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82-637: (Redirected from Vmax ) VMAX , Vmax or V max may refer to: V max (maximum voltage/velocity) [ edit ] V max , the maximum voltage attained in the action potential . V max , maximum aortic velocity, the maximum speed of blood flow in the aorta of the heart, also less commonly noted as AoV max Maximal rate in Michaelis–Menten kinetics See V Speeds for aircraft speeds VMAX, V-Max or Vmax [ edit ] Yamaha V-Max and VMAX , motorcycles EMC Symmetrix , VMAX Series,

164-647: A gene . Figure 3 shows the important ion channels involved in the cardiac action potential, the current (ions) that flows through the channels, their main protein subunits (building blocks of the channel), some of their controlling genes that code for their structure, and the phases that are active during the cardiac action potential. Some of the most important ion channels involved in the cardiac action potential are described briefly below. Hyperpolarization-activated cyclic nucleotide-gated channels (HCN channels) are located mainly in pacemaker cells, these channels become active at very negative membrane potentials and allow for

246-617: A +2 charge is leaving the cell (by the Ca ) therefore there is a net charge of +1 entering the cell). This calcium is then pumped back into the cell and back into the SR via calcium pumps (including the SERCA ). This phase consists of a rapid, positive change in voltage across the cell membrane ( depolarization ) lasting less than 2 ms in ventricular cells and 10–20 ms in SAN cells. This occurs due to

328-411: A data storage product line from EMC Corporation Maximum Velocity (V-Max) , an Italian movie Vmax cinemas of Event Cinemas and Village Cinemas , features larger screens and enhanced visual and audio quality VMaX (Véhicule Manœuvrant Expérimental) a French hypersonic glide vehicle Topics referred to by the same term [REDACTED] This disambiguation page lists articles associated with

410-478: A duration of 20–40 msec would give an isoelectric wave and anything under 20 msec would result in a negative T-wave. Early repolarization is a phenomenon that can be seen in ECG recordings of ventricular cells where there is an elevated ST segment, also known as a J wave. The J wave is prominent when there is a larger outward current in the epicardium compared to the endocardium. It has been historically considered to be

492-443: A net flow of positive charge into the cell. In non-pacemaker cells (i.e. ventricular cells), this is produced predominantly by the activation of Na channels , which increases the membrane conductance (flow) of Na (g Na ). These channels are activated when an action potential arrives from a neighbouring cell, through gap junctions . When this happens, the voltage within the cell increases slightly. If this increased voltage reaches

574-421: A net outward positive current, corresponding to negative change in membrane potential , thus allowing more types of K channels to open. These are primarily the rapid delayed rectifier K channels (I Kr ) and the inwardly rectifying K current, I K1 . This net outward, positive current (equal to loss of positive charge from the cell) causes the cell to repolarize. The delayed rectifier K channels close when

656-403: A normal variant in cardiac rhythm but recent studies show that it is related to an increased risk of cardiac arrest. Early repolarization occurs mainly in males and is associated with a larger potassium current caused by the hormone testosterone . Additionally, although the risk is unknown, African American individuals seem more likely to have the early repolarization more often. As mentioned in

738-428: A pore through which ions (including Na , Ca and K ) can pass. As potassium is highest within the cell, it is mainly potassium that passes through. This increased potassium in the neighbour cell causes the membrane potential to increase slightly, activating the sodium channels and initiating an action potential in this cell. (A brief chemical gradient driven efflux of Na+ through the connexon at peak depolarization causes

820-456: A protein, called a G s -protein (s for stimulatory). Activation of this G-protein leads to increased levels of cAMP in the cell (via the cAMP pathway ). cAMP binds to the HCN channels (see above), increasing the funny current and therefore increasing the rate of depolarization, during the pacemaker potential. The increased cAMP also increases the opening time of L -type calcium channels, increasing

902-496: A receptor located on the outside of the pacemaker cell, called an M2 muscarinic receptor . This activates a G i -protein (I for inhibitory), which is made up of 3 subunits (α, β and γ) which, when activated, separate from the receptor. The β and γ subunits activate a special set of potassium channels, increasing potassium flow out of the cell and decreasing membrane potential, meaning that the pacemaker cells take longer to reach their threshold value. The G i -protein also inhibits

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984-425: A selective pharmacological blocker for voltage gated K channels. The lack of repolarization means that neuron stays at a high voltage, which slows sodium channel deactivation to a point where there is not enough inwards Na current to depolarize and sustain firing. The structure of the voltage gated K channel is that of six transmembrane helices along the lipid bilayer . The selectivity of this channel to voltage

1066-405: Is a stage of an action potential in which the cell experiences a decrease of voltage due to the efflux of potassium (K ) ions along its electrochemical gradient. This phase occurs after the cell reaches its highest voltage from depolarization. After repolarization, the cell hyperpolarizes as it reaches resting membrane potential (−70 mV in neuron). Sodium (Na ) and potassium ions inside and outside

1148-510: Is affected, but not controlled by the autonomic nervous system . The sympathetic nervous system (nerves dominant during the body's fight-or-flight response ) increase heart rate (positive chronotropy ), by decreasing the time to produce an action potential in the SAN. Nerves from the spinal cord release a molecule called noradrenaline , which binds to and activates receptors on the pacemaker cell membrane called β1 adrenoceptors . This activates

1230-433: Is characterized by inward S4 motion. The switch from depolarization into repolarization is dependent on the kinetic mechanisms of both voltage gated K and Na channels . Although both voltage gated Na and K channels activate at roughly the same voltage (−50 mV ), Na channels have faster kinetics and activate/deinactivate much more quickly. Repolarization occurs as the influx of Na decreases (channels deinactivate) and

1312-496: Is known as repolarization . Another important ion is calcium (Ca ) , which can be found inside the cell in the sarcoplasmic reticulum (SR) where calcium is stored, and is also found outside of the cell. Release of Ca from the SR, via a process called calcium-induced calcium release , is vital for the plateau phase of the action potential (see phase 2, below) and is a fundamental step in cardiac excitation-contraction coupling . There are important physiological differences between

1394-405: Is known as the all-or-none law . The influx of calcium ions (Ca ) through L-type calcium channels also constitutes a minor part of the depolarisation effect. The slope of phase 0 on the action potential waveform (see figure 2) represents the maximum rate of voltage change of the cardiac action potential and is known as dV/dt max . In pacemaker cells (e.g. sinoatrial node cells ), however,

1476-441: Is known as the absolute refractory period during which it is impossible for the cell to produce another action potential. This is immediately followed, until the end of phase 3, by a relative refractory period, during which a stronger-than-usual stimulus is required to produce another action potential. These two refractory periods are caused by changes in the states of sodium and potassium channels . The rapid depolarization of

1558-473: Is less steep than that in the non-pacemaker action potential waveform. This phase begins with the rapid inactivation of the Na channels by the inner gate (inactivation gate), reducing the movement of sodium into the cell. At the same time potassium channels (called I to1 ) open and close rapidly, allowing for a brief flow of potassium ions out of the cell, making the membrane potential slightly more negative. This

1640-513: Is mediated by four of these transmembrane domains (S1–S4) – the voltage sensing domain. The other two domains (S5, S6) form the pore by which ions traverse. Activation and deactivation of the voltage gated K channel is triggered by conformational changes in the voltage sensing domain. Specifically, the S4 domain moves such that it activates and deactivates the pore. During activation, there is outward S4 motion, causing tighter VSD-pore linkage. Deactivation

1722-441: Is referred to as a 'notch' on the action potential waveform. There is no obvious phase 1 present in pacemaker cells. This phase is also known as the "plateau" phase due to the membrane potential remaining almost constant, as the membrane slowly begins to repolarize. This is due to the near balance of charge moving into and out of the cell. During this phase delayed rectifier potassium channels (I ks ) allow potassium to leave

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1804-491: Is responsible for the large duration of the action potential and is important in preventing irregular heartbeat (cardiac arrhythmia). There is no plateau phase present in pacemaker action potentials. During phase 3 (the "rapid repolarization" phase) of the action potential, the L-type Ca channels close, while the slow delayed rectifier (I Ks ) K channels remain open as more potassium leak channels open. This ensures

1886-479: Is strongly recommended. In addition, a patient may be more prone to atrial fibrillation if the individual has early repolarization syndrome and is under sixty years of age. Patients who suffer from obstructive sleep apnea can experience impaired cardiac repolarization, increasing the morbidity and mortality of the condition greatly. Especially at higher altitudes, patients are much more susceptible to repolarization disturbances. This can be somewhat mitigated through

1968-515: Is the classic athletic heart syndrome . Sustained training of athletes causes a cardiac adaptation where the resting SAN rate is lower (sometimes around 40 beats per minute). This can lead to atrioventricular block , where the signal from the SAN is impaired in its path to the ventricles. This leads to uncoordinated contractions between the atria and ventricles, without the correct delay in between and in severe cases can result in sudden death. The speed of action potential production in pacemaker cells

2050-436: Is the property of the specialized conductive muscle cells of the heart to generate spontaneous cardiac action potentials. Automaticity can be normal or abnormal, caused by temporary ion channel characteristic changes such as certain medication usage, or in the case of abnormal automaticity the changes are in electrotonic environment , caused, for example, by myocardial infarction . The standard model used to understand

2132-424: Is thought to be due to a group of channels, referred to as HCN channels (Hyperpolarization-activated cyclic nucleotide-gated) . These channels open at very negative voltages (i.e. immediately after phase 3 of the previous action potential; see below) and allow the passage of both K and Na into the cell. Due to their unusual property of being activated by very negative membrane potentials, the movement of ions through

2214-496: The Goldman-Hodgkin-Katz voltage equation . However, pacemaker cells are never at rest. In these cells, phase 4 is also known as the pacemaker potential . During this phase, the membrane potential slowly becomes more positive, until it reaches a set value (around -40 mV; known as the threshold potential) or until it is depolarized by another action potential, coming from a neighboring cell. The pacemaker potential

2296-515: The T-tubule membrane of ventricular cells, whereas the T-type channels are found mainly within atrial and pacemaker cells , but still to a lesser degree than L-type channels. These channels respond to voltage changes across the membrane differently: L-type channels are activated by more positive membrane potentials, take longer to open and remain open longer than T-type channels. This means that

2378-456: The atria to contract, to the atrioventricular node (AVN) , which slows down conduction of the action potential from the atria to the ventricles . This delay allows the ventricles to fully fill with blood before contraction. The signal then passes down through a bundle of fibres called the bundle of His , located between the ventricles, and then to the Purkinje fibers at the bottom (apex) of

2460-458: The pacemaker cells of the sinoatrial node , that spontaneously generate the cardiac action potential and those non-pacemaker cells that simply conduct it, such as ventricular myocytes ). The specific differences in the types of ion channels expressed and mechanisms by which they are activated results in differences in the configuration of the action potential waveform, as shown in figure 2. Cardiac automaticity also known as autorhythmicity ,

2542-434: The selectivity filter of the K channel pore. Repolarization typically results from the movement of positively charged K ions out of the cell. The repolarization phase of an action potential initially results in hyperpolarization , attainment of a membrane potential, termed the afterhyperpolarization , that is more negative than the resting potential . Repolarization usually takes several milliseconds. Repolarization

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2624-449: The threshold potential (approximately −70 mV) it causes the Na channels to open. This produces a larger influx of sodium into the cell, rapidly increasing the voltage further to around +50 mV, i.e. towards the Na equilibrium potential. However, if the initial stimulus is not strong enough, and the threshold potential is not reached, the rapid sodium channels will not be activated and an action potential will not be produced; this

2706-437: The Ca current through the channel, speeding up phase 0. The parasympathetic nervous system ( nerves dominant while the body is resting and digesting) decreases heart rate (negative chronotropy ), by increasing the time taken to produce an action potential in the SAN. A nerve called the vagus nerve , that begins in the brain and travels to the sinoatrial node, releases a molecule called acetylcholine (ACh) which binds to

2788-409: The HCN channels is referred to as the funny current (see below). Another hypothesis regarding the pacemaker potential is the 'calcium clock'. Calcium is released from the sarcoplasmic reticulum within the cell. This calcium then increases activation of the sodium-calcium exchanger resulting in the increase in membrane potential (as a +3 charge is being brought into the cell (by the 3Na ) but only

2870-449: The T-type channels contribute more to depolarization (phase 0) whereas L-type channels contribute to the plateau (phase 2). In the heart's conduction system electrical activity that originates from the sinoatrial node (SAN) is propagated via the His - Purkinje network, the fastest conduction pathway within the heart. The electrical signal travels from the sinoatrial node, which stimulates

2952-429: The action potential in the atria and ventricles . Similar to skeletal muscle, the resting membrane potential (voltage when the cell is not electrically excited) of ventricular cells is around −90 millivolts (mV; 1 mV = 0.001 V), i.e. the inside of the membrane is more negative than the outside. The main ions found outside the cell at rest are sodium (Na ), and chloride (Cl ), whereas inside

3034-472: The action potential is a fundamental property of cardiac cells and alterations can lead to severe cardiac diseases including cardiac arrhythmia and sometimes sudden death. Action potential activity within the heart can be recorded to produce an electrocardiogram (ECG). This is a series of upward and downward spikes (labelled P, Q, R, S and T) that represent the depolarization (voltage becoming more positive) and repolarization (voltage becoming more negative) of

3116-475: The action potential, characteristically generated by the influx of Na through voltage gated Na channels, there is a period of repolarization in which the Na channels are inactivated while K channels are activated. Further study of K channels shows that there are four types which influence the repolarization of the cell membrane to re-establish the resting potential. The four types are K v 1, K v 2, K v 3 and K v 4. The K v 1 channel primarily influences

3198-452: The atrial diastole phase when the current undergoes hyperpolarization. Specifically, these channels are activated when Ca binds to calmodulin (CaM) because the N-lobe of CaM interacts with the channel's S4/S5 linker to induce conformational change. When these K channels are activated, the K ions rush out of the cell during the peak of its action potential causing the cell to repolarize as

3280-415: The cAMP pathway therefore reducing the sympathetic effects caused by the spinal nerves. Antiarrhythmic drugs are used to regulate heart rhythms that are too fast. Other drugs used to influence the cardiac action potential include sodium channel blockers , beta blockers , potassium channel blockers , and calcium channel blockers . Repolarization In neuroscience , repolarization refers to

3362-454: The cardiac action potential is that of the ventricular myocyte. Outlined below are the five phases of the ventricular myocyte action potential, with reference also to the SAN action potential. In the ventricular myocyte, phase 4 occurs when the cell is at rest, in a period known as diastole . In the standard non-pacemaker cell the voltage during this phase is more or less constant, at roughly -90 mV. The resting membrane potential results from

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3444-401: The cell and K into the cell to restore the original resting ion concentrations. Blockages in repolarization can arise due to modifications of the voltage-gated K channels. This is demonstrated with selectively blocking voltage gated K channels with the antagonist tetraethylammonium (TEA). By blocking the channel, repolarization is effectively stopped. Dendrotoxins are another example of

3526-438: The cell and two K into the cell. Another example is the sodium-calcium exchanger which removes one Ca from the cell for three Na into the cell. During this phase the membrane is most permeable to K , which can travel into or out of cell through leak channels, including the inwardly rectifying potassium channel. Therefore, the resting membrane potential is mostly equal to K equilibrium potential and can be calculated using

3608-455: The cell are moved by a sodium potassium pump, ensuring that electrochemical equilibrium remains unreached to allow the cell to maintain a state of resting membrane potential. In the graph of an action potential, the hyper-polarization section looks like a downward dip that goes lower than the line of resting membrane potential. In this afterhyperpolarization (the downward dip), the cell sits at more negative potential than rest (about −80 mV) due to

3690-449: The cell it is mainly potassium (K ). The action potential begins with the voltage becoming more positive; this is known as depolarization and is mainly due to the opening of sodium channels that allow Na to flow into the cell. After a delay (known as the absolute refractory period ), the action potential terminates as potassium channels open, allowing K to leave the cell and causing the membrane potential to return to negative, this

3772-479: The cell while L-type calcium channels (activated by the influx of sodium during phase 0) allow the movement of calcium ions into the cell. These calcium ions bind to and open more calcium channels (called ryanodine receptors) located on the sarcoplasmic reticulum within the cell, allowing the flow of calcium out of the SR. These calcium ions are responsible for the contraction of the heart. Calcium also activates chloride channels called I to2 , which allow Cl to enter

3854-408: The cell would slowly lose its membrane potential. The second purpose, intricately linked to the first, is to keep the intracellular concentration more or less constant, and in this case to re-establish the original chemical gradients, that is to force the sodium and calcium which previously flowed into the cell out of it, and the potassium which previously flowed out of the cell back into it (though as

3936-400: The cell, during phase 0, causes the membrane potential to approach sodium's equilibrium potential (i.e. the membrane potential at which sodium is no longer drawn into or out of the cell). As the membrane potential becomes more positive, the sodium channels then close and lock, this is known as the "inactivated" state. During this state the channels cannot be opened regardless of the strength of

4018-504: The cell. Increased calcium concentration in the cell also increases activity of the sodium-calcium exchangers, while increased sodium concentration (from the depolarisation of phase 0) increases activity of the sodium-potassium pumps. The movement of all these ions results in the membrane potential remaining relatively constant, with K outflux, Cl influx as well as Na /K pumps contributing to repolarisation and Ca influx as well as Na /Ca exchangers contributing to depolarisation. This phase

4100-414: The change in membrane potential that returns it to a negative value just after the depolarization phase of an action potential which has changed the membrane potential to a positive value. The repolarization phase usually returns the membrane potential back to the resting membrane potential . The efflux of potassium (K ) ions results in the falling phase of an action potential. The ions pass through

4182-447: The channel. The pore formed by an ion channel is aqueous (water-filled) and allows the ion to rapidly travel across the membrane. Ion channels can be selective for specific ions, so there are Na , K , Ca , and Cl specific channels. They can also be specific for a certain charge of ions (i.e. positive or negative). Each channel is coded by a set of DNA instructions that tell the cell how to make it. These instructions are known as

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4264-486: The conduction of cell to cell depolarization, not potassium.) These connections allow for the rapid conduction of the action potential throughout the heart and are responsible for allowing all of the cells in the atria to contract together as well as all of the cells in the ventricles. Uncoordinated contraction of heart muscles is the basis for arrhythmia and heart failure. Ion channels are proteins that change shape in response to different stimuli to either allow or prevent

4346-422: The depolarization period of a neuron. When the K v 4 channel is blocked, the action potential becomes broader, resulting in an extended repolarization period, delaying the neuron from being able to fire again. The rate of repolarization closely regulates the amount of Ca ions entering the cell. When large quantities of Ca ions enter the cell due to extended repolarization periods, the neuron may die, leading to

4428-442: The depolarization phase. However, as the membrane potential continues to become more positive, the channel begins to allow the passage of K out of the cell. This outward flow of potassium ions at the more positive membrane potentials means that the K ir can also aid the final stages of repolarisation. The voltage-gated potassium channels (K v ) are activated by depolarization. The currents produced by these channels include

4510-421: The development of stroke or seizures. The K v 1 channels are found to contribute to repolarization of pyramidal neurons , likely associated with an upregulation of the K v 4 channels. The K v 2 channels were not found to contribute to repolarization rate as blocking these channels did not result in changes in neuron repolarization rates. Another type of K channel that helps to mediate repolarization in

4592-432: The efflux of K ions increases as its channels open. The decreased conductance of sodium ions and increased conductance of potassium ions cause the cell's membrane potential to very quickly return to, and past the resting membrane potential, which causes the hyperpolarization due to the potassium channels closing slowly, allowing more potassium to flow through after the resting membrane potential has been reached. Following

4674-399: The excitatory stimulus—this gives rise to the absolute refractory period. The relative refractory period is due to the leaking of potassium ions, which makes the membrane potential more negative (i.e. it is hyperpolarised), this resets the sodium channels; opening the inactivation gate, but still leaving the channel closed. Because some of the voltage-gated sodium ion channels have recovered and

4756-434: The flow of K into the cell. This influx of potassium, however, is larger when the membrane potential is more negative than the equilibrium potential for K (~-90 mV). As the membrane potential becomes more positive (i.e. during cell stimulation from a neighbouring cell), the flow of potassium into the cell via the K ir decreases. Therefore, K ir is responsible for maintaining the resting membrane potential and initiating

4838-424: The flux of ions having flowed into the cell (e.g. sodium and calcium), the flux of ions having flowed out of the cell (e.g. potassium, chloride and bicarbonate), as well as the flux of ions generated by the different membrane pumps, being perfectly balanced. The activity of these pumps serve two purposes. The first is to maintain the existence of the resting membrane potential by countering the depolarisation due to

4920-494: The heart, causing ventricular contraction. In addition to the SAN, the AVN and Purkinje fibres also have pacemaker activity and can therefore spontaneously generate an action potential. However, these cells usually do not depolarize spontaneously, simply because action potential production in the SAN is faster. This means that before the AVN or Purkinje fibres reach the threshold potential for an action potential, they are depolarized by

5002-420: The high-frequency firing that mammalian neurons require. Areas with dense K v 3 channels include the neocortex , basal ganglia , brain stem and hippocampus as these regions create microsecond action potentials that requires quick repolarization. Utilizing voltage-clamp data from experiments based on rodent neurons, the K v 4 channels are associated with the primary repolarization conductance following

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5084-502: The human atria is the SK channel , which are K channels which are activated by increases in Ca concentration. "SK channel" stands for a small conductance calcium activated potassium channel, and the channels are found in the heart. SK channels specifically act in the right atrium of the heart, and have not been found to be functionally important in the ventricles of the human heart. The channels are active during repolarization as well as during

5166-415: The increase in membrane voltage is mainly due to activation of L-type calcium channels. These channels are also activated by an increase in voltage, however this time it is either due to the pacemaker potential (phase 4) or an oncoming action potential. The L-type calcium channels are activated more slowly than the sodium channels, therefore, the depolarization slope in the pacemaker action potential waveform

5248-537: The influx of Ca ions are exceeded by K ions leaving the cell continuously. In the human ventricles , repolarization can be seen on an ECG ( electrocardiogram ) via the J-wave (Osborn), ST segment , T wave and U wave . Due to the complexity of the heart, specifically how it contains three layers of cells ( endocardium , myocardium and epicardium ), there are many physiological changes effecting repolarization that will also affect these waves. Apart from changes in

5330-420: The leakage of ions not at the electrochemical equilibrium (e.g. sodium and calcium). These ions not being at the equilibrium is the reason for the existence of an electrical gradient, for they represent a net displacement of charges across the membrane, which are unable to immediately re-enter the cell to restore the electrical equilibrium. Therefore, their slow re-entrance in the cell needs to be counterbalanced or

5412-400: The membrane potential is restored to about -85 to -90 mV, while I K1 remains conducting throughout phase 4, which helps to set the resting membrane potential Ionic pumps as discussed above, like the sodium-calcium exchanger and the sodium-potassium pump restore ion concentrations back to balanced states pre-action potential. This means that the intracellular calcium is pumped out, which

5494-451: The membrane, which usually occurs from neighboring cells, through gap junctions. They allow for a rapid flow of sodium into the cell, depolarizing the membrane completely and initiating an action potential. As the membrane potential increases, these channels then close and lock (become inactive). Due to the rapid influx sodium ions (steep phase 0 in action potential waveform) activation and inactivation of these channels happens almost at exactly

5576-440: The movement of specific ions across a membrane. They are said to be selectively permeable. Stimuli, which can either come from outside the cell or from within the cell, can include the binding of a specific molecule to a receptor on the channel (also known as ligand-gated ion channels ) or a change in membrane potential around the channel, detected by a sensor (also known as voltage-gated ion channels ) and can act to open or close

5658-480: The oncoming impulse from the SAN This is called "overdrive suppression". Pacemaker activity of these cells is vital, as it means that if the SAN were to fail, then the heart could continue to beat, albeit at a lower rate (AVN= 40-60 beats per minute, Purkinje fibres = 20-40 beats per minute). These pacemakers will keep a patient alive until the emergency team arrives. An example of premature ventricular contraction

5740-616: The passage of both Na and K into the cell (which is a movement known as a funny current, I f ). These poorly selective, cation (positively charged ions) channels conduct more current as the membrane potential becomes more negative (hyperpolarised). The activity of these channels in the SAN cells causes the membrane potential to depolarise slowly and so they are thought to be responsible for the pacemaker potential. Sympathetic nerves directly affect these channels, resulting in an increased heart rate (see below). These sodium channels are voltage-dependent, opening rapidly due to depolarization of

5822-453: The plateau phase of the action potential, and are named based on the speed at which they activate: slowly activating I Ks , rapidly activating I Kr and ultra-rapidly activating I Kur . There are two voltage-gated calcium channels within cardiac muscle: L-type calcium channels ('L' for Long-lasting) and T-type calcium channels ('T' for Transient, i.e. short). L-type channels are more common and are most densely populated within

5904-404: The potassium is mostly at the electrochemical equilibrium, its chemical gradient will naturally reequilibrate itself opposite to the electrical gradient, without the need for an active transport mechanism). For example, the sodium (Na ) and potassium (K ) ions are maintained by the sodium-potassium pump which uses energy (in the form of adenosine triphosphate (ATP) ) to move three Na out of

5986-589: The previous section, early repolarization is known as appearing as elevated wave segments on ECGs. Recent studies have shown a connection between early repolarization and sudden cardiac death , which is identified as early repolarization syndrome. The condition is shown in both ventricular fibrillation without other structural heart defects as well as an early depolarization pattern, which can be seen on ECG. The primary root of early repolarization syndrome stems from malfunctions of electrical conductance in ion channels, which may be due to genetic factors. Malfunctions of

6068-400: The repolarization of the axon. The K v 2 channel is characteristically activated slower. The K v 4 channels are characteristically activated rapidly. When K v 2 and K v 4 channels are blocked, the action potential predictably widens. The K v 3 channels open at a more positive membrane potential and deactivate 10 times faster than the other K v channels. These properties allow for

6150-406: The same time. During the inactivation state, Na cannot pass through (absolute refractory period). However they begin to recover from inactivation as the membrane potential becomes more negative (relative refractory period). The two main types of potassium channels in cardiac cells are inward rectifiers and voltage-gated potassium channels. Inwardly rectifying potassium channels (K ir) favour

6232-552: The slow inactivation of voltage gated K delayed rectifier channels, which are the primary K channels associated with repolarization. At these low voltages, all of the voltage gated K channels close, and the cell returns to resting potential within a few milliseconds. A cell which is experiencing repolarization is said to be in its absolute refractory period. Other voltage gated K channels which contribute to repolarization include A-type channels and Ca -activated K channels . Protein transport molecules are responsible for Na out of

6314-405: The structure of the heart that effect repolarization, there are many pharmaceuticals that have the same effect. On top of that, repolarization is also altered based on the location and duration of the initial action potential . In action potentials stimulated on the epicardium, it was found that the duration of the action potential needed to be 40–60 msec to give a normal, upright T-wave, whereas

6396-750: The syndrome include fluctuating sodium, potassium, and calcium currents. Changes in these currents may result in overlap of myocardial regions undergoing different phases of the action potential simultaneously, leading to risk of ventricular fibrillation and arrhythmias . Upon being diagnosed, most individuals do not need immediate intervention, as early repolarization on an ECG does not indicate any life-threatening medical emergency. Three to thirteen percent of healthy individuals have been observed to have early repolarization on an ECG. However, patients who display early repolarization after surviving an event of early repolarization syndrome (a sudden-cardiac death experience), an implantable cardioverter-defibrillator (ICD)

6478-470: The title VMAX . If an internal link led you here, you may wish to change the link to point directly to the intended article. Retrieved from " https://en.wikipedia.org/w/index.php?title=VMAX&oldid=1193187012 " Category : Disambiguation pages Hidden categories: Short description is different from Wikidata All article disambiguation pages All disambiguation pages Cardiac action potential Rate dependence of

6560-441: The transient out potassium current I to1 . This current has two components. Both components activate rapidly, but I to,fast inactivates more rapidly than I to, slow . These currents contribute to the early repolarization phase (phase 1) of the action potential. Another form of voltage-gated potassium channels are the delayed rectifier potassium channels. These channels carry potassium currents which are responsible for

6642-439: The voltage-gated potassium ion channels remain open, it is possible to initiate another action potential if the stimulus is stronger than a stimulus which can fire an action potential when the membrane is at rest. Gap junctions allow the action potential to be transferred from one cell to the next (they are said to electrically couple neighbouring cardiac cells ). They are made from the connexin family of proteins, that form

6724-499: Was responsible for cardiac myocyte contraction. Once this is lost, the contraction stops and the heart muscles relax. In the sinoatrial node, this phase is also due to the closure of the L-type calcium channels, preventing inward flux of Ca and the opening of the rapid delayed rectifier potassium channels (I Kr ). Cardiac cells have two refractory periods , the first from the beginning of phase 0 until part way through phase 3; this

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