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Chest pain
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Chest pain
Synonym
Pectoralgia, stethalgia, thoracalgia, thoracodynia
Potential location of pain from a heart attack
Specialty
Emergency medicine, internal medicine
Types
Cardiac, noncardiac
Chest pain is pain in any region of the chest. Chest pain may be a symptom of a number of serious disorders and is, in general, considered a medical emergency. Chest pain can be differentiated into heart-related and non heart related chest pain.[1][2][3] Cardiac chest pain is called angina pectoris. Some causes of noncardiac chest pain include gastrointestinal, musculoskeletal, or lung issues.[4] Even though chest pain may not be related to a heart problem, noncardiac chest pain can still be due to significant disease.[3] Chest pain can present with different types of pain and associated symptoms which may vary with a person's age, sex, and previous medical conditions.[1] Determining the cause of chest pain is through review of a person's medical history, a physical exam, and other medical tests.[1][4] Management of chest pain is based on the underlying cause.[1][4]
Chest pain is a common presenting problem:
In the United States, an estimated 6-8 million people per year present to the emergency department with chest pain.[4][1]
An estimated 50-70% of patients presenting with chest pain in the emergency department will be placed in an observation unit or admitted to the hospital.[1]
2 million people are admitted annually for workup of acute coronary syndrome (ACS).[5]
Approximately 8 billion dollars are used annually to evaluate complaints of chest pain.[3]
Children with chest pain account for 0.3% to 0.6% of pediatric emergency department visits.[6]
Contents
[hide]
1 Presentation
2 Differential diagnosis
2.1 Cardiovascular
2.2 Respiratory
2.3 Gastrointestinal
2.4 Chest wall
2.5 Psychological
2.6 Others
3 Diagnostic approach
3.1 History taking
3.2 Physical examination
3.3 Clinical risk scores
3.4 Medical tests
4 Management
4.1 Prehospital care
4.2 Hospital care
4.3 Outpatient care
5 Epidemiology
6 References
7 External links
Presentation[edit]
Chest pain may present in different ways depending upon the underlying diagnosis. Chest pain may also vary from person to person based upon age, sex, weight, and other differences.[1] Chest pain may present as a stabbing, burning, aching, sharp, or pressure-like sensation in the chest.[4][1] Chest pain may also radiate, or move, to several other areas of the body. This may include the neck, left or right arms, cervical spine, back, and upper abdomen.[7] Other associated symptoms with chest pain can include nausea, vomiting, dizziness, shortness of breath, anxiety, and sweating.[4][1] The type, severity, duration, and associated symptoms of chest pain can help guide diagnosis and further treatment.
Differential diagnosis[edit]
Causes of chest pain range from non-serious to serious to life-threatening.[8]
In adults the most common causes of chest pain include: gastrointestinal (42%), coronary artery disease (31%), musculoskeletal (28%), pericarditis (4%) and pulmonary embolism (2%).[9] Other less common causes include: pneumonia, lung cancer, and aortic aneurysms.[9] Psychogenic causes of chest pain can include panic attacks, however, this is a diagnosis of exclusion.[10]
In children, the most common causes for chest pain are musculoskeletal (76-89%), exercise-induced asthma (4-12%), gastrointestinal illness (8%), and psychogenic causes (4%).[11] Chest pain in children can also have congenital causes.
Cardiovascular[edit]
A blockage of coronary arteries can lead to a heart attack
Acute coronary syndrome
Stable or unstable angina
Myocardial infarction ("heart attack") - People usually complained of a pressure or squeezing sensation over the chest.[1] Other associated symptoms are: excessive sweating, nausea, vomiting, and weakness.[1] Chest pain is more commonly associated with anterior infarction because of left ventricular impairment; inferior infarction is more commonly associated with nausea, vomitng, and excessive sweating due to irritation of vagus nerve; lateral infarction is associated with left arm pain.[12]
Prinzmetal's angina - Chest pain is caused by coronary vasospasm. More common in women younger than 50 years. Person usually complain of chest pain at rest. It may occur early in the morning which awaken person from sleep.[12]
Cocaine abuse - This condition is suspected when a person with few or no risk of arteriosclerosis presented with non-traumatic chest pain. Ingestion of cocaine can cause vasoconstriction of coronary arteries, thus producing chest pain similar to heart attack. Symptoms can appear within one hour of cocaine use.[12]
Aortic stenosis - This condition happens when the person has underlying congenital bicuspid valve, aortic sclerosis, or history of rheumatic fever. Chest pain usually happens during physical activity. Syncope is a late symptom. Signs and symptoms of heart failure may also present. On auscultation, loud ejection systolic murmur can be best heard at the right second intercostal space and radiates to the carotid artery in the neck. Splitting of second heart sound is heard in severe stenosis.[12]
Hypertrophic cardiomyopathy - It is the hypertrophy of interventricular septum that causes outflow obstruction of left ventricle. Dyspnea and chest pain commonly occurs during daily activities. Sometimes, syncope may happen. On physical examination, significant findings include: loud systolic murmur and palpable triple apical impulse due to palpable presystolic fourth heart sound.[12]
Aortic dissection is characterized by severe chest pain that radiates the back. It is usually associated with Marfan's syndrome and hypertension. On examination, murmur of aortic insufficiency can be heard with unequal radial pulses.[12][13]
Pericarditis - This condition can be the result of viral infection such as coxsackie virus and echovirus, tuberculosis, autoimmune disease, uremia, and after myocardial infarction (Dressler syndrome). The chest pain is often pleuritic in nature (associated with respiration) which is aggravated when lying down and relieved on sitting forward, sometimes, accompanied by fever. On auscultation, pericardial friction rub can be heard.[12]
cardiac tamponade
Arrhythmia - atrial fibrillation and a number of other arrhythmias can cause chest pain.
Myocarditis
Mitral valve prolapse syndrome - Those affected are usually thin females presented with chest pain which is sharp in quality, localized at the apex, and relieved when lying down. Other symptoms include: shortness of breath, fatigue, and palpitations. On auscultation, midsystolic click followed by late systolic murmur can be heard, louder when person is in standing position.[12]
Aortic aneurysm
Respiratory[edit]
Bronchitis
Pulmonary embolism - Common signs and symptoms are shortness of breath, pleuritic chest pain, blood in sputum during cough (haemoptysis), and lower limb swelling. Risk factors includes: recent surgery, malignancy, and bedridden state. Source of embolus usually comes from venous thromboembolism.[12]
Pneumonia
Hemothorax
Pneumothorax - Those who are at a higher risk of developing pneumothorax are tall, thin, male smoker who had underlying lung diseases such as emphysema. Those affected can have a sharp chest pain which radiates to the shoulder of the same side. Physical examination revealed absent breath sounds and hyperresonance on the affected side of the chest.[12]
Pleurisy - an inflammation that can cause painful respiration
Tuberculosis
Tracheitis
Lung malignancy
Gastrointestinal[edit]
GERD is a common cause of chest pain in adults
Gastroesophageal reflux disease (GERD) - The pain is aggravated when lying down or after meals. Persons may describe this as a heartburn. Besides, they may also complain of tasting bitter contents from the stomach.[12]
Achalasia, nutcracker esophagus, and other motility disorders of the esophagus
Diffuse esophageal spasm - Unlike cardiac chest pain, esophageal pain is not related to activity. The pain is usually associated with swallowing of hot or cold water.[12]
Esophageal rupture - Those affected usually complained of sudden, severe, and constant pain that starts from the neck to the upper abdomen. The pain is aggravated by swallowing. On examination, neck swelling and crepitations can be felt due to subcutaneous emphysema as free air is entering from esophagus into the subcutaneous tissue.[12]
Esophagitis - There are many causes of esophagitis. Esophagitis caused by Candida albicans is usually found in chemotherapy or HIV patients. Medication such as nonsteroidal anti-inflammatory drug (NSAIDs) and alendronate can induce esophagitis if not swallowed properly.[12]
Functional dyspepsia
Hiatus hernia
Jackhammer esophagus
Acute cholecystitis - Characterized by positive Murphy's sign where the person had a cessation of inhalation when the doctor placed his finger at the right subcostal region of the abdomen.[12]
Acute pancreatitis - History of alcohol abuse, cholelithiasis (stones in the gallbladder), and hypertriglyceridemia are risk factors for pancreatitis. It is a constant, boring pain in the upper abdomen.[12]
Perforated peptic ulcer - Sudden onset of severe pain in the upper abdomen which later developed into peritonitis (inflammation of tissues that lines the abdominal organs).[12]
Chest wall[edit]
Costochondritis or Tietze's syndrome - an inflammation of costochondral junction. Any movements or palpation of the chest can reproduce the symptoms.[12]
Spinal nerve problem
Fibromyalgia
Chest wall problems
Radiculopathy
Precordial catch syndrome - another benign and harmless form of a sharp, localized chest pain often mistaken for heart disease
Breast conditions
Herpes zoster commonly known as shingles - It is usually described as a burning sensation over the chest in a unilateral dermatome distribution. However, diagnosis can be difficult because the pain usually appears before the characteristic rash is visible.[12]
Tuberculosis
Osteoarthritis
Bornholm disease
Psychological[edit]
Panic attack - Chest pain is a common symptom of panic attacks, with as high as 78% of persons describing chest pain with their worst panic attacks.[10] Overall chest pain is a symptom of up to 48% of sudden-onset panic attacks, and 10% of gradual-onset panic attacks.[10]
Anxiety
Clinical depression
Somatization disorder
Hypochondria
Others[edit]
Hyperventilation syndrome often presents with chest pain and a tingling sensation of the fingertips and around the mouth.
Da costa's syndrome
Carbon monoxide poisoning
Sarcoidosis
Lead poisoning
Prolapsed intervertebral disc
Thoracic outlet syndrome
Adverse effect from certain medications
Diagnostic approach[edit]
History taking[edit]
Knowing a person's risk factors can be extremely useful in ruling in or ruling out serious causes of chest pain. For example, heart attack and thoracic aortic dissection are very rare in healthy individuals under 30 years of age, but significantly more common in individuals with significant risk factors, such as older age, smoking, hypertension, diabetes, history of coronary artery disease or stroke, positive family history (premature atherosclerosis, cholesterol disorders, heart attack at early age), and other risk factors. Chest pain that radiates to one or both shoulders or arms, chest pain that occurs with physical activity, chest pain associated with nausea or vomiting, chest pain accompanied by diaphoresis or sweating, or chest pain described as "pressure," has a higher likelihood of being related to acute coronary syndrome, or inadequate supply of blood to the heart muscle, but even without these symptoms chest pain may be a sign of acute coronary syndrome.[14] Other clues in the history can help lower the suspicion for myocardial infarction. These include chest pain described as "sharp" or "stabbing", chest pain that is positional or pleuritic in nature, and chest pain that can be reproduced with palpation.[15][16] However, both atypical and typical symptoms of acute coronary syndrome can occur, and in general a history cannot be enough to rule out the diagnosis of acute coronary syndrome.[16] In some cases, chest pain may not even be a symptom of an acute cardiac event. An estimated 33% of persons with myocardial infarction in the United States do not present with chest pain, and carry a significantly higher mortality as a result of delayed treatment.[17]
Physical examination[edit]
Careful medical history and physical examination is essential in separating dangerous from trivial causes of disease, and the management of chest pain may be done on specialized units (termed medical assessment units) to concentrate the investigations. Occasionally, invisible medical signs will direct the diagnosis towards particular causes, such as Levine's sign in cardiac ischemia.[18] However, in the case of acute coronary syndrome, a third heart sound, diaphoresis, and hypotension are the most strongly associated physical exam findings.[19] However these signs are limited in their prognostic and diagnostic value.[4] Other physical exam findings suggestive of cardiac chest pain may include hypertension, tachycardia, bradycardia, and new heart murmurs.[4] Chest pain that is reproducible during the physical exam with contact of the chest wall is more indicative of non-cardiac chest pain, but still cannot completely rule out acute coronary syndrome.[20] For this reason, in general, additional tests are required to establish the diagnosis.
In the emergency department the typical approach to chest pain involves ruling out the most dangerous causes: heart attack, pulmonary embolism, thoracic aortic dissection, esophageal rupture, tension pneumothorax, and cardiac tamponade. By elimination or confirmation of the most serious causes, a diagnosis of the origin of the pain may be made. Often, no definite cause will be found and reassurance is then provided.[8]
Clinical risk scores[edit]
The Global Registry of Acute Coronary Events score (GRACE score) and the Thrombosis in Myocardial Infarction score (TIMI score) performed at time of admission may help stratify persons into low, intermediate and high risk groups for acute coronary syndrome.[1] However the GRACE and TIMI scores do not provide management guidelines for risk-stratified persons. The HEART score, stratifies persons into low-risk and high-risk groups, and recommends either discharge or admission based upon the score.[1]
HEART Score[21][22]
Criteria
Point Value
History
Highly suspicious +2
Moderately suspicious +1
Slightly suspicious 0
ECG
Significant ST-depression +2
Nonspecific repolarization disturbance +1
Normal 0
Age
≥ 65 +2
45-65 +1
≤ 45 0
Risk factors*
≥ 3 risk factors or history of atherosclerotic disease +2
1-2 risk factors +1
No risk factors known 0
Troponin
≥ 3× normal limit +2
1-3× normal limit +1
≤ normal limit 0
*Risk factors include hypercholesterolemia, hypertension, diabetes mellitus, smoking, and obesity
Cumulative score:
0-3: 2.5% risk of adverse cardiac event. Patient's can be discharged with follow-up.
4-6: 20.3% risk of adverse cardiac event. Patients should be admitted to the hospital for trending of troponin and provocative testing.
≥7: 72.7% risk of adverse cardiac event, suggesting early invasive measures with these patients and close coordination with inpatient cardiology.
If acute coronary syndrome ("heart attack") is suspected, many people are admitted briefly for observation, sequential ECGs, and measurement of cardiac enzymes in the blood over time. On occasion, further tests on follow up may determine the cause.
Medical tests[edit]
On the basis of the above, a number of tests may be ordered:[23]
An electrocardiogram (ECG)
Chest radiograph or chest x rays are frequently performed
Echocardiography can be useful in patients with known cardiac disease or aortic dissection[4][24]
CT scanning is used in the diagnosis of aortic dissection[24]
V/Q scintigraphy or CT pulmonary angiogram (when a pulmonary embolism is suspected)[4]
Blood tests:
Troponin I or T (to indicate myocardial damage)
Complete blood count
Electrolytes and renal function (creatinine)
Liver enzymes
Creatine kinase (and CK-MB fraction in many hospitals)
D-dimer (when suspicion for pulmonary embolism is present but low)
serum lipase to exclude acute pancreatitis
Management[edit]
Management of chest pain varies with the underlying cause of the pain and the stage of care.
Prehospital care[edit]
Chest pain is a common symptom encountered by emergency medical services. Aspirin increases survival in people with acute coronary syndrome and it is reasonable for EMS dispatchers to recommend it in people with no recent serious bleeding.[25] Supplemental oxygen was used in the past for most people with chest pain but is not needed unless the oxygen saturations are less than 94% or there are signs of respiratory distress.[26][25] Entonox is frequently used by EMS personnel in the prehospital environment.[27] However, there is little evidence about its effectiveness.[25][28]
Hospital care[edit]
Hospital care of chest pain begins with initial survey of a person's vital signs, airway and breathing, and level of consciousness.[1][4] This may also include attachment of ECG leads, cardiac monitors, intravenous lines and other medical devices depending on initial evaluation.[4] After evaluation of a person's history, risk factors, physical examination, laboratory testing and imaging, management begins depending on suspected diagnoses.[4] Depending upon the diagnosis, a person may be placed in the intensive care unit, admitted to the hospital, or be treated outpatient.[4] For persons with suspected cardiac chest pain or acute coronary syndrome, or other emergent diagnoses such as pneumothorax, pulmonary embolism, or aortic dissection, admission to the hospital is most often recommended for further treatment.[4]
Outpatient care[edit]
For people with non-cardiac chest pain, cognitive behavioral therapy (CBT) might be helpful on an outpatient basis. A 2015 Cochrane review found that CBT might reduce the frequency of chest pain episodes the first three months after treatment.[29] For persons with chest pain due to gastroesophageal reflux disease (GERD), a proton-pump inhibitor (PPI) has been shown to be the most effective treatment.[30] However, PPI treatment has been shown to be no better than placebo in persons with noncardiac chest pain not caused by GERD.[30] For musculoskeletal causes of chest pain, manipulation therapy or chiropractic therapy, acupuncture, or a recommendation for increased exercise are often used as treatment.[30] Studies have shown conflicting results on the efficacy of these treatments.[30] A combination therapy of nonsteroidal anti-inflammatory drugs (NSAIDs) and manipulation therapy with at-home exercises has been shown to be most effective in treatment of musculoskeletal chest pain.[7]
Epidemiology[edit]
Chest pain is a common presenting problem. Overall chest pain is responsible for an estimated 6% of all emergency department in the United States and is the most common reason for hospital admission.[16] Chest pain is also very prevalent in primary care clinics, representing 1-3% of all visits with primary care physicians.[31] The rate of emergency department visits in the US for chest pain decreased 10% from 1999 to 2008.[32] but a subsequent increase of 13% was seen from 2006-2011.[33] Less than 20% of all cases of chest pain admissions are found to be due to coronary artery disease.[34] The rate of chest pain as a symptom of acute coronary syndrome varies among populations based upon age, sex, and previous medical conditions.[17] In general, women are more likely than men to present without chest pain (49% vs. 38%) in cases of myocardial infarction.[17]
References[edit]
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Jump up ^ "Entonox for the Treatment of Undiagnosed Chest Pain: Clinical Effectiveness and Guidelines" (PDF). Canadian Agency for Drugs and Technologies in Health. Retrieved 12 July 2011.
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^ Jump up to: a b c d Burgstaller JM, Jenni BF, Steurer J, Held U, Wertli MM (2014-08-11). "Treatment efficacy for non-cardiovascular chest pain: a systematic review and meta-analysis". PLOS One. 9 (8): e104722. doi:10.1371/journal.pone.0104722. PMC 4128723  . PMID 25111147.
Jump up ^ Stochkendahl MJ, Christensen HW (March 2010). "Chest pain in focal musculoskeletal disorders". The Medical Clinics of North America. 94 (2): 259–73. doi:10.1016/j.mcna.2010.01.007. PMID 20380955.
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External links[edit]
Classification
V · T · D
ICD-10: R07
ICD-9-CM: 786.5
MeSH: D002637
DiseasesDB: 16537
External resources
MedlinePlus: 003079

[show]
v
t
e
Symptoms and signs relating to the cardiovascular system (R00–R03, 785)
Chest pain
Referred pain
Angina
Aerophagia
Auscultation
Heart sounds
Split S2
S3
S4
Gallop rhythm
Heart murmur
Systolic
Diastolic
Continuous
Pericardial friction rub
Heart click
Bruit
carotid
Pulse
Tachycardia
Bradycardia
Pulsus tardus et parvus
Pulsus paradoxus
doubled
Pulsus bisferiens
Dicrotic pulse
Pulsus bigeminus
Pulsus alternans
Pulse deficit
Vascular disease
Gangrene
Other
Palpitations
Apex beat
Cœur en sabot
Jugular venous pressure
Cannon A waves
Hyperaemia
Shock
Cardiogenic
Hypovolemic
Distributive
Septic
Neurogenic
[show]
v
t
e
Symptoms and signs relating to the respiratory system (R04–R07, 786)
Medical examination and history taking
Auscultation
Stethoscope
Respiratory sounds
Stridor
Wheeze
Crackles
Rhonchi
Stertor
Squawk
Pleural friction rub
Fremitus
Bronchophony
Terminal secretions
Elicited findings
Percussion
Pectoriloquy
Whispered pectoriloquy
Egophony
Breathing
Rate
Apnea
Prematurity
Dyspnea
Hyperventilation
Hypoventilation
Hyperpnea
Tachypnea
Hypopnea
Bradypnea
Pattern
Agonal respiration
Biot's respiration
Cheyne–Stokes respiration
Kussmaul breathing
Ataxic respiration
Other
Respiratory distress
Respiratory arrest
Orthopnea/Platypnea
Trepopnea
Aerophagia
Asphyxia
Breath holding
Mouth breathing
Snoring
Other
Chest pain
In children
Precordial catch syndrome
Pleurisy
Nail clubbing
Cyanosis
Cough
Sputum
Hemoptysis
Epistaxis
Silhouette sign
Post-nasal drip
Hiccup
COPD
Hoover's sign
asthma
Curschmann's spirals
Charcot–Leyden crystals
chronic bronchitis
Reid index
sarcoidosis
Kveim test
pulmonary embolism
Hampton hump
Westermark sign
pulmonary edema
Kerley lines
Hamman's sign
Golden S sign
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Phosphorus cycle
From Wikipedia, the free encyclopedia
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Phosphorus Cycle on land
The phosphorus cycle is the biogeochemical cycle that describes the movement of phosphorus through the lithosphere, hydrosphere, and biosphere. Unlike many other biogeochemical cycles, the atmosphere does not play a significant role in the movement of phosphorus, because phosphorus and phosphorus-based compounds are usually solids at the typical ranges of temperature and pressure found on Earth. The production of phosphine gas occurs in only specialized, local conditions.
On the land, phosphorus gradually becomes less available to plants over thousands of years, because it is slowly lost in runoff. Low concentration of phosphorus in soils reduces plant growth, and slows soil microbial growth - as shown in studies of soil microbial biomass. Soil microorganisms act as both sinks and sources of available phosphorus in the biogeochemical cycle.[1] Locally, transformations of phosphorus are chemical, biological and microbiological: the major long-term transfers in the global cycle, however, are driven by tectonic movements in geologic time.[2]
Humans have caused major changes to the global phosphorus cycle through shipping of phosphorus minerals, and use of phosphorus fertilizer, and also the shipping of food from farms to cities, where it is lost as effluent.
Contents
[hide]
1 Phosphorus in the environment
1.1 Ecological function
1.2 Biological function
1.3 Process of the cycle
1.4 Phosphatic minerals
2 Human influences
3 See also
4 References
5 External links
Phosphorus in the environment[edit]
The aquatic phosphorus cycle
Ecological function[edit]
Phosphorus is an essential nutrient for plants and animals. Phosphorus is a limiting nutrient for aquatic organisms. Phosphorus forms parts of important life-sustaining molecules that are very common in the biosphere. Phosphorus does not enter the atmosphere, remaining mostly on land and in rock and soil minerals. Eighty percent of the mined phosphorus is used to make fertilizers. Phosphates from fertilizers, sewage and detergents can cause pollution in lakes and streams. Overenrichment of phosphate in both fresh and inshore marine waters can lead to massive algae blooms which, when they die and decay, leads to eutrophication of fresh waters only. An example of this is the Canadian Experimental Lakes Area. These freshwater algal blooms should not be confused with those in saltwater environments. Recent research suggests that the predominant pollutant responsible for algal blooms in salt water estuaries and coastal marine habitats is Nitrogen.[3]
Phosphorus occurs most abundantly in nature as part of the orthophosphate ion (PO4)3−, consisting of a P atom and 4 oxygen atoms. On land most phosphorus is found in rocks and minerals. Phosphorus rich deposits have generally formed in the ocean or from guano, and over time, geologic processes bring ocean sediments to land. Weathering of rocks and minerals release phosphorus in a soluble form where it is taken up by plants, and it is transformed into organic compounds. The plants may then be consumed by herbivores and the phosphorus is either incorporated into their tissues or excreted. After death, the animal or plant decays, and phosphorus is returned to the soil where a large part of the phosphorus is transformed into insoluble compounds. Runoff may carry a small part of the phosphorus back to the ocean. Generally with time (thousands of years) soils become deficient in phosphorus leading to ecosystem retrogression.[4]
Biological function[edit]
The primary biological importance of phosphates is as a component of nucleotides, which serve as energy storage within cells (ATP) or when linked together, form the nucleic acids DNA and RNA. The double helix of our DNA is only possible because of the phosphate ester bridge that binds the helix. Besides making biomolecules, phosphorus is also found in bone and the enamel of mammalian teeth, whose strength is derived from calcium phosphate in the form of Hydroxylapatite. It is also found in the exoskeleton of insects, and phospholipids (found in all biological membranes).[5] It also functions as a buffering agent in maintaining acid base homeostasis in the human body.[6]
Process of the cycle[edit]
Phosphates move quickly through plants and animals; however, the processes that move them through the soil or ocean are very slow, making the phosphorus cycle overall one of the slowest biogeochemical cycles.[2][7]
Initially, phosphate weathers from rocks and minerals, the most common mineral being apatite. Overall small losses occur in terrestrial environments by leaching and erosion, through the action of rain. In soil, phosphate is adsorbed on iron oxides, aluminium hydroxides, clay surfaces, and organic matter particles, and becomes incorporated (immobilized or fixed). Plants and fungi can also be active in making P soluble.[citation needed]
Unlike other cycles, P is not normally found in the air as a gas; it only occurs under highly reducing conditions as the gas phosphine PH3.[citation needed]
Phosphatic minerals[edit]
The availability of phosphorus in an ecosystem is restricted by the rate of release of this element during weathering. The release of phosphorus from apatite dissolution is a key control on ecosystem productivity. The primary mineral with significant phosphorus content, apatite [Ca5(PO4)3OH] undergoes carbonation.[2][8]
Little of this released phosphorus is taken up by biota (organic form), whereas a larger proportion reacts with other soil minerals. This leads to precipitation into unavailable forms in the later stage of weathering and soil development. Available phosphorus is found in a biogeochemical cycle in the upper soil profile, while phosphorus found at lower depths is primarily involved in geochemical reactions with secondary minerals. Plant growth depends on the rapid root uptake of phosphorus released from dead organic matter in the biochemical cycle. Phosphorus is limited in supply for plant growth. Phosphates move quickly through plants and animals; however, the processes that move them through the soil or ocean are very slow, making the phosphorus cycle overall one of the slowest biogeochemical cycles.[2][7]
Low-molecular-weight (LMW) organic acids are found in soils. They originate from the activities of various microorganisms in soils or may be exuded from the roots of living plants. Several of those organic acids are capable of forming stable organo-metal complexes with various metal ions found in soil solutions. As a result, these processes may lead to the release of inorganic phosphorus associated with aluminium, iron, and calcium in soil minerals. The production and release of oxalic acid by mycorrhizal fungi explain their importance in maintaining and supplying phosphorus to plants.[2][9]
The availability of organic phosphorus to support microbial, plant and animal growth depends on the rate of their degradation to generate free phosphate. There are various enzymes such as phosphatases, nucleases and phytase involved for the degradation. Some of the abiotic pathways in the environment studied are hydrolytic reactions and photolytic reactions. Enzymatic hydrolysis of organic phosphorus is an essential step in the biogeochemical phosphorus cycle, including the phosphorus nutrition of plants and microorganisms and the transfer of organic phosphorus from soil to bodies of water.[1] Many organisms rely on the soil derived phosphorus for their phosphorus nutrition.[citation needed]
Human influences[edit]
Nutrients are important to the growth and survival of living organisms, and hence, are essential for development and maintenance of healthy ecosystems. Humans have greatly influenced the phosphorus cycle by mining phosphorus, converting it to fertilizer, and by shipping fertilizer and products around the globe. Transporting phosphorus in food from farms to cities has made a major change in the global Phosphorus cycle. However, excessive amounts of nutrients, particularly phosphorus and nitrogen, are detrimental to aquatic ecosystems. Waters are enriched in phosphorus from farms' run-off, and from effluent that is inadequately treated before it is discharged to waters. Natural eutrophication is a process by which lakes gradually age and become more productive and may take thousands of years to progress. Cultural or anthropogenic eutrophication, however, is water pollution caused by excessive plant nutrients; this results in excessive growth in the algal population; when this algae dies its putrefaction depletes the water of oxygen.Such eutrophication may also give rise to toxic algal bloom.Both these effects cause animal and plant death rates to increase as the plants take in poisonous water while the animals drink the poisoned water. Surface and subsurface runoff and erosion from high-phosphorus soils may be major contributing factors to this fresh water eutrophication. The processes controlling soil Phosphorus release to surface runoff and to subsurface flow are a complex interaction between the type of phosphorus input, soil type and management, and transport processes depending on hydrological conditions.[10][11]
Repeated application of liquid hog manure in excess to crop needs can have detrimental effects on soil phosphorus status. Also, application of biosolids may increase available phosphorus in soil.[12] In poorly drained soils or in areas where snowmelt can cause periodic waterlogging, dereducing conditions can be attained in 7–10 days. This causes a sharp increase in phosphorus concentration in solution and phosphorus can be leached. In addition, reduction of the soil causes a shift in phosphorus from resilient to more labile forms. This could eventually increase the potential for phosphorus loss. This is of particular concern for the environmentally sound management of such areas, where disposal of agricultural wastes has already become a problem. It is suggested that the water regime of soils that are to be used for organic wastes disposal is taken into account in the preparation of waste management regulations.[13]
Human interference in the phosphorus cycle occurs by overuse or careless use of phosphorus fertilizers. This results in increased amounts of phosphorus as pollutants in bodies of water resulting in eutrophication. Eutrophication devastates water ecosystems by inducing anoxic conditions.[14]
See also[edit]
Peak phosphorus
Planetary boundaries
References[edit]
^ Jump up to: a b Turner B.L et al. (2003) Organic phosphorus in the environment. CABI publishing
^ Jump up to: a b c d e Schlesinger W.H. Biogeochemistry: An analysis of global change. (1991)
Jump up ^ https://www.soils.org/discover-soils/soils-in-the-city/green-infrastructure/important-terms/eutrophication
Jump up ^ Peltzer, D.A. et al. 2010. Understanding ecosystem retrogression. Ecological Monographs 80; 509-529.
Jump up ^ http://www.enviroliteracy.org/article.php/480.html
Jump up ^ Voet D and Voet J.G. (2003) Biochemistry pg 607-608.
^ Jump up to: a b Oelkers E.H (2008) Phosphate mineral reactivity: from global cycles to sustainable development Mineralogical Magazine 72: 337 - 340.
Jump up ^ Filippelli G.M (2002) The Global Phosphorus Cycle. Reviews in Mineralogy and geochemistry 48: 391 – 425
Jump up ^ Harrold S.A. and Tabatabai M.A (2006) Release of Inorganic Phosphorus from Soils by Low-Molecular-Weight Organic Acids. Communications in soil science and plant analysis, volume, issue 9 & 10
Jump up ^ Branom J.R and Sarkar D (2004) Phosphorus bioavailability in sediments of a sludge-disposal lake. Environmental Geoscience 11: 42 - 52
Jump up ^ Schelde K et al. (2006) Effects of Manure Application and Plowing on Transport of Colloids and Phosphorus to Tile Drains. 5: 445 - 458.
Jump up ^ "The effects of incubation on phosphorus desorption properties, phosphorus availability, and salinity of biosolids-amended soils". Environmental Earth Sciences. 69: 899–908. doi:10.1007/s12665-012-1975-6.
Jump up ^ Ajmone-Marsan. F et al. (2005) Phosphorus transformations under reduction in long-term manured soils.
Jump up ^ Conley, Daniel J.; et al. (2009). "Controlling Eutrophication: Nitrogen and Phosphorus". Science. 323: 1014–1015. CS1 maint: Explicit use of et al. (link)
External links[edit]
Part III of "Matter cycles": The phosphorus cycle, Lenntech Water treatment & air purification, Holding B.V. 2006
Environmental Literacy Council - Phosphorus Cycle
Monitoring and assessing water quality, section 5.6 Phosphorus - EPA
Prentice Hall Biology, Kenneth R. Miller and Joseph Levine 2001
Katie Corbin-Soil Microbiology
Environmental Literacy Council: Phosphorus Cycle
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