Many, if not most antiarrhythmic drugs, even with differing pharmacologic properties, are capable of myocardial depression. That this has not occurred commonly with most drugs currently available may reflect several factors. These may include depression of myocardial function which is not clinically overt or which is masked by preexisting cardiac decompensation, limitation of dosages because of the difficulty in accurately determining a therapeutic endpoint, and the lack of physician awareness of the effects of these drugs on myocardial performance. However, as techniques for monitoring and quantifying arrhythmia permit more aggressive drug therapy, and as more drugs become available for clinical use, the incidence of clinically overt myocardial depression from anti-arrhythmic therapy will undoubtedly rise. Hopefully, awareness of the hemodynamic effects of these drugs and applications of new technology permitting accurate, noninvasive assessment of left ventricular function will identify and hence limit the occurrence of toxic hemodynamic effects, as well as permit the usage of maximum dosages of antiarrhythmic drugs when warranted by clinical circumstances.