \n \nDosage per protocol(s): \n2.18 \nObstetrical Complications", + "Pralodoxime": "Pralidoxime Chloride (2PAM) \n \nClassification: \nCholinesterase reactivator \n \n \nGeneral: \n \nPralidoxime chloride is a cholinesterase reactivator used as an antidote for organophosphate \nbased pesticides and nerve agents. As a group, pesticides and nerve agents are referred to \ncholinesterase inhibitors. Cholinesterase inhibitors phosphorylate and inactivate cholinesterase. \nCholinesterase is the enzyme responsible for the breakdown of the neurotransmitter \nacetylcholine (Ach). When cholinesterase is inhibited, Ach accumulates and activates muscarinic \nand nicotinic receptors. Activation of muscarinic receptors results in miosis (pupillary \nconstriction), bradycardia, bronchial secretion and increased secretions, increased GI motility, \nrelaxation of the urinary sphincter, contraction of the bladder, and increased secretions \n(salivation, lacrimation). Activation of nicotinic receptors at the neuromuscular junction results \nin muscular contraction (fasciculations and weakness). If the offending agent is able to cross the \nblood brain barrier (BBB), it will affect the cholinergic receptors in the central nervous system \n(CNS). The effects can be tremor, anxiety, restlessness, seizures, or coma. Due to their lipid \nsolubility, organophosphates rapidly cross the blood brain barrier. Because pralidoxime does not \ncross the BBB, it is not effective in reversing the CNS effects of cholinesterase inhibitors. \nPralidoxime is usually administered with atropine sulfate, which is a muscarinic agonist, because \nit blocks the effects of excess Ach, but only at muscarinic receptors (it has no effect on nicotinic \nreceptors located at the neuromuscular junction). \n \n Protocol Indication(s): \n \n1. \nOrganophosphate or nerve agent exposure with signs/symptoms \n \nContraindications: \n1. \nKnown hypersensitivity \n \nPrecautions: \n1. \nRepeat dosing may be required. \n2. \nShould not be used as prophylaxis \n \n \n \nSignificant adverse/side effects: \n \n1. \nDizziness \n2. \nHeadache \n3. \nNausea \nSignificant adverse/side effects: \n \n4. \nTachycardia \n5. \nWeakness \n6. \nHypertension \n7. \nBlurred vision \n \nDosage per protocol(s): \n4.19 \nNerve Agent or Organophosphate Exposure", + "Prednisone": "Prednisolone (Orapred) \n \n \n \n \n \nClassification: \nSteroid (synthetic glucocorticoid) \nGeneral: \nPrednisolone is a synthetic glucocorticoid steroid. Glucocorticoid receptors are found in virtually \nevery cell in the body and exert a powerful physiologic effect on every body system. \nGlucocorticoids stimulate the formation of glucose (gluconeogenesis) and cause the breakdown \nof protein into amino acids (catabolism). Because prednisolone inhibits the inflammatory and \nimmunologic response, it is useful in the management of allergic and anaphylactic reactions and \nin the management of disease processes that involve airway inflammation or edema (i.e. reactive \nairway disease, asthma). In reversing asthmatic obstruction, glucocorticoids probably have \nmultiple actions including the reduction of inflammatory mucosal edema, bronchial smooth \nmuscle reaction, bronchial vasoconstriction, and decreasing capillary permeability. They may \nalso restore the responsiveness of asthmatic patients to beta agonist. \n \nProtocol Indication(s): \n \n1. \nAsthma/reactive airway disease \n2. \nAllergic and anaphylactic reactions \n \nContraindications: \n1. \nKnown hypersensitivity to any steroid \n2. \nSystemic fungal infections \n \nPrecautions: \n \nNone \n \nSignificant adverse/side effects: \n1. \nHyperglycemia \n2. \nImmunosuppression \n3. \nNausea/vomiting \n4. \nEdema \n \nDosage per protocol(s): \n2.04 \nAllergic Reaction - Anaphylaxis - Pediatric \n \n \n \n \n \n \n2.08 \nRespiratory Distress (Asthma/RAD/Croup) - Pediatric", + "Procainamide": "Procainamide (Pronestyl) \n \n \n \n \n \n \n \nClassification: \nAntiarrhythmic (class 1A) \nGeneral: \nProcainamide is a class IA antiarrhythmic useful in the management of atrial and ventricular \narrhythmias. Class I antiarrhythmic agents block sodium entry into the cell during depolarization. \nClass I agents are subcategorized into three groups (IA, IB, IC) based on their degree of sodium \nblockade. IA agents slow the rate of rise of phase 0 and prolong the relative refractory period of \nthe ventricle thus prolonging the repolarization time. Procainamide raises the ventricular \nfibrillation threshold. Procainamide has mild post ganglionic effects and may cause hypotension \nsecondary to peripheral vasodilation. Procainamide is used in the management of atrial \nfibrillation and flutter, paroxysmal supraventricular tachycardia, ventricular tachycardia, and \nrefractory ventricular fibrillation. Procainamide may convert atrial fibrillation to a sinus rhythm. \nProtocol Indication(s): \n1. \nRefractory ventricular fibrillation/tachycardia \n2. \nWide complex tachycardia \n \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nHypotension (SBP <100mmHg) \n3. \nHeart rate <60 \n4. \nAV block > 1st degree in absence of a pacemaker \n5. \nPreexisting QT prolongation or torsade\u2019s de pointes \n \nPrecautions: \n \n1. \nUse with caution in heart failure \n2. \nAdministration should be stopped when one of the following occurs: arrhythmia resolves, \n \nhypotension ensues, or the QRS widens by >50%, or 17 mg/kg is administered \n \nSignificant adverse/side effects: \n1. \nHypotension \n2. \nAV block \n3. \nBradycardia \n4. \nQRS/QT prolongation \n \nDosage per protocol(s): \n3.04 \nCardiac Arrest - Adult \n \n \n \n \n3.07 \nWide Complex Tachycardia - Adult \n \n \nNotes: \n\uf0b7 The 2015 AHA ECC Guidelines recommend procainamide, amiodarone or sotalol for the \ntreatment of stable ventricular tachycardia. However, a higher class of recommendation is \ngiven to procainamide compared to amiodarone and sotalol.", + "Promethazine": "Promethazine (Phenergan) \n \n \n \n \n \n \n \n \nClassification: \nPhenothiazine \n \nGeneral: \n \nPromethazine is a phenothiazine with antiemetic properties. Promethazine blocks dopaminergic \n(D1 and D2) receptors in the brain. Promethazine also exerts a strong \u03b1 adrenergic effect and \ncompetes with histamine for the H1 receptor (antihistamine). Promethazine\u2019s antiemetic effect \nis thought to take place in the chemoreceptor trigger zone (CTZ), which is an area of the vomiting \ncenter (area postrema) of the brain. Due to its antihistamine effects, promethazine is \nsometimes used in the management of motion sickness. Promethazine has weak antipsychotic \neffects as compared to other phenothiazines. \n \nProtocol Indication(s): \n1. \nNausea and vomiting \n \nContraindications: \n \n1. \nKnown hypersensitivity \n2. \nParkinson\u2019s disease \n3. \nNarrow angle glaucoma \n \nPrecautions: \n1. \nPromethazine is an irritant drug that can lead to serious vascular injury and potential \ngangrene with the need for tissue grafting and/or amputation if it is inadvertently \nextravasated or given intra-arterially. \n2. \nPromethazine lowers the seizure threshold and should be used cautiously in patients with \na history of seizures. \n3. \nPromethazine for injection contains metabisulfites, which may cause anaphylaxis; this \nreaction is more likely to occur in patients with a history of asthma. \n4. \nDue to its potential sedating effect, promethazine should not be used when sedation is \nnot desirable. \n \nSignificant adverse/side effects: \n \n1. \nSedation \n2. \nExtrapyramidal/dystonic reactions \n3. \nHypotension (particularly in volume depleted patients) \n \nSignificant adverse/side effects: \n \n4. \nTachycardia \n5. \nBlurred vision \n6. \nDry mouth \n7. \nNeuroleptic malignant syndrome \n8. \nParadoxical excitation (particularly in pediatric and geriatric patients) \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult", + "Proparacaine": "Proparacaine Hydrochloride 0.5% Ophthalmic Solution \n \n \n \n \n \n \n \n \n \nClassification: \nLocal anesthetic (ester group) \n \nGeneral: \n \nProparacaine is a local anesthetic belonging to the ester subgroup of local anesthetics. \nProparacaine blocks sodium ion channels required for the initiation and conduction of neuronal \nimpulses thereby affecting corneal local anesthesia. Proparacaine is used as a topical ophthalmic \nanesthetic to facilitate ocular irrigation and to provide analgesia in cases of ultraviolet keratitis \n(corneal flash burns). Maximal corneal anesthesia is achieved within 20 seconds of installation, \nwith anesthetic effects lasting 15\u201320 minutes. Like tetracaine, because proparacaine belongs to \nthe ester group of local anesthetics, it can be administered with minimal concern for \nallergic/anaphylactic reaction in patients with an allergy to any of the local anesthetics belonging \nto the amide group (lidocaine, bupivacaine, mepivacaine, prilocaine). \n \nProtocol Indication(s): \n1. \nKnown hypersensitivity \n2. \nChemical ocular exposure requiring irrigation \n3. \nCorneal flash burns \n \nContraindications: \nNone \n \nPrecautions: \n1. \nPatients should be advised that their eyes will be insensitive up to 20 minutes and that \ncare should be taken to avoid ocular contact. \n \nSignificant adverse/side effects: \n \n1. \nCorneal injury due to insensitivity \n2. \nTransient stinging or burning \n3. \nConjunctival redness \n4. \nOcular discomfort \n \nDosage per protocol(s): \n4.11 \nOcular Trauma and Emergencies", + "Pseudoephedrine": "Pseudoephedrine Hydrochloride (Sudafed) \n \n \n \n \n \n \n \nClassification: \n\u03b1 adrenergic receptor agonist \n \n \nGeneral: \nPseudoephedrine is an alpha adrenergic receptor agonist that is used as a nasal decongestant. It \nproduces vasoconstriction by stimulating alpha receptors within the mucosa of the respiratory \ntract resulting in the temporary reduction of swelling associated with inflammation of the \nmucous membranes. Systemically, pseudoephedrine may result in a mild increase of the heart \nrate. \n \nProtocol Indication(s): \n \n1. \nEar or sinus squeeze associated with diving \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nHypertension \n3. \nPatient taking monoamine oxidase inhibitors (MAOIs) \n4. \nBenign prostatic hyperplasia (BPH) \n5. \nGlaucoma \n \nPrecautions: \n \nNone \n \nSignificant adverse/side effects: \n1. \nAnxiety \n2. \nRestlessness \n3. \nInsomnia \n4. \nIncreased heart rate \n \nDosage per protocol(s): \n4.15 \nDiving Emergencies", + "Rocuronium": "Rocuronium (Zemuron) \n \n \n \n \n \n \n \n \nClassification: \nNon-depolarizing neuromuscular blocking agent \n \nGeneral: \n \nRocuronium competes with acetylcholine (Ach) for binding at nicotinic receptors at the \nneuromuscular junction preventing depolarization of the muscle cell membrane and inhibiting \nmuscular contraction. Because these agents compete with Ach at the receptor, they are called \ncompetitive blockers. Rocuronium is used to facilitate endotracheal intubation and to facilitate \nventilation in the patient with and advanced airway in place. Rocuronium does not cross the \nblood brain barrier and have no sedating or analgesic properties and therefore, sedation and \nanalgesia must be administered at the time as it is. Rocuronium has an onset of action of 1-3 \nminutes and has a 30-40 minute duration of action (dose dependent). \n \nProtocol Indication(s): \n1. \nFacilitation of ventilation in a patient with an advanced airway in place. \n2. \nAlternative for rapid sequence intubation when succinylcholine is contraindicated \n(restricted use for this purpose) \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nLack of ability continuously monitor waveform capnography. \n \n \nPrecautions: \n1. \nRocuronium should only be administered by providers skilled in advanced airway \nmanagement, including performing cricothyrotomy. \n2. \nAdvanced airway placement must be confirmed by the presence of a capnographic \nwaveform for \u22656 breaths prior to administration and waveform capnography must be \ncontinuously monitored following the administration of rocuronium. \n3. \nProviders must be vigilant for signs of unintentional awareness (patient is awake, but \nunder paralysis) or pain perception requiring additional sedation/analgesia. Signs may \ninclude tachycardia, hypertension, ocular tearing. \n4. \nRocuronium should be dosed on ideal body weight. \n \nSignificant adverse/side effects: \n \nNone of clinical significance. \n \nDosage per protocol(s): \n2.07 \nPatient Comfort - Adult", + "Sodium bicarbonate": "Sodium Bicarbonate (NaHCO3) \n \n \n \n \n \n \nClassification: \nAlkalizing (buffering) agent \n \nGeneral: \n \nSodium bicarbonate is a naturally occurring buffering agent which binds free hydrogen (H+) ions \nto form carbonic acid, which is a weak acid that dissociates to carbon dioxide (CO2) and water \n(H2O). CO2 can then be excreted by the lungs and H2O can be excreted by the kidney. Excretion \nof CO2 by the lungs requires adequate minute ventilation, if minute ventilation is inadequate, \nparadoxical acidosis can occur. The brain is especially subject to the effects of paradoxical \nacidosis because CO2 diffuses across the blood brain barrier more rapidly than does sodium \nbicarbonate. Historically, sodium bicarbonate was used to empirically treat presumed metabolic \nacidosis during cardiac arrest. The routine administration of sodium bicarbonate in cardiac arrest \nis not recommended, even in the event of a \u201cprolonged downtime\u201d. Acidosis associated with \ncardiac arrest is often a result of a respiratory and metabolic etiology and is best treated by the \nrestoration of ventilation and perfusion. In the rare circumstance of severe preexisting \nmetabolic acidosis, sodium bicarbonate administration may be considered in cardiac arrest. In \nthe EMS setting, sodium bicarbonate is primarily used in the management of suspected \nhyperkalemia, crush injury/syndrome, sodium channel blocker toxicity, and cardiac arrest \nassociated with excited delirium. When sodium bicarbonate is administered in the setting of \nhyperkalemia, H+ ions move from the intracellular space to the extracellular space and potassium \n(K+) shifts from the extracellular space (serum) to the intracellular space to maintain electrical \nneutrality of the cell. The exact mechanism of sodium bicarbonate as an antidote for sodium \nchannel blocker toxicity is not completely understood. It is believed the mechanism may be \ntwofold: 1. Alkalization (higher pH) promotes dissociation of the drug from sodium channels; 2. \nThe sodium load plays a more important role by helping to drive sodium through both blocked \nand unblocked channels. In crush injury (CI)/crush syndrome (CS), alkalization with sodium \nbicarbonate helps prevent acute kidney injury secondary to myoglobin and uric acid deposition \nin kidneys. It also combats hyperkalemia associated with CI/CS. In excited delirium, sodium \nbicarbonate may be used to help correct associated acidosis, prevent or minimize acute kidney \ninjury from rhabdomyolysis, and may be beneficial if hyperkalemia is present. \n \nProtocol Indication(s): \n1. \nHyperkalemia \n2. \nSodium channel blocker toxicity (tricyclic antidepressants and others) \n3. \nCrush injury/syndrome \n \nContraindications: \nNone when the above indications are present \nPrecautions: \n1. \nSodium bicarbonate precipitates and interacts with multiple medications. Therefore, it \nshould not be given or mixed with any other medications. \n2. \nFlush IV line prior to and after administration. \n \n3. \nIn neonates and children <2 years of age, a 4.2% solution of sodium bicarbonate should \nbe used and administered slowly. \n4. \nSodium bicarbonate may cause tissue necrosis, ulceration, and sloughing. \n \nSignificant adverse/side effects: \n \n1. \nMetabolic alkalosis \n2. \nParadoxical acidosis \n3. \nExacerbation of heart failure \n4. \nHypernatremia \n5. \nHypokalemia \n6. \nHypocalcemia \n \nDosage per protocol(s): \n2.11 \nDialysis Emergencies and Renal Failure \n \n \n \n \n2.25 \nExcited Delirium \n \n \n \n \n4.09 \nCrush Injury/Crush Syndrome \n \n \n \n \n4.18 \nToxicological Emergencies - Adult \n \n \n \n \n \n \n4.18 \nToxicological Emergencies - Pediatric \nNotes: \n \n\uf0b7 Medications with sodium channel blocking properties include: tricyclic antidepressants \n(TCA), \nquinidine, \nprocainamide, \nflecanide, \nencanide, \nbupivicane, \npropranolol, \ncarbamazepine, quinine, and diphenhydramine. \n\uf0b7 Typical ECG findings associated with sodium channel blocker (TCA) toxicity include QRS/QTI \nprolongation, ventricular dysrhythmias, and a late R wave in lead aVR.", + "Sodium chloride 0.9%": "Sodium Chloride 0.9% (NaCl 0.9%) \n \n \n \n \n \n \n \nClassification: \nCrystalloid \nGeneral: \nSodium Chloride 0.9% is an unbalanced crystalloid fluid. While often referred to as \u201cnormal \nsaline\u201d, it contains a supraphysiologic concentration of chloride (154 mEq/L, 1.5 times that of \nplasma), 154 mEq/L of sodium, and it has a pH of 5.7 (the pH of plasma is 7.4). Simply stated, \n\u201cNormal saline is not normal\u201d. Unlike Lactated Ringers solution (LR), it does not contain an \nanion buffer. It has a strong ion difference (SID) of 0. The SID is the difference between the \nconcentrations of strong cations and strong anions. While a detailed explanation of the SID is \nbeyond the scope of this guide, it is useful to know that the administration of a resuscitation fluid \nwith a SID less than the serum bicarbonate level (normal range 22\u201326\u202fmmol/L) will lead to a more \nacidotic state (\u2193pH) and the administration of a resuscitation fluid with a SID greater than the \nserum bicarbonate level leads to a more alkalotic state (\u2191pH). The table below compares the \nelectrolyte composition and SID of LR and NaCl 0.9% to human blood plasma (concentrations are \nin mEq/L): \n \n \nSodium (Na+) \nChloride (Cl-) \nPotassium (K+) \nCalcium (Ca++) \nLactate \nSID \nPlasma \n1-2 \n+40 \nNaCl 0.9% 154 \nLR \n+28 \n \nThere is some recent data that suggests that outcomes may be worse in patients who receive \nfluid resuscitation with NaCl 0.9% v. those who receive fluid resuscitation with LR or other \nbuffered resuscitation fluids. Specifically, resuscitation with NaCl 0.9% was associated with an \nincrease in acute kidney injury, hyperchloremic metabolic acidosis, and increased mortality. For \nthis reason, LR was chosen as the fluid of choice for patients requiring large volume fluid \nresuscitation. NaCl 0.9% should only be used in patients requiring limited fluid administration. \n \nProtocol Indication(s): \n \n1. \nDehydration \n2. \nHypovolemia \n3. \nShock \n4. \nOcular irrigation \n \n \n \n \nContraindications: \n1. \nProfound liver failure (LR may increase the lactate level, but it should be noted that the \nlactate in LR is in the form of sodium lactate, not lactic acid and it will not make the patient \nmore acidotic). \n \nPrecautions: \n \n1. \nFluids should be administered judiciously to patients with evidence of or a history of heart \nfailure. \n2. \nBecause LR is slightly hypotonic, large volumes may increase intracranial pressure. \n3. \nThe calcium in LR can bind to the citrated anticoagulant in blood products and lead to \ninactivation of anticoagulant and promote the formation of clots in donor blood. For this \nreason, LR is contraindicated as a diluent for red blood cell transfusions. \n \nSignificant adverse/side effects: \n1. \nFluid overload \n2. \nMetabolic alkalosis \n3. \nIncreased intracranial pressure (large volumes, primarily of concern in patients with \nalready increased intracranial pressure). \n \nDosage per protocol(s): \n1.01 \nRoutine Patient Care \n2.20 \nGeneral Shock and Hypotension - Adult \n2.20 \nGeneral Shock and Hypotension - Pediatric \n2.21 \nHemorrhagic Shock - Adult \n2.21 \nHemorrhagic Shock - Pediatric \n2.22 \nSeptic Shock - Adult \n2.22 \nSeptic Shock - Pediatric \n3.03 \nCardiac Arrest - Adult \n3.03 \nCardiac Arrest - Pediatric \n4.06 \nTraumatic Cardiac Arrest - Adult \n4.06 \nTraumatic Cardiac Arrest - Pediatric \n4.07 \nThermal Burns - Adult \n4.07 \nThermal Burns - Pediatric \n4.11 \nOcular Trauma and Emergencies \n4.22 \nRadiation Incident \n7.44 \nOcular Irrigation - Morgan Lens\u00a9", + "Sodium chloride 3%": "Sodium Chloride 3% (Hypertonic Saline) \n \n \n \n \n \n \n \nClassification: \nElectrolyte solution \n \nGeneral: \n \nHypertonic (3%) saline (HTS) is a solution of 3% sodium chloride and sterile water. It is \nhyperosmolar with an osmolality of 1027 mOsml/L. HTS draws water from the extravascular \nspace to the intravascular space. This effect is useful in reducing intracranial volume, thereby \nreducing intracranial pressure. Secondarily, HTS may also increase the mean arterial pressure \n(MAP) by increasing intravascular volume, augmenting cerebral perfusion pressure (CPP). HTS \nis used in the management of increased intracranial pressure with clinical evidence (altered \nmental status (GCS <8), abnormal motor posturing, unilateral or bilateral dilation of pupils, +/- \nbradycardia and/or hypertension) suggesting brain herniation. Use of HTS in the setting of \nincreased ICP is usually a bridge to surgical or other interventions as the effect on ICP is transient. \nIn other settings, HTS is utilized for the correction of hypernatremia. Use this purpose requires \nthe ability to measure the serum sodium. \n \nProtocol Indication(s): \n1. \nAcute neurologic event with evidence of increased ICP \n \nContraindications: \n1. \nKnown hypersensitivity \n \nPrecautions: \n1. \nHTS should not be administered with blood products. \n \nSignificant adverse/side effects: \n \n1. \nHypervolemia \n2. \nIrritation at injection site \n3. \nPhlebitis \n \nDosage per protocol(s): \n2.01 \nAcute Neurologic Event with Evidence of Increased ICP", + "Sodium thiosulfate": "Sodium Thiosulfate \n \n \n \n \n \n \n \n \nClassification: \nAntidote \n \n \nGeneral: \n \nSodium thiosulfate is used as an antidote for cyanide toxicity. Cyanide is a cellular asphyxiant \nwhich disrupts metabolism dependent on metal-containing enzymes. In particular, it binds to \nferric iron present in the cytochrome oxidase system disrupting oxidative phosphorylation \n(oxidative phosphorylation is the final metabolic pathway of cellular respiration). Cells then \nshift to anaerobic metabolism which results in the production of lactic acid, which is manifested \nclinically as metabolic acidosis. Sodium thiosulfate donates a sulfur atom necessary for the \ntransformation of cyanomethemoglobin to thiocyanate, thus increasing the endogenous \ndetoxification of cyanide. Thiocyanate is then excreted in the urine. Sodium thiosulfate is often \nused in conjunction with sodium nitrite, which binds with cyanide to form cyanomethemoglobin. \n \nProtocol Indication(s): \n \n1. \nCyanide toxicity (known or suspected) \n \nContraindications: \n \nNone \n \nPrecautions: \n \n1. \nSodium thiosulfate should not be administered concurrently in the same intravenous line \nwith hydroxocobalamin. \n2. \nSodium thiosulfate may contain trace impurities of sodium sulfite, however this should \nnot deter its administration for treatment of life threatening cyanide toxicity, even if the \npatient is sulfite-sensitive. \n \nSignificant adverse/side effects: \n1. \nNausea \n2. \nVomiting \n3. \nHeadache \n4. \nHypotension \n \n \nDosage per protocol(s): \n4.18 \nToxicological Emergencies - Adult \n \n \n \n \n4.18 \nToxicological Emergencies - Pediatric", + "Succinylcholine (restricted use)": "Succinylcholine (Anectine) \nRESTRICTED USE AGENT MEDICATION \nClassification: \nDepolarizing neuromuscular blocking agent \nGeneral: \nSuccinylcholine is a depolarizing neuromuscular blocking agent used for rapid sequence \nintubation/medication assisted intubation (RSI/MAI). Succinylcholine occupies nicotinic \nreceptors at the neuromuscular junction and mimics the effect of acetylcholine (Ach). This \nresults in depolarization of the receptors leading to transient muscular fasciculations (twitching). \nThe receptors are then rendered incapable of responding to depolarization and flaccid paralysis \nensues. Paralysis lasts until the succinylcholine diffuses from the neuromuscular junction back \ninto the vascular compartment where it is hydrolyzed (broken down due to a reaction with water) \nby psuedocholinesterase, an enzyme produced in the liver and found in blood plasma. The \naction of succinylcholine is not limited to the receptors located at the neuromuscular junction. It \nmay stimulate cardiac muscarinic receptors, leading to bradycardia. Bradycardia is most \ncommonly observed following repeat dosing. Less commonly, succinylcholine administration \nmay cause histamine release, leading to flushing, hypotension, and tachycardia. Under normal \nconditions, the administration of succinylcholine results in a 0.5-1.0 mEq/L increase in the serum \npotassium. Patients with certain pathological conditions are at increased risk for hyperkalemia \nfollowing the administration of succinylcholine. In most of these conditions, this is thought to \nbe due to an up regulation of junctional and extrajunctional cholinergic receptors. These \nconditions include spinal cord injury with paralysis, CVA with paralysis, progressive \nneuromuscular disorders (multiple sclerosis, amyotrophic lateral sclerosis, Guillain-Barre \nSyndrome), immobility, myopathies, muscular dystrophies, burns, and crush injury. Receptor \nup regulation does not occur immediately, but occurs over a short period of time. \nSuccinylcholine is considered safe if administered within 24 hours of onset in some of these \nconditions (see below). The onset of action for succinylcholine is 45 seconds and the duration \nof action is 8-12 minutes. \n \nProtocol Indication(s): \n \n1. \nRapid sequence intubation/medication assisted intubation \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nPersonal or family history of malignant hyperthermia \n3. \nBurns (>24hrs) \n4. \nCrush injury (>24hrs) \n5. \nSpinal cord injury with paralysis (>24hrs) \n6. \nCVA with paralysis (>24hrs) \nContraindications: \n7. \nHyperkalemia \n8. \nIntra-abdominal infection \n9. \nRhabdomyolysis \n10. \nAmyotrophic lateral sclerosis \n11. \nProlonged immobilization \n12. \nInherited myopathies \n13. \nMuscular dystrophy \n \nPrecautions: \n \n1. \nSuccinylcholine should only be administered by providers skilled in advanced airway \nmanagement, including performing cricothyrotomy. Use of succinylcholine is restricted \nto paramedics participating in a CEMS approved medication assisted intubation program. \n 2. \nWhen using succinylcholine or any other neuromuscular blocking agent for the facilitation \nof endotracheal intubation, the airway must be assessed for difficulty and a plan must be \ndeveloped in the event intubation is unsuccessful and ventilation is not possible. A back-\nup airway device (i.e. supraglottic airway, etc.) and equipment to perform a \ncricothyrotomy must be immediately available. \n3. \nFollowing the IV administration of succinylcholine, the intubating provider should wait a \nfull minute prior to performing direct laryngoscopy to ensure optimal intubating \nconditions are present. \n \nSignificant adverse/side effects: \n1. \nMalignant hyperthermia (see notes section below) \n2. \nHyperkalemia \n3. \nFasciculations \n4. \nIncreased intraocular pressure (not of clinical significance, airway takes priority) \n5. \nBradycardia (usually associated with repeat dosing) \n6. \nIncreased ICP (see notes section below) \n \nDosage per protocol(s): \n5.04 \nRapid Sequence Intubation/Medication Assisted \n \n \nIntubation \n \n \nNotes: \n\uf0b7 When compared to other available neuromuscular blocking agents, succinylcholine has the \nfastest onset of action and the shortest duration of action. \n \n \n \nNotes: \n \n\uf0b7 Malignant hyperthermia (MH) is a rare condition characterized by a genetic skeletal muscle \nmembrane abnormality. In a patient with a susceptibility to MH, an acute event or exposure \ntriggers an abnormal release of calcium from the sarcoplasmic reticulum (a storage site for \ncalcium) in the muscle cells, which results in a sustained muscle contraction and thus an \nabnormal increase in metabolism and heat production. The muscle cells eventually are \ndepleted of adenosine triphosphate (ATP) the source of cellular energy, and die, releasing \nlarge amounts of potassium into the bloodstream, causing hyperkalemia, followed by \nventricular (cardiac) arrhythmias. Myoglobin is also released from the muscle cells and may \nbe cause acute kidney injury (AKI). Patients with MH are also at risk for coagulopathies. \n\uf0b7 Succinylcholine is known to be a trigger of MH, particularly when administered in conjunction \nwith a halogenated anesthetic. MH is less commonly associated with succinylcholine when \nit is not used in conjunction with a halogenated anesthetic. \n\uf0b7 Clinical manifestations of MH include hypercarbia (increasing EtCO2), acidosis, sinus \ntachycardia, masseter muscle spasm, muscular rigidity, and hyperthermia. \n\uf0b7 The management MH includes discontinuing the triggering agent, rapid cooling, managing \nacidosis, and administering the antidote medication Dantrolene. \n\uf0b7 In animal studies, when succinylcholine is administered in the setting of increased ICP, a \ntransient increase in the ICP is observed. This occurs during the fasciculation phase, but is \nnot believed to be directly related to the fasciculations. The clinical significance of this \ntransient effect is unknown. Due to succinylcholine\u2019s rapid onset, consistent and reliable \neffects, and short duration of action, it is the recommended neuromuscular blocking agent \nfor RSI of the head injured patient. \n\uf0b7 Succinylcholine is safe in myasthenia gravis.", + "Terbutaline": "Terbutaline (Breathine, Bricanyl) \n \nClassification: \nBeta adrenergic agonist (\u03b22 selective) \n \nGeneral: \n \nTerbutaline is \u03b22 selective adrenergic receptor agonist used in the management of \nbronchospasm. Terbutaline stimulates \u03b22 receptors resulting in an increase in cyclic adenosine \nmonophosphate (cAMP), which leads to the activation of protein kinase A inhibiting \nphosphorylation of myosin and lowering intracellular ionic calcium concentrations, resulting in \nrelaxation of bronchial smooth muscle (bronchodilation) and relaxation of uterine and vascular \nsmooth muscle. Increasing cAMP concentrations also inhibits the release of mediators from \nmast cells in the airway. Because it relaxes vascular smooth muscle, some peripheral \nvasodilation may also occur, which may be reflected by a decrease in the diastolic blood pressure. \nAs a result of sympathomimetic stimulation, an intracellular shift of potassium may occur. This \nmay result in a small (approximately 0.5 mEq/L) decrease in the serum potassium concentration. \nThis is generally not of clinical concern, unless large doses of beta agonist are being administered. \nTerbutaline has little or no effect on alpha adrenergic receptors and may be preferred over \nepinephrine for the management of reversible bronchospasm in patients with hypertension or a \nhistory of cardiovascular disease. The effects of terbutaline are observed within minutes after \nadministration and persist for 4-6 hours. \n \nProtocol Indication(s): \n1. \nBronchospasm (asthma/RAD/COPD) \n \nContraindications: \n1. \nKnown hypersensitivity \n \nPrecautions: \n1. \nUse with caution in patients with myocardial ischemia. \n \nSignificant adverse/side effects: \n \n1. \nTachycardia \n2. \nPalpitations/cardiac ectopy \n3. \nTremor \n4. \nHeadache \n5. \nNausea/vomiting \n \nDosage per protocol(s): \n2.08 \nRespiratory Distress (Asthma/COPD/RAD)", + "Tetracaine": "Tetracaine 0.5% Ophthalmic Solution \n \n \n \n \n \n \n \n \nClassification: \nLocal anesthetic (ester group) \n \nGeneral: \n \nTetracaine is a local anesthetic belonging to the ester subgroup of local anesthetics. Tetracaine \nblocks sodium ion channels required for the initiation and conduction of neuronal impulses \nthereby affecting corneal local anesthesia. Tetracaine is used as a topical ophthalmic anesthetic \nto facilitate ocular irrigation and to provide analgesia in cases of ultraviolet keratitis (corneal flash \nburns). Maximal corneal anesthesia is achieved within 10\u201320 seconds after instillation, with \nanesthetic effects lasting 10\u201320 minutes. Because tetracaine belongs to the ester group of local \nanesthetics, it can be administered with minimal concern for allergic/anaphylactic reaction in \npatients with an allergy to any of the local anesthetics belonging to the amide group (lidocaine, \nbupivacaine, mepivacaine, prilocaine). \n \nProtocol Indication(s): \n1. \nChemical ocular exposure requiring irrigation \n2. \nCorneal flash burns \n \nContraindications: \nNone \n \nPrecautions: \n1. \nPatients should be advised that their eyes will be insensitive up to 20 minutes and that \ncare should be taken to avoid ocular contact. \n \nSignificant adverse/side effects: \n \n1. \nCorneal injury due to insensitivity \n2. \nTransient stinging or burning \n3. \nConjunctival redness \n4. \nOcular discomfort \n \nDosage per protocol(s): \n4.11 \nOcular Trauma and Emergencies", + "Thiamine": "Thiamine \n \n \n \n \n \n \n \n \n \nClassification: \nVitamin (B1) \n \nGeneral: \n \nThiamine is a component of the B complex. Thiamine exists in the body in the form of thiamine \npyrophosphate (TTP). TTP catalyzes several reactions responsible in the glycolytic and Krebs cycle \nresponsible for the metabolism of glucose. Without TTP a significant amount of energy available \nin glucose cannot be obtained. The brain is very sensitive to thiamine deficiency, which may \noccur in alcoholics and malnourished patients. The two major syndromes of concern associated \nwith thiamine deficiency are Wernicke\u2019s encephalopathy and Korsakoff\u2019s syndrome. Wernicke\u2019s \nencephalopathy is characterized by confusion, ataxia (unstable gait), opthalmoplegia (paralysis \nof the extra ocular muscles), and nystagmus (constant involuntary eye movement). Wernicke\u2019s \nresponds rapidly to thiamine administration. If Wernicke\u2019s syndrome is left untreated, it can \nprogress to Korsakoff\u2019s syndrome, which is characterized by learning and memory impairment \nout of proportion to other cognitive functions in an otherwise alert and responsive patient. \nBecause the normal metabolism of glucose results in the consumption of TTP, the administration \nof a glucose load to a patient with marginal TTP stores may precipitate symptoms of thiamine \ndeficiency. Thiamine is administered prior to or with dextrose in patients at high risk for thiamine \ndeficiency (alcoholics and malnourished patients). \n \nProtocol Indication(s): \n1. \nCo-administration with glucose to malnourished patients or patients with a history of \nalcohol abuse \n \nContraindications: \n1. \nKnown hypersensitivity \n \nPrecautions: \n1. \nWhile very uncommon, allergic reactions have been reported. \n \nSignificant adverse/side effects: \n \nNone \n \nDosage per protocol(s): \n2.10 \nDiabetic Emergencies - Adult", + "Tissue Plasminogen Activator (tPA)": "Tissue Plasminogen Activator (t-PA) \n \n \n \n \n \n \n \nClassification: \nFibrinolytic \n \nGeneral: \n \nTissue plasminogen activator (t-PA) is a fibrinolytic agent. When tissue injury occurs, platelets \nrespond and adhere to the site of injury. Platelets and injured tissue release chemical mediators \nthat promote aggregation (clumping of platelets) and result in activation of the coagulation \ncascade. Activation of the coagulation cascade results in the formation of thrombin. Thrombin \nconverts fibrinogen to fibrin. Fibrin strands become cross-linked forming a fibrous mesh which \nentangles platelets over the wound creating a clot. t-PA binds to fibrin in a clot and converts \nfibrin bound plasminogen to plasmin. Plasmin initiates local fibrinolysis causing the clot to \ndissolve. While the activity of t-PA is relatively specific to fibrin-bound plasminogen, systemic \nbleeding complications may occur following the administration of t-PA. t-PA is primarily used in \nthe management of ischemic stroke, myocardial infarction, and pulmonary embolus. It is also \nused to restore function in central venous lines and other devices that have become occluded by \na clot. In patients with ischemic stroke, the window for the administration of systemic IV t-PA is \nwithin 3 hours after the time the patient was last seen normal, but in some patients the window \nmay be increased up to 4.5 hours. \n \nProtocol Indication(s): \n1. \nIschemic stroke \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nBP >185/110 on repeated measurements at time of treatment (not responsive to anti- \nhypertensive medications) \n3. \nSignificant head trauma or prior stroke in the previous 3 months \n4. \nPresentation suggestive of subarachnoid hemorrhage (even if head CT is negative for \nhemorrhage) \n5. \nArterial puncture at a non-compressible site in previous 7 days \n6. \nHistory of previous intracranial hemorrhage, intracranial neoplasm, AVM, or aneurysm \n7. \nRecent intracranial or intraspinal surgery \n8. \nActive internal bleeding \n9. \nPlatelet count <100,000 \n10. \nHeparin received within 48 h resulting in abnormally elevated aPTT \n11. \nCurrent use of an oral anticoagulant with INR >1.7 or PT >15s \n12. \nCurrent use of a thrombin inhibitor or direct 10a inhibitor with elevated sensitive \nlaboratory tests \nContraindications: \n13. \nBlood glucose concentration <50 mg/dL \n14. \nCT evidence of multilobar infarction (hypodensity >1/3 cerebral hemisphere) \n15. \nAdditional exclusionary criteria for the administration beyond 3 hours following the onset \nof stroke symptoms include: age >80 yo, use of oral anticoagulants (regardless of INR), \nbaseline NIHSS score >25, imaging evidence of ischemic injury involving more than one \nthird of the MCA territory, or a history of both stroke and diabetes mellitus. \n16. \nMinor or rapidly improving stroke symptoms (relative) \n17. \nPregnancy (relative) \n18. \nSeizure at onset with postictal residual neurological impairments (relative) \n19. \nMajor surgery or serious trauma within previous 14 days (relative) \n20. \nRecent (within 21 days) gastrointestinal or urinary tract hemorrhage (relative) \n21. \nRecent (within 3 mo) acute myocardial infarction (relative) \n \nPrecautions: \n1. \nFor any acute worsening of neurologic condition, or if patient develops severe headache, acute \nhypertension, nausea, or vomiting (suggestive of ICH), discontinue the t-PA infusion and contact \nmedical control for further instructions including decision to adjust antihypertensive agents \nand/or diversion to nearest hospital. \n2. \nPatients should have frequent monitoring of their BP (generally every 5 minutes in the \nEMS/transport setting) while receiving t-PA. \n3. \nThe following procedures should not be performed within 24 hours of t-PA administration \n(unless lifesaving): arterial or central venous punctures/lines, IM injections, nasogastric \ntubes, or urinary catheter insertion. \n4. \nDo not give any antithrombotic drugs (including heparin, warfarin, aspirin, clopidogrel, \ndipyridamole, ticlopidine, or NSAIDS) for 24 hrs. following t-PA administration. \n5. \nMild orolingual angioedema may be seen in a small percentage of patients receiving t-PA. It is \ntypically mild and transient, and affects the contralateral side from the hemisphere of ischemic \ninjury. \n6. \nSevere angioedema is a rare occurrence, but may occur. If the patient develops stridor, \nimmediately discontinue the infusion, provide appropriate airway management and \ncontact medical control. \n7. \nMinor bleeding may occur after t-PA administration. Oozing at IV sites, ecchymosis (particularly \nunder BP cuffs), and gingival bleeding are frequently seen. In these cases, there is no need to stop \nthe infusion, monitor for further or more extensive bleeding. \n8. \nMajor systemic bleeding (GI, GU) may require that the infusion be discontinued. If this \noccurs, contact medical control. \n9. \nIf hypotension develops after infusion of t-PA, consider tamponade physiology. \n \n \n \nSignificant adverse/side effects: \n \n1. \nBleeding (minor and major, including intracerebral hemorrhage) \n2. \nAngioedema \n3. \nArrhythmias (when administered for STEMI, reperfusion related) \n \nDosage per protocol(s): \n2.13 \nt-PA for Acute Ischemic Stroke \nNotes: \n\uf0b7 The current use of aspirin, NSAIDs or antiplatelet drugs (dipyridamole, ticlopidine, \nclopidogrel) are not contraindications to t-PA administration. \n\uf0b7 The dose of t-PA for acute ischemic stroke is 0.9 mg/kg (maximum dose =90 mg). 10% of the \ndose is administered as an IV bolus over 1 minute and the remainder is infused over 1 hour. \nFor dose determination, the patient\u2019s actual (measured) body weight should be used. \n\uf0b7 Verify with the sending hospital that the excess tPA has been withdrawn from the tPA bottle \nand wasted, so that the tPA bottle will be empty when the full dose is finished infusing. For \nexample, if the total dose is 70 mg, then there would be an extra 30 cc that has been \nwithdrawn and wasted since a 100 mg bottle of tPA contains 100cc of fluid when \nreconstituted. \n\uf0b7 When pump alarms to signify that the infusion is complete (bottle is empty) there will still be \nsome tPA left in the tubing which must be infused. Remove the IV tubing connector from the \nt-PA bottle and attach it to a newly spiked bag of 0.9% NS and re-start the infusion at the \nsame rate. The pump will stop automatically when the preset volume has been infused (the \ntotal volume must equal or exceed the amount of residual t-PA in the administration set).", + "Tranexamic acid (TXA)": "Tranexamic Acid (TXA) \n \n \n \n \n \n \n \n \n \n \nClassification: \nAnti-fibrinolytic \n \nGeneral: \n \nTXA is a synthetic derivative of lysine that inhibits fibrinolysis by blocking the lysine binding sites \non plasminogen. Part of the physiologic response to trauma and surgery in any patient is the \nformation and subsequent breakdown (fibrinolysis) of clots. In some cases, clot breakdown can \nbecome excessive (hyper-fibrinolysis) thus causing increased hemorrhage. TXA inhibits both \nplasminogen activation and plasmin activity thus preventing clot breakdown rather than \npromoting new clot formation. Other potential mechanisms of action including decreasing the \nsystemic inflammatory response to trauma are being explored. \n \nProtocol Indication(s): \n1. Patients with blunt or penetrating trauma (including extremity trauma) with signs of \nsignificant hemorrhage (SBP < 90 mm Hg, HR > 110 BPM); or who are considered in paramedic \njudgment to be at high risk of significant hemorrhage (external or internal) \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nTime elapsed from injury >3 hours \n3. \nAge <16 years \n4. \nIsolated closed head injury \n5. \nPregnancy \u226524 weeks \n6. \nPatient who has or will receive prothrombin complex concentrate (PCCs), or factor VIIa \n \ncomplex concentrates \n \nPrecautions: \n1. \nTXA should be used cautiously in the setting of urinary tract bleeding as ureteral \n \nobstruction due to clotting has been reported. \n2. \nDo not administer in the same IV/IO as blood products or penicillin. \n3. \nA second (maintenance) dose must be given over 8 hours. EMS providers must clearly \n \ncommunicate to the receiving facility staff that a loading does was administered in the \n \nfield. \n \n \n \n \n \nSignificant adverse/side effects: \n \n1. \nHypotension (if given IV push) \n2. \nNausea/vomiting \n3. \nDiarrhea \n \nDosage per protocol(s): \n2.21 \nHemorrhagic Shock - Adult", + "Vecuronium": "Vecuronium (Norcuron) \n \n \n \n \n \n \n \n \nClassification: \nNon-depolarizing neuromuscular blocking agent \n \nGeneral: \n \nVecuronium competes with acetylcholine (Ach) for binding at nicotinic receptors at the \nneuromuscular junction preventing depolarization of the muscle cell membrane and inhibiting \nmuscular contraction. Because these agents compete with Ach at the receptor, they are called \ncompetitive blockers. Vecuronium is used to facilitate ventilation in the patient with an \nadvanced airway in place. Vecuronium does not cross the blood brain barrier and has no sedating \nor analgesic properties and therefore, sedation and analgesia must be administered prior to or \nat the same time it is administered. Vecuronium has an onset of action of 2-4 minutes and has \na 30-40 minute duration of action (dose dependent). \n \nProtocol Indication(s): \n1. \nFacilitation of ventilation in a patient with an advanced airway in place \n \nContraindications: \n1. \nKnown hypersensitivity \n2. \nLack of ability continuously monitor waveform capnography. \n \n \nPrecautions: \n1. \nVecuronium should only be administered by providers skilled in advanced airway \nmanagement, including performing cricothyrotomy. \n2. \nAdvanced airway placement must be confirmed by the presence of a capnographic \nwaveform for \u22656 breaths prior to administration and waveform capnography must be \ncontinuously monitored following the administration of vecuronium. \n3. \nProviders must be vigilant for signs of unintentional awareness (patient is awake, but \nunder paralysis) or pain perception requiring additional sedation/analgesia. Signs may \ninclude tachycardia, hypertension, ocular tearing. \n4. \nVecuronium should be dosed on ideal body weight. \n \nSignificant adverse/side effects: \n \nNone of clinical significance. \n \nDosage per protocol(s): \n2.07 \nPatient Comfort \u2013 Adult" + }, + { + "document title": "Clinical Procedures", + "protocol title": "Surgical Cricothyrotomy", + "overview": "Advanced airway procedures and competency are the cornerstones of paramedicine. True competency involves knowing not only how to control the airway, but when to control the airway, and selecting the best method to do so. A surgical cricothyrotomy should be performed only as a last resort when an airway cannot be definitively secured via oral / nasal intubation or rescue airway device insertion AND the airway cannot be maintained with BLS adjuncts or procedures.", + "indications": "1. Total airway obstruction not relieved by any other means.\n2. Airway compromise from injuries that make oral or nasal intubation impractical.\n3. No alternative airway device / maneuver is successful.\n4. The patient cannot be oxygenated or ventilated by any other means.", + "contraindications": "1. Patient less than 8 years old (If less than 8 years old, refer to Needle Cricothyrotomy Clinical Procedure).\n2. Airway able to be maintained via BLS airway management procedures.", + "complications": "\u2022 Bleeding\n\u2022 Incorrect or unsuccessful tube placement\n\u2022 Pneumothorax and / or pneumomediastinum\n\u2022 Tracheal perforation\n\u2022 Vocal cord injury\n\u2022 Aspiration\n\u2022 Subcutaneous emphysema\n\u2022 Esophageal and / or tracheal perforation\n\u2022 Infection leading to cellulitis and / or sepsis\n\u2022 Phrenic nerve and / or brachial plexus injury", + "protocol for management": "1. Prepare all equipment for surgical cricothyrotomy:\n a. All appropriate BSI should be worn to include eye protection, mask, and gloves\n b. Adult bag valve mask (BVM) connected to 100% oxygen\n c. Appropriately sized ET tube. Shorten ET tube length by cutting tube just ABOVE point at which cuff inflation line attaches to tube. Remove BVM hub from discarded portion and attach to shortened tube\n d. Attach 10 cc syringe to ET tube and pre-inflate cuff of tube to ensure no leaks, then deflate, leaving syringe attached\n e. \u00bd\u201d silk tape, torn into two 8\u201d strips to secure tube upon successful cricothyrotomy\n f. Connect capnography sensor to monitor\n g. Check that capnography sensor is working properly and attach to end of shortened ET tube\n h. Suction setup, turned on, and within reach\n i. Sterile scalpel (# 10 preferred)\n j. Antiseptic solution\n k. Several 4 x 4s, opened\n2. Once all equipment is prepared, a surgical cricothyrotomy attempt should be made.\n a. Identify the cricothyroid membrane, located subcutaneously between the thyroid cartilage ( Adam\u2019s apple) superiorly and the cricoid cartilage inferiorly\n b. Cleanse the intended site of procedure with antiseptic solution\n c. Stabilize the site by placing thumb and index finger of non-dominate hand on either side of the trachea, stretching the skin across the cricoid membrane\n d. While stabilizing the trachea, use your dominant hand to make a 3 - 4 cm vertical incision through the skin, midline over the cricoid membrane. The skin will spread as the incision is made\n e. Bleeding will occur, use 4 x 4s as needed to maintain clear visual field\n f. After visual identification of the cricoid membrane, make a 1 cm horizontal incision by puncturing the cricoid membrane with the scalpel\n g. Remove scalpel while continuing to hold traction. Turn scalpel over, insert handle into trachea and rotate to enlarge opening. NEVER enlarge incision with scalpel blade\n h. Remove scalpel and insert \u201chook\u201d or hemostat into tracheal opening to keep insertion site patent. As a last resort, use the index finger of your non-dominant hand, inserting the tip of the finger into the site just enough to keep tracheal incision open. If opening is lost, it can be extremely difficult to relocate definitively, possibly causing false passage of the tube along the outside of the trachea\n i. Insert shortened ET tube into trachea via incision site. ET tube should only be inserted until the tube cuff can no longer be visualized\n j. Inflate cuff with 8 - 10 cc of air, ventilate patient with BVM, and check monitor for distinct capnography waveform and numerical value\n k. If no capnography waveform is present, check equipment (capnography working correctly, no kinks, attached securely) and recheck for proper placement (possible false passage in tracheal lining)\n l. If capnography waveform is present, continue placement confirmation:\n \u2022 Observe chest rise upon ventilation\n \u2022 Auscultate for bilateral breath sounds\n \u2022 Auscultate abdomen for absent epigastric sounds\n \u2022 Note condensation in the tube with expirations\n m. If breath sounds are not heard equally, adjust tube for possible left or right main-stem intubation by pulling tube out one (1) centimeter. Reassess lung sounds. In trauma patients, also assess for possible pneumothorax\n n. Once lung sounds have been confirmed, secure ET tube with \u00bd\u201d strips of tape crossed around tube and taped to neck. Reassess lung sounds and capnography readings\n o. Reassess tube placement after all movement of patient or change in capnography readings", + "pearls": "1. Make incision as small as possible to avoid extensive hemorrhage.\n2. If an appropriately sized tracheostomy tube is available, and provider is familiar with placement, use in place of modified ET tube. Once tracheostomy tube is inserted, remove obturator, attach capnography, and continue procedure as outlined above. Secure tube with included tie strap." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Synchronized Cardioversion", + "overview": "Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart, at a specific moment in the cardiac cycle to treat hemodynamically significant supraventricular (or narrow complex) tachycardias, including : atrial fibrillation and atrial flutter. It is also used in the emergent treatment of wide complex tachycardias, including ventricular tachycardia, when a pulse is present.", + "indications": "Synchronized cardioversion is indicated for any type of unstable tachycardia with serious signs and symptoms directly related to the tachycardia.", + "contraindications": "1. Asystole\n2. Ventricular Fibrillation\n3. Polymorphic Ventricular Tachycardia (Torsades de Pointes)", + "protocol for management": "1. Remove all clothing covering the patient\u2019s chest and dry if necessary. If the patient has excessive chest hair, shave hair to ensure proper adhesion.\n2. Attach 4 - Lead ECG electrodes for monitoring during cardioversion.\n3. Connect the multi function pacing / defibrillation pads to the monitor multi-function cable (if not already connected).\n4. Open the pad packaging and apply one edge of the pad securely to the patient. Roll the pad smoothly from that edge to the other being careful not to trap any air pockets between the gel and skin. Poor adherence and / or air under the multi-function pads can lead to the possibility of arcing and skin burns.\n5. If it is not possible to place the back multi- function pad on the patient\u2019s back, place it on the standard apex position of the apex-sternum configuration. Effective defibrillation will result, but pacing with the device is usually less effective.\n6. If possible initiate IV / IO assess patient and consider sedation with Midazolam 0.1 mg / kg slow IVP, maximum single dose 5.0 mg.\n7. Prepare for cardioversion to pulseless arrhythmias; prepare for resuscitation / CPR.\n8. Turn the monitor on and select the lead you wish to view.\n9. Ready the monitor for defibrillation, and then select the desired energy level.\n10. Press the SYNC key. The selected energy level is displayed on the monitor. Refer to the Cardiac Care Protocols for appropriate energy settings as well as specific manufacturer settings/recommendations.\n11. A SYNC marker should be displayed above each detected R-wave to indicate where discharge will occur.\n12. Press the CHARGE button and wait for the SHOCK button to enable.\n13. Press and hold SHOCK until energy is delivered to the patient. The discharge will occur with the next marked R-wave. ( NOTE: MONITORS AUTOMATICALLY DEFAULT BACK TO DEFIBRILLATION MODE, FOLLOWING EACH SYNCHRONIZED SHOCK).\n14. If additional countershocks are necessary, re-adjust the energy level as necessary, press SYNC, and repeat steps 10 - 13. Note: SYNC should be displayed prior to pressing the CHARGE button.\n15. If it is necessary to disarm the charged defibrillator, changing the selected energy level should discharge internally all stored energy by the defibrillator." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Nasal Intubation", + "overview": "Advanced airway procedures and competency are the cornerstones of paramedicine. \nTrue competency involves knowing not only how to control the airway, but when to \ncontrol the airway, and selecting the best method to do so. While orotracheal \nintubation is the gold standard of securing the airway, it is not the only means available \nto advanced life support providers. Nasal intubation, if not done correctly may cause \nhemorrhaging from the nasal passages leading to an uncontrolled airway and \naspiration.", + "indications": "1. Respiratory failure with decreasing level of consciousness, signs of hypoxia, or \ndeep coma. \n2. Respiratory failure trismus. \n3. Trauma patients without significant mid-facial trauma or mid-face instability.", + "contraindications": "1. Patient has mid-face instability or frontal lobe head trauma or suspected basilar \nskull fracture. \n2. The patient is apneic and / or in cardiac arrest. \n3. The patient is known or is suspected to have increased intracranial pressure \n(ICP). \n4. Diabetic emergency or suspected narcotic overdose unless patient has not \nresponded to treatment per protocol and the airway is not maintainable with \nBLS adjuncts. \n5. There is a known ingestion of a caustic substance.", + "protocol for management": "1. Explain procedure to patient, if appropriate. \n2. Patient should be pre-oxygenated, if tolerated, with an appropriately sized Bag \nValve Mask at a rate of 12 - 20 breaths per minute. The patient\u2019s SpO 2 should \nbe raised as much as possible with manual ventilations prior to intubation \nattempt. \n3. Visually inspect each nare for foreign bodies or large polyps. Insert an \nappropriately sized nasopharyngeal airway (NPA), lubricated with a water \nbased lubricant (KY Jelly), into the patient\u2019s larger nare, usually the right nare. \n4. Prepare all equipment for intubation: \n a. Appropriately sized, non-styletted, ET tube with 10 cc syringe \nattached \n b. Pre-inflate cuff of tube to ensure no leaks, then deflate, leaving \nsyringe attached \n a. Starting at the distal tip of tube, bevel out, curl tightly around gloved \nfinger and hold to assist in forming curvature of tube \n c. Second ET tube, one (1) size smaller for unanticipated smaller nare \npassage way \n d. 1/2\u201d silk tape torn into two 4\u201d strips to secure tube upon successful \nintubation \n e. Capnography sensor connected to monitor \n f. Suction setup turned on and within reach for use with vomited gastric \nsecretions \n g. One (1) 15 mL bottle of Neo-Synephrine (if available) \n h. One (1) 5.0 mL uro-jet of Lidocaine 2% Jelly (if available) \n i. All appropriate BSI / PPE should be worn, to include eye protection, \nmask, and gloves \n5. Place patient in position of comfort. \n6. Once the determination has been made by the provider that the patient has \nbeen sufficiently pre-oxygenated, the NPA should be removed and an \nintubation attempt should be made. \n7. Remove the NPA and apply two (2) full \u201csquirts\u201d of Neo -Synephrine (if \navailable) in nare determined to be used for intubation ensuring to coat full \nlength of nare. \n8. Insert Lidocaine uro-jet (if available) tip in nare determined to be used for \nintubation, pushing tip into nose to rear of nare and pulling out while injecting \njelly solution. \n9. Check that capnography sensor is working properly; attach to end of ET tube. \n10. Insert the ET tube on a flat plane, bevel up, into nare, advancing tube gently, \nbut firmly, into nasal pharynx. \n11. If resistance is met, cephalad traction or rotation of tube may facilitate passage \nof tube past superior turbinate/ sphenoid sinus in rear of nose. Use only \ngentle, firm pressure to advance the tube. DO NOT FORCE TUBE IF \nRESISTANCE IS MET. \n12. Once tube has passed superior turbinate, continue advancing tube into lower \nairway until reaching the glottic opening (patient will gag), pull tube back slightly \nuntil gagging stops. \n13. Hold tube in place and listen to patient respirations through end of tube, \nwatching capnography waveform on monitor. \n14. While listening to air movement through the tube, advance tube into trachea \nwhen sound is loudest (inspiration). Continue to watch capnography waveform \nduring insertion, as it should not change. \n15. If no waveform is present, pull tube back to glottic opening and attempt again. \nIf intubation is unsuccessful a second time, remove tube and continue BLS \nairway interventions. \n16. If capnography waveform is present, inflate tube cuff with 5 - 10cc of, attach \nBVM and ventilate patient. Attempt to ven tilate with patient\u2019s spontaneous \nrespirations. \n17. Continue placement confirmation: \n \uf0b7 Observe chest rise upon ventilation \n \uf0b7 Auscultate for bilateral lung sounds \n \uf0b7 Auscultate abdomen for absent epigastric sounds \n \uf0b7 Note condensation in the tube with passive exhalation \n18. If breath sounds are not heard equally, adjust tube for possible left or right \nmain-stem intubation by pulling tube out one (1) centimeter. Reassess lung \nsounds. In trauma patients, also assess for possible pneumothorax. \n19. Once lung sounds confirmed, secure ET tube with strips of tape and reassess \nlung sounds and capnography readings. \n20. Reassess the tube placement after all movement of patient or change in \ncapnography readings." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Patient Restraint \n(Proposed: Behavioral/Patient Restraint)", + "overview": "This procedure is to be used when it is determined that the only way to administer \nproper patient care is through the use of restraints.", + "indications": "1. Safe & controlled access for medical procedures when involuntary patient \ninterference or resistance is reasonably anticipated. \n2. Evaluation or treatment of combative persons when illness or trauma is \nsuspected to be the cause of the combativeness. \n3. Involuntary treatment of persons without capacity to refuse treatment.", + "contraindications": "1. When any other form of transport without restraint is available.", + "protocol for management": "1. Attempt to obtain verbal control of the situation. \n2. Determine if restraints will be needed by provider. \n3. Try to identify other causes for combativeness. \n4. Request Police response for assistance. \n5. INFORM Patient that you intend to restrain them and WHY (do not use this \ntechnique as a threat). \n6. The minimum number of providers needed to restrain a patient is three (3 ); \nhowever five (5) providers are recommend ed. These five (5) people allow one \n(1) to control each extremity and one (1) for the patient\u2019s head / airway. \n7. Apply restraints. ALL restraints used by EMS will be soft restraints. If police \nrestrain the patient with hard restraints, a police officer MUST ride in the \nambulance with the patient to the hospital. \n8. Soft restraints should be applied so that the circulation of the extremity is not \nimpaired. It is recommended that providers use triangular bandages. Doubled 6-\nply roller gauze (3 inch), sheets, and commercial soft restraint are acceptable \nalternatives. Document physical assessment findings / injuries discovered before \nrestraints were applied. \n9. ALL Patients will be transported in the Supine Position. \na. Place patient onto stretcher. \nb. Apply chest belt first. This belt goes under the patient\u2019s arms. It should \nas high as possible on the patient\u2019s chest . \nc. Apply thigh belt second. This belt should be applied above the patient\u2019s \nknees. \nd. Apply abdominal / waist strap and shoulder straps. \ne. Insure that once the belt it tightened, it does not cause respiratory \ndistress and that the patient can still take full inspiratory breaths. \nf. Apply 4-point restraints last. (Each arm and leg as necessary). The 5-\npoint belt restraints may be enough restraint to control patient. \ng. It is recommended to restrain the arms above the wrists and the legs \nabove the ankles. \nh. It is recommended that the dominant arm of the patient be restrained \nabove his head. \n i. Tie all restraints to \u201cT -Posts\u201d so tha t the restraint cannot slide. \n10. Once restrained, the patient should remain restrained until arrival at the receiving \nfacility. \n11. Circulatory checks should be performed distal to the restraints every 15 minutes. \n12. If a patient begins to have a seizure, CUT / RELEASE THE RESTRAINTS \nIMMEDIATELY. \n13. When a patient is restrained, documentation must include the following: \na. Evidence of patient\u2019s need for restraint. \nb. That the treatment and necessity of the restraints was in the patient\u2019s \nbest interest. \nc. Type of restraint employed and which extremities were restrained. \nd. Injuries that occurred during or after the restraint. \ne. Circulation checks every 15 minutes recorded with patient vital signs.", + "pearls": "1. There are reversible, medically treatable conditions that can cause violen t \nbehavior in patients. Providers should consider these causes (hypoglycemia, \nhypovolemia, overdoses, psychosis, etc.) when restraining a patient. Refer to \nthe Medical Patient Care Protocols: Altered Mental Status." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Capnography", + "overview": "Capnography (PETCO 2 monitoring) is a non -invasive method of measuring CO 2 in exhaled gases. By tracking the carbon dioxide in a patient\u2019s exhaled breath, capnography enables paramedics to objectively evaluate a patient\u2019s ventilatory status (and indirectly circulatory and metabolic status), while utilizing clinical judgment to assess and treat their patients. Capnography is to be used as an additional tool to compliment sound clinical skills and patient assessment and is to be used on all intubated patients.", + "usage requirement": "Capnography is an absolute requirement in all patients that have been intubated or had a supra -glottic airway placed , or had a cricothyrotomy performed. 100% compliance is the goal .", + "protocol for management": "1. Ensure all airway management equipment in working order and attached appropriately. \n2. Attach capnography sensor to the endotracheal tube, or airway device, ventilate patient several times, and check monitor for distinct waveform and numerical value. \n3. If no waveform is present, suspect esophageal intubation. Remove tube and continue in airwa y algorithm. \n4. Once tube placement is verified, record the time, waveform, and CO 2 reading. Be sure to note these times on your ePCR. \n5. Provide ventilatory assistance to maintain CO 2 readings at 35 - 45 Torr (4.6% to 5.9%). \n6. End tidal CO 2 monitoring is consider ed a vital sign and should be documented as such with serial vital signs (blood pressure, heart rate, respiratory rate, SPO 2,) at least every 5 minutes.", + "capnogram waveform description": "The capnogram waveform begins before exhalation and ends with inspiration. Breathing out comes before breathing in. \n\nA\uf0aeB is post inspiration / dead space exhalation \nB is the start of alveolar exhalation \nB\uf0aeC is the exhalation upstroke where dead space gas mixes with lung gas \nC\uf0aeD is the continuation of exhalation, or the plateau (all the gas is alveolar now, rich in CO 2) \nD is the end -tidal value (the peak concentration) \nD\uf0aeA is the inspiration washout.", + "pearls": "1. Sensor and readings not affected by administering drugs down ET tube. \n2. Water, secretions, or vomitus accumulating in sensor can cause inaccurate readings. \n3. The sensor is easily damaged and should be replaced if inaccurate readings occur. \n4. An increasing e nd-tidal CO 2 may be the first sign of return of spontaneous circulation (ROSC) because readings within the normal values may indicate organ perfusion. If you see the CO 2 value \u201cshoot up\u201d, stop CPR and check for pulses. End tidal will often overshoot baseline values wh en circulation is restored due to carbon dioxide washout from the tissues. \n5. Capnography should be used in patients that have been orally / nasally intubated, had a dual lumen / supraglottic airway inserted or had a surgical cricothyrotomy performed .", + "causes of increased etco2": "Leak in vent circuit\nIncreased metabolic rate\nSodium Bicarbonate\nAdministration\nHypoventilation\nCOPD\nRebreathing\nSeizures\nMuscular paralysis\nFever\nSepsis\nRespiratory depression", + "causes of decreased etco2": "Hypothermia\nHypotension\nPulmonary hypoperfusion\nCardiac arrest\nVentilatory disconnect\nEsophageal intubation\nHyperventilation\nComplete airway obstruction\nLeak around ET cuff\nHemorrhage\nPoor sampling\nPulmonary embolism", + "clinical insights and waveform interpretation": "8. While capnography is a direct measurement of ventilation in the lungs, it also indirectly measures metabolism and circulation. For example, an increased metabolism will increase the production of carbon dioxide increasing the ETCO 2. A decrease in cardiac output will lower the delivery of carbon dioxide to the lungs decreasing the ETCO 2. \n9. Bronchospasm and obstructive lung disease will produce a characteristic \u201cshark fin\u201d wave form, as the patient has to struggle to exhale, creating a sloping \u201cB -C\u201d upstroke. The shape is caused by uneven alveolar emptying. \n10. It has been suggested that in wheezing patients with HF (because the alveoli are still, for the most part, emptying equally), the wave form should be upright. This can help assist your clinical judgment when attempting to differentiate between obstructive airway wheezing such as COPD and the \"cardiac asthma\" of heart failure ( HF)." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Transcutaneous Pacing", + "overview": "Non-invasive external transcutaneous cardiac pacing is basically providing an electrical signal to make the heart beat when the body\u2019s conduction system fails. The body\u2019s anatomical pacemaker, the sino- atrial node, provides the heart\u2019s \u201cintrinsic\u201d rhythm. When this internal pacemaker fails or is compromised and the body becomes hemodynamically unstable, transcutaneous pacing is the appropriate therapy. It is accomplished by delivering pulses of electric current through the patient\u2019s chest, which stimulates the heart to contract.", + "indications": "1. Mobitz Type II second-degree AV block\n2. Third-degree AV block\n3. Hemodynamically unstable bradycardia with signs and symptoms of low perfusion or shock.", + "contraindications": "None in the presence of indications above", + "protocol for management": "1. Remove all clothing covering the patient\u2019s chest and dry if necessary. If the patient has excessive chest hair, shave hair to ensure proper adhesion.\n2. Attach 4 - Lead ECG electrodes for monitoring during pacing. Adjust the ECG size and lead for a convenient waveform display. Verify proper R-wave detection according to the specific indication given by your device.\n3. Connect the multi function pacing / defibrillation pads to the monitor multi-function cable (if not already connected).\n4. Open the pad packaging and apply one edge of the pad securely to the patient. Roll the pad smoothly from that edge to the other being careful not to trap any air pockets between the gel and skin. Poor adherence and / or air under the multi-function pads can lead to the possibility of arcing and skin burns.\n5. Apply the multi-function pads in the apex/ lateral position of the anterior-lateral configuration. Be sure to check your specific manufacturer\u2019s recommendations for pad placement\n6. Turn on the pacing function on your device.\n7. Set the PACER RATE to a value 10 - 20 ppm higher than the patient\u2019s intrinsic rate. If no intrinsic rate exists, use 100 ppm. The pacer rate increments or decrements by a value of 2 ppm on the display when you turn the knob.\n8. Increase the PACER OUTPUT ( mA) until capture is noted. The output mA value will be displayed on the screen.", + "determine capture": "Capture refers to the state when the heart is being paced by the monitor rather than the body\u2019s own pacemaker mechanism. Capture consists of two parts: electrical and mechanical capture. You MUST verify capture both electrically and mechanically to ensure appropriate circulatory support of the patient.", + "electrical capture": "Electrical capture means that the monitor is delivering sufficient electrical current to stimulate the heart as seen on the ECG tracing. The shape and the size of the paced ECG waveforms can vary depending on the patient and the ECG lead configuration. Electrical capture is obtained when : (1) Each stimulus marker is followed by a wide QRS complex, (2) There is no underlying intrinsic rhythm, and (3) An extended and sometimes enlarged T-wave appears.\nTypical ECG tracings of effective pacing", + "mechanical capture": "Mechanical capture is confirmed when the patient\u2019s pulse matches the displayed pace rate. Because pacing stimuli generally causes muscular contractions that can be mistaken for a pulse, you should never take a pulse on the left side of the body to confirm mechanical capture. Pectoral muscle contractions due to pacing also do not indicate mechanical capture. To avoid mistaking muscular response to pacing stimuli for arterial pulsations, use ONLY : (1) Femoral artery, or (2) Right brachial or radial artery for confirming mechanical capture.\nOnce capture has been confirmed, the optimum therapeutic threshold must be determined. The ideal output current is the lowest value that maintains mechanical capture. This is usually 10% above threshold. Threshold is the minimum current that must be exceeded to begin producing ventricular capture.", + "checking underlying patient rhythm": "Follow the manufacturer\u2019s directions for your specific device to check and determine the patient\u2019s underlying rhythm.", + "asynchronous pacing": "Some devices allow for the delivery of asynchronous pacing. If ECG electrodes are not available or there is some circumstance that prevents or interferes with the surface ECG, it may be necessary to operate the pacemaker asynchronously. Asynchronous pacing should ONLY be performed in an emergency when NO OTHER ALTERNATIVES EXIST. Follow the manufacturer\u2019s instructions for your specific device to deliver asynchronous pacing.\nNOTE: Pace stimuli is also delivered asynchronously whenever there is an ECG lead off condition. Be aware that there is no ECG activity on the display when pacing by this method; you must use other means of determining capture such as checking the patient\u2019s pulse. When pacing asynchron ously with an ECG LEAD OFF condition, set the rate and output at the known capture level or high enough (100mA) to presume capture.", + "pediatric pacing": "Non-invasive external transcutaneous cardiac pacing of pediatric patients is done in an identical manner to adult pacing. Smaller size pediatric multi-function pads should be used for patients weighing less than 33 lbs / 15 kg. Continuous pacing of neonates can cause skin burns. If it is necessary to pace for more than 30 minutes, periodic inspection of the underlying skin is strongly advised.", + "pearls": "1. The outcome of prolonged bradycardic or asystolic cardiac arrest is poor, even with non-invasive pacing. Indiscriminate pacing of this rhythm is unwarranted, particularly as a late effort in the resuscitatio n.\n2. Human studies have shown that the average current necessary for external pacing is between 65 - 100 milliamperes.\n3. Pulse duration is the time of impulse stimulation. Early non-invasive pacemakers used short-duration (1 - 2 milliseconds) impulses. The action potential (electrical impulse including depolarizing and repolarizing) of cardiac muscle cells is longer than that for skeletal muscle, requiring 20 - 40 milliseconds to reach maximum effect. Studies have found that increasing the duration from 1 to 4 milliseconds resulted in a three-fold reduction in threshold (the current required for stimulation) to produce capture. Increasing the current from 4 to 40 milliseconds further halves the threshold.\n4. Transcutaneous pacing may be uncomfortable for the patient. Sedation and pain management should be considered, as needed.\n5. Prolonged transcutaneous pacing may cause burns to the skin. If possible, pacing should not be continued more than 30 minutes if at all possible." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Orogastric Tube", + "overview": "An oral gastric tube is used to decompress the stomach of air and / or gastric contents\nafter intubation.", + "indications": "Decompression of air and suctioning of gastric contents of a cardiac or respiratory arrest\npatient after endotracheal intubation, King LTS-D, or other appropriate alternate airway\ndevice, has been performed and placement verified.", + "contraindications": "1. Known or suspected esophageal varices\n2. Esophageal stricture\n3. Esophagectomy or partial gastrectomy\n4. Gastric bypass\n5. Penetrating neck trauma", + "protocol for management": "1. Estimate the length of the tube needed to reach the stomach by measuring the\ntube from the corner of the mouth to the earlobe and down to the xiphoid\nprocess. Mark the length with tape.\n2. Lubricate the OG tube (16F) with water-soluble lubricant (KY Jelly).\n3. Insert the tube through the oropharynx until the marked depth is reached.\n4. If the tube coils in the posterior pharynx, direct laryngoscopy can be utilized to\nplace the tube in the esophagus.\n5. Verify placement. Using a 60 ml catheter tip syringe, instill 30 ml of air into the\ntube while auscultating over the epigastrum for sound of rushing air.\n6. Aspirate for gastric contents and assess for cloudy, green, tan, brown, bloody, or\noff-white colored contents consistent with gastric contents.\n7. Secure tube with tape and leave the blue air vent open to atmosphere.\n8. Attach the tube to continual low suction (approximately 60 mmHg) using onboard\nsuction.\n9. If suction is not readily available, connect the empty 60 ml syringe to the tube\nwhile keeping the blue air vent open to atmosphere. This will allow the sump\nfunction of the tube to continue working until suction can be applied and will also\nprevent gastric contents from leaking from the tube.\n10. If you cannot place the OG tube quickly (no more than 2 attempts), forego the\nprocedure. DO NOT DELAY TRANSPORT." + }, + { + "document title": "Clinical Procedures", + "protocol title": "12-Lead ECG Acquisition", + "overview": "The 12-lead ECG analysis is useful in the diagnosis and treatment of patients with acute myocardial infarction (AMI). 12-lead ECG analysis is also useful in the interpretation and documentation of other transient cardiac arrhythmias that may occur. When used in the pre-hospital setting, the 12-lead analysis results can be of assistance in diagnosis and treatment decisions once the patient has arrived in the hospital emergency department.", + "signs and symptoms for 12 lead acquisition": "At a minimum, both ALS and BLS providers should obtain a 12-lead for the following patient complaints:\n- Chest pain/tightness\n- Difficulty Breathing\n- Nausea\n- Stroke/neuro symptoms\n- Altered mental status with no obvious cause\n- General feelings of malaise in diabetic and/or geriatric and/or female patients", + "protocol for management": "Electrode Placement\n1. Proper skin preparation and use of proper electrodes is essential for good signal quality. If necessary, prepare the patient\u2019s skin for electrode application by shaving excess hair at electrode site, cleaning oily skin with an alcohol pad, or using benzoine tincture for excessive diaphoresis.\n2. When acquiring a 12-Lead ECG , place the patient in a supine o r semi -fowlers position. Discuss the need to hold still. American Heart Associa tion (AHA) recommends placing the electrodes anywhere along the wrists and ankles . Conversely, w hen it is difficult for the patient to remain motionless due to shivering, muscle tremors, or ambulance movement place limb electrodes on patient\u2019s thorax for better results, per International Electrotechnical Commission (IEC) recommendation.\n3. Placement of the electrodes used to perform a 12-Lead ECG requires proper knowledge of anatomy and precise application for an accurate analysis. Proper placement is as follows:\nV1: Fourth intercostal space, right sternal margin.\nV2: Fourth intercostal space, left sternal margin.\nV3: Fifth rib, midway between leads V2 and V4.\nV4: Fifth intercostal space, mid-clavicular line.\nV5: Left anterior axillary line, at the horizontal level of V4.\nV6: Left mid-axillary line, at the horizontal level as V4 and V5\nLocating the V1 position (fourth intercostal space) is critically important because it is the reference point for locating the placement of the remaining V-leads. To locate the V1 position:\n1. Place your finger on top of the jugular notch.\n2. Move your finger slowly downward approximately 1.5 inches (3.8 centimeters) until you feel a slight horizontal ridge or elevation. This is the \u201cAngle of Louis,\u201d where the manubrium joins the body of the sternum.\n3. Locate the second intercostal space on the patient\u2019s right, lateral to and just below the \u201cAngle of Louis.\u201d\n4. Move your finger down two more intercostal spaces to the fourth intercostal space which is the V1 position.\nWhen placing electrodes on female patients, ALWAYS place leads V3 - V6 under the breast rather than on the breast", + "normal ecg parameters": "P-R Interval 0.12 - 0.20 sec\nQRS Duration 0.08 - 0.12 sec\nQTc Interval 0.35 - 0.43 sec\n**Anything greater than 0.44 sec is considered prolonged **", + "considerations for right sided and posterior 12 lead electrode placement": "Right ventricular infarct may complicate up to 40-50% of all inferior AMIs and 13% of all anterior AMIs. When assessing a patient presenting with AMI it is important to ascertain whether it involves the right ventricle as this may alter your treatment or the receiving facilities treatment upon your arrival. It is recommended, although not mandatory, that a right-sided and / or posterior 12-Lead ECG be obtained if ST elevation is noted in Leads II, III, AVL, AVF, or V1. Time is muscle and transport should not be delayed to obtain a right-sided or posterior 12-Lead ECGs.\nTwo ways to obtain a right-sided 12- Lead ECG are noted below, the first being a \u201cquick look\u201d and the second being a full right sided ECG.\nPosterior Lead Placement\nModified Lead V4R\nBasically, this is lead V4 moved to the right side of the chest (mid-clavicular line, fifth inter-costal space).\nWhen Lead V4R shows at least 1 mm of ST segment elevation in the presence of inferior STEMI, it\u2019s a highly sensitive marker for right ventricular involvement.\nWhen printed out, this ECG should be marked as V4R for clarification.\nRight-Sided and Posterior Lead Definitions:\nV4R \u2013 Fifth inter-costal space at the left right mid-clavicular line (Lead V3).\nV5R \u2013 Right anterior axillary line, horizontal line from V4R (Lead V2).\nV6R \u2013 Right mid-axillary line, horizontal line from V5R (Lead V1).\nV7 \u2013 Left posterior axillary line, horizontal line from V6R (Lead V5).\nV8 \u2013 Left mid-scapular line, horizontal line from V7 (Lead V5).\nV9 \u2013 Left para-spinal line, horizontal line from V8 (Lead V6).", + "considerations for reviewing 12 lead ecg printout results": "The ECG data can be viewed in three different ways:\nECG Strip The unit displays a 12 -lead strip with 10 seconds of ECG data, in four staggered 2.5 second segments.\nInterpretation The unit displays the results of interpretation of the ECG recording by the 12 -lead program.\nMeasurements The unit displays measurements based on all 12 -leads.\nThe global measurements include heart rate, PR i nterval, QRS duration, QT, and the QTc.\nMeasurement Description\nHeart Rate Frequency is shown in beats per minute. Normal adult range is 60 - 100.\nPR Interval This time interval is between the beginning of the P wave and the beginning of the QRS complex. It is sometimes referred to as PQ duration. Smaller values indicate premature excitation of the ventricles and larger values indicate conduction defects in th e atrioventricular (AV) node.\nQRS Duration Duration of the QRS complex in milliseconds. Larger values indicate ventricular conduction defects.\nQT, QTc Duration Time in milliseconds from the beginning of the QRS complex to the end of T wave. The QTc value is the QT corrected for heart rate to estimate the value it would have been if the heart rate were 60 beats per minute. Abnormal values can be due to an electrolyte im balances or drugs. A short QT may be due to hyperkalemia and long QT due to hypocalcemia, or quinidine -like drugs (procainamide, amiodarone).\nQRS axis This is the axis of the QRS complex. Smaller than -30 is called left axis deviation; larger than 90 is a right axis deviation. Deviations can be due to conduction blocks or hypertrophy" + }, + { + "document title": "Clinical Procedures", + "protocol title": "Pulse Oximetry", + "overview": "Assessment and maintenance of a patent airway is an important skill required of every \npre-hospital provider. Pulse Oximetry (Pulse Ox, SpO 2) is a non-invasive method of \nmeasuring the oxygen saturation of arterial blood, thus providing an evaluation of \nventilatory status. Oxygen saturation is only part of the picture. The assessment of the \nventilatory status remains one of clinical judgment. The principle behind pulse oximetry \nis relatively basic. A probe is applied to the patient and a beam of light is passed \nthrough the tissues to a photo-detector on the other half of the probe. The photo-\ndetector senses the amount of light absorbed by the oxyhemoglobin molecules in the \narterial blood as it passes through the tissues beneath the probe. This information is \ntransmitted to the processing unit of the oximeter, and the percentage of oxygen \nsaturation is displayed.", + "device types and waveform recognition": "Reusable Pulse Oximeter\nPediatric Disposable Pulse Oximeter\nPulse Oximetry Waveforms Recognition\nNormal SpO2 Waveform\nNoise Artifact Waveform\nLow Perfusion Waveform\nMotion Artifact Waveform\nPhoto courtesy of biomedsearch.com\n**Make sure the SPO 2 sensor is correctly positioned to achieve the \noptimum wave form**", + "pearls": "1. ALWAYS TREAT THE PATIENT NOT THE PULSE OXIMETER . Never withhold \noxygen from a patient in respiratory distress regardless of the SpO 2 reading.\n2. A SpO 2 reading and corresponding HR on the monitor should be confirmed with \nmanual pulse check and visualization of proper SpO 2 waveform on monitor.\n3. Patients found with possible carbon monoxide poisoning will have an \ninaccurately high SpO 2 reading due to the binding of carbon monoxide with \nhemoglobin. Carbon monoxide has a binding affinity for hemoglobin 240 times \ngreater than that of oxygen, causing decreased oxygen delivery to the tissue.\n4. Remember that the pulse oximeter only measures arterial oxygen saturation. It \ndoes not measure the actual PaO 2, nor does it measure the PCO 2 or the pH. It \nalso does not assess ventilation. A patient with COPD who has a normal hypoxic \ndrive may have an excellent PaO 2 when given 100% oxygen, but will soon \nhypoventilate and have dangerously high CO 2 levels while maintaining a high \nPO 2.\n5. Pulse oximetry is considered the \u201cfourth vital sign\u201d and should be assessed and \ndocumented when available for use.\n6. The device must sense a pulse to calculate the oxygen saturation. States of \ndecreased cardiac output, such as : bradycardia, tachycardia, hypotension, and \ncardiac arrest will greatly limit the probes ability to sense the pulse. Episodes of \nvasoconstriction, such as shock of hypothermia will also have a similar effect." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Supraglottic Airway", + "overview": "Supraglottic airways such as the King LTS- D and LMA Supreme are designed for use as a primary or alternate airway device utilized for airway control in the unconscious patient when oral intubation attempts have failed or are unfeasible. ODEMSA does not advocate for one particular device over another.", + "king ltd ltsd device name": "King LTD / LTSD", + "king ltd ltsd indications": "1. Can be used as the primary airway for cardiac arrest.\n2. Any patient requiring intubation when oral ET intubation has failed or insertion of oral ET intubation is unfeasible.", + "king ltd ltsd contraindications": "1. Patient has an intact gag reflex.\n2. Patient is less than three (3) feet tall.\n3. Patient has a known or suspected underlying esophageal and / or laryngeal disease.\n4. Significant damage to the cricoid cartilage or larynx (fractured larynx) is noted upon exam.\n5. Transection of the patient\u2019s trachea is noted upon exam.\n6. Patient has known or suspected foreign body airway obstruction.\n7. There is significant damage noted to the maxillofacial region.\n8. There is a known ingestion of a caustic substance.", + "king ltd ltsd sizing": "Size Connector Color Patient Criteria\n2 (Green) 35 - 45 inches 12 - 25 kg\n2.5 (Orange) 41 - 51 inches 25 - 35 kg\n3 (Yellow) 4 - 5 feet N/A\n4 (Red) 5 - 6 feet N/A\n5 (Purple) > 6 feet N/A", + "king ltd ltsd management protocol": "1. Gently bend the distal portion of the King LTS-D airway to aid in insertion.\n2. Lubricate the distal portion of the tube with a water-based lubricant (KY Jelly) to aid insertion.\n3. Using the thumb and forefinger of your non-dominant hand, grasp the tongue and jaw and gently lift the jaw in an anterior and distal motion, unless contraindicated by C-spine precautions or patient position. Using a lateral approach, introduce the tip into the corner of the mouth.\n4. Insert the tube following the natural curve of the oropharynx until the proximal end of the King LTS-D airway lies flush with the patient\u2019s teeth. DO NOT FORCE THE TUBE INTO PLACE.\n5. Using the large syringe provided, inflate the cuff of the King LTS-D airway with the appropriate volume:\nSize Connector Color Patient Criteria\n2 (Green) 25 - 35 ml\n2.5 (Orange) 30 - 40 ml\n3 (Yellow) 45 - 60 ml\n4 (Red) 60 - 80 ml\n5 (Purple) 70 - 90 ml\n6. Attach the Bag Valve Mask to the King LTS-D airway and evaluate compliance. While bagging patient, gently withdraw the tube until ventilation becomes easy and free-flowing.\n7. Attach capnography sensor, ventilate patient several times, and check monitor for distinct waveform and numerical value. If no waveform is present, check equipment as outlined in Capnography Clinical Procedure. If capnography is working but no waveform is present, remove King LTS-D, oxygenate patient with bag valve mask, and reattempt insertion.\n8. Continue placement confirmation:\n- Observe chest rise upon ventilation\n- Auscultate for bilateral lung sounds\n- Auscultate abdomen for absent epigastric sounds\n- Note condensation in the tube with passive exhalation\n9. If successful tube placement cannot be confirmed, remove the tube and ventilate using basic airway skills.\n10. Secure the King LTS-D airway with a tube holder device and reassess placement.", + "lma supreme device name": "LMA Supreme", + "lma supreme indications": "1. Can be used as the primary airway for cardiac arrest.\n2. Any patient requiring intubation when oral ET intubation has failed or insertion of oral ET intubation is unfeasible.", + "lma supreme contraindications": "1. Patient has an intact gag reflex.\n2. Patients with inadequate mouth opening to permit insertion.\n3. Patient has a known or suspected underlying esophageal and/ or laryngeal disease.\n4. Patients who have ingested caustic substances.\n5. There is a known ingestion of a caustic substance.", + "lma supreme management protocol": "1. Lubricate the posterior surface of the mask and airway tube just prior to insertion.\n2. Stand behind or besides the patient\u2019s head.\n3. Place the head in the neutral or slight \u201csniffing\u201d position (Sniffing = extension of head & flexion of neck).\n4. Hold the device as shown in the illustration above.\n5. Slide inwards using a slightly diagonal approach (direct the tip away from the midline).\n6. Continue to slide inwards rotating the hand in a circular motion so that the device follows the curvature behind the tongue.\n7. Resistance should be felt when the distal end of the device meets the upper esophageal sphincter. The device is now fully inserted.\n8. Secure the device.\n9. Attach capnography sensor, ventilate patient several times, and check monitor for distinct waveform and numerical value. If no waveform is present, check equipment as outlined in Capnography Clinical Procedure. If capnography is working but no waveform is present, remove LMA Supreme, oxygenate patient with bag valve mask, and reattempt insertion.\n10. Continue placement confirmation:\n- Observe chest rise upon ventilation\n- Auscultate for bilateral lung sounds\n- Auscultate abdomen for absent epigastric sounds\n11. If successful tube placement cannot be confirmed, remove the tube and ventilate using basic airway skills." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Continuous Positive Airway Pressure (CPAP)", + "overview": "Continuous Positive Airway Pressure (CPAP) has been shown to rapidly improve vital signs and gas exchange, reduce the work of breathing, decrease the sense of dyspnea, and decrease the need for endotracheal intubation in patients who suffer from shortness of breath from asthma, chronic obstructive pulmonary disease (COPD), pulmonary edema, heart failure (HF), and pneumonia. In patients with HF, CPAP improves hemodynamics by reducing left ventricular pre-load and after-load.", + "indications": "1. Any patient experiencing dyspnea or hypoxemia secondary to asthma, COPD, pulmonary edema, HF, pneumonia, or inhalation injury secondary to CO / CN exposure and:\n a. Is awake and able to follow commands\n b. Is > 12 years old and is able to fit the CPAP mask to their face properly\n c. Has the ability to maintain an open airway\n d. Has a systolic BP > 90 mmHg\n e. Exhibits two or more of the following:\n \uf0b7 Has a spontaneous respiratory rate > 25 breaths per minute\n \uf0b7 SpO 2 < 94% at any time\n \uf0b7 Use of accessory muscle usage during respiration", + "contraindications": "1. Patient < 12 years old.\n2. Patient suspected of having a pneumothorax or has suffered trauma to the chest.\n3. Respiratory or cardiac arrest.\n4. Patient has a tracheostomy.\n5. Patient has agonal respirations.\n6. Patient showing signs of shock associated with cardiac insufficiency.\n7. Unconsciousness.\n8. Persistent nausea / vomiting.\n9. Facial anomalies / stroke / obtundation / facial trauma.\n10. Patient has active vomiting, upper GI bleeding or a history of recent gastric surgery.", + "protocol for management": "1. Prepare all equipment for CPAP initiation and application:\n a. Connect CPAP to portable/ ambulance oxygen supply\n b. Connect CPAP mask to airflow hose and airflow hose to CPAP machine\n c. Connect capnography sensor to monitor\n d. Do not delay CPAP application to setup in-line nebulizer attachment\n e. Assure airflow is present and machine is working properly by placing hand over mask opening and checking pressure\n f. If not previously initiated, place patient on continuous pulse oximetry and cardiac monitoring (if provider\u2019s certification allows)\n2. Once all equipment is prepared, CPAP should be supplied to patient:\n a. Explain the procedure to the patient\n b. Place mask to patient face assuring proper fit and seal over mouth and nose\n c. Refer to manufacturer\u2019s instructions for set up of your specific device\n d. Hold mask in place and secure with provided straps. Mask / seal should be tight but not uncomfortable for patient. Check for air leaks, mask / straps may need to be adjusted for proper fit\n e. If patient present with wheezing, setup nebulizer medications per protocol and apply as inline treatment\n f. Monitor and document the patient\u2019s respiratory response to treatment\n g. Check monitor for distinct capnography waveform and numerical value. If no waveform is present, check equipment as outlined in Capnography Clinical Procedure\n h. Vital signs should be checked and documented every 5 minutes while on CPAP\n i. All medications per applicable medical treatment protocol should be given in conjunction with CPAP use. CPAP does not replace medication use\n j. Continue to coach patient as needed to keep mask in place, readjust as needed\n k. Notify intended receiving hospital as soon as possible of patient status and CPAP application so a CPAP device can be brought to Emergency Department prior to patient arrival\n l. If respiratory status deteriorates, remove CPAP, assist patient spontaneous respirations with Bag Valve Mask, and prepare for nasal / oral intubation", + "considerations": "1. CPAP therapy needs to be continuous and should not be removed once applied unless patient cannot tolerate mask, patient respiratory drive declines, or patient begins to vomit.\n2. Upon arrival at hospital, advocate for patient to remain on CPAP and do not remove CPAP until hospital equivalent respiratory therapy is ready to be placed on patient.\n3. Watch patient for gastric distention, which may result in vomiting.\n4. Procedure may be performed on patient with a valid Pre-Hospital Do Not Resuscitate order.\n5. Due to changes in pre-load and after-load of the heart during CPAP therapy, a complete set of vital signs must be obtained every five minutes.\n6. Due to existing high intra-thoracic pressures present with these types of patients it is imperative that the lowest possible pressures be used during treatment to prevent possible development of a pneumothorax from lung over inflation." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Medication Administration Cross-Check", + "overview": "In line with developing a Culture of Safety, the medication cross-check procedure is a critical component of improving the care we deliver, and keeping our patients safe. As providers, we must appreciate that the measures developed to create barriers, redundancy, and recovery are not attempts to \u201cdumb down\u201d the care we provide, but to address the ubiquitous vulnerabilities of human cognition so that our patients are more than one human error away from harm. The Medication Administration Cross-Check is an attempt to do just that; to insert one more layer of protection for the patient from predictable patterns and frequency of human errors.", + "indications": "1. Any time a medication is to be administered.", + "contraindications": "1. None", + "protocol initiation statement": "The AIC initiates the procedure check by stating \u201cCross -check.\u201d Provider #2 responds that he/she is, \u201cReady.\u201d It is important to avoid using ambiguous responses like, \u201cOkay,\u201d since they may be interpreted many different ways.", + "two provider procedure details": "The attendant in charge (AIC) obtains intended medication and confirms correct drug.\na. Second Provider verifies and states, \u201cCheck.\u201d\nThe attendant in charge (AIC) confirms expiration date.\nb. Second Provider verifies and states, \u201cCheck.\u201d\nThe attendant in charge (AIC) confirms correct concentration.\nc. Second Provider verifies and states, \u201cCheck.\u201d\nThe attendant in charge (AIC) confirms correct route of administration.\nd. Second Provider verifies and states, \u201cCheck.\u201d\nThe attendant in charge (AIC) confirms correct amount of medication to be given.\ne. Second Provider verifies and states, \u201cCheck.\u201d\nThe attendant in charge (AIC) confirms no allergies or prior reactions to the medication.\nf. Second Provider verifies and states, \u201cCheck.\u201d\nThe attendant in charge (AIC) confirms V/S are appropriate.\ng. Second Provider verifies and states, \u201cCheck.\u201d\nThe attendant in charge (AIC) confirms there are no other contraindications.\nh. Second Provider verifies and states, \u201cCheck.\u201d\nUpon the cross-check procedure being completed, the AIC should then administer the medication.", + "medication terminology note": "*Terms such as \u201camp\u201d or \u201cvial\u201d should be avoided, as this may lead to an incorrect dosage administration. By providing a specific amount, the false notion that the contents of a vial are a \u201cdose\u201d is avoided and directs the provider\u2019s attention to exactly how much medication they intend to deliver.", + "two provider summary": "Provider #1 | Provider #2\nCorrect drug name | Check\nExpiration date valid | Check\nConcentration & volume in vial | Check\nRoute of administration | Check\nVolume to be given | Calculate & crosscheck\nNo prior allergy or reaction | Check\nVital signs appropriate | Check\nNo other contraindications | Check\nADMINISTER THE MEDICATION", + "one provider procedure details": "1. When and AIC must medicate a patient alone (e.g. administering during transport to a hospital), the provider should follow and confirm the medication using a modified version of the established shelf-check procedure on the 1 Provider Medication Administration Cross-Check card.\n2. The AIC must confirm by reading the label that it is the intended medication to administer.\n3. The AIC must confirm by reading the label that the medication is not expired.\n4. The AIC must confirm by reading the label that the concentration by volume in the container.\n5. The AIC must confirm by calculating the amount of medication to be given.\n6. The AIC must repeat each of the above actions to cross-check.\n7. The AIC must verify the patient\u2019s vital signs are appropriate and confirm any drug allergies.\n8. Upon the self-check procedure being completed, the AIC should then administer the medication.", + "one provider summary": "Action |\nCorrect drug name | Verify\nExpiration date valid | Verify\nConcentration & volume in vial | Verify\nRoute of administration | Verify\nVolume to be given | Calculate\nREPEAT EACH OF THE ABOVE STEPS TO CROSSCHECK\nNo prior allergy or reaction | Verify\nVital signs appropriate | Verify\nNo other contraindications | Verify\nADMINISTER THE MEDICATION", + "pearls": "1. It is essential that both providers participate in an engaged manner and do not participate passively.\n2. If a discrepancy, disagreement, or a need for clarification is encountered at any step in the process, it must be resolved prior to continuing the cross-check procedure.\n3. The cross-check confirmation has been created to be effective regardless of provider #2\u2019s level of certification and/or knowledge of pharmacology. The drug name, concentration and expiration date can all be verified by visual verification of the information printed on the drug label.", + "interruption guideline": "IF AT ANY TIME THE PROCESS IS INTERRUPTED DURING A TWO PROVIDER AND ESPECIALLY A ONE PROVIDER CROSS-CHECK, THE PROCESS SHOULD START AGAIN FROM THE BEGINNING." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Needle Thoracentesis", + "overview": "A needle decompression is a life saving procedure used to relieve a tension \npneumothorax. A tension pneumothorax is usually the result of blunt or penetrating \ntrauma to the chest but may also be spontaneous. A simple pneumothorax develops \ninto a tension pneumothorax as the pressure in the pleural space exceeds the outside \natmospheric pressure. This increase of pressure within the pleural space further \ncollapses the lung on the involved side and forces the mediastinum to the unaffected \nside decreasing the blood flow to the heart and placing pressure on the unaffected \nlung.", + "indications": "1. Any patient exhibiting signs/ symptoms of respiratory distress due to blunt \nforce or penetrating chest trauma that also has a complaint of: \na. Increasing respiratory distress and \nb. Decreasing or absent breath sounds unilaterally or bilaterally with \nrespirations and \nc. Decreased SpO 2 despite oxygen therapy and \nd. Increasing tachycardia \n2. Any trauma arrest involving chest trauma that resuscitation is being attempted \nshould have bilateral needle decompression performed as soon as possible to \neliminate hemo / pneumothorax as a cause of traumatic arrest. \n3. Consider in the setting of refractory pulseless electrical activity (PEA).", + "protocol for management": "1. Prepare all equipment for needle thoracentesis: \na. Over 8 years old: 14g x 3.75\u201d angiocath with 10 ml syringe attached. \nb. Under 8 years old: 18g x 1.25\u201d angiocath with 10 ml syringe attached. \nc. \u00bd\u201d silk tape torn into 5\u201d length to use to stabilize catheter. \n2. Once all equipment is prepared, needle thoracentesis should be performed. \na. Locate proper insertion site, 2nd inter-costal space at the mid-clavicular \nline of the affected side of the chest. \nb. Prep insertion site with betadine using aseptic technique, if available. \nc. Insert angiocath with syringe attached into second inter-costal space \njust over 3rd rib to avoid inter-costal nerves and vessels located on the \ninferior portion of the rib border. \nd. Advance the catheter 1 - 2 inches (3/4 - 1 inch in patients less than 8 \nyears old) through the chest wall while pulling back gently on plunger \nof syringe. Tension should be felt on the plunger until the needle \nenters the pleural space. A \u201cpop\u201d or \u201cgive\u201d may also be felt. Once \nneedle has entered pleural space, do not advance needle any further. \ne. Advance catheter while withdrawing the needle until the catheter is \nflush with the skin. \n3. Listen for a gush or \u201c hiss\u201d of air, which confirms placement and diagnosis. \nNote: This may not always be heard due to severity of injury or missed due to \nsurrounding noise. \n4. Dispose of needle properly and never reinsert into the catheter . \n5. Secure catheter by wrapping strip of tape around hub and taping to chest. \n6. Reassess lung sounds and document procedure, whether air or blood was \nexpelled, improvement of vital signs, and success/ failure in PPCR. \n7. Continue to reassess during transport as tension pneumothorax may reoccur.", + "signs and symptoms": "***PROGRESSIVE SIGNS AND SYMPTOMS OF TENSION PNEUMOTHORAX*** \nEARLY \n\uf0b7 Unilaterally decreased \nor absent breath \nsounds \n\uf0b7 Continued increased \ndyspnea and \ntachypnea despite \ntreatment \n\uf0b7 Increasing heart rate \nwith decreasing SpO 2 \nPROGRESSIVE \n\uf0b7 Increasing tachypnea \nand dyspnea \n\uf0b7 Tachycardia and \nsubcutaneous \nemphysema \n\uf0b7 Increasing difficulty \nventilating an intubated \npatient \nLATE \n\uf0b7 Jugular vein distention \n\uf0b7 Tracheal deviation \n\uf0b7 Tympany \n\uf0b7 Signs o f acute hypoxia \n\uf0b7 Narrowing pulse \npressure", + "considerations": "PEARLS: \n1. Catheter may become occluded after initial decompression. Full procedure \nmay need to be repeated if occlusion occurs. If additional procedures are \nnecessary, placement of these catheters should be near the original site. \n2. A partially filled syringe of saline (i.e., 5 mL in a 10 mL syringe) may be \napplied to the catheter when available as a visual aide to confirm placement. \nIf air is present, bubbles will be seen in the syringe." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Oral Intubation", + "overview": "Advanced airway procedures and competency are the cornerstones of paramedicine. True competency involves knowing not only how to control the airway, but when to control the airway, and selecting the best method to do so.", + "attempt limit": "Only one (1) attempt at oral intubation should be attempted. If unsuccessful, an alternative airway device should be inserted without delay.", + "indications absolute": "1. Hypoxia or obtunded patients\n2. Respiratory Arrest\n3. Cardiac Arrest", + "indications strongly consider with": "1. Any patient with a decreased level of consciousness with compromised ability to manage their airway\n2. Airway burns or edema\n3. HF, acute asthma, COPD, or other respiratory failure\n4. with diminished respiratory drive\n5. Suspected intracranial hemorrhage or closed head injury\n6. Patients who fail to respond to positive pressure ventilation\n7. GCS < 8 without reversible causes", + "contraindications": "1. An intact gag reflex\n2. Patients that have a tracheostomy or stoma", + "protocol for management": "1. Patient should be pre-oxygenated with appropriately sized Bag Valve Mask at a rate of 12 - 20 breaths per minute with an appropriately sized oropharyngeal airway in place. The patient\u2019s SpO 2 should be raised as much as possible with manual ventilations prior to intubation attempt.\n2. Patient airway should be assessed and documented for ability / difficulty of oral intubation via Mallampati classification and prepare for possible use of rescue airway device. Once visualization of the lower airway has been obtained, assessment of difficulty can again be made using the Cormack & LeHane classification. The higher the classification, the more difficult the intubation.\n3. Prepare all equipment for intubation:\na. Appropriately sized Macintosh or Miller (provider choice) intubation blade and handle\nb. Appropriately sized ET Tube with stylet and 10 ml syringe attached\nc. Pre-inflate cuff of tube to ensure no leaks, then deflate, leaving syringe attached\nd. Bend tube and stylet into a crescent or \u201chockey stick\u201d shape and ensure that the stylet is at least one (1) centimeter proximal to the end of the tube\ne. Have immediately available a second ET tube, one (1) size smaller for unanticipated smaller trachea\nf. Adult or pediatric tube holder\ng. Capnography sensor connected to monitor\nh. Suction setup turned on and within reach for use with vomited gastric secretions\ni. An alternative airway device should be within reach and ready for use in case of failed intubation\nj. All appropriate BSI / PPE should be worn to include eye protection, mask, and gloves\n4. Once the determination has been made by the provider that the patient has been sufficiently pre- oxygenated, the OPA should be removed and an intubation attempt should be made:\na. Position the patient\u2019s head in the \u201csniffing position\u201d (unless C-spine injury is suspected)\nb. Insert the intubation blade into the mouth, lifting the tongue and sweeping it to the left. Suction, as necessary, to create a clear field of view of t he lower airway\nc. Insert the laryngoscope blade into the pharynx and visualize the glottic opening and epiglottis by properly seating the blade in the correct position:\n \uf0b7 Macintosh blade should be inserted until the tip is seated in the vallecula\n \uf0b7 Miller blade should be inserted until covering the epiglottis\nd. When maneuvering airway with blade, do not use teeth as a fulcrum, as this may cause breakage of teeth, increased intubation difficulty, and / or possible airway obstruction.\ne. Lift the laryngoscope upward and forward, without changing the angle of the blade, to expose the vocal cords. Do not lift using prying motion.\nf. Once vocal cords are visualized, do not change position of blade. Insert ET tube into the pharynx and between the vocal cords, anterior to the arytenoid cartilages, until the wide black mark on the distal end of the tube has passed through the vocal cords, approximately 1 inch in the adult and 5 - 10 mm in the child.\ng. Without releasing tube, remove laryngoscope blade. Inflate ET tube cuff with 5 - 10 cc of air via attached syringe.\nh. Attach capnography sensor, ventilate patient several times, and check monitor for distinct waveform and numerical value. If no waveform is present, check equipment as outlined in Capnography Clinical Procedure . If capnography is working but no waveform is present, remove ET tube, and immediately insert an alternative airway device.\ni. If capnography waveform is present, continue placement confirmation:\n \uf0b7 Observe chest rise upon ventilation\n \uf0b7 Auscultate for bilateral lung sounds\n \uf0b7 Auscultate abdomen for absent epigastric sounds\n \uf0b7 Note condensation in the tube with passive exhalation\n ***Continually assess the placement of the ET tube***\nj. If breath sounds are not heard equally, deflate cuff and adjust tube for possible left or right main-stem intubation by pulling tube out one (1) centimeter. Inflate cuff and reassess lung sounds. In trauma patients, also assess for possible pneumothorax.\nk. Once lung sounds confirmed, document centimeter mark at teeth (depth), and secure ET tube with tube holder and reassess lung sounds and capnography readings.\nl. Reassess the tube placement after all movement of patient or change in capnography readings." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Mechanically-Assisted External Chest Compression Device", + "overview": "When treating patients in sudden cardiac arrest, consistent, continuous, high-quality chest compressions are critical to survival. Several devices are now available that provide mechanically-assisted external chest compression, allowing for effective, non-invasive cardiac support during cardiac arrest resuscitation. ODEMSA does not advocate the use of one device over another.", + "indications": "Medical origin Cardiac Arrest.", + "contraindications": "Vary based on the specifics parameters of the device. Follow the manufacturer\u2019s recommendations for contraindications.", + "protocol for management": "1. After assessing patient\u2019s condition, begin manual CPR.\n2. Attach defibrillation / pacing pads.\n3. Prepare the mechanically-assisted external chest compression device for deployment.\n4. Apply mechanically-assisted external chest compression device, according to the manufactur er\u2019s recommendations. WHILE APPLYING DEVICE, ATTEMPT TO LIMIT INTERRUPTIONS IN MANUAL CHEST COMPRESSION TO LESS THAN 10 SECONDS.\n5. As quickly as possible, engage operation of the device.\n6. Ventilate the patient as directed according to manufacturer\u2019s recommendations.\n7. Every effort should be made to not stop compressions unless absolutely necessary.\n8. Positive pressure ventilation can be performed synchronously with any decompression once an advanced airway is in place.\n9. To access the patient, or to pause the device for any reason, press the Stop / Cancel or pause button.\n10. Defibrillate the patient when indicated, according to the manufacturer\u2019s recommendations.\n11. Pause compressions to reassess the patient and check for a pulse.", + "note": "Any time failure occurs, manual external chest compressions should be resumed IMMEDIATELY, whilst troubleshooting the device." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Intraosseous Access", + "overview": "Intraosseous vascular infusion is a method of gaining access to the circulatory system by using a specialized trocar that is placed into the cavity of a long bone. Within the bone marrow, is a network of venous sinusoids that drain into the venous system, thereby accepting fluids or medications infused through an intraosseous access site. Although an IO can be used to infuse any fluid or medication, a drawback to its use may include slower than normal infusion rates due to anatomy of the IO space. To improve the infusion flow, a pressure bag should be used with all fluids administered via IO. Proper BSI precautions and aseptic technique should be used at all times.", + "indications": "1. Intravenous fluids or medications are needed and a peripheral IV cannot be established in one (1) attempt or ninety (90) seconds AND the patient exhibits one or more of the following:\n a. An altered mental status (GCS of 8 or less)\n b. Respiratory compromise (SpO2 80% after appropriate therapy, respiratory rate < 10 or > 40 per minute)\n c. Hemodynamic instability (Systolic BP of < 90 mmHg)\n2. Intraosseous access may be considered PRIOR to peripheral IV attempts in the following situations:\n a. Cardiac arrest (medical or trauma)\n b. Profound hypovolemia with altered mental status\n c. Patient in extremis, with immediate need for delivery of medications, and / or fluids.", + "contraindications": "1. Suspected narcotic overdose and / or hypoglycemia.\n2. Fracture of the bone selected for IO insertion.\n3. Excessive tissue at insertion site or inability to locate anatomical landmarks.\n4. Previous significant orthopedic procedures in area selected for IO insertion (IO within 24 hours, knee replacement, and surgically implanted hardware). Look for scars.\n5. Signs of infection in area selected for IO insertion (redness, skin lesions).\n6. Osteogenesis imperfecta (severe congenital bone degenerative disorders if known).", + "protocol for management": "1. Assemble and prepare all equipment:\n a. IO device\n b. Cleansing agent\n c. Syringe for aspiration and flushing\n d. Fluid and administration tubing\n e. Materials to secure site\n2. Prepare and position the patient.\n3. Select a site for insertion of the intraosseous access device. The site should be readily accessible and should be a site approved for use by the device manufacturer and agency operational medical director.\n4. Once the proper area of insertion has been located, clean the site and the immediate surrounding area with betadine, or other acceptable cleansing agent, allowing a large sterile field to work in.\n5. Stabilize the site with non-dominant hand, making sure hands and fingers are out of the path of the insertion.\n6. Insert the device, according to manufacturer\u2019s instructions for use.\n7. Aspirate the site with a syringe, as directed by the device manufacturer, to ensure accurate placement. Upon aspiration, a small volume of blood or marrow indicated correct medullary placement of the trocar.\n8. Flush the site with a small volume of saline (10 \u2013 20 mL). If the patient is alert, you may administer 0.5 mg / kg to a max dosage of 20 - 40mg of lidocaine (or as otherwise approved by the agency medical director) through the IO site for control of pain associated with infusion pressure within the bone cavity.\n9. Secure site according to device manufacturer\u2019s recommendations.\n10. Infuse fluid at the appropriate rate. A pressure bag may be necessary to obtain an adequate flow rate." + }, + { + "document title": "Clinical Procedures", + "protocol title": "Tourniquet", + "overview": "If external bleeding from an extremity cannot be controlled by pressure, application of a\ntourniquet is the next step in hemorrhage control. Tourniquets that are narrow and\nband-like are more likely to result in damage to arteries and superficial nerves and\nshould be avoided. Wider tourniquets are more effective at controlling bleeding, and\nthey control hemorrhage at a lower pressure. A tourniquet should be applied just\nproximal to the hemorrhage, regardless of location on extremity. Other devices are\navailable, including commercial devices for use in place of the manual tourniquet. \n\n***The application of a tourniquet increases the risk of loss of limb* **", + "indications": "Extremity hemorrhage that cannot be controlled with basic or pressure bandaging", + "contraindications": "1. Any hemorrhage that can be controlled by a basic or pressure bandage.", + "protocol for management": "The technique for application of a manual tourniquet is as follows:\n\n1. Fold a cravat into a\nwidth of about four (4)\ninches (10 cm) and\nwrap cravat twice\naround the affected\nextremity.\n\n2. Tighten the bandage\nmanually and tie a knot\nsecuring it in place.\n\n3. Place a metal or plastic\nrod on top of the knot,\nand tie a second knot\nsecuring the rod in\nplace.\n\n4. Twist the rod until\nbleeding has stopped\nand the distal pulse is\neliminated.\n\n5. Tie the ends of the rod\nin place and reassess\nfor pulse and bleeding.\n\n6. Place a piece of 2\u201d\ntape above the\ntourniquet and record\nthe time of application\non the tape.", + "pearls": "1. The tourniquet should be placed around a solid piece of bone, if possible,\nproximal to the uncontrolled hemorrhage. Placing the tourniquet over a solid\npiece of bones will aid in the tourniquet\u2019s ability to tamponade the hemorrhage.\n2. The tourniquet should be placed as close proximally to the wound as possible to\nminimize further extremity damage.\n3. The tourniquet must be marked with the time of application. Do not write on the\nactual tourniquet.\n4. Consider Pain Management Protocol in conjunction with the application of a\ntourniquet. Be vigilant of the patient\u2019s hemodynamic status." + }, + { + "document title": "Administration", + "protocol title": "Infection Control - Exposure", + "overview": "Each agency is responsible for identifying a designated infection control officer. This person shall have been formally trained for this position and shall be knowledgeable in proper procedures and current regulations and laws regarding governing disease transmission.\n\nIn 1990, the Ryan White Comprehensive AIDS Resources Emergency Act, Public Law 101 - 381, was enacted into law. Although this law deals primarily with funding for HIV / AIDS programs throughout the country, Subpart B contains key provisions for fire / EMS personnel regarding notification of possible exposure to communicable diseases. This portion of the law, often referred to as the Ryan White Notification Law, requires every emergency response entity in the country to have a designated infection control officer (DICO) to serve as the liaison between emergency responders involved in exposure incidents and medical facilities to which the source patients in the exposures are transported. This covers emergency responders including firefighters, EMTs, paramedics, police officers, and volunteers. The law also outlines the role and responsibilities for this individual, which are extensive and comprehensive. Since this individual is charged with the post-exposure follow-up and deals with infection control issues, the DICO title seemed appropriate.\n\nThe law requires medical facilities to provide the disease status of source patients as soon as possible and no later than 48 hours after an exposure has been reported to the facilities by the DICO of the responder involved in the exposure. The law also requires that medical facilities contact the DICO of the transporting entity that delivered a patient suspected for or diagnosed with pulmonary tuberculosis. The law also affords coverage to fire / EMS agencies that were not covered under the Occupational Safety and Health Administration's (OSHA's) Bloodborne Pathogen Standard ( 29 CFR 1910.1030 ).1", + "blood borne pathogens": "Includes but are not limited to: \n1. HIV \n2. Hepatitis B \n3. Hepatitis C \n4. Syphilis", + "airborne pathogens": "Include but are not limited to: \n1. Tuberculosis \n2. Measles (Rubeola) \n3. Varicella", + "other less common pathogens": "Include but are not limited to: \n1. Malaria \n2. Rabies \n3. Neisseria Meningitis \n4. Plague \n5. Hemorrhagic fevers \n6. Diphtheria \n7. Rubella \n8. SARS", + "management protocol": "1. Determine if exposure has occurred. Body fluids should have visible blood before exposure should be considered. Routes of exposure include direct injection (needle stick), through non intact skin (cuts and abrasions), and through mucous membranes (eyes and mouth). If the exposure is a sharps injury, let the area bleed freely and wash the area with soap and water or the waterless hand wash solution. If the exposure was a splash to eye, nose, or mouth, flush the area for 10 minutes with water. \n2. Consult with / notify your designated infection control officer (DICO) with any exposure or infection control questions. \n3. The DICO shall contact the facility to initiate testing required by federal and state rules and regulations. \n4. The facility shall notify the DICO or designee with results as required by federal and state rules and regulations. \n5. The DICO shall arrange follow up and prophylaxis based on the results as guided by the most recent CDC recommendations. \n\nEach agency must develop a comprehensive infection control plan and designate an infection control officer.", + "ems provider initial actions for exposure": "Initial Action for EMS Provider in Event of Potential Exposure:\n\nQuestion: Did an EMS Exposure Occur?\n\nIf Exposure was Airborne:\n- Notify hospital staff of possible exposure.\n- Notify the Designated Infection Control Officer.\n- Designated Infection Control Officer to arrange for follow-up as needed.\n\nIf Exposure was Percutaneous (through the skin):\n- Let area bleed freely.\n- Notify hospital staff of possible exposure.\n- Notify the Designated Infection Control Officer.\n- Designated Infection Control Officer to arrange for follow-up as needed.\n\nIf Exposure was to eyes, nose or mouth:\n- Flush affected area w/flowing water for at least 10 minutes.\n- Notify hospital staff of possible exposure.\n- Notify the Designated Infection Control Officer.\n- Designated Infection Control Officer to arrange for follow-up as needed.\n\nIf Exposure was to non-intact skin:\n- Remove any contaminated clothing.\n- Notify hospital staff of possible exposure.\n- Notify the Designated Infection Control Officer.\n- Designated Infection Control Officer to arrange for follow-up as needed.\n\nFor all other exposure determinations or questions contact Designated Infection Control Officer Immediately." + }, + { + "document title": "Administration", + "protocol title": "Traumatic Cease Resuscitation", + "overview": "The primary purpose of a traumatic cease resuscitation protocol is to reduce the likelihood of injuring pre-hospital providers and to prevent injury to the public whom we serve while transporting non-viable patients to receiving facilities.", + "considerations": "If a trauma patient presents with one or more of the following conditions, then the pre-hospital provider should consider termination of treatment or do not resuscitate. In cases of hypothermia or submersion, follow the appropriate protocol.", + "signs and symptoms": "The conditions are:\n\uf0b7 Decapitation.\n\uf0b7 100% full thickness burns without signs / symptoms of life.\n\uf0b7 Obvious mortal wounds (i.e., crushing injuries to the head or chest, gunshot wounds to the head o r chest with massive tissue destruction or loss) without signs / symptoms of life.\n\uf0b7 Blunt or penetrating trauma with no signs of life when first responders arrive.\n\uf0b7 Greater than 30 minute transport time to any receiving facility with a pediatric cardiac arrest.", + "protocol for management adult": "1. WHEN IN DOUBT, RESUSCITATE!\n2. The responding pre-hospital provider should perform a routine patient assessment.\n3. Once the provider determines that the patient is without life (no pulse, no respirations), the provider will verify the patient\u2019s condition with another pre-hospital provider.\n4. If both providers agree, they will note the time of death and follow local protocols concerning notification of law enforcement or the medical examiner.\n5. At the provider\u2019s discretion, the cardiac monitor may be attached for the purpose of printing a rhythm strip to document a non-perfusing rhythm. At no time during the assessment phase should other ALS procedures / treatments be started. DO NOT initiate IV lines, intubate, etc. ALS procedures indicate that a patient needs to be transported to the closest appropriate hospital.", + "protocol for management pediatric": "1. WHEN IN DOUBT, RESUSCITATE!\n2. Almost all pediatric cardiac arrest patients should have the benefit of full resuscitative efforts, including transport.\n3. If the pediatric patient presents with any of the indications for Traumatic Cease Resuscitation and the pediatric patient remains in cardiac arrest after initial BLS resuscitative efforts, contact the receiving facility and establish on-line medical control for orders to cease resuscitation.\n4. Note the time of death and request law enforcement response.", + "special circumstances": "1. Remember there are several special circumstances (hypothermia, electrocution, etc.) that warrant patient transport. Any patient, who may benefit from advanced life support, should receive such." + }, + { + "document title": "Administration", + "protocol title": "Interfacility Transfers", + "indications": "An interfacility transfer is defined as \u201cthe movement of a patient, directed by p hysician orders, from one facility to another , for the purpose of specialty care ; after initial and / or stabilizing care has been provided by the transferring facility.", + "protocol for management": "1. The interfacility transport should be performed by an appropriately equipped and appropriately staffed ambulance / aircraft.\n2. The transferring physician/institution (or designee) will provide the EMS agency, prior to dispatch, a patient report that includes the patient\u2019s condition and any special treatment the patient is receiving.\n3. The clinical level of care should be maintained throughout transport. Additional staff (RN, Respiratory Therapist, MD, etc.) may be required.\n4. The Attendant in Charge (AIC) should request a brief patient report from the health care personnel on scene, and should obtain the pertinent records to go with the patient (i.e., face sheet, transport sheet, lab work, x-rays, etc.)\n5. If the patient has a valid Do Not Resuscitate order, a written order (including a Prehospital DNR order) must accompany the patient.\n6. Assessment by the AIC should be kept to a minimum and should not delay transport. Also, the AIC will have access to information necessary to provide appropriate care during transport.\n7. If the ambulance / aircraft crew arrives and the patient\u2018s condition has deteriorated to a life-threatening situation where immediate intervention is necessary, stabilizing effort should be initiated by the transferring hospital staff. EMS should not initiate transfer of a patient who is unstable.\n8. An ALS provider may monitor and administer nonstandard medications prescribed by the patient\u2019s tra nsferring physician with on-line Medical Control as needed during transfer.\n9. The administration of any medications not covered by protocol will be recorded on the Prehospital Patient Care Report, noting the name of the transferring physician, time that Medical Control was contacted, and dosage of the medication and route administered." + }, + { + "document title": "Administration", + "protocol title": "Management", + "overview": "An orderly management of the emergency scene will improve any level of pre-hospital patient care. Although questions concerning authority (i.e., on-scene physician and response by more than one EMS agency) can arise, they should be settled quickly and quietly.", + "protocol for management": "1. Upon arrival at the scene, NIMS (National Incident Management System) shall be used and the Incident Commander (or designee) shall have authority for patient care and management at the scene of an emergency.\n2. Authority for management of the emergency scene, exclusive of medical control over the patient, will rest with the appropriate on-scene public safety officials (i.e., police, fire, and rescue). It is recommended that scene management be negotiated in advance of emergencies by local agreements and written protocols.\n3. If other medical professionals are at the emergency scene offer or provide assistance in patient care, the following will apply:\n a. Medical professionals who offer their assistance at the scene should be asked to identify themselves and their level of training. The pre-hospital provider should request that the medical professional provide proof of her / his identity if that person wants to continue to assist with patient care after the ambulance has arrived.\n b. Physicians are the only medical professional who may assume control of the patient\u2019s care. Pre -hospital providers should recognize the knowledge and expertise of other medical professionals and use them, if needed, for the best patient care possible. Any bystander claiming to be a physician must show credentials to EMS on scene prior to being allowed to provide patient care. All medical professionals who assist or offer assistance should be treated with courtesy and respect.\n c. The authority of the pre- hospital provider\u2019s procedures rests in these pre -hospital Patient Care Protocols adopted by the EMS agency and the agency Operational Medical Director (OMD).\n d. A physician at the scene who renders care to the patient prior to arrival of an EMS unit may retain medical authority for the patient if the physician desires. The pre-hospital provider shall advise the physician who wants to supervise o r to direct patient care that, in order to so, the physician MUST accompany the patient to the receiving hospital to maintain continuity of patient care. Documentation of these events will be complete and will include the physician\u2019s name.\n e. If there is a conflict about patient care or treatment protocols, the pre-hospital provider will contact on-line medical control or, if practical, the agency OMD for further instructions. Under no circumstances should this conflict interfere with prudent patient care.\n4. The levels of pre-hospital EMS certification currently recognized by the Commonwealth of Virginia are:\n\nCore Certifications\n a. First Responder / EMR\n b. Emergency Medical Technician -Basic / EMT\n c. Emergency Medical Technician \u2013Enhanced / Advanced EMT\n d. Emergency Medical Technician \u2013Intermediate\n e. Emergency Medical Technician -Paramedic / Paramedic\n\nSpecialty Certifications\n a. Pediatric Neonatal Critical Care Transport Paramedic\n b. Critical Care Emergency Medical Technician \u2013 Paramedic\n c. Certified Flight Paramedic" + }, + { + "document title": "Administration", + "protocol title": "Infection Control - PPE", + "overview": "In order to protect patients, healthcare providers, and their families, pre-hospital providers must be familiar with, and act in accordance with, effective infection control measures for airborne and bloodborne pathogens. Infection control is the responsibility of all members of the EMS system. The ultimate goal is a safe environment for patients and everyone else involved in the healthcare system.\n\nEach agency is responsible for identifying a designated infection control officer. This person shall have been formally trained for this position and shall be knowledgeable in current regulations and laws governing infection control practices.", + "standard precautions": "1. Standard precautions should be observed with every patient. This includes, but is not limited to, starting IVs, intubation, suctioning, caring for trauma patients, nebulizer treatments, OB emergencies.\n2. Body fluids include: blood, saliva, sputum, vomitus or other gastric secretions, urine, feces, cerebrospinal fluids, breast milk, serosanguinous fluid, semen and / or bodily drainage.", + "protocol for management": "1. Wear appropriate protective gloves on every patient. Change gloves between patients or if gloves become contaminated or torn.\n2. Wash hands after any patient contact, even when gloves have been us ed.\n3. Wear gown if soiling of clothing or of exposed skin with blood or body fluids is likely. Gowns must be impervious to fluids.\n4. Wear appropriate mask and eye protection if aerosolization or spattering of body fluids is likely to occur, (e.g., during suctioning, nebulizer treatments, insertion of endotracheal tubes and other invasive procedures ); or when a patient displays signs and symptoms suggestive of an infection with an airborne or respiratory route of transmission; or if the provider has been told the patient has an infection with a respiratory component.\n5. Use airway adjuncts whenever respiratory assistance is indicated. Adjuncts include pocket masks with one-way valves, shields and Bag-Valve Masks (BVM). BVMs should be the first choice when ventilating a patient.\n6. Contaminated equipment:\n a. Place contaminated disposable equipment in an appropriately marked biohazard bag. Dispose in a location approved for biohazard waste or served by an agency licensed to haul biohazard waste.\n b. Render non- disposable equipment safe for handling before putting it back in service. Follow manufacturers' recommendations for proper cleaning and decontamination procedures. CDC may also provide information on current decontamination of equipment.\n c. Use a high-level disinfecting solution on non-disposable equipment, (i.e., laryngoscope blades), before re-using the items.\n7. In the field, place linens soiled with body fluids in appropriately marked biohazard bags. In the hospital, ask and determine the appropriate container and place soiled linens in it. Remove linen from biohazard bag before placing in linen container. Always wear appropriate protective gloves when handling soiled linens.\n8. Dispose of needles, syringes and sharp items in a rigid, puncture-resistant container, red in color or bearing the universal biohazard symbol. Do not bend or shear needles. Recapping contaminated needles is only permitted by a single-handed method and is NOT recommended.\n9. Do not leave sharps or any contaminated items in any Drug Box.\n10. Place any specimen to be left at the hospital in double-bagged, zip-lock-type bags with the universal biohazard label attached to the outer bag. Attach a specimen label to the outer bag. When in doubt, check with the Charge Nurse.\n11. Wipe up body fluid spills promptly. Wear gloves when cleaning up spills. Decontaminate with a disinfectant approved by the Environmental Protection Agency (EPA) and CDC. Dispose of gloves and cleaning items in an appropriately marked biohazard bag.\n12. Regularly clean and disinfect the interior of emergency vehicles and any on-board equipment. Follow agency procedures for cleaning and disinfecting solutions in accordance with manufacturers' guidelines and Center for Disease Control (CDC) recommendations.\n13. Discard unused articles, medications and equipment only when those items have been opened or in some way have been contaminated with blood and / or body fluids.\n14. Consult with your designated infection control officer with any actual or potential exposure or any infection control questions" + }, + { + "document title": "Administration", + "protocol title": "DNR", + "overview": "Pre-hospital providers may, at times, withhold cardiopulmonary resuscitation (CPR) and\nadvanced cardiac life support (ACLS) due to a patient\u2019s pre -determined wishes. For\nresuscitative efforts to be withheld, a valid state of Virginia Durable Do Not Resuscitate\n(DDNR) order must be present.", + "protocol for management": "1. The responsible pre-hospital\nprovider should perform routine\npatient assessment, resuscitation\nand / or intervention efforts until the\nDDNR or other alternate form of\nDNR status is confirmed. Alternate\nforms of DNR orders include:\na. EMS-DNR order (old format)\nwritten after July 1, 1999.\nb. DNR order written for a patient\ncurrently admitted to a licensed\nhealth care facility. EMS\npersonnel may recognize these\norders only while the patient is in\nthe facility. The DNR may\nappear in different forms\nincluding prescription forms,\nfacility DNR forms, and patient\nrecords. All DNR formats must\ncontain: Patient name, physician\nname, DNR determination, and\ndate of issue.\nc. DNR order written for the purpose of transfer. EMS personnel may recognize\nthese orders during transport. DNR may appear in different forms including :\nprescription forms, facility DNR forms, and patient records. All DNR formats\nmust contain: Patient name, physician name, DNR determination, and date of\nissue.\nNOTE: Many times pre-hospital providers are presented with a Living Will. Living Wills\nare NOT recognized in the pre-hospital setting due to the fact that it is not a\nphysician ordered DNR and therefore does not fit into the accepted \u201calternate DNR\norder. \u201d\n2. Request the original DDNR form.\n3. Determine that the DDNR order is intact and not defaced.\n4. The provider should verify the identity of the DDNR patient through the family\nmembers or friends at the scene, or with appropriate photo identification (e.g.,\ndriver\u2019s license).\n5. Once validity is verified, resuscitation efforts may be ceased or withheld.\nDocument all pertinent information on ePCR form including:\na. DDNR form number\nb. Patient name\nc. Physician name\nd. Date of issue\ne. Method of identification", + "prohibited resuscitation measures with ddnr": "1. Cardiopulmonary Resuscitation (CPR).\n2. Endotracheal intubation or other advanced airway management. This does\nNOT include CPAP.\n3. Artificial ventilation.\n4. Defibrillation.\n5. Cardiac resuscitation medications.", + "encouraged comfort measures": "1. Airway (excluding intubation or advanced airway management).\n2. Suction.\n3. Supplemental oxygen delivery devices including CPAP.\n4. Pain medications or intravenous fluids.\n5. Bleeding control.\n6. Patient positioning.\n7. Other therapies deemed necessary to provide comfort care or to alleviate pain.", + "ddnr orders may be revoked by": "1. The patient, by destroying the EMS-DDNR form or alternate DNR form or by\nverbally withdrawing consent to the order.\n2. The authorized decision-maker for the patient.", + "revisions in the virginia ddnr vs ems dnr": "1. DDNR program, adopted by the Virginia State Board of Health, became\neffective on January 3, 2000. Once issued, the DDNR orders do not expire.\n2. DDNR forms may be honored in any facility, program or organization operated\nor licensed by the State Board of Health or by the Department of Mental Health,\nMental Retardation and Substance Abuse Services, or operated, licensed or\nowned by another state agency.\n3. DDNR orders can now be written for anyone, regardless of health condition or\nage. Inclusion of minors is a significant change in the emergency DDNR order.", + "alternate forms of ddnr identification": "1. DDNR bracelets and necklaces are available and can be honored in place of the\nVirginia Durable DNR Order form by emergency medical services providers.\nOnly approved necklaces or bracelets can be honored. These alternative forms\nof identification must have the following information:\na. Patient\u2019s full legal name.\nb. Durable DNR number from the Virginia DDNR form or a unique to the\npatient number that the vendor has assigned.\nc. The words \u201cVirginia Durable Do Not Resuscitate\u201d.\nd. The vendor\u2019s 24 hour phone number.\ne. The phys ician\u2019s name and phone number.\n2. MOLST ( Medical Orders for Life-Sustaining Treatment) and POLST\n(Physician Orders for Life-Sustaining Treatment) forms can be honored in\nplace of the Virginia Durable DNR Order form by emergency medical services\nproviders." + }, + { + "document title": "Administration", + "protocol title": "Minors", + "overview": "Pre-hospital providers are called to treat young patients and occasionally, there is no parent or other person responsible for the minor. Minors, in the eyes of the law, are generally considered to be incapable of self-determination; and therefore require parental or guardian consent for treatment / transport. That being said, generally one of three situations present: (1) Emancipated Minor ( Very rare), (2) A concept of Mature Minor emerges, or (3) the patient is a bona fide Minor.", + "guideline": "Whenever delay in providing medical or surgical treatment to a minor may adversely affect such minor\u2019s recovery and no person authorized in this section to consent to such treatment for such minor is available within a reasonable time under the circumstances, no liability shall be imposed upon qualified emergency medical services personnel as defined in \u00a7 32.1-111.1 at the scene of an accident, fire or other emergency, a licensed health professional, or a licensed hospital by reason of lack of consent to such medical or surgical treatment. However, in the case of a minor 14 years of age or older that is physically capable of giving consent, such consent shall be obtained first.1\n\nA pregnant minor shall be deemed an adult for the sole purpose of giving consent for herself and her child to surgical and medical treatment relating to the delivery of her child when such surgical or medical treatment is provided during the delivery of the child or the duration of the hospital admission for such delivery; thereafter, the minor mother of such child shall also be deemed an adult for the purpose of giving consent to surgical and medical treatment for her child.1\n\nAuthority of Parents, Guardians or Others : Parents have the authority to direct or refuse to allow treatment of their children. A court appointed guardian, and any adult person standing in loco parentis , also has the same authority. \u201cIn loco parentis\u201d is defined as \u201c[I]n the place of a parent; instead of a parent; charged, fictitiously, with a parent\u2019s rights, duties, and responsibilities.\u201d Black\u2019s Law Dictionary, 708 ( 5th ed. 1979). 1987 - 88 Va. Op. Atty. Gen. 617 \u201cFurthermore, I would point out that \u00a754 -325.2(6) allows any person standing \u201cin locos parentis\u201d to consent to medical treatment for a minor child. This signifies, in my judgment, an intent to allow any responsible adult person, who acts in the place of a parent, to consent to the treatment of a minor child, particularly in emergency situations.\u201d 1983 -84 VA. Op. Atty. Gen. 219 . Such a person may be a relative, schoolteacher or principle, school bus driver, baby-sitter, neighbor, or other adult person in whose care of the child has been entrusted.2\n\nIn situations where parental involvement is impractical or problematic, OR the patient is unconscious and/or lacks mental capacity to consent to care, the pre -hospital provider may treat and/or transport.", + "persons subject to policy under age 14": "A person that is under the age of 14 shall be treated and transported unless a parent or guardian or person in locos parentis advises otherwise. Do not delay treatment or transport for extended periods simply trying to contact a parent or guardian. If you believe that treatment is necessary, but the parent or guardian or person in locos parentis refuses to allow treatment, medical control should be consulted. 2", + "persons subject to policy aged 14 to 18": "A person between the ages of 14 and 18 may refuse treatment and transport, unless a parent or guardian or person in locos parentis advises otherwise. If you believe that treatment is necessary, but the person refuses, an attempt should be made to contact a parent or guardian, and medical control should be consulted. If you believe that treatment is necessary, but the parent or guardian or person in locos parentis refuses to allow treatment, medical control should be consulted.2", + "emancipation": "Emancipation is a court ordered decree. The circumstances under which a minor may petition for emancipation are as follows: A minor who has reached his / her sixteenth birthday and is residing in this Commonwealth, AND (i) the minor has entered into a valid marriage, whether or not that marriage has been terminated by dissolution; or (ii) the minor is on active duty with any of the armed forces of the United States of America; or (iii) the minor willingly lives separate and apart from his parents or guardian, with the consent or acquiescence of the parents or guardian, and that the minor is or is capable of supporting himself and competently managing his own financial affairs. If the courts determine that an emancipation order is appropriate and subsequently issues such order, the emancipated minor is legally able to consent to medical, dental, or psychiatric care, without parental consent, knowledge, or liability. Once emancipation has been granted by the courts, DMV issues identification indicating the emancipation degree, that identification should be readily available for your review.", + "consent mental capacity requirements": "In situations where the parent / guardian or emancipated minor possess sufficient mental capacity to formulate decisions regarding medical care / treatment, consent shall be obtained prior to initiating care. Mental capacity means that the individual rendering the consent, is informed and possesses sufficient ability to be able to understand: \n\u2022 The general nature of the injury / illness \n\u2022 Nature and purpose of proposed treatment \n\u2022 Risks and consequences of proposed treatment \n\u2022 Probability that treatment will be successful \n\u2022 Feasible treatment alternatives and have the ability to make a voluntary choice among the alternatives \n\u2022 Prognosis if treatment is not given", + "handling refusal of care": "In situations where the parent / guardian or emancipated min or demonstrates sufficient mental capacity to formulate decisions and subsequently refuses the offer of care; yet in the provider\u2018s judgment is in need of medical attention, the provider should first attempt to discern the reasons for the patients\u2019 refusal of consent. Often it is something so inconsequential, that reason and common sense often prevail and once you have provided assistance with whatever is the basis of concern (i.e., patient needs to call someone to look after a pet, etc) the patient often consents to treatment / transport. If unable to influence the parent / guardian or patient, contact on-line Medical Control for additional guidance.", + "pearls": "1. Always act in the best interest of the patient - EMS providers must strike a balance between abandoning the patient and forcing care.\n2. All states allow parental consent for treatment of a minor to be waived in the event of a medical emergency. The circumstances that should be present in order for such an emergency include the patient being incapacitated to the point of being unable to give an informed choice, the circumstances are life-threatening or serious enough that immediate treatment is required, and it would be impossible or imprudent to try to get consent from someone regarding the patient. In these cases, consent of the parent is presumed, since otherwise the minor would suffer avoidable injury.\n3. If a minor is injured or ill and no parent contact is possible, the provider should contact on-line Medical Control for additional instructions. \n4. Refer to the appropriate Pediatric Protocol sections and consider the following in regard to transport: \na. Transport conscious children with a parent unless it interferes with proper patient care. \nb. In cases of major trauma or cardiopulmonary arrest, exercise judgment in allowing parents to accompany the child in the ambulance .\nc. Allow the parent to hold and / or touch the child whenever possible and safe to do so. \nd. Both parent and child will respond best to open and honest dialogue." + }, + { + "document title": "Administration", + "protocol title": "Patient Destination", + "purpose": "To provide for a defined, consistent policy for the destination of ambulance patients consistent with quality patient care and regional medical protocols within the ODEMSA region this includes Planning Districts 13, 14, 15 and 19.", + "policy elements": "1. Stable patients should be transported to the patient\u2019s destination of choice if allowed by local EMS agency policies and by available resources .\n\n2. All unstable ambulance patients (resulting from requests for emergency assistance which result in transport) normally will be transported to the closest appropriate hospital emergency department unless otherwise directed by the on-line medical control physician and/ or by medical control during a declared diversion. The closest appropriate hospital is defined as the hospital closest to the location of the patient that can provide the level of care needed by the patient . The medical control physician is defined as the attending emergency department physician at the hospital contacted by the ambulance Attendant -in-Charge (AIC) or a person designated by the AIC. Medical C ontrol Hospital is defined as that hospital designated to direct ambulance movements in line with ODEMSA\u2019s Hospital Diversion Policy as most recently revised. \n\n3. Patients who meet certain criteria as severe trauma patients, as defined in the Old Dominion EMS Alliance Trauma Care System Plan, usually will be transported directly to a T rauma Center unless redirected by the M edical Control Physician in accordance with the Trauma Care System Plan.\n\n4. Individual EMS agencies and/or EMS systems are responsible for determining operational policies related to the most effective ambulance deployment and utilization patterns. This may include policies allowing transport of stable patients to hospitals of the patient\u2019s choice. \n\n5. In mass casualty incident (MCI) situations, the current Central Virginia Mass Casualty Incident Plan and its EMS Mutual Aid Response Guide, as most recently revised, will govern patient transportation and hospital destination(s). \n\n6. Other policies and protocols related to patient transport and ambulance- to-hospital communications are defined in the ODEMSA Pre- hospital Patient Care Protocols and the Hospital Diversion Policy as most recently revised." + }, + { + "document title": "Administration", + "protocol title": "Cease Resuscitation", + "overview": "Prehospital termination of resuscitation guidelines have been developed by the Ontario Prehospital Life Support (OPALS) study group. In their BLS prediction rule, EMT with defibrillation capabilities could consider patients with the following for termination of resuscitation: 1. No return of spontaneous circulation prior to transport 2. No shock was given 3. The arrest was not witnessed by EMS personnel. In applying the BLS rule 37.4% of the cardiac arrest cases would have been transported. There were a very small number of cases of survival to hospital discharge in patients who the BLS rule would have recommended termination of resuscitation. The OPALS group developed a more conservative ALS prediction rule in which providers could consider patients with the following for termination of resuscitation: 1. No return of spontaneous circulation prior to transport 2. No shock was given 3. The arrest was not witnessed by EMS personnel 4. The arrest was not witnessed by bystander 5. No bystander CPR. If CPR has been initiated and circumstances arise where the pre-hospital provider believes resuscitative efforts may not be indicated, cease resuscitation orders may be requested via on-line medical control.", + "indications for not initiating cpr": "Under existing Virginia EMS practice standards, prehospital providers should initiate cardiopulmonary resuscitation (CPR) on all patients without vital signs UNLESS the patient presents with one or more of the following conditions: a. Decapitation b. 100% full thickness burn (incineration) c. Putrefied, decayed, or decomposed body d. Advanced lividity e. Rigor mortis f. Obvious mortal wounds, i.e. crushing injuries to head and/or chest g. A valid state of Virginia EMS_DDNR approved order h. Asystole as a presenting rhythm in an unwitnessed arrest.", + "criteria for requesting cease resuscitation orders after cpr initiated": "The provider should confirm that the patient is pulseless and apneic. Prior to contacting medical control, the following criteria should be met: a. No return of spontaneous circulation prior to transport b. No shock was given or indicated c. The arrest was not witnessed by EMS personnel d. The arrest was not witnessed by bystander e. No bystander CPR f. 15 minutes of CPR g. ETCO 2 is less than 10.", + "special considerations": "Patients who are hypothermic or who are victims of cold water drownings should receive appropriate resuscitative efforts. Patients with electrical injuries, including those struck by lightning, may initially be tetanic, or stiff, and should receive appropriate resuscitative efforts.", + "procedure for ceasing resuscitation": "1. Once all prerequisites have been met, the provider should then contact Medical Control so that the on-line physician can decide to continue or stop resuscitative efforts. Providers should begin contact with Medical Control with the statement: \"This is a potential cease- resuscitation call.\u201d The provider should review why resuscitative efforts may not be indicated (i.e., end-stage cancer). The provider then should report interventions and, if directed by on-line Medical Control, stop resuscitative efforts. 2. If a patient is determined to be dead on the scene (DOA) or if the cessation of resuscitative efforts is authorized by on-line Medical Control, law enforcement authorities should be requested to respond if indicated. 3. Document specific findings, such as signs of death, on the ePCR form. Include name of physician who ordered resuscitation efforts ended and log the time of the order. 4. Be attentive to the emotional needs of the patient's survivors when dealing with them. If possible, leave survivors in the care of family and / or friends." + }, + { + "document title": "Administration", + "protocol title": "Patient Refusal", + "overview": "If a patient (or the person responsible for a minor patient) refuses secondary care and / or ambulance transport to a hospital after pre-hospital providers have been called to the scene, the following procedures should be completed:", + "definition adult": "A person at least eighteen (18) years of age.", + "definition minor": "A person less than eighteen (18) years of age.", + "definition emancipated minor": "A person under the age of eighteen (18) is emancipated if any of the following conditions met:\na. Married or previously married\nb. On active military duty\nc. Has received a declaration of emancipation from the Commonwealth of Virginia", + "definition mental capacity": "A person who is alert, oriented, and has the capacity to understand the circumstances surrounding their illness or impairment, and the possible risks associated with refusing treatment and / or transport. The patient\u2019s judgment is also not significantly impaired by illness, injury or drugs / alcohol intoxication. Patients who have attempted suicide, verbalized suicidal intent, or if other factors lead pre-hospital care personnel to suspect suicidal intent, should not be regarded as having capacity and may not decline transport to a medical facility.", + "protocol for management": "1. Complete an initial assessment and complete set of vital signs of the patient, with particular attention to the patient\u2019s neurological status.\n2. Determine the patient\u2019s capacity to make a valid judgment concerning the extent of their illness or injury. If the provider has doubts about whether the patient is competent to refuse, the provider should contact on-line medical control.\n3. Clearly explain to the patient and all responsible parties the possible risks and / or overall concerns with regards to refusing care.\n4. Perform appropriate medical care with the consent of the patient.\n5. Complete an ePCR form, clearly documenting the initial assessment findings and the discussions with all involved persons regarding the possible consequences of refusing additional pre-hospital care and/or transportation. A third party should witness the form and discussion. If no such party is available then a second EMS provider should witness this.\n6. After the form has been completed, have the patient or the person responsible for a minor patient sign the refusal form provided on the ePCR form. This procedure should be witnessed by at least one other individual.\n7. Any person who calls for any type of assistance should have a refusal form completed unless, upon evaluation, the caller denies any injury or illness and none is suspected. This includes motor vehicle accidents. Furthermore, a refusal should always be completed if the original caller was the complainant (1st party), as a complaint originally existed prior to EMS arrival.", + "pearls": "1. An adult or emancipated minor, who has demonstrated possessing sufficient \u201cmental capacity\u201d for making decisions, has the right to determine the course of their medical care, including the refusal of care. These patients must be advised of the risks and consequences resulting from refusal of medical care.\n2. All patients, under the age of 14 years, must have a parent or legal representative to refuse evaluation, treatment, and / or transport for an emergency condition. In Virginia, patients 14 years of age or older can refuse treatment and transport (see protocol for Minors).\n3. A patient determined by EMS personnel or On-line Medical Control to lack \u201cmental capacity\u201d may not refuse care against medical advice or be released at scene. Mental illness, drugs, alcohol intoxication, or physical/mental impairment may significantly impair a patient\u2019s capacity. Patients who have attempted suicide, verbalized suicidal intent, or if other factors lead EMS personnel to suspect suicidal intent, should generally, not be regarded as having demonstrated sufficient \u201cmental capacity.\n4. At no time, should EMS personnel put themselves in danger by attempting to treat and / or transport a patient who refuses care.", + "source organization": "Created, Developed, and Produced by the Old Dominion EMS Alliance" + }, + { + "document title": "Administration", + "protocol title": "Documentation", + "overview": "Under existing Virginia law, all licensed emergency medical services agencies are\nrequired to \u201cparticipate in the pre-hospital patient care reporting procedures by making\navailable \u2026 the minimum data set on forms .\u201d Licensed EMS agencies, pre -hospital\nproviders and the Commonwealth of Virginia are required to keep patient information\nconfidential.", + "protocol for management": "1. An electronic patient care report (ePCR) will be completed for each patient\n encounter. The report must be completed and sent to the appropriate facility\n within the following 12 hours. ODEMSA, at the request of the region, has\n developed a MIVT report for documenting patient care to assist the hospital\n between the time when the patient is delivered to the ED and when the patient\n care report is received. A copy of the MIVT is included in these protocols.\n2. Each ePCR will include documentation of:\n a. The evaluation and care of the patient during pre-hospital care.\n b. The patient\u2019s refusal of the evaluation. \n c. The patient\u2019s encounter to protect the local EMS system and its personnel\n from undue risk and liability.\n3. A patient is defined as any individual that requests evaluation by EMS. If an\n individual is not legally competent due to age, injury, chronic illness, intoxication,\n etc., always err on the side of patient safety and assume an implied request for\n evaluation.\n4. All patient encounters, which result in some component of an evaluation, must\n have an ePCR completed.\n5. All patients who refuse any component of the evaluation or treatment, should\n have a refusal signed and documentation of the refusal noted in the narrative.\n6. All patients who are not transported by EMS should have a refusal completed.\n7. When utilized effectively, the ePCR allows great detail in documentation by using\n the pre-loaded information coupled with notes. However, this does not eliminate\n the need for a narrative to be completed. No ePCR will be considered complete\n without a written narrative that \u201cpaints\u201d an accurate picture of the scene, patient\n presentation, and all occurrences during the interaction with that patient.\n8. When a patient is transported, a copy of the MIVT report should be left at the\n receiving hospital. Also, some facilities have printing capability and providers\n can print ePCRs before leaving the facility. It is imperative that reports are\n completed and uploaded in a timely manner as these reports may influence the\n patient\u2019s care at the receiving facility and will be placed in the patient\u2019s\n permanent medical record once received." + }, + { + "document title": "Administration", + "protocol title": "Diversion", + "contraindications": "Patients with STEMI, Acute Stroke, Airway Obstruction, Uncontrolled Airway, \nUncontrolled Bleeding, who are in Extremis or with CPR in progress, should be taken \nimmediately to the closest appropriate hospital , without regard to the hospital\u2019s diversion \nstatus.", + "diversion override decisions": "Prehospital EMS providers may overrule diversion if a patient is in extremis, or for \nsignificant weather / traffic delays, mechanical problems, etc. An EMS provider who \nbelieves an acute decompensation is likely to occur if the patient is diverted to a more \ndistant hospital ALWAYS has the option to take that patient to the closest Emergency \nDepartment regardless of the diversion status.", + "note ems communication and patient care": "Early c ontact and notification by the EMS ambulance crew to the \nreceiving facility is essential for optimal patient care. It is highly \nrecommended that the ambulance Attendant in Charge (AIC) use the regional \nMIVT Report format when providing the receiving facili ty with pre -arrival \ninformation on the patient. Once an EMS unit has marked enroute and a \nreport has been given to the receiving facility, any later change in diversion \nstatus of the receiving facility will not affect that ambulance. \n\nThe Attendan t-in-Charge also has the option to ask via radio or \nphone to speak directly to an Emergency Department physician. \nGood clinical sense and optimal patient care are the ultimate \nconsiderations.", + "categories of hospital status": "A. OPEN - When a hospital has full capacity for receiving its usual patient \nload. \n\nB. DIVERSION \u2013 When a hospital is unable to handle certain types of patients. \nSubcategories are listed below. \n\n1. Adult Medical / Surgical \u2013 includes Minor Trauma . \n2. Major Trauma \u2013 means the operating rooms and surgeons are \ncompletely full. Reference: Trauma Triage Schematic \u2013 Appendix E. \n3. Labor & Delivery (L & D) \u2013 Pre-Term is defined as active labor \nbefore 36 weeks. \n4. Psychiatric \u2013 divided into three areas: \na) Child & Adolescent Psych \u2013 age infant < 18 \nb) Adult Psych \u2013 age 18 to 64 \nc) Geriatric Psych \u2013 age 65 and over \n5. Pediatric \u2013 For the purposes of this Hospital Diversion Policy , \npediatric is defined as under the age of 18. \n\nC. OUT OF SERVICE - Critical or catastrophic circumstances result in \noperational shutdown. Hospital cannot receive any new patients by EMS \nor any other means.", + "medical control hospital details": "The primary Medical Control Hospital will be the Virginia \nCommonwealth University Medical Center, or an identified \nalternate facility, as specified in the Central Virginia MCI \nPlan. If VCU cannot handle Medical Control, the identified \nalternate facilities, in order, are : (1) Chippenham Medical \nCenter and (2) Southside Regional Medical Center." + }, + { + "document title": "Administration", + "protocol title": "Mass Gathering", + "scope": "This policy and its related protocol are intended for use only in gatherings of\nlarge numbers of persons such as races, concerts and rallies, and in those\ncircumstances / situations approved by the EMS Agency\u2019s operational medical\ndirector (OMD). It is designed to give clear patient care guidelines to EMS\nproviders in the ODEMSA region, and allow them the option of treating patients\nwith minor injuries and / or medical complaints without transporting patients to a\nmedical facility. The OMD must approve the use of this policy for each event\nbefore it is implemented.\n\nIt is intended for use only when the number of anticipated patients could quickly\noverwhelm existing EMS or hospital resources to provide appropriate patient\ncare. This policy will apply to any patient that meets the patient profile (below)\nthat requires basic first aid only.\n\nEMS providers are expected to use good clinical judgment and complete\ndocumentation. Providers may transport any patient to a medical facility\nregardless of the patient\u2019s chief complaint, presenting symptoms, or clinical\nassessment according to ODEMSA Prehospital Patient Care Protocols.\n\nAny patient, who asks to be transported to a medical facility, even if the EMS\nprovider feels that the patient could be treated and released under this policy, will\nbe transported.\n\nAny patient, for whom the E911 System has been appropriately activated, may\nbe transported to the hospital for further evaluation.", + "patient profile (those patients who may be treated with this protocol)": "A. Patient history and examination will be reliable:\n1. Alert and oriented x 3\n2. No suggestion of drug, alcohol or other substance\nusage/abuse\n3. No suggestion of psychological/psychiatric problems\n4. No head injury (including loss of consciousness or\naltered mental status)\n5. Patient is able to communicate adequately and to\nunderstand what is being communicated to him/her\nB. Injuries sustained where mechanism of injury is very low risk for\nsignificant injury.\nC. Patient has no spinal injury, pain, tenderness or deformity on\nexam, and has a normal sensory/motor exam.\nD. Patient does not exhibit signs of chest pains or shortness of\nbreath.\nE. Patient will have vital signs within age specific normal limits.", + "general exclusion criteria": "A. Any patient with a pain scale assessment higher than a \u201c5\u201d on a 1 to 10 scale\nB. Any patient who does not meet all requirements in the Patient Profile section\nC. Any patient who requests transportation to a medical facility\nD. Any patient for whom the E911 System has been appropriately activated", + "indications and treatments": "Minor complaints / injuries may include the following, but are not limited to:\n\n12 - 12A: Minor Wounds\nIndications:\nAny minor injury requiring simple wound disinfection and bandage application:\nContraindications:\na. Any signs or symptoms of infection (redness, swelling, fever, drainage)\nb. Any wound to facial area, unless it is a simple abrasion\nc. Any deep, jagged or gaping wound\nd. Any uncontrolled bleeding from the wound\ne. Any wound exposing subcutaneous tissue / structure\nA. Any patient with a pain scale assessment higher than a \u201c5\u201d on a 1 to 10 scale\nB. Any patient who does not meet all requirements in the Patient Profile section\nC. Any patient who requests transportation to a medical facility\nD. Any patient for whom the E911 System has been appropriately activated\n1. Perform a general assessment.\n2. Clean abrasions, simple avulsions and small lacerations\nnot requiring suturing with normal saline.\n***Note: ensure that the patient has had Tetanus Toxoid immunization within the last\nfive (5) years. If not current, the patient must be referred within 72 hours from the\nincident to his/her own physician. ***\n\n12 - 12B: Request for over the counter medications for c/o headache or\nsimple muscle type pain\nIndications:\nRequest for over the counter medications for c/o headache, or simple muscle\ntype pain\nContraindications:\na. Any neurological deficits with headache\nb. Any history of allergies to approved medications\nc. Any request for ASA for complaint of chest pain (These patients must\nbe referred to the hospital for further evaluation. ASA may be given\nunder the ALS protocol for chest pain)\nd. Any patient requesting ASA or Ibuprofen with a history of asthma\n1. Perform a general patient assessment.\n2. Assess patient for allergies.\n3. Administer Tylenol, Ibuprofen, or ASA as requested by\nthe patient per manufacturer dosage recommendation.\n\n12 - 12C: Soft Tissue Injury without signs or symptoms of a fracture\nIndications:\nSoft tissue injury without signs or symptoms of a fracture\nContraindications:\na. Any signs or symptoms of a fracture (deformity, excessive swelling,\ndiscoloration, any open wounds over the site, or decreased range of\nmotion)\nb. Any neurological deficits (numbness or tingling distally, delayed\ncapillary refill, or decreased pulses distally)\nc. Any severe pain or swelling requiring splinting\nd. Any injury associated with vascular deficits distal to the injury\n1. Perform a general assessment.\n2. Elevate the affected area and apply a cold / ice pack.\n3. Provide education on removal of cold pack within 20\nminutes of placement.\n\n12 - 12D: Insect Stings\nIndications:\nAny patient with an insect sting\nContraindications:\na. Any patient with a history of allergies to insect stings\nb. Any insect sting on the face or neck\nc. Any patient that exhibits signs of respiratory distress, tightness in throat\nor chest, dizziness, rash, fainting, nausea / vomiting, or difficulty\nswallowing\nd. Any swelling of the face, lips or eyelids\ne. Hypotension\nf. Presence of hives or other obvious symptoms of a more generalized\nallergic reaction\n1. Perform a general assessment.\n2. Assess patient for previous allergies to bee stings.\n3. Remove the stinger by scraping with a blunt edged\nobject. Do not remove with tweezers as squeezing may\nrelease more of the poison into the surrounding tissue.\n4. Wash the area thoroughly with soap and water.\n5. Monitor airway for allergic reaction / swelling.\nNOTE: Stingers NOT removed will continue to release venom into the tissue for a long\nas 20 minutes.\n\n12 - 12E: Tick Bites\nIndications:\nAny patient with a tick bite\nContraindications:\na. Any tick that appears to have been embedded for longer than 24 hours\nb. Any signs or symptoms of infection present\nc. If the tick does not appear to have been removed whole and the head\nremains embedded in the skin, the patient must be sent to a physician\nor medical facility that day\n1. Perform a general assessment.\n2. Remove the tick gently by using tweezers to grasp the\ntick firmly at its head, next to the patient\u2019s skin. Pull\nfirmly and steadily on the tick until it lets go.\n3. Swab the bite with alcohol.\n4. Inspect the tick to ensure that the head has been\nremoved successfully.\n5. Educate patient on signs / symptoms of Lyme Disease\n(bull\u2019s eye rash, fever, headache, joint pain) and Rocky\nMountain Spotted Fever (purple to red rash on trunk and\nextremities, fever and headache).\n\n12 - 12F: Minor Animal Bite\nIndications: Minor Animal Bites\nAny patient with a minor animal bite\nContraindications:\na. Any facial involvement\nb. Any wound that will not stop bleeding after 15 minutes of direct pressure\nc. The attacking animal was wild or behaving strangely\nd. Animal immunization status is unknown, or the animal cannot be found\n1. Perform a general assessment.\n2. Wash the area of the bite carefully with soap and water.\n3. Apply antibiotic cream and a sterile dressing.\n4. Ensure that the patient has had Tetanus Toxoid\nimmunization within the last five (5) years.\n***NOTE: If not current with Tetanus immunization, the patient must be referred within\n72 hours from the incident to his / her own physician.***\n5. Report bite (as required under State and local laws) to\neither local animal control or the local health department.\nIf possible to do so without endangering anyone, detain\nor take steps to identify the biting animal. If the animal is\ndeceased, the carcass should be immediately turned\nover to animal control.\n6. Refer the patient to their primary care physician for\nfollow up treatment because the risk of infection needs\nto be closely monitored.\n\n12 - 12G: Non-traumatic Nose Bleeds\nIndications:\nNon-traumatic nose bleeds\nContraindications:\na. Any medical causes ( i.e., hypertension, history of hemophilia )\nb. Currently on blood thinner medication\nc. Bleeding uncontrolled for longer than 10 minutes after treatment\nd. Any nosebleed caused by a direct traumatic injury\n1. Perform a general assessment (rule out any medical\ncauses).\n2. Lean the patient slightly forward to avoid swallowing\nblood.\n3. Apply firm pressure below the bony part of the nose for\n10 minutes.\n4. Reassess. If bleeding continues, transport to a medical\nfacility.\n\n12 - 12H: 1st Degree Burns\nIndications:\n1st degree burns\nContraindications:\na. Any 2nd or 3rd degree burns\nb. Any burns to the face, eyes, mouth, hands, or genital areas\nc. Any burn too large to cover with a bandage\nd. Any burn caused by electricity or an explosion\n1. Perform a general assessment.\n2. Run cool water over the burned area or hold a cold\ncompress on the burn. Do NOT use ice.\n3. Cover loosely with a sterile bandage.\n4. Offer extra fluids.\n\n12 - 12I: Eye Irritation / FB on the surface of the eye\nIndications:\nEye irritations\nContraindications:\na. Any embedded foreign body\nb. Any eye irritation due to chemical exposure\nc. Any eye irritation due to trauma\n1. Perform a general assessment.\n2. Flush the affected eye with sterile saline solution. Flush\nfor up to 15 minutes, checking the eye every five (5)\nminutes to see if the foreign body has been flushed out.\n3. Encourage the patient not to touch or rub the affected\neye.\n4. If the foreign material cannot be removed by flushing, or\nthe eye remains irritated after flushing, transport to a\nmedical facility.\n\n12 - 12J: Splinter Removal\nIndications:\nSplinter Removal\nContraindications:\na. If the splinter is too large or went deeply into the skin\nb. Any signs of infection\nc. If the splinter is unable to be removed\n1. Perform a general assessment.\n2. Remove the splinter from the skin by pulling at the same\nangle that it entered with a pair of tweezers.\n3. Wash with soap and water.\n4. Apply antibiotic ointment and a sterile dressing.\n5. If a splinter is not easily removed, refer the patient to a\nphysician for removal.\n\n12 - 12K: Heat Exhaustion / Heat Cramps (heat related illness)\nIndications:\nHeat exhaustion / cramps (heat related illness)\nContraindications:\na. Heat stroke (a life threatening condition where the body loses the\nability to regulate its own temperature). Signs and symptoms\ninclude:\ni. Hot, red, dry skin, but NOT sweaty\nii. Confusion, delirium, hallucinations\niii. Seizures\niv. Syncopal episode\nv. Frequent uncontrolled vomiting\nvi. Difficulty breathing\nvii. Elevated internal body temperature (>103\u00b0)\nb. Patients experiencing the above symptoms should be rapidly\ncooled, an IV of NS established, and transported immediately to\nthe closest emergency department (See ODEMSA protocol\nHyperthermia / Heat Stroke )\nc. Any patient with complaint of chest pains or dyspnea\nd. Any patient with a BP < 90mmHg systolic\ne. Any patient over the age of 70, or under the age of 13\n1. Perform a general assessment.\n2. Place patient in a cool area to rest.\n3. Exam Remove any excess clothing.\n4. Sponge the patient\u2019s skin with cool water. Consider the\nuse of fans, if available, to aid in the cooling process.\n5. Apply cold packs to the forehead and / or back of neck.\nConsider the application of these packs to the axillae\nand groin to further enhance the cooling effects in\nseverely symptomatic patients.\n6. Provide cold water for drinking.\n7. Initiate IV fluid bolus for patients with persistent\nsymptoms, despite above cooling efforts Bolus with 250\n- 500 cc over 10 - 20 minutes.\n8. Reevaluate symptoms. Repeat once as needed.\n9. Appropriately document findings. Patients who show\nsignificant improvement with cessation of symptoms may\nbe released.\n10. Provide the patient with education related to prevention\nof future heat related illness and / or symptoms.\n11. Patients will be transported to a medical facility\nimmediately for symptoms that persist after a total of one\n(1) liter of normal saline.\n12. Patients will be transported to a medical facility\nimmediately for symptoms which persist for more than\none (1) hour despite treatment.", + "patient assessment and documentation": "A. Documentation is required for each patient and should be done on\na PPCR, ODEMSA Treat and Release for Minor Injuries form, or\nother locally developed form. This form, when complete, will\ninclude:\n1. Chief complaint\n2. Vital signs (including pain scale)\n3. Primary assessment with particular attention to the\npatient\u2019s neurological status\n4. Clinical assessment\n5. Treatment rendered\n6. Education of follow up care\nB. Providers\u2019 assessment skills should be renewed and reviewed on\na regular basis.", + "patient referrals": "In all cases where patients are treated and released under this policy and\nprotocol, there will be clear documentation and explanation to the patient or\nresponsible party of the absolute need for the patient to be reevaluated by the\npatient\u2019s own physical or medical facility of choice for definitive medical care.\n\nThis policy and protocol is not intended to provide definitive care to any patient.\nRather, it is intended to provide a mechanism by which basic first aid may be\nadministered acutely, with physician follow up at the patient\u2019s earliest\nconvenience.", + "performance improvement": "It is recommended that participating agency\u2019s quality assurance / performance\nimprovement policy stipulate that both during and upon completion of each event\nwhere the use of the Treat and Release Patient Care Policy and Protocol has\nbeen authorized, the OMD conduct a random review of the charts generated for\nthe appropriateness of documentation, treatment and disposition of the patient.\nThe sample size should be large enough to assure that appropriate care by all\nproviders is being rendered.", + "reporting": "It is recommended that clinical / performance improvement or administrative\nissues regarding the mass gathering guideline be reported back to the ODEMSA\nMedical Control Committee for quality assurance and performance improvement\npurposes." + } +] \ No newline at end of file