Electropharmacology of antiarrhythmic drugs

Cardiac arrhythmias may be caused by abnormalities of impulse initiation, impulse propagation, or a combination of the two. The specific mechanisms that may induce arrhythmias are reviewed, as are the means whereby antiarrhythmic drugs might be expected to modify arrhythmias. The cellular electrophysiologic effects of the following antiarrhythmic drugs are discussed: quinidine, procainamide, disopyramide, lidocaine, tocainide, mexiletine, phenytoin, beta-blocking and slow-channel-blocking drugs, aprindine, bretylium, ethmozin, and amiodarone. A knowledge of the similarities and differences of their actions on the determinants of conduction, on repolarization and refractoriness, on automatic mechanisms, and on afterdepolarizations, when considered in the context of the mechanism of clinically occurring tachyarrhythmias, may provide the correct framework for the choice of an appropriate agent for the control of an individual disorder of rhythm. However, it is emphasized that neither the precise mechanism of various dysrhythmias nor the fundamental basis for the salutary action of antiarrhythmic compounds is completely understood.