The administration of antiarrhythmic drugs is determined largely on the basis of empiricism, and the experience of individual physicians and the results of clinical studies are probably the two major factors determining the approach to treatment. Although much effort has been expended in learning the mechanisms of action of antiarrhythmic drugs, the applicability to clinical treatment of the knowledge attained has been limited. Nonetheless, recent advances in our understanding of the biology of the cardiac cell, of the factors that predispose to arrhythmias and of drug-receptor interactions, have not only provided new insights into the mechanisms whereby specific drugs exert their effects, but promise to provide means for designing and testing compounds whose actions will be more specific and more predictable than is presently the case. This paper will review some of the advances that have been made and will consider some of their implications.