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Cardiac Arrhythmias: Difference between revisions
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''Sébastien Krul, MD | ''Sébastien Krul, MD'' | ||
=Introduction= | |||
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A basic knowledge of the cardiac action potential and cardiac conduction system facilitates understanding of cardiac arrhythmias. The effects and side-effects of anti-arrhythmic drugs are depended on the influence on ion channels involved in the generation and/or perpetuation of the cardiac action potential. | A basic knowledge of the cardiac action potential and cardiac conduction system facilitates understanding of cardiac arrhythmias. The effects and side-effects of anti-arrhythmic drugs are depended on the influence on ion channels involved in the generation and/or perpetuation of the cardiac action potential. | ||
==Cardiac Action Potential== | ==Cardiac Action Potential== | ||
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 the type and structure of ion channels, the various parts of the heart 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). The changes in the membrane potential due to the movement of ions produce an action potential which lasts only 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.<cite>Kleber</cite> | 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 the type and structure of ion channels, the various parts of the heart 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). The changes in the membrane potential due to the movement of ions produce an action potential which lasts only a few hundreds of milliseconds. Disorders in single channels can lead to arrhythmias, as seen in the section [[Primary_Arrhythmias|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.<cite>Kleber</cite> | ||
In summary during the depolarization, sodium ions (Na<sup>+</sup>) stream into the cytoplasm of 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 by coupling with the muscle fibers. During repolarization the cell returns to the resting membrane potential, due to the passive efflux of K<sup>+</sup>(Figure 1). In detail the (ventricular) action potential can be divided in five phases: <Cite>Berne,Braunwald</Cite> | In summary during the depolarization, sodium ions (Na<sup>+</sup>) stream into the cytoplasm of 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 by coupling with the muscle fibers. During repolarization the cell returns to the resting membrane potential, due to the passive efflux of K<sup>+</sup>(Figure 1). In detail the (ventricular) action potential can be divided in five phases: <Cite>Berne,Braunwald</Cite> | ||
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===Re-entry=== | ===Re-entry=== | ||
Re-entry or circus movement is a multicellular mechanism of arrhythmia. Important criteria for the development of re-entry are a circular pathway with an area in this circle of unidirectional block and a trigger to induce the re-entry movement. Re-entry can arise when an impulse enters the circuit, follows the circular pathway and is conducted through an unidirectional (slow conducting) pathway. Whilst the signal is in this pathway the surrounding myocardium repolarizes. If the surrounding myocardium has recovered from the refractory state, the impulse that exits the area of unidirectional block can reactivate this recovered myocardium. This process can repeat itself and thus form the basis of a re-entry tachycardia. Slow conduction and/or a short refractory period facilitate re-entry. The reason of unidirectional block can be anatomical (atrial flutter, AVNRT, AVRT) or functional (myocardial ischemia) or a combination of both.<Cite>deBakker,Janse</Cite> | Re-entry or circus movement is a multicellular mechanism of arrhythmia. Important criteria for the development of re-entry are a circular pathway with an area in this circle of unidirectional block and a trigger to induce the re-entry movement. Re-entry can arise when an impulse enters the circuit, follows the circular pathway and is conducted through an unidirectional (slow conducting) pathway. Whilst the signal is in this pathway the surrounding myocardium repolarizes. If the surrounding myocardium has recovered from the refractory state, the impulse that exits the area of unidirectional block can reactivate this recovered myocardium. This process can repeat itself and thus form the basis of a re-entry tachycardia. Slow conduction and/or a short refractory period facilitate re-entry. The reason of unidirectional block can be anatomical ([[Tachycardia|atrial flutter, AVNRT, AVRT]]) or functional (myocardial ischemia) or a combination of both.<Cite>deBakker,Janse</Cite> | ||
=References= | =References= | ||