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Cardiac Arrhythmias: Difference between revisions
→Cardiac Action Potential
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The cardiac action potential is a result of ions flowing through different ion channels. Ion channels are passages for ions (mainly Na<sup>+</sup>, K<sup>+</sup>, Ca<sup>2+</sup> and Cl<sup>-</sup>) that facilitate movement through the cell membrane. Changes in the structure of these channels can open, inactivate or close these channels and thereby control the flow of ions into and out of the myocytes. Due to differences in expression of the type and structure of ion channels, the various parts of the cardiac conduction system have slightly different action potential characteristics. Ion channels are mostly a passive passageway, where movement of ions is caused by the electrochemical gradient. In addition to these passive ion channels a few active trigger-dependent channels exist that open or close in response to certain stimuli (for instance acetylcholine or ATP). These changes in the membrane potential produce and action potential lasting a few hundreds of milliseconds. Disorders in single channels can lead to arrhythmias, as seen in the section [[Primary_Arrhythmias]]. The action potential is propagated throughout the myocardium by the depolarization of the immediate environment of the cells and through intracellular coupling with gap-junctions. | The cardiac action potential is a result of ions flowing through different ion channels. Ion channels are passages for ions (mainly Na<sup>+</sup>, K<sup>+</sup>, Ca<sup>2+</sup> and Cl<sup>-</sup>) that facilitate movement through the cell membrane. Changes in the structure of these channels can open, inactivate or close these channels and thereby control the flow of ions into and out of the myocytes. Due to differences in expression of the type and structure of ion channels, the various parts of the cardiac conduction system have slightly different action potential characteristics. Ion channels are mostly a passive passageway, where movement of ions is caused by the electrochemical gradient. In addition to these passive ion channels a few active trigger-dependent channels exist that open or close in response to certain stimuli (for instance acetylcholine or ATP). These changes in the membrane potential produce and action potential lasting a few hundreds of milliseconds. Disorders in single channels can lead to arrhythmias, as seen in the section [[Primary_Arrhythmias]]. The action potential is propagated throughout the myocardium by the depolarization of the immediate environment of the cells and through intracellular coupling with gap-junctions. | ||
In summary during the depolarization, sodium ions (Na<sup>+</sup>) stream into the cell followed by a influx of calcium (Ca<sup>2+</sup>) ions (both from the inside (sarcoplasmatic reticulum) and outside of the cell). These Ca<sup>2+</sup> ions cause the actual muscular contraction. Shortly thereafter potassium (K<sup>+</sup>) ions flow out of the cell, causing repolarization. During repolarization the ion | In summary during the depolarization, sodium ions (Na<sup>+</sup>) stream into the cell followed by a influx of calcium (Ca<sup>2+</sup>) ions (both from the inside (sarcoplasmatic reticulum) and outside of the cell). These Ca<sup>2+</sup> ions cause the actual muscular contraction. Shortly thereafter potassium (K<sup>+</sup>) ions flow out of the cell, causing repolarization. During repolarization the ion concentrations return to their resting concentrations, due to the passive efflux of K<sup>+</sup> and active exchange of Na<sup>+</sup> with Ca<sup>2+</sup> (Figure 1). In detail the (ventricular) action potential can be divided in five phases: | ||
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[[File:AP.png|thumb|500px|'''Figure 1.''' The cardiac action potential and relevant ion channels.]] | [[File:AP.png|thumb|500px|'''Figure 1.''' The cardiac ventricular action potential and relevant ion channels.]] | ||
===Phase 0: Rapid Depolarization=== | ===Phase 0: Rapid Depolarization=== | ||
Rapid depolarization is started once the membrane potential reaches a certain threshold (about -70 to -60 mV), independent of the size of the depolarizing stimulus. This produces a rapid influx of Na<sup>+</sup> and a rapid upstroke of the action potential. At higher potentials (-40 to -30) Ca<sup>2+</sup> influx participates in the upstroke. In sinus node and AV node a slower upstroke can be observed (Figure | Rapid depolarization is started once the membrane potential reaches a certain threshold (about -70 to -60 mV), independent of the size of the depolarizing stimulus. This produces a rapid influx of Na<sup>+</sup> and a rapid upstroke of the action potential. At higher potentials (-40 to -30) Ca<sup>2+</sup> influx participates in the upstroke. In the sinus node and AV node a slower upstroke can be observed (Figure 2). This is because the upstroke in these cells is mainly mediated by the slower acting Ca<sup>2+</sup> ion channels. The slower activation produces a slower upstroke. | ||
===Phase 1: Early Rapid Repolarization=== | ===Phase 1: Early Rapid Repolarization=== | ||