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Cardiac physiology
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Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.
Contents
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1 Blood flow
2 Cardiac muscle
2.1 Structure of cardiac muscle
3 Electrical conduction
3.1 Sinoatrial (SA) node
3.2 Atrioventricular (AV) node
3.2.1 Bundle of His, bundle branches, and Purkinje fibers
3.3 Membrane potentials and ion movement in cardiac conductive cells
3.4 Membrane Potentials and ion movement in cardiac contractile cells
3.5 Calcium ions
3.6 Comparative rates of conduction system firing
4 Cardiac cycle
4.1 Pressures and flow
4.2 Phases of the cardiac cycle
4.2.1 Atrial systole and diastole
4.2.2 Ventricular systole
4.2.3 Ventricular diastole
5 Heart sounds
6 Heart rate
6.1 Cardiovascular centres
6.2 Factors influencing heart rate
7 Cardiac output
7.1 Stroke volume
7.2 Preload
7.3 Afterload
7.4 Contractility
8 See also
9 References
Blood flow[edit]
Main articles: Cardiac cycle and Heart valve
Blood flow through the valves
3D echocardiogram viewed from the top, with the upper part of the ventricles removed and the mitral valve clearly visible (cusps are not clear and pulmonary valve not visible). On the left are two, two-dimensional views showing tricuspid and mitral valves (above) and aortic valve (below).
Blood flow diagram of the human heart. Blue components indicate de-oxygenated blood pathways and red components indicate oxygenated pathways.
The heart functions as a pump and acts as a double pump in the cardiovascular system to provide a continuous circulation of blood throughout the body. This circulation includes the systemic circulation and the pulmonary circulation. Both circuits transport blood but they can also be seen in terms of the gases they carry. The pulmonary circulation collects oxygen from the lungs and delivers carbon dioxide for exhalation. The systemic circuit transports oxygen to the body and returns relatively deoxygenated blood and carbon dioxide to the pulmonary circuit.[1]
Blood flows through the heart in one direction, from the atria to the ventricles, and out through the pulmonary artery into the pulmonary circulation, and the aorta into the systemic circulation. The pulmonary artery (also trunk) branches into the left and right pulmonary arteries to supply each lung. Blood is prevented from flowing backwards (regurgitation) by the tricuspid, bicuspid, aortic, and pulmonary valves.
The function of the right heart, is to collect de-oxygenated blood, in the right atrium, from the body via the superior vena cava, inferior vena cava and from the coronary sinus and pump it, through the tricuspid valve, via the right ventricle, through the semilunar pulmonary valve and into the pulmonary artery in the pulmonary circulation where carbon dioxide can be exchanged for oxygen in the lungs. This happens through the passive process of diffusion. In the left heart oxygenated blood is returned to the left atrium via the pulmonary vein. It is then pumped into the left ventricle through the bicuspid valve and into the aorta for systemic circulation. Eventually in the systemic capillaries exchange with the tissue fluid and cells of the body occurs; oxygen and nutrients are supplied to the cells for their metabolism and exchanged for carbon dioxide and waste products[1] In this case, oxygen and nutrients exit the systemic capillaries to be used by the cells in their metabolic processes, and carbon dioxide and waste products will enter the blood.[1]
The ventricles are stronger and thicker than the atria, and the muscle wall surrounding the left ventricle is thicker than the wall surrounding the right ventricle due to the higher force needed to pump the blood through the systemic circulation. Atria facilitate circulation primarily by allowing uninterrupted venous flow to the heart, preventing the inertia of interrupted venous flow that would otherwise occur at each ventricular systole.[2]
Cardiac muscle[edit]
Main article: Cardiac muscle
Cardiac muscle tissue has autorhythmicity, the unique ability to initiate a cardiac action potential at a fixed rate - spreading the impulse rapidly from cell to cell to trigger the contraction of the entire heart. This autorhythmicity is still modulated by the endocrine and nervous systems.[1]
There are two types of cardiac muscle cell: cardiomyocytes which have the ability to contract easily, and modified cardiomyocytes the pacemaker cells of the conducting system. The cardiomyocytes make up the bulk (99%) of cells in the atria and ventricles. These contractile cells respond to impulses of action potential from the pacemaker cells and are responsible for the contractions that pump blood through the body. The pacemaker cells make up just (1% of cells) and form the conduction system of the heart. They are generally much smaller than the contractile cells and have few of the myofibrils or myofilaments which means that have limited contractibility. Their function is similar in many respects to neurons.[1] The bundle of His and Purkinje fibres are specialised cardiomyocytes that function in the conduction system.
Structure of cardiac muscle[edit]
Details of intercalated discs
Cardiomyocytes, are considerably shorter and have smaller diameters than skeletal myocytes. Cardiac muscle (like skeletal muscle) is characterized by striations - the stripes of dark and light bands resulting from the organised arrangement of myofilaments and myofibrils in the sarcomere along the length of the cell. T (transverse) tubules are deep invaginations from the sarcolemma (cell membrane) that penetrate the cell, allowing the electrical impulses to reach the interior. In cardiac muscle the T-tubules are only found at the Z-lines.[1] When an action potential causes cells to contract, calcium is released from the sarcoplasmic reticulum of the cells as well as the T tubules. The calcium release triggers sliding of the actin and myosin fibrils leading to contraction.[3] A plentiful supply of mitochondria provide the energy for the contractions. Typically, cardiomyocytes have a single, central nucleus, but can also have two or more.[1]
Cardiac muscle cells branch freely and are connected by junctions known as intercalated discs which help the synchronized contraction of the muscle.[4] The sarcolemma (membrane) from adjacent cells bind together at the intercalated discs. They consist of desmosomes, specialized linking proteoglycans, tight junctions, and large numbers of gap junctions that allow the passage of ions between the cells and help to synchronize the contraction. Intercellular connective tissue also helps to strongly bind the cells together, in order to withstand the forces of contraction.[1]
Cardiac muscle undergoes aerobic respiration patterns, primarily metabolizing lipids and carbohydrates. Oxygen from the lungs attaches to haemoglobin and is also stored in the myoglobin, so that a plentiful supply of oxygen is available. Lipids, and glycogen are also stored within the sarcoplasm and these are broken down by mitochondria to release ATP. The cells undergo twitch-type contractions with long refractory periods followed by brief relaxation periods when the heart fills with blood for the next cycle.[1]
Electrical conduction[edit]
Main articles: Electrical conduction system of the heart and Cardiac action potential
Transmission of a cardiac action potential through the heart's conduction system
It is not very well known how the electric signal moves in the atria. It seems that it moves in a radial way, but Bachmann's bundle and coronary sinus muscle play a role in conduction between the two atria, which have a nearly simultaneous systole.[5][6][7] While in the ventricles, the signal is carried by specialized tissue called the Purkinje fibers which then transmit the electric charge to the myocardium.[8]
If embryonic heart cells are separated into a Petri dish and kept alive, each is capable of generating its own electrical impulse followed by contraction. When two independently beating embryonic cardiac muscle cells are placed together, the cell with the higher inherent rate sets the pace, and the impulse spreads from the faster to the slower cell to trigger a contraction. As more cells are joined together, the fastest cell continues to assume control of the rate. A fully developed adult heart maintains the capability of generating its own electrical impulse, triggered by the fastest cells, as part of the cardiac conduction system. The components of the cardiac conduction system include the atrial and ventricular syncytium, the sinoatrial node, the atrioventricular node, the bundle of His (atrioventricular bundle), the bundle branches, and the Purkinje cells.[1]
Sinoatrial (SA) node[edit]
Main article: SA node
Diagrammatic conduction system of the heart
Normal sinus rhythm is established by the sinoatrial (SA) node, the heart's pacemaker. The SA node is a specialized grouping of cardiomyocytes in the upper and back walls of the right atrium very close to the opening of the superior vena cava. The SA node has the highest rate of depolarization.[1]
This impulse spreads from its initiation in the SA node throughout the atria through specialized internodal pathways, to the atrial myocardial contractile cells and the atrioventricular node. The internodal pathways consist of three bands (anterior, middle, and posterior) that lead directly from the SA node to the next node in the conduction system, the atrioventricular node. The impulse takes approximately 50 ms (milliseconds) to travel between these two nodes. The relative importance of this pathway has been debated since the impulse would reach the atrioventricular node simply following the cell-by-cell pathway through the contractile cells of the myocardium in the atria. In addition, there is a specialized pathway called Bachmann's bundle or the interatrial band that conducts the impulse directly from the right atrium to the left atrium. Regardless of the pathway, as the impulse reaches the atrioventricular septum, the connective tissue of the cardiac skeleton prevents the impulse from spreading into the myocardial cells in the ventricles except at the atrioventricular node.[1] The electrical event, the wave of depolarization, is the trigger for muscular contraction. The wave of depolarization begins in the right atrium, and the impulse spreads across the superior portions of both atria and then down through the contractile cells. The contractile cells then begin contraction from the superior to the inferior portions of the atria, efficiently pumping blood into the ventricles.[1]
Atrioventricular (AV) node[edit]
Main article: AV node
The atrioventricular (AV) node is a second cluster of specialized myocardial conductive cells, located in the inferior portion of the right atrium within the atrioventricular septum. The septum prevents the impulse from spreading directly to the ventricles without passing through the AV node. There is a critical pause before the AV node depolarizes and transmits the impulse to the atrioventricular bundle. This delay in transmission is partially attributable to the small diameter of the cells of the node, which slow the impulse. Also, conduction between nodal cells is less efficient than between conducting cells. These factors mean that it takes the impulse approximately 100 ms to pass through the node. This pause is critical to heart function, as it allows the atrial cardiomyocytes to complete their contraction that pumps blood into the ventricles before the impulse is transmitted to the cells of the ventricle itself. With extreme stimulation by the SA node, the AV node can transmit impulses maximally at 220 per minute. This establishes the typical maximum heart rate in a healthy young individual. Damaged hearts or those stimulated by drugs can contract at higher rates, but at these rates, the heart can no longer effectively pump blood.[1]
Bundle of His, bundle branches, and Purkinje fibers[edit]
Arising from the AV node, the bundle of His, proceeds through the interventricular septum before dividing into two bundle branches, commonly called the left and right bundle branches. The left bundle branch has two fascicles. The left bundle branch supplies the left ventricle, and the right bundle branch the right ventricle. Since the left ventricle is much larger than the right, the left bundle branch is also considerably larger than the right. Portions of the right bundle branch are found in the moderator band and supply the right papillary muscles. Because of this connection, each papillary muscle receives the impulse at approximately the same time, so they begin to contract simultaneously just prior to the remainder of the myocardial contractile cells of the ventricles. This is believed to allow tension to develop on the chordae tendineae prior to right ventricular contraction. There is no corresponding moderator band on the left. Both bundle branches descend and reach the apex of the heart where they connect with the Purkinje fibers. This passage takes approximately 25 ms.[1]
The Purkinje fibers are additional myocardial conductive fibers that spread the impulse to the myocardial contractile cells in the ventricles. They extend throughout the myocardium from the apex of the heart toward the atrioventricular septum and the base of the heart. The Purkinje fibers have a fast inherent conduction rate, and the electrical impulse reaches all of the ventricular muscle cells in about 75 ms. Since the electrical stimulus begins at the apex, the contraction also begins at the apex and travels toward the base of the heart, similar to squeezing a tube of toothpaste from the bottom. This allows the blood to be pumped out of the ventricles and into the aorta and pulmonary trunk. The total time elapsed from the initiation of the impulse in the SA node until depolarization of the ventricles is approximately 225 ms.[1]
Membrane potentials and ion movement in cardiac conductive cells[edit]
Action potentials are considerably different between conductive and contractive cardiomyocytes. While sodium Na+ and potassium K+ ions play essential roles, calcium ions Ca2+ are also critical for both types of cell. Unlike skeletal muscles and neurons, cardiac conductive cells do not have a stable resting potential. Conductive cells contain a series of sodium ion channels that allow a normal and slow influx of sodium ions that causes the membrane potential to rise slowly from an initial value of −60 mV up to about –40 mV. The resulting movement of sodium ions creates spontaneous depolarization (or prepotential depolarization).[1]
At this point, calcium channels open and Ca2+ enters the cell, further depolarizing it at a more rapid rate until it reaches a value of approximately +5 mV. At this point, the calcium ion channels close and potassium channels open, allowing outflux of K+ and resulting in repolarization. When the membrane potential reaches approximately −60 mV, the K+ channels close and Na+ channels open, and the prepotential phase begins again. This process gives the autorhythmicity to cardiac muscle.[1]
The prepotential is due to a slow influx of sodium ions until the threshold is reached followed by a rapid depolarization and repolarization. The prepotential accounts for the membrane reaching threshold and initiates the spontaneous depolarization and contraction of the cell; there is no resting potential.[1]
Membrane Potentials and ion movement in cardiac contractile cells[edit]
There is a distinctly different electrical pattern involving the contractile cells. In this case, there is a rapid depolarization, followed by a plateau phase and then repolarization. This phenomenon accounts for the long refractory periods required for the cardiac muscle cells to pump blood effectively before they are capable of firing for a second time. These cardiac myocytes normally do not initiate their own electrical potential, although they are capable of doing so, but rather wait for an impulse to reach them.[1]
Contractile cells demonstrate a much more stable resting phase than conductive cells at approximately −80 mV for cells in the atria and −90 mV for cells in the ventricles. Despite this initial difference, the other components of their action potentials are virtually identical. In both cases, when stimulated by an action potential, voltage-gated channels rapidly open, beginning the positive-feedback mechanism of depolarization. This rapid influx of positively charged ions raises the membrane potential to approximately +30 mV, at which point the sodium channels close. The rapid depolarization period typically lasts 3–5 ms. Depolarization is followed by the plateau phase, in which membrane potential declines relatively slowly. This is due in large part to the opening of the slow Ca2+ channels, allowing Ca2+ to enter the cell while few K+ channels are open, allowing K+ to exit the cell. The relatively long plateau phase lasts approximately 175 ms. Once the membrane potential reaches approximately zero, the Ca2+ channels close and K+ channels open, allowing K+ to exit the cell. The repolarization lasts approximately 75 ms. At this point, membrane potential drops until it reaches resting levels once more and the cycle repeats. The entire event lasts between 250 and 300 ms.[1]
The absolute refractory period for cardiac contractile muscle lasts approximately 200 ms, and the relative refractory period lasts approximately 50 ms, for a total of 250 ms. This extended period is critical, since the heart muscle must contract to pump blood effectively and the contraction must follow the electrical events. Without extended refractory periods, premature contractions would occur in the heart and would not be compatible with life.[1]

(a) There is long plateau phase due to the influx of calcium ions. The extended refractory period allows the cell to fully contract before another electrical event can occur.
(b) The action potential for heart muscle is compared to that of skeletal muscle.[1]
Calcium ions[edit]
Calcium ions play two critical roles in the physiology of cardiac muscle. Their influx through slow calcium channels accounts for the prolonged plateau phase and absolute refractory period. Calcium ions also combine with the regulatory protein troponin in the troponin complex. Both roles enabling the myocardium to function properly.[1]
Approximately 20 percent of the calcium required for contraction is supplied by the influx of Ca2+ during the plateau phase. The remaining Ca2+ for contraction is released from storage in the sarcoplasmic reticulum.[1]
Comparative rates of conduction system firing[edit]
The pattern of prepotential or spontaneous depolarization, followed by rapid depolarization and repolarization just described, are seen in the SA node and a few other conductive cells in the heart. Since the SA node is the pacemaker, it reaches threshold faster than any other component of the conduction system. It will initiate the impulses spreading to the other conducting cells. The SA node, without nervous or endocrine control, would initiate a heart impulse approximately 80–100 times per minute. Although each component of the conduction system is capable of generating its own impulse, the rate progressively slows from the SA node to the Purkinje fibers. Without the SA node, the AV node would generate a heart rate of 40–60 beats per minute. If the AV node were blocked, the atrioventricular bundle would fire at a rate of approximately 30–40 impulses per minute. The bundle branches would have an inherent rate of 20–30 impulses per minute, and the Purkinje fibers would fire at 15–20 impulses per minute. While a few exceptionally trained aerobic athletes demonstrate resting heart rates in the range of 30–40 beats per minute (the lowest recorded figure is 28 beats per minute for Miguel Indurain, a cyclist)–for most individuals, rates lower than 50 beats per minute would indicate a condition called bradycardia. Depending upon the specific individual, as rates fall much below this level, the heart would be unable to maintain adequate flow of blood to vital tissues, initially resulting in decreasing loss of function across the systems, unconsciousness, and ultimately death.[1]
Cardiac cycle[edit]
Main article: Cardiac cycle
Cardiac cycle shown against ECG
The period of time that begins with contraction of the atria and ends with ventricular relaxation is known as the cardiac cycle. The period of contraction that the heart undergoes while it pumps blood into circulation is called systole. The period of relaxation that occurs as the chambers fill with blood is called diastole. Both the atria and ventricles undergo systole and diastole, and it is essential that these components be carefully regulated and coordinated to ensure blood is pumped efficiently to the body.[1]
The cardiac cycle as correlated to the ECG
Pressures and flow[edit]
Fluids, move from regions of high pressure to regions of lower pressure. Accordingly, when the heart chambers are relaxed (diastole), blood will flow into the atria from the higher pressure of the veins. As blood flows into the atria, the pressure will rise, so the blood will initially move passively from the atria into the ventricles. When the action potential triggers the muscles in the atria to contract (atrial systole), the pressure within the atria rises further, pumping blood into the ventricles. During ventricular systole, pressure rises in the ventricles, pumping blood into the pulmonary trunk from the right ventricle and into the aorta from the left ventricle.[1]
Phases of the cardiac cycle[edit]
At the beginning of the cardiac cycle, both the atria and ventricles are relaxed (diastole). Blood is flowing into the right atrium from the superior and inferior venae cavae and the coronary sinus. Blood flows into the left atrium from the four pulmonary veins. The two atrioventricular valves, the tricuspid and mitral valves, are both open, so blood flows unimpeded from the atria and into the ventricles. Approximately 70–80 percent of ventricular filling occurs by this method. The two semilunar valves, the pulmonary and aortic valves, are closed, preventing backflow of blood into the right and left ventricles from the pulmonary trunk on the right and the aorta on the left.[1]
Atrial systole and diastole[edit]
Contraction of the atria follows depolarization, represented by the P wave of the ECG. As the atrial muscles contract from the superior portion of the atria toward the atrioventricular septum, pressure rises within the atria and blood is pumped into the ventricles through the open atrioventricular (tricuspid, and mitral or bicuspid) valves. At the start of atrial systole, the ventricles are normally filled with approximately 70–80 percent of their capacity due to inflow during diastole. Atrial contraction, also referred to as the "atrial kick," contributes the remaining 20–30 percent of filling. Atrial systole lasts approximately 100 ms and ends prior to ventricular systole, as the atrial muscle returns to diastole.[1]
Ventricular systole[edit]
Ventricular systole follows the depolarization of the ventricles and is represented by the QRS complex in the ECG. It may be conveniently divided into two phases, lasting a total of 270 ms. At the end of atrial systole and just prior to atrial contraction, the ventricles contain approximately 130 mL blood in a resting adult in a standing position. This volume is known as the end diastolic volume (EDV) or preload.[1]
Initially, as the muscles in the ventricle contract, the pressure of the blood within the chamber rises, but it is not yet high enough to open the semilunar (pulmonary and aortic) valves and be ejected from the heart. However, blood pressure quickly rises above that of the atria that are now relaxed and in diastole. This increase in pressure causes blood to flow back toward the atria, closing the tricuspid and mitral valves. Since blood is not being ejected from the ventricles at this early stage, the volume of blood within the chamber remains constant. Consequently, this initial phase of ventricular systole is known as isovolumic contraction, also called isovolumetric contraction.[1]
In the second phase of ventricular systole, the ventricular ejection phase, the contraction of the ventricular muscle has raised the pressure within the ventricle to the point that it is greater than the pressures in the pulmonary trunk and the aorta. Blood is pumped from the heart, pushing open the pulmonary and aortic semilunar valves. Pressure generated by the left ventricle will be appreciably greater than the pressure generated by the right ventricle, since the existing pressure in the aorta will be so much higher. Nevertheless, both ventricles pump the same amount of blood. This quantity is referred to as stroke volume. Stroke volume will normally be in the range of 70–80 mL. Since ventricular systole began with an EDV of approximately 130 mL of blood, this means that there is still 50–60 mL of blood remaining in the ventricle following contraction. This volume of blood is known as the end systolic volume (ESV).[1]
Ventricular diastole[edit]
Ventricular relaxation, or diastole, follows repolarization of the ventricles and is represented by the T wave of the ECG. It too is divided into two distinct phases and lasts approximately 430 ms.[1]
During the early phase of ventricular diastole, as the ventricular muscle relaxes, pressure on the remaining blood within the ventricle begins to fall. When pressure within the ventricles drops below pressure in both the pulmonary trunk and aorta, blood flows back toward the heart, producing the dicrotic notch (small dip) seen in blood pressure tracings. The semilunar valves close to prevent backflow into the heart. Since the atrioventricular valves remain closed at this point, there is no change in the volume of blood in the ventricle, so the early phase of ventricular diastole is called the isovolumic ventricular relaxation phase, also called isovolumetric ventricular relaxation phase.[1]
In the second phase of ventricular diastole, called late ventricular diastole, as the ventricular muscle relaxes, pressure on the blood within the ventricles drops even further. Eventually, it drops below the pressure in the atria. When this occurs, blood flows from the atria into the ventricles, pushing open the tricuspid and mitral valves. As pressure drops within the ventricles, blood flows from the major veins into the relaxed atria and from there into the ventricles. Both chambers are in diastole, the atrioventricular valves are open, and the semilunar valves remain closed. The cardiac cycle is complete.[1]
Heart sounds[edit]
Main article: Heart sounds
One of the simplest methods of assessing the heart's condition is to listen to it using a stethoscope.[1] In a healthy heart, there are only two audible heart sounds, called S1 and S2. The first heart sound S1, is the sound created by the closing of the atrioventricular valves during ventricular contraction and is normally described as "lub". The second heart sound, S2, is the sound of the semilunar valves closing during ventricular diastole and is described as "dub".[1] Each sound consists of two components, reflecting the slight difference in time as the two valves close.[9] S2 may split into two distinct sounds, either as a result of inspiration or different valvular or cardiac problems.[9] Additional heart sounds may also be present and these give rise to gallop rhythms. A third heart sound, S3 usually indicates an increase in ventricular blood volume. A fourth heart sound S4 is referred to as an atrial gallop and is produced by the sound of blood being forced into a stiff ventricle. The combined presence of S3 and S4 give a quadruple gallop.[1]
The x-axis reflects time with a recording of the heart sounds. The y-axis represents pressure.[1]
Heart murmurs are abnormal heart sounds which can be either pathological or benign and there are numerous kinds.[10] Murmurs are graded by volume, from 1) the quietest, to 6) the loudest, and evaluated by their relationship to the heart sounds and position in the cardiac cycle.[9] Phonocardiograms can record these sounds.[1] Murmurs can result from narrowing (stenosis), regurgitation or insufficiency of any of the main heart valves but they can also result from a number of other disorders, including atrial and ventricular septal defects.[9] One example of a murmur is Still's murmur, which presents a musical sound in children, has no symptoms and disappears in adolescence.[11]
A different type of sound, a pericardial friction rub can be heard in cases of pericarditis where the inflamed membranes can rub together.[12]
Heart rate[edit]
Main article: Heart rate
The resting heart rate of a newborn can be 120 beats per minute (bpm) and this gradually decreases until maturity and then gradually increases again with age. The adult resting heart rate ranges from 60-100 bpm. Exercise and fitness levels, age and basal metabolic rate can all affect the heart rate. An athlete's heart rate can be lower than 60bpm. During exercise the rate can be 150bpm with maximum rates reaching from 200 and 220 bpm.[1]
Cardiovascular centres[edit]
Autonomic innervation of the heart
The wave of depolarization in a normal sinus rhythm shows a stable resting HR. Following parasympathetic stimulation, HR slows. Following sympathetic stimulation, HR increases.[1]
The normal sinus rhythm of the heart rate is generated by the SA node. It is also influenced by central factors through sympathetic and parasympathetic nerves[3]:116–22 of the two paired cardiovascular centres of the medulla oblongata. Activity is increased via sympathetic stimulation of the cardioaccelerator nerves, and inhibited via parasympathetic stimulation by the vagus nerve. During rest vagal stimulation normally predominates as, left unregulated, the SA node would initiate a sinus rhythm of approximately 100 bpm.[1]
Both sympathetic and parasympathetic stimuli flow through the paired cardiac plexus near the base of the heart. Without any nervous stimulation, the SA node would establish a sinus rhythm of approximately 100 bpm. Since resting rates are considerably less than this, it becomes evident that parasympathetic stimulation normally slows HR.[1] The cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia (the cervical ganglia plus superior thoracic ganglia T1–T4) to both the SA and AV nodes, plus additional fibers to the atria and ventricles. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (also known as noradrenaline) at the neuromuscular junction of the cardiac nerves. This shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increased heartrate. It opens chemical or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions.[1] Norepinephrine binds to the beta–1 receptor. High blood pressure medications are used to block these receptors and so reduce the heart rate.[1]
The cardiovascular centres receive input from a series of visceral receptors with impulses traveling through visceral sensory fibers within the vagus and sympathetic nerves via the cardiac plexus. Among these receptors are various proprioreceptors, baroreceptors, and chemoreceptors, plus stimuli from the limbic system which normally enable the precise regulation of heart function, via cardiac reflexes. Increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. The cardiovascular centres monitor these increased rates of firing, suppressing parasympathetic stimulation or increasing sympathetic stimulation as needed in order to increase blood flow.[1]
Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.[1]
There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase HR. The opposite is also true.[1]
Factors influencing heart rate[edit]
In addition to the autonomic nervous system, other factors can affect this. These include epinephrine, norepinephrine, and thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and pH balance .[1]
Table 1: Major factors increasing heart rate and force of contraction[1]
Factor
Effect
Cardioaccelerator nerves Release of norepinephrine
Proprioreceptors Increased rates of firing during exercise
Chemoreceptors Decreased levels of O2; increased levels of H+, CO2, and lactic acid
Baroreceptors Decreased rates of firing, indicating falling blood volume/pressure
Limbic system Anticipation of physical exercise or strong emotions
Catecholamines Increased epinephrine and norepinephrine
Thyroid hormones Increased T3 and T4
Calcium Increased Ca2+
Potassium Decreased K+
Sodium Decreased Na+
Body temperature Increased body temperature
Nicotine and caffeine Stimulants, increasing heart rate
Table 2: Factors decreasing heart rate and force of contraction[1]
Factor
Effect
Cardioinhibitor nerves (vagus) Release of acetylcholine
Proprioreceptors Decreased rates of firing following exercise
Chemoreceptors Increased levels of O2; decreased levels of H+ and CO2
Baroreceptors Increased rates of firing, indicating higher blood volume/pressure
Limbic system Anticipation of relaxation
Catecholamines Decreased epinephrine and norepinephrine
Thyroid hormones Decreased T3 and T4
Calcium Decreased Ca2+
Potassium Increased K+
Sodium Decreased Na+
Body temperature Decrease in body temperature
Factors that increase heart rate also trigger an increase in stroke volume. As with skeletal muscles the heart can increase in size and efficiency with exercise.[1] Thus endurance athletes such as marathon runners may have a heart that has hypertrophied by up to 40%.[3]:1063–64 The difference between maximum and minimum cardiac outputs is known as the cardiac reserve and this measures the residual capacity to pump blood.[1] Heart rates may reach up to 185–195 in exercise, depending on how fit a person is.[3]
Cardiac output[edit]
Main article: Cardiac output
Cardiac output as shown on an ECG
Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle (stroke volume, SV) in one minute. To calculate this, multiply stroke volume (SV), by heart rate (HR), in beats per minute.[1] It can be represented by the equation: CO = HR x SV[1]
SV is normally measured using an echocardiogram to record end diastolic volume (EDV) and end systolic volume (ESV), and calculating the difference: SV = EDV – ESV. SV can also be measured using a specialized catheter, but this is an invasive procedure and far more dangerous to the patient. A mean SV for a resting 70-kg (150-lb) individual would be approximately 70 mL. There are several important variables, including size of the heart, physical and mental condition of the individual, sex, contractility, duration of contraction, preload or EDV, and afterload or resistance. Normal range for SV would be 55–100 mL. An average resting HR would be approximately 75 bpm but could range from 60–100 in some individuals.[1] Using these numbers, (which refer to each ventricle, not both) the mean CO is 5.25 L/min, with a range of 4.0–8.0 L/min.[1]
Major Factors Influencing Cardiac Output - Cardiac output is influenced by heart rate and stroke volume, both of which are also variable.[1]
SVs are also used to calculate ejection fraction, which is the portion of the blood that is pumped or ejected from the heart with each contraction. To calculate ejection fraction, SV is divided by EDV. Despite the name, the ejection fraction is normally expressed as a percentage. Ejection fractions range from approximately 55–70 percent, with a mean of 58 percent.[1]
Stroke volume[edit]
Major Factors Influencing Stroke Volume - Multiple factors affect preload, afterload, and contractility, and are the major considerations influencing SV.[1]
Summary of Major Factors Influencing Cardiac Output - The primary factors influencing HR include autonomic innervation plus endocrine control. Not shown are environmental factors, such as electrolytes, metabolic products, and temperature. The primary factors controlling SV include preload, contractility, and afterload. Other factors such as electrolytes may be classified as either positive or negative inotropic agents.[1]
Many of the factors that regulate the heart rate also affect cardiac function by altering the stroke volume. While a number of variables are involved, stroke volume is dependent upon the difference between end diastolic volume and end systolic volume. The three primary factors involved are preload, afterload and contractility.[1]
Preload[edit]
Main article: Preload (cardiology)
Preload is another way of expressing EDV. Therefore, the greater the EDV, the greater the preload. A main factor is ventricular filling time. The faster the contractions are, the shorter the filling time and both the EDV and preload are lower.[1]
The relationship between ventricular stretch and contraction has been stated in the Frank-Starling mechanism which says that the force of contraction is directly proportional to the initial length of muscle fibre. So that the greater the stretch of the ventricle the greater the contraction. Any sympathetic stimulation to the venous system will increase venous return to the heart and ventricular filling.[1]
Afterload[edit]
The ventricles must develop a certain tension to pump blood against the resistance of the vascular system. This tension is called afterload. When the resistance is increased particularly due to stenotic valve damage the afterload must necessarily increase. A decrease in normal vascular resistance can also occur. Different cardiac responses operate to restore homeostasis of the pressure and blood flow.[1]
Contractility[edit]
The ability of the myocardium to contract, (its contractility), controls the stroke volume which determines the end systolic volume. The greater the contraction the greater the stroke volume and the smaller the end systolic volume. Positive or negative inotropic factors via sympathetic and parasympathetic stimulation respectively, can increase or decrease the force of contractions. Sympathetic stimulation triggers the release of norepinephrine from the cardiac nerves and also stimulates the adrenal cortex to secrete both epinephrine and norepinephrine. These secretions increase the heart rate, subsequent metabolic rate and contractility. Parasympathetic stimulation stimulates the release of acetylcholine (ACh) from the vagus nerve which decreases contractility, and stroke volume which increases end systolic volume.
Several synthetic drugs have been developed that can act either as a stimulant or inhibitor inotrope. The stimulant inotropes, such as Digoxin, cause higher concentrations of calcium ions which increase contractility. Excess calcium (hypercalcemia) is also a positive inotrope. Drugs that are negative inotropes include beta blockers and calcium channel blockers. Hypoxia, acidosis, hyperkalemia are also negative inotropic agents.
Table 3: Cardiac response to decreasing blood flow and pressure due to decreasing cardiac output[1]
Baroreceptors (aorta, carotid arteries, venae cavae, and atria)
Chemoreceptors (both central nervous system and in proximity to baroreceptors)
Sensitive to
Decreasing stretch[1] Decreasing O2 and increasing CO2, H+, and lactic acid[1]
Target
Parasympathetic stimulation suppressed[1] Sympathetic stimulation increased[1]
Response of heart
Increasing heart rate and increasing stroke volume[1] Increasing heart rate and increasing stroke volume[1]
Overall effect
Increasing blood flow and pressure due to increasing cardiac output; hemostasis restored[1] Increasing blood flow and pressure due to increasing cardiac output; hemostasis restored[1]
Table 4: Cardiac response to increasing blood flow and pressure due to increasing cardiac output[1]
Baroreceptors (aorta, carotid arteries, venae cavae, and atria)
Chemoreceptors (both central nervous system and in proximity to baroreceptors)
Sensitive to
Increasing stretch[1] Increasing O2 and decreasing CO2, H+, and lactic acid[1]
Target
Parasympathetic stimulation increased[1] Sympathetic stimulation suppressed[1]
Response of heart
Decreasing heart rate and decreasing stroke volume[1] Decreasing heart rate and decreasing stroke volume[1]
Overall effect
Decreasing blood flow and pressure due to decreasing cardiac output; hemostasis restored[1] Decreasing blood flow and pressure due to decreasing cardiac output; hemostasis restored[1]
See also[edit]
Cardiovascular System Dynamics Society
References[edit]
^ Jump up to: a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg bh bi bj bk bl bm bn bo bp bq br bs bt bu bv bw bx by bz ca cb cc cd ce cf cg Betts, J. Gordon (2013). Anatomy & physiology. pp. 787–846. ISBN 1938168135. Retrieved 11 August 2014.
Jump up ^ Anderson, RM. The Gross Physiology of the Cardiovascular System (2nd ed., 2012). See "Chapter 1: Normal Physiology."
^ Jump up to: a b c d Hall, Arthur C. Guyton, John E. (2005). Textbook of medical physiology (11th ed.). Philadelphia: W.B. Saunders. p. 106. ISBN 978-0-7216-0240-0.
Jump up ^ Pocock, Gillian (2006). Human Physiology (Third ed.). Oxford University Press. p. 85. ISBN 978-0-19-856878-0.
Jump up ^ Antz, Matthias; et al. (1998). "Electrical Conduction Between the Right Atrium and the Left Atrium via the Musculature of the Coronary Sinus". Circulation. 98 (17): 1790–95. doi:10.1161/01.CIR.98.17.1790. PMID 9788835.
Jump up ^ De Ponti, Roberto; et al. (2002). "Electroanatomic Analysis of Sinus Impulse Propagation in Normal Human Atria". Journal of Cardiovascular Electrophysiology. 13 (1): 1–10. doi:10.1046/j.1540-8167.2002.00001.x. PMID 11843475.
Jump up ^ "SA node definition – Medical Dictionary definitions of popular medical terms easily defined on MedTerms". Medterms.com. 27 April 2011. Retrieved 7 June 2012.
Jump up ^ "Purkinje Fibers". Biology.about.com. 9 April 2012. Retrieved 7 June 2012.
^ Jump up to: a b c d Talley, Nicholas J.; O'Connor, Simon. Clinical Examination. Churchill Livingstone. pp. 76–82. ISBN 9780729541985.
Jump up ^ Dorland's (2012). Dorland's Illustrated Medical Dictionary (32nd ed.). Elsevier Saunders. p. 1189. ISBN 978-1-4160-6257-8.
Jump up ^ Newburger, Jane (2006). Nadas' Pediatric Cardiology 2nd Edition. Philadelphia: Elsevier. p. 358. ISBN 978-1-4160-2390-6.
Jump up ^ Cantarini L, Lopalco G; et al. (Oct 2014). "Autoimmunity and autoinflammation as the yin and yang of idiopathic recurrent acute pericarditis". Autoimmun Rev. 14: 90–97. doi:10.1016/j.autrev.2014.10.005. PMID 25308531.
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Limitless (TV series)
From Wikipedia, the free encyclopedia
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Limitless
Genre
Science fiction
Comedy drama
Thriller
Based on
Limitless
Developed by
Craig Sweeny
Starring
Jake McDorman
Jennifer Carpenter
Hill Harper
Mary Elizabeth Mastrantonio
Composer(s)
Paul Leonard-Morgan
Country of origin
United States
Original language(s)
English
No. of seasons
1
No. of episodes
22 (list of episodes)
Production
Executive producer(s)
Bradley Cooper
Todd Phillips
Ryan Kavanaugh
Tucker Tooley
Tom Forman
Heather Kadin
Marc Webb
Craig Sweeny
Alex Kurtzman
Roberto Orci
Production location(s)
New York City
Camera setup
Single-camera
Running time
43–45 minutes
Production company(s)
K/O Paper Products
Relativity Television
Action This Day!
Critical Content
CBS Television Studios
Distributor
CBS Television Distribution
Release
Original network
CBS
Picture format
HDTV 1080i
Original release
September 22, 2015 (2015-09-22) – April 26, 2016 (2016-04-26)
External links
Website
Limitless is an American comedy-drama television series based on the 2011 film of the same name, which originally aired on CBS from September 22, 2015, to April 26, 2016.[1][2][3][4] It stars Jake McDorman as Brian Finch, who discovers the power of a mysterious nootropic drug by the name of NZT-48. This drug unlocks the full potential of the human brain and gives its user enhanced mental faculties.
It is a spinoff to the film of the same name, which in turn was based on the novel The Dark Fields, and takes place four years after the events of the movie.
The series was ordered by CBS on May 8, 2015. On October 23, 2015, CBS picked up Limitless for a full season of 22 episodes.[5] On May 18, 2016, CBS confirmed Limitless would not be part of the network's 2016–2017 lineup, and on May 25, 2016, CBS executive Craig Sweeny announced the series had been cancelled after one season.[6]
Contents
1 Premise
2 Cast
2.1 Main
2.2 Recurring
3 Episodes
4 Broadcast
5 Reception
5.1 Ratings
6 References
7 External links
Premise[edit]
Brian Finch (McDorman), a 28-year-old burnout and struggling musician, is introduced to NZT-48, a miracle drug that gives him access to every neuron in his brain. For twelve hours after taking the pill, he becomes the smartest person in the world, able to perfectly recall every detail of his life and capable of prodigious leaps of intuition and reasoning. With the mysterious US Senator Eddie Morra (Bradley Cooper) providing him with an immunity shot to counteract NZT's deadly side effects, Brian uses his enhanced abilities to help FBI agent Rebecca Harris (Jennifer Carpenter). The FBI doesn't know about the shot and Brian has to keep both worlds separate.
Cast[edit]
Main[edit]
Jake McDorman as Brian Finch[7]
Jennifer Carpenter as FBI Special Agent Rebecca Harris[8]
Hill Harper as FBI Special Agent Spelman Boyle,[9][10] named for Spelman College.
Mary Elizabeth Mastrantonio as FBI Special Agent in Charge Nasreen "Naz" Pouran, of Iranian origin,[11] commander of the Cross Jurisdictional Command (CJC) team[12]
Recurring[edit]
Bradley Cooper as U.S. Senator Edward "Eddie" Morra, the original main character from the film[13]
Analeigh Tipton as Shauna, Brian's ex-girlfriend
Ron Rifkin as Dennis Finch, Brian's father
Blair Brown as Marie Finch, Brian's mother
Megan Guinan as Rachel Finch, Brian's sister
Tom Degnan as FBI Agent Jason[14] "Ike", Mike's partner and Brian's bodyguard
Michael James Shaw as FBI Agent Daryl "Mike", Ike's partner and Brian's bodyguard
Colin Salmon as Jarrod Sands, a former MI6 officer who now works as a fixer for Morra[15]
Desmond Harrington as SWAT Agent Casey Rooks
Georgina Haig as Piper Baird
Michael Devine as James "Tech" Padgett
Episodes[edit]
No.
Title
Directed by
Written by
Original air date
U.S. viewers
(millions)
1
"Pilot" Marc Webb Craig Sweeny September 22, 2015 (2015-09-22) 9.86[16]
When his father becomes seriously ill, Brian Finch realises he has not reached the goals that he had set for his life. His friend Eli offers him a pill of NZT, which helps Brian excel in his temp job and discover the true nature of his father's disease. When Brian finds Eli dead from a gunshot, he becomes the main suspect in an FBI murder investigation. Looking for more NZT, Brian tracks down one of Eli's coworkers and gets shot in the leg by the real murderer. He passes out, and awakes to find himself with Senator Eddie Morra, who offers him access to both NZT and a drug to counter its dangerous side effects, on the condition that he will not tell the FBI. The FBI wants to find out who created NZT and how to counter the side effects, and FBI agent Rebecca Harris offers Brian a consultant position with the Bureau. Brian insists that they first help his father get an immediate liver transplant. Agent Harris reveals a personal reason behind her involvement in the investigation: she suspects that her father was using NZT before he was found dead in a river.
2
"Badge! Gun!" Marc Webb Craig Sweeny & Marc Webb September 29, 2015 (2015-09-29) 9.73[17]
Brian begins work with the FBI, only to be stuck behind a desk as an analyst while they monitor his use of NZT, since they are unaware he is using the enzyme to counter the side effects. Restless, he works his way into an assassination case investigated by Harris and Boyle, but leaves the facility against orders to find evidence, and nearly gets himself fired. Together they unravel a plot to target an army general with a genetically-engineered virus. Meanwhile, Brian tries to learn more about Senator Eddie Morra, and draws a blank. Morra's nurse starts taking care of Brian's father in order to monitor Brian.
3
"The Legend of Marco Ramos" Guillermo Navarro Matthew Federman & Stephen Scaia October 6, 2015 (2015-10-06) 9.57[18]
With his daily NZT pill, Brian helps the FBI find a sniper who shot a former FBI agent. He also has a chance encounter with Shauna (Analeigh Tipton), a former love interest, and starts up a new relationship with her. One of Morra's henchmen, Mr. Sands, calls himself Brian's new boss and threatens to harm Brian's friends and family if Brian does not comply with his every request on behalf of Morra's interests. To protect Shauna, Brian breaks up with her.
4
"Page 44" Doug Aarniokoski Mark Goffman October 13, 2015 (2015-10-13) 8.03[19]
Brian receives his first confidential case investigating a Chinese spy. However, when his new online friend Arthur Maciel is framed for the murder of a former business partner, Rebecca helps Brian look into the police investigation instead. Mr. Sands asks Brian to find out how much the FBI knows about NZT and threatens to withhold the counter-effect drug until he has their files. Afraid of committing treason and not wanting to betray Rebecca, Brian fabricates a file. Sands has Brian's father infected with a virus, forcing Brian to steal the real files. Rebecca goes to an exhibition of her father's last paintings and Brian finds her father in the NZT files.
5
"Personality Crisis" Joshua Butler Sallie Patrick October 20, 2015 (2015-10-20) 7.90[20]
After recovering all of the files the FBI has on NZT which includes information about suspected users past & present, one of which being Rebecca's late father, Brian very badly wants to tell her, but worries that telling her will blow his cover. He keeps himself from telling her by making videos from his NZT self to his non-NZT self. Also, Brian accidentally meddles in Rebecca's personal life while learning self-defense from her secret boyfriend, FBI Agent Casey Rooks (who incidentally does not know about NZT) by making him suspicious about how Brian was able to pick up self-defense technique so quickly.
6
"Side Effects May Include..." Doug Aarniokoski Jenna Richman October 27, 2015 (2015-10-27) 7.45[21]
After Brian tells Rebecca about the file, they start digging deeper into her father's involvement with NZT. Sands, however, wants Rebecca gone and attempts to blackmail Brian by withholding the immunity shot, into framing her so she loses her job at the FBI. Brian hopes that whoever created NZT might be able to provide him with a way to counteract the side effects. He eventually tracks down Andrew Epperly, a Ubient scientist who received the NZT formula anonymously, and tried it on his father who was suffering from Alzheimer's, as well as on several others, among whom Rebecca's father. Rebecca confronts Epperly, and he reveals he faked his death after NZT started circulating on the streets. Finally, Morra gives Brian the shot and five extra NZT pills. He explains he was testing his moral compass, and whether he is "somebody who just takes orders like Sands, or if he is somebody who has character".
7
"Brian Finch's Black Op" Aaron Lipstadt Taylor Elmore November 3, 2015 (2015-11-03) 7.86[22]
Brian fakes being sick when Mike & Ike show up for his morning NZT pill in order to create his own version of Ferris Bueller's Day Off with one of the five NZT pills Senator Morra gave him. However, the CIA abducts him before he is even able to leave his apartment to borrow his NZT-enhanced capabilities for a black-ops mission without Naz's clearance nor knowledge, infuriating her and forcing the CIA agent handling the case to return Brian. It becomes clear near the end of the mission that Brian will most likely be killed by the CIA mercenaries who kidnapped him, as the mission has gone off-script. Brian thinks quickly on his feet to get out alive, even with his NZT dose wearing off, and finally manages to escape.
8
"When Pirates Pirate Pirates" Peter Werner Kari Drake November 10, 2015 (2015-11-10) 7.09[23]
Naz is taken into custody because she is under suspicion of funding international group of terrorists. She paid a known terrorist to help with the release of her niece from Southeast-Asian pirates. This brings the whole NZT program at the FBI to a halt and Brian briefly retreats to Naz's home (his new safe house). Together with Naz's daughter, he plans to find a solution using a pill from his stash. They negotiate with the pirates. With the help of Sands, they get Naz out of detention and reinstate her back into her position.
9
"Headquarters!" Doug Aarniokoski Story by : Frances Brennand Roper
Teleplay by : Craig Sweeny November 17, 2015 (2015-11-17) 7.52[24]
Brian begs Naz for his own office which he calls his "headquarters!" To earn it, he sends agents out to track down the FBI's top ten Most Wanted. But, when this endeavor causes too much attention, Naz shuts down the search. Brian meets with his father, who feels they have become increasingly estranged, so Brian tells him about NZT.
10
"Arm-ageddon" Leslie Libman Dennis Saavedra Saldua November 24, 2015 (2015-11-24) 6.53[25]
Brian is asked by Agent Boyle to help his U.S ranger friend whose brain-controlled prosthetic arm appears to have killed his wife against his will. Meanwhile, Brian's father betrays his confidence to a lawyer, leading to danger that Morra will certainly find out.
11
"This is Your Brian on Drugs" Steven A. Adelson Sallie Patrick December 15, 2015 (2015-12-15) 6.70[26]
Agent Casey Rooks and his team steal the NZT pills for themselves, triggering an internal investigation. Rebecca faces relationship issues with Casey and Mike and Ike's allegiance to Finch is tested. After Brian figures out Casey stole the NZT pills, Casey holds Brian at gunpoint, but Boyle shoots him in the head before he could have pulled the trigger on him.
12
"The Assassination of Eddie Morra" Christine Moore Matthew Federman & Stephen Scaia January 5, 2016 (2016-01-05) 7.30[27]
Senator Edward Morra is victim of an assassination attempt while giving a speech at the Intrepid Sea, Air & Space Museum in Manhattan. Sands informs Brian that a woman named Piper Baird is behind the failed attempt on the Senator's life. Piper is a former associate of Morra's, who was involved in the development of the immunity shot. She began questioning the Senator's motives and went rogue, breaking into one of his R&D facilities and stealing a year's supply of the enzyme. Upon finding Piper, Brian has doubts about the intentions of Morra and Sands. Eventually, he helps her fake her death so that she can go into hiding. Towards the end of the episode, the Senator announces his candidacy for President of the United States.
13
"Stop Me Before I Hug Again" Edward Ornelas Jenna Richman January 19, 2016 (2016-01-19) 6.33[28]
Brian needs to find a serial killer. In the process, he finds out an innocent man is in jail, convicted of a series of murders. Brian sets out to prove the man's innocence and catch the real killer. Meanwhile, Brian realizes that Morra's coat from the assassination attempt, on which is Morra's blood, is still in the evidence locker and if tested, Morra will be exposed as an NZT user. After informing Sands, he brings in another coat with Morra's blood without NZT inside it and manages to fool the evidence clerk into letting him in, where he covertly switches the coat just as Rebecca, who is investigating Morra, goes in to retrieve the coat.
14
"Fundamentals of Naked Portraiture" Guy Ferland Story by : Dennis Saavedra Saldua & Craig Sweeny
Teleplay by : Sallie Patrick & Craig Sweeny February 9, 2016 (2016-02-09) 6.39[29]
Brian gets a new bodyguard, Spike. The FBI investigates the death of a programmer who was working on a type of artificial intelligence and who may have been selling secrets to the enemy. Rebecca asks Finch to follow him to the evidence locker again, but Brian is hesitant as the clerk will recognize him. However, just before they are about to make the trip, they hear that the evidence clerk has suddenly died from eating food laced with peanuts (to which he was allergic).
15
"Undercover!" Peter Werner Taylor Elmore February 16, 2016 (2016-02-16) 6.01[30]
Following the theft of the FBI's list of undercover agents, Finch goes undercover with one of them who does not want to come in due to being very close to catching the human traffickers she has been investigating, until she grows romantic feelings for him due to his help. Elsewhere, Brian meets with Sands, who admits that he murdered the evidence clerk's death in order to prevent Brian from being exposed, but Brian argues that Rebecca is now even more suspicious of the circumstances. Sands decides to meet with Rebecca and offers her a job within Morra's organization, but she declines.
16
"Sands, Agent of Morra" Rich Lee Gregory Weidmann & Geoff Tock February 23, 2016 (2016-02-23) 5.87[31]
Brian is visited by his sister, Rachel, for hanging out. However, Brian is suddenly visited by Sands, who is injured. After stitching him up, he swears Rachel to secrecy and goes with Sands to help him out, who is being forced to murder his former army colleagues because he needs to save his son. Coincidentally, Rebecca and Boyle are on a case where a boy of a wealthy political family has been kidnapped, who just happens to be Sands' son. Elsewhere, Rachel has to cover-up for Brian when Ike checks up, but she ends up sleeping with him.
17
"Close Encounters" Maja Vrvilo Kari Drake March 8, 2016 (2016-03-08) 5.40[32]
Amidst a large-scale blackout in Manhattan, Brian tracks down whoever stole an estimated $8 million in cash from the mutilated money vault. Meanwhile, Mike and Ike hear Brian's mother blurt out that there was an injured agent lying in his apartment. To make matters worse, Brian is confronted by his mother about NZT after Rachel produces his spare NZT pills, and she ostracizes him from the family after his father, who is also his attorney, refuses to tell her more after his NZT pills are confiscated. Brian, who covertly steals the pills back, decides to leave and leaves Rebecca an apology note.
18
"Bezgranichnyy" John Behring Matthew Federman & Stephen Scaia March 15, 2016 (2016-03-15) 5.63[34]
Brian, wanting to finally rid himself of Morra's influence on him, travels to St. Petersburg, Russia, where he reconnects with Piper and helps her steal the last ingredient she needs to synthesize the enzyme that protects against NZT damage from the highly secured vault of an eco-friendly Russian millionaire. Meanwhile, Naz launches a search for Brian after finding out that he stole some spare NZT pills.
The title of this episode is Russian for "limitless."[33]
19
"A Dog's Breakfast" Lexi Alexander Jenna Richman March 22, 2016 (2016-03-22) 6.64[35]
Returning from Russia, Brian is placed under increased surveillance by both the FBI and by Sands, while Rebecca, with help from Mike and Ike, starts her own investigation about Brian's meetings with Sands. He solves the case of a man who was murdered and had his kidney stolen. Sands gets to Piper before Brian can and acquires her supply of the enzyme while forcing her to make NZT. Brian comes clean about Piper to Senator Morra, who tells him that Sands has gone AWOL. Meanwhile, after witnessing Brian's visit to Morra, Rebecca goes to his house with handcuffs and demands that Brian explain his connection with Morra.
20
"Hi, My Name Is Rebecca Harris" Holly Dale Mark Goffman April 5, 2016 (2016-04-05) 6.07[36]
When Rebecca confronts Brian about his lies, he admits everything to her about spying for Morra and that Sands killed her father. She then takes his NZT pill for that day and they find Houston's burn book that Brian hid with the information about the NZT purge. This leads them to a former Morra employee who was addicted to NZT and she gives them a cigarette butt with the DNA of the killer. As they leave her trailer, Harris is shot by a sniper sent by Sands to kill them and Brian does field surgery to heal her. They then go visit Huston and attempt to communicate with him in his coma using a homemade EEG machine. With the information gathered, they lure out Sands and arrest him.
21
"Finale: Part One!" Paul Edwards Sallie Patrick & Taylor Elmore April 19, 2016 (2016-04-19) 5.63[37]
When NZT floods the streets of New York City and threatens to become a national epidemic, the FBI partners with the DEA in a city-wide manhunt to find the lab producing the drug. Also, Brian has trouble adjusting to his new reality when he lacks the resources to continue searching for Piper.
22
"Finale: Part Two!!" Douglas Aarniokoski Craig Sweeny & Taylor Elmore April 26, 2016 (2016-04-26) 5.71[38]
Sands enacts a plan regarding Canada's Northwest Passage, as Boyle and Harris fail to save the diplomat Sands orders assassinated. Using details taken from the killer's testimony, Brian and the CJC close in on Sands' real NZT lab. When the lab is raided, Brian learns Piper was there but is gone, while Sands is shot by Rebecca and sent to the hospital. After Brian returns to his parents' house, he learns Piper is there with a permanent NZT immunity shot, but that she has to keep moving so the cure doesn't fall into the wrong hands. Brian returns to the CJC with his own squad to tackle new cases, while Senator Morra is still missing.
Broadcast[edit]
The premiere of Limitless was broadcast in the U.S. on CBS on September 22, 2015.[2] In Canada, the show was simulcast with the American broadcast, which was aired on Global.[39] In Brazil, the TV station Space aired the series on October 1, 2015.[40] The series premiered in Australia on Network Ten on October 11, 2015.[41] In Italy, the series aired on January 3, 2016 on Rai 2. In the United Kingdom and Ireland, the series aired on February 17, 2016 on Sky One.
Reception[edit]
Limitless received mixed reviews from television critics. The review aggregator website Rotten Tomatoes reports a 57% approval rating with an average rating of 6.39/10 based on 47 reviews. The website's critics' consensus reads, "Even with a likable hero, Limitless cannot overcome its credulity-straining premise and shaky, hole-riddled narrative."[42] On Metacritic, the series holds an average score of 57 (out of 100 points) based on 30 critics.[43]
Ratings[edit]
No.
Title
Air date
Rating/share
(18–49)
Viewers
(millions)
DVR
(18–49)
DVR viewers
(millions)
Total
(18–49)
Total viewers
(millions)
1 "Pilot" September 22, 2015 1.9/6 9.86[16] 1.3 4.40 3.2 14.26[44]
2 "Badge! Gun!" September 29, 2015 1.9/7 9.73[17] 1.2 4.10 3.1 13.84[45]
3 "The Legend of Marcos Ramos" October 6, 2015 1.7/6 9.57[18] 1.1 3.53 2.8 13.11[46]
4 "Page 44" October 13, 2015 1.4/5 8.03[19] 1.2 3.64 2.6 11.67[47]
5 "Personality Crisis" October 20, 2015 1.4/4 7.90[20] 1.2 3.63 2.6 11.53[48]
6 "Side Effects May Include..." October 27, 2015 1.4/4 7.45[21] 1.1 3.41 2.5 10.86[49]
7 "Brian Finch's Black Op" November 3, 2015 1.5/5 7.86[22] 1.1 3.27 2.6 11.13[50]
8 "When Pirates Pirate Pirates" November 10, 2015 1.5/5 7.09[23] 1.0 3.20 2.5 10.30[51]
9 "Headquarters!" November 17, 2015 1.4/5 7.52[24] 1.1 3.54 2.5 11.07[52]
10 "Arm-ageddon" November 24, 2015 1.3/4 6.53[25] 0.9 3.15 2.2 9.68[53]
11 "This is Your Brian on Drugs" December 15, 2015 1.3/4 6.63[26] 1.0 3.39 2.3 10.02[54]
12 "The Assassination of Eddie Morra" January 5, 2016 1.4/5 7.40[27] 0.9 2.83 2.3 10.13[55]
13 "Stop Me Before I Hug Again" January 19, 2016 1.2/4 6.33[28] 1.2 3.50 2.4 9.83[56]
14 "Fundamentals of Naked Portraiture" February 9, 2016 1.3/4 6.39[29] 1.0 3.19 2.3 9.57[57]
15 "Undercover!" February 16, 2016 1.2/4 6.01[30] 1.0 3.05 2.2 9.06[58]
16 "Sands, Agent of Morra" February 23, 2016 1.1/4 5.87[31] 1.0 2.93 2.1 8.79[59]
17 "Close Encounters" March 8, 2016 1.1/4 5.40[32] 1.0 3.05 2.1 8.45[60]
18 "Bezgranichnyy" March 15, 2016 1.1/4 5.63[34] 0.8 2.70 1.9 8.33[61]
19 "A Dog's Breakfast" March 22, 2016 1.3/5 6.64[35] 0.9 2.81 2.2 9.46[62]
20 "Hi, My Name is Rebecca Harris..." April 5, 2016 1.1/4 6.07[36] 0.9 2.74 2.0 8.81[63]
21 "Finale: Part One!" April 19, 2016 1.1/4 5.63[37] 0.8 2.49 1.9 8.12[64]
22 "Finale: Part Two!!" April 26, 2016 1.1/4 5.71[38] 0.8 2.52 1.9 7.99[65]
References[edit]
Jump up ^ Andreeva, Nellie (May 8, 2015). "'Limitless', 'Rush Hour', 'Criminal Minds' Spinoff, 'Code', 'Life' Among CBS Orders". Deadline Hollywood. Retrieved August 7, 2015.
^ Jump up to: a b Evry, Max (June 9, 2015). "CBS Announces Fall Premiere Dates, Including Supergirl and Limitless". Comingsoon. Retrieved August 7, 2015.
Jump up ^ Ausiello, Michael (June 9, 2015). "CBS Fall Premiere Dates: Supergirl Gets Big October Launch". TVLine. Retrieved August 7, 2015.
Jump up ^ "EXCLUSIVE: 'Limitless' Is Paying Homage to 'Ferris Bueller's Day Off' and This Opening Scene Is Perfection!]". Entertainment Tonight. Retrieved January 3, 2016.
Jump up ^ Andreeva, Nellie (October 23, 2015). "'Limitless' Receives Full-Season Order From CBS, 'Code Black' Gets 6 Scripts". Deadline.com. Retrieved October 23, 2015.
Jump up ^ Wagmeister, Elizabeth (May 25, 2016). "'Limitless' Showrunner Confirms CBS Cancellation". Variety. Retrieved May 26, 2016.
Jump up ^ Andreva, Nellie (March 11, 2015). "Jake McDorman to Topline CBS Pilot Limitless Based on 2011 Movie". Deadline Hollywood. Retrieved August 7, 2015.
Jump up ^ Andreeva, Nellie (March 12, 2015). "Jennifer Carpenter to Co-Star in CBS Pilot Limitless". Deadline Hollywood. Retrieved August 7, 2015.
Jump up ^ Boyle, Spelman. "When Pirates Pirate Pirates". Limitless.
Jump up ^ Andreeva, Nellie (March 17, 2015). "Hill Harper Joins CBS Pilot Limitless". Deadline Hollywood. Retrieved August 7, 2015.
Jump up ^ Andreeva, Nellie (March 17, 2015). "Mary Elizabeth Mastrantonio Joins CBS Pilot Limitless". Deadline Hollywood. Retrieved August 7, 2015.
Jump up ^ McNutt, Myles (February 17, 2016). "Limitless Adds 'Romantic Caper' to Its Growing Bag of Tricks". Exclamation Point. The A.V. Club. Retrieved February 17, 2016.
Jump up ^ Andreeva, Nellie (May 13, 2015). "Bradley Cooper To Recur On CBS Series Limitless". deadline.com. Retrieved August 7, 2015.
Jump up ^ Finch, Rachel. "Sands, Agent of Morra". Limitless.
Jump up ^ Andreeva, Nellie (July 24, 2015). "Colin Salmon Joins CBS Drama Limitless". deadline.com. Retrieved August 7, 2015.
^ Jump up to: a b Kondolojy, Amanda (September 23, 2015). "Tuesday Final Ratings: 'The Voice', 'NCIS', 'Limitless' & 'The Muppets' Adjusted Up; 'Best Time Ever' Adjusted Down". TV by the Numbers. Retrieved September 23, 2015.
^ Jump up to: a b Dixon, Dani (September 30, 2015). "Tuesday Final Ratings: 'The Voice', + 'NCIS', Adjusted Up; 'Best Time Ever' Adjusted Down". TV by the Numbers. Retrieved September 30, 2015.
^ Jump up to: a b Porter, Rick (October 7, 2015). "Tuesday final ratings: 'The Muppets,' 'NCIS' and 'Scream Queens' adjusted up, 'Flash' and 'iZombie' hold". TV by the Numbers. Retrieved October 7, 2015.
^ Jump up to: a b Porter, Rick (October 14, 2015). "Tuesday Final Ratings: 'The Flash' and 'NCIS' Adjusted Up; 'Chicago Fire' Holds". TV by the Numbers. Retrieved October 14, 2015.
^ Jump up to: a b Porter, Rick (October 21, 2015). "Tuesday final ratings: 'NCIS' and 'Limitless' adjusted up, 'Chicago Fire' adjusted down". TV by the Numbers. Retrieved October 21, 2015.
^ Jump up to: a b Porter, Rick (October 28, 2015). "Tuesday final ratings: 'Fresh Off the Boat,' 'The Flash' and 'NCIS' adjust up, 'Wicked City' stays under 1.0". TV by the Numbers. Retrieved October 28, 2015.
^ Jump up to: a b Porter, Rick (November 4, 2015). "Tuesday final ratings: 'Fresh Off the Boat' and 'Best Time Ever' adjust up". TV by the Numbers. Retrieved November 4, 2015.
^ Jump up to: a b Porter, Rick (November 11, 2015). "Tuesday final ratings: 'Chicago Fire' adjusts down, 'NCIS' adjusts up". TV by the Numbers. Retrieved November 11, 2015.
^ Jump up to: a b Porter, Rick (November 18, 2015). "Tuesday final ratings: 'Flash' and 'NCIS' adjust up, 'Chicago Med' premiere holds". TV by the Numbers. Retrieved November 18, 2015.
^ Jump up to: a b Porter, Rick (November 25, 2015). "Tuesday final ratings: 'NCIS' adjusts up, everything else steady". TV by the Numbers. Retrieved November 25, 2015.
^ Jump up to: a b Porter, Rick (December 16, 2015). "Tuesday final ratings: 'NCIS: New Orleans' adjusts up, 'Voice' finale holds". TV by the Numbers. Retrieved December 17, 2015.
^ Jump up to: a b Porter, Rick (January 6, 2016). "Tuesday final ratings: 'NCIS' and 'NCIS: New Orleans' adjust up". TV by the Numbers. Retrieved January 6, 2016.
^ Jump up to: a b Porter, Rick (January 21, 2016). "Tuesday final ratings: 'Chicago Fire' and 'Hollywood Game Night' adjust up". TV by the Numbers. Retrieved January 21, 2016.
^ Jump up to: a b Porter, Rick (February 10, 2016). "Tuesday final ratings: 'Muppets,' 'iZombie,' 'NCIS: New Orleans' and 'Grinder' all adjust down". TV by the Numbers. Retrieved February 10, 2016.
^ Jump up to: a b Porter, Rick (February 17, 2016). "Tuesday final ratings: 'Hollywood Game Night' and 'iZombie' adjust down". TV by the Numbers. Retrieved February 17, 2016.
^ Jump up to: a b Porter, Rick (February 24, 2016). "Tuesday final ratings: 'Agent Carter' adjusts up". TV by the Numbers. Retrieved February 24, 2016.
^ Jump up to: a b Porter, Rick (March 9, 2016). "Tuesday Final Ratings: 'Limitless' and 'NCIS: New Orleans' rerun adjust up". TV by the Numbers. Retrieved March 9, 2016.
Jump up ^ "What is the Russian word for unlimited?". WordHippo.
^ Jump up to: a b Porter, Rick (March 16, 2016). "Tuesday Final Ratings: 'Crowded' adjusts down". TV by the Numbers. Retrieved March 16, 2016.
^ Jump up to: a b Porter, Rick (March 23, 2016). "Tuesday Final Ratings: 'The Voice' adjusts up". TV by the Numbers. Retrieved March 23, 2016.
^ Jump up to: a b Porter, Rick (April 6, 2016). "Tuesday Final Ratings: 'The Voice' adjusts up, 'Chicago Fire' adjusts down". TV by the Numbers. Retrieved April 6, 2016.
^ Jump up to: a b Porter, Rick (April 20, 2016). "Tuesday Final Ratings: 'NCIS' and 'The Flash' adjust up, 'Containment' adjusts down". TV by the Numbers. Retrieved April 20, 2016.
^ Jump up to: a b Porter, Rick (April 27, 2016). "Tuesday final ratings: 'The Voice' adjusts up, 'Containment' adjusts down". TV by the Numbers. Retrieved April 27, 2016.
Jump up ^ Limitless | Watch Limitless TV Series Online - Global TV, retrieved September 11, 2015
Jump up ^ "Canal Space estreia a inédita Limitless no Brasil nesta quinta". Ligado em Séries. September 29, 2015.
Jump up ^ Knox, David (September 28, 2015). "Airdate: Limitless". TV Tonight. Retrieved September 28, 2015.
Jump up ^ "Limitless: Season 1". Rotten Tomatoes. Retrieved April 10, 2017.
Jump up ^ "Limitless (2015) - Season 1 Reviews". Metacritic. Retrieved October 14, 2015.
Jump up ^ Andreeva, Nellie (October 11, 2015). "'Empire' Hits New High, Leads Premiere Week L+7 Ratings Gains With 'Blindspot'". Deadline. Retrieved October 11, 2015.
Jump up ^ Porter, Rick (October 19, 2015). "Broadcast Live +7 ratings, week 2: 'The Blacklist' premiere joins 'Empire' and 'Blindspot' atop the charts". TV by the Numbers. Retrieved October 19, 2015.
Jump up ^ Porter, Rick (October 31, 2015). "Broadcast Live +7 ratings, week 3: 'Quantico' more than doubles, 'Empire' and 'Blindspot' score biggest gains". TV by the Numbers. Retrieved October 31, 2015.
Jump up ^ Porter, Rick (November 4, 2015). "Broadcast Live +7 ratings, week 4: 'Jane the Virgin' premiere doubles, 'Empire' and 'Blindspot' top charts for Oct. 12-18". TV by the Numbers. Retrieved November 4, 2015.
Jump up ^ Porter, Rick (November 9, 2015). "Broadcast Live +7 ratings, week 5: 'Empire' and 'Blindspot' have biggest toal gains, 5 shows double". TV by the Numbers. Retrieved November 9, 2015.
Jump up ^ Porter, Rick (November 16, 2015). "Broadcast Live +7 ratings: 'Big Bang Theory' and 'Blindspot' top week 6, 'Quantico' doubles in 18-49 and viewers". TV by the Numbers. Retrieved November 16, 2015.
Jump up ^ Porter, Rick (November 23, 2015). "Broadcast Live +7 ratings, week 7: 'Elementary' is still a strong DVR show". TV by the Numbers. Retrieved November 23, 2015.
Jump up ^ Porter, Rick (December 1, 2015). "Broadcast Live +7 ratings, week 8: 'Empire,' 'Big Bang Theory' and 'Quantico' top charts for Nov. 9-15". TV by the Numbers. Retrieved December 1, 2015.
Jump up ^ Porter, Rick (December 7, 2015). "Broadcast Live +7 ratings, week 9: 'Big Bang Theory' makes the biggest gains". TV by the Numbers. Retrieved December 7, 2015.
Jump up ^ Porter, Rick (December 14, 2015). "Broadcast Live +7 ratings, week 10: 'Blindspot' is officially* the biggest gainer in Thanksgiving week". TV by the Numbers. Retrieved December 14, 2015.
Jump up ^ Porter, Rick (January 5, 2016). "Broadcast Live +7 ratings: 'Big Bang Theory' and 'Jane the Virgin' lead a light week 13". TV by the Numbers. Retrieved January 6, 2015.
Jump up ^ Porter, Rick (January 25, 2016). "Broadcast Live +7 ratings: 'Shades of Blue' premiere gets a good lift in week 16". TV by the Numbers. Retrieved January 25, 2016.
Jump up ^ Porter, Rick (February 8, 2016). "Broadcast Live +7 ratings: 'X-Files' premiere dominates week 18, 'Limitless' doubles". TV by the Numbers. Retrieved February 8, 2016.
Jump up ^ Porter, Rick (February 29, 2016). "Broadcast Live +7 ratings: 'How to Get Away with Murder,' 5 other shows double in a DVR-heavy week 21". TV by the Numbers. Retrieved February 29, 2016.
Jump up ^ Porter, Rick (March 7, 2016). "Broadcast Live +7 ratings: 'The Blacklist' and 'The Big Bang Theory' lead week 22". TV by the Numbers. Retrieved March 7, 2016.
Jump up ^ Porter, Rick (March 14, 2016). "Broadcast Live +7 ratings: 'Big Bang Theory' has biggest week 23 gain, 'Jane the Virgin' and 3 others double". TV by the Numbers. Retrieved March 14, 2016.
Jump up ^ Porter, Rick (March 28, 2016). "Broadcast Live +7 ratings: 'The Big Bang Theory' and 'Quantico' lead week 25". TV by the Numbers. Retrieved March 28, 2016.
Jump up ^ Porter, Rick (April 5, 2016). "Broadcast Live +7 ratings: 'Modern Family' and 'Blindspot' gain the most for March 14–20". TV by the Numbers. Retrieved April 5, 2016.
Jump up ^ Porter, Rick (April 11, 2016). "Broadcast Live +7 ratings: 'Modern Family' tops the week of March 21–27, 4 shows double". TV by the Numbers. Retrieved April 11, 2016.
Jump up ^ Porter, Rick (April 25, 2016). "Broadcast Live +7 ratings: 'Empire' and 'Big Bang Theory' stay on top for April 4–10". TV by the Numbers. Retrieved April 25, 2016.
Jump up ^ Porter, Rick (May 9, 2016). "Broadcast Live +7 ratings: 'Empire' and 'Big Bang Theory' lead for April 18–24, 5 shows double". TV by the Numbers. Retrieved May 10, 2016.
Jump up ^ Porter, Rick (May 17, 2016). "Broadcast Live +7 ratings: 'Big Bang Theory,' 'Empire' and 'Blacklist' lead for April 25-May 1". TV by the Numbers. Retrieved May 19, 2016.
External links[edit]
Official website
Limitless on IMDb
Retrieved from "https://en.wikipedia.org/w/index.php?title=Limitless_(TV_series)&oldid=864736204"
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