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Cardiac Arrhythmias: Difference between revisions
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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 thereby creating the substrate for a re-entry circuit (see below). | * 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 Ca<sup>2+</sup> handling of the cell is probably 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 | * 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 probably 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. | ||
==Disorders of Impulse Conduction== | ==Disorders of Impulse Conduction== | ||
Conduction block or conduction delay is a frequent cause of bradyarrhythmias, however | Conduction block or conduction delay is a frequent cause of bradyarrhythmias, however tachyarrhythmias can also result from conduction block when this block produces a reentrant circuit. Conduction block can develop in different (physiological) conditions. It is important to assess the cause of conduction block as explained in the section of [[bradycardia]], for it is important in the treatment of the conduction delay or block. | ||
===Reentry=== | ===Reentry=== | ||
Reentry or circus movement can arise when an area is slowly conducting thereby | Reentry or circus movement can arise when an area is slowly conducting thereby still propagating the activation while the rest of the heart depolarizes. When the surrounding myocardium has recovered from this refractory state, and can be stimulated, the impulse in the slow conducting zone can reactivate the heart when it exits the area of slow conduction. 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= | ||