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Cardiac Arrhythmias: Difference between revisions
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===Triggered Activity=== | ===Triggered Activity=== | ||
Triggered activity is activity 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). | Triggered activity is activity 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). | ||
* In early afterdepolarizations depolarization occurs during the action potential (phase 2 and 3) by a diversity of causes. Early afterdepolarizations can increase duration of the repolarization phase of the action potential. This increase can create heterogeneity in refractoriness | * In early afterdepolarizations depolarization occurs during the action potential (phase 2 and 3) by a diversity of causes. Early afterdepolarizations can increase duration of the repolarization phase of the action potential. This increase can create heterogeneity in refractoriness thereby creating the substrate for a re-entry circuit (see below). | ||
* Delayed afterdepolarizations occur after the cell has recovered after completion of repolarization. In delayed afterdepolarization an abnormal Ca2+ handling of the cell is probably responsible for the afterdepolarizations due to release of Ca<sup>2+</sup> from the storage of Ca2<sup>+</sup> in the sarcoplasmatic reticulum. The accumulation of Ca<sup>2+</sup> increases membrane potential and thus depolarizes the cell when it reaches a certain threshold. | * Delayed afterdepolarizations occur after the cell has recovered after completion of repolarization. In delayed afterdepolarization an abnormal Ca2+ handling of the cell is probably responsible for the afterdepolarizations due to release of Ca<sup>2+</sup> from the storage of Ca2<sup>+</sup> in the sarcoplasmatic reticulum. The accumulation of Ca<sup>2+</sup> increases membrane potential and thus depolarizes the cell when it reaches a certain threshold. | ||
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===Reentry=== | ===Reentry=== | ||
Reentry or circus movement can arise when an area is slowly conducting thereby remaining active while the rest of the heart depolarizes. When the rest of the heart has recovered from this refractory state, and can be reactivated, the impulse in the slow conducting zone can activate the heart. This process can repeat itself and thus form the basis of a reentry tachycardia. These areas of slow conduction can be anatomical or functional or a combination of both. Examples of reentry tachycardias are atrial flutter | Reentry or circus movement can arise when an area is slowly conducting thereby remaining active while the rest of the heart depolarizes. When the rest of the heart has recovered from this refractory state, and can be reactivated, the impulse in the slow conducting zone can activate the heart. This process can repeat itself and thus form the basis of a reentry tachycardia. These areas of slow conduction can be anatomical or functional or a combination of both. Examples of reentry tachycardias are atrial flutter and ventricular tachycardias originating from an infarct zone. | ||
=References= | =References= | ||
# Braunwald's Heart Disease, 8th edition. Edited by Douglas P. Zipes. Philadelphia, Pa.: W.B. Saunders, 2008 | # Braunwald's Heart Disease, 8th edition. Edited by Douglas P. Zipes. Philadelphia, Pa.: W.B. Saunders, 2008 | ||
[[Cardiodrugstemplate]] | [[Cardiodrugstemplate]] | ||