IV. ANTIARRHYTHMIC AGENTS
Figure 11 illustrates how myocardial cells generate an action potential in phase zero through a fast influx of sodium ions into cells. This increases the resting potential and voltage of the cell (depolarization). During phase three the cell returns to its resting potential with an efflux of potassium ions. Some antiarrhythmic agents produce their effects by decreasing the rate at which sodium enters the myocardial cell during phase zero. Thus, generation of the action potential of an abnormal impulse is dampened and does not reach sufficient magnitude to produce abnormal beats. Quinidine, disopyramide, procainamide, flecainide, and propafenone decrease the rate at which sodium enters myocardial cells. Beta-adrenergic blocking agents, lido-caine, and several antiarrhythmic agents decrease the rate of automaticity of abnormal rhythms by depressing phase four of the action potential (as indicated by the arrow in Fig. 3). Amiodarone and a unique beta-blocker, sotalol, cause prolongation of the action potential (phase two) and retard the generation of an abnormal impulse. Most important, an increase in the absolute refractory period(phases one and two), protects the heart from dangerous impulse stimuli. During a 20–30 ms vulner¬able period in phase three a strong electrical stimulus or ventricular ectopic beat can readily trigger ventricular tachycardia and ventricular fibrillation.