Antiarrhythmic drugs may either decrease or increase the likelihood of ventricular fibrillation. Although reliable data suggest reasonable mechanisms for the antiarrhythmic action of several drugs, much less information is available to indicate the mechanisms by which drugs are arrhythmogenic. Antiarrhythmic action may result from suppression of precipitating events such as inappropriately timed premature impulses or runs of excessively rapid impulses and from modification of the conditions predisposing to random reentry. Increases in the likelihood of fibrillation may result from opposite effects on precipitating events or from drug-induced increase in the likelihood of random reentry. One factor that very likely is involved in the latter is the presence of local differences in the electrical activity of myocardial cells that cause significant local differences in the tonic and use-dependent actions of antiarrhythmic drugs.