Every myocardial cell has intrinsic pacemaker activity (automaticity) with the potential to initiate electrical impulses. The varying rates at which the threshold potential is reached normally allows a co-ordinated progressive depolarization, beginning in the SA mode. Transient factors may alter the normal hierarchy of automaticity, either producing an accelerated rate (sinus tachycardia, escape rhythm, accelerated atrioventricular nodal rhythms) or triggering abnormal depolarizations (oscillations of phase 3/4 of the action potential may reach threshold level characterized by conditions producing the long QT syndrome ( Table d), causing early or late after-depolarizations).
Early after-depolarizations are associated with class IA antiarrhythmic drugs, acidosis, hypokalemia, hypoxia, and catecholamines. Delayed after-depolarizations are associated with digoxin therapy and postmyocardial infarction.
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