Mechanism of Action-Amiodarone

During normal sinus rhythm (Panel A), myocardial activation is initiated in the sinus node, with a resulting coordinated wavefront of depolarization that spreads across both atria (arrows) to the atrioventricular node and specialized conduction system (green). Atrial fibrillation (Panel B) is triggered by atrial premature depolarizations arising in the region of the pulmonary veins (red asterisk) and propagates in an irregular and unsynchronized pattern (arrows). The resulting pattern of ventricular activation is irregular (as shown on the electrocardiographic recording). Amiodarone (Panel C) has several electrophysiological effects. Chief among these in the control of atrial fibrillation is the effect on the potassium channel blockade, which slows repolarization, thus prolonging the action potential and the refractoriness of the myocardium. Waves of depolarization are more likely to encounter areas of myocardium that are unresponsive; thus, propagation is prevented. Although the prolongation of the action potential is most apparent on the electrocardiogram as an effect on the ventricular myocardium (prolonged QT interval), a similar effect occurs in the atria.

NEJM. Zimetbaum 356 (9): 935, Figure 1 March 1, 2007