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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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===Ventricle=== | ===Ventricle=== | ||
The ventricle is activated through the dense network of Purkinje fibers originating from the bundle branches. They penetrate the myocardium and are the starting point of the ventricular activation. The left ventricular areas first excited are the anterior and posterior paraseptal wall and the central left surface of the interventricular septum. The last part of the left ventricle to be activated is the posterobasal area. Septal activation starts in the middle third of the left side of the interventricular septum, and at the lower third at the junction of the septum and posterior wall. Activation of the right ventricle starts near the anterior papillary muscle 5 to 10 | The ventricle is activated through the dense network of Purkinje fibers originating from the bundle branches. They penetrate the myocardium and are the starting point of the ventricular activation. The left ventricular areas first excited are the anterior and posterior paraseptal wall and the central left surface of the interventricular septum. The last part of the left ventricle to be activated is the posterobasal area. Septal activation starts in the middle third of the left side of the interventricular septum, and at the lower third at the junction of the septum and posterior wall. Activation of the right ventricle starts near the anterior papillary muscle 5 to 10 milliseconds after onset of the left ventricle.<cite>Durrer</cite> | ||
=Mechanisms of Arrhythmia= | =Mechanisms of Arrhythmia= | ||
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[[File:Mechanisms.svg|right|thumb|400px|'''Figure 3.''' The different mechanisms of arrhythmia.]] | [[File:Mechanisms.svg|right|thumb|400px|'''Figure 3.''' The different mechanisms of arrhythmia.]] | ||
Structural abnormalities or electric changes in the cardiomyocytes can impede impulse formation or change cardiac propagation, therefore facilitating arrhythmias. Arrhythmogenic mechanisms can arise in single cells (automaticity, triggered activity), but other mechanisms require multiple cells for arrhythmica induction (re-entry). We briefly discuss the | Structural abnormalities or electric changes in the cardiomyocytes can impede impulse formation or change cardiac propagation, therefore facilitating arrhythmias. Arrhythmogenic mechanisms can arise in single cells (automaticity, triggered activity), but other mechanisms require multiple cells for arrhythmica induction (re-entry). We briefly discuss the pathophysiological mechanisms of the main causes of arrhythmia. <Cite>Coronel</Cite> | ||
== Abnormal Impulse Formation== | == Abnormal Impulse Formation== | ||
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===Triggered Activity=== | ===Triggered Activity=== | ||
Triggered activity is | Triggered activity is depolarization of a cell triggered by a preceding activation. Due to early or delayed afterdepolarizations the membrane potential depolarizes and, when reaching a threshold potential, activates the cell. These afterdepolarizations are depolarizations of the membrane potential initiated by the preceding action potential. Depending on the phase of the action potential in which they arise, they are defined as early or late afterdepolarizations (figure 3). | ||
* A disturbance of the balance in influx and efflux of ions during the plateau phase (phase 2 or 3) of the action potential is responsible for the early afterdepolarizations. Multiple ion currents can be involved in the formation of early after depolarizations depending on the triggering mechanism. Early afterdepolarizations can develop in cells with an increased duration of the repolarization phase of the action potential, as the plateau phase is prolonged. | * A disturbance of the balance in influx and efflux of ions during the plateau phase (phase 2 or 3) of the action potential is responsible for the early afterdepolarizations. Multiple ion currents can be involved in the formation of early after depolarizations depending on the triggering mechanism. Early afterdepolarizations can develop in cells with an increased duration of the repolarization phase of the action potential, as the plateau phase is prolonged. The prolonged repolarization might reactivate the Ca2+ channels that have recovered from activation at the beginning of the repolarization. Otherwise disparity in action potential duration of surrounding myocytes can destabilize the plateau phase through adjacent depolarizing currents. | ||
* Delayed afterdepolarizations occur after the cell has recovered after completion of repolarization. In delayed afterdepolarization an abnormal Ca<sup>2+</sup> handling of the cell is responsible for the afterdepolarizations due to release of Ca<sup>2+</sup> from the storage of Ca<sup>2+</sup> in the sarcoplasmatic reticulum. The accumulation of Ca<sup>2+</sup> increases membrane potential and depolarizes the cell until it reaches a certain threshold, thereby creating an action potential. A high heart rate can result in the accumulation of intracellular Ca<sup>2+</sup> and induce delayed afterdepolarizations. | * Delayed afterdepolarizations occur after the cell has recovered after completion of repolarization. In delayed afterdepolarization an abnormal Ca<sup>2+</sup> handling of the cell is responsible for the afterdepolarizations due to release of Ca<sup>2+</sup> from the storage of Ca<sup>2+</sup> in the sarcoplasmatic reticulum. The accumulation of Ca<sup>2+</sup> increases membrane potential and depolarizes the cell until it reaches a certain threshold, thereby creating an action potential. A high heart rate can result in the accumulation of intracellular Ca<sup>2+</sup> and induce delayed afterdepolarizations. | ||
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===Re-entry=== | ===Re-entry=== | ||
Re-entry or circus movement is a | 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= | ||