Triggered activity is postulated to cause certain cardiac arrhythmias. The term triggered activity was coined to identify “arrhythmias” triggered by one or more preceding action potentials. Triggered activity is easily distinguishable from reentrant mechanisms because it can be elicited in isolated, small multicellular cardiac preparations and in single cells, experimental conditions where reentry is impossible. Triggered activity differs as well from abnormal (enhanced) automaticity, since the latter is thought to occur spontaneously without the requirement of a trigger. Triggered activity is caused by afterdepohrizatwns. These are low frequency (around 5 Hz) depolarizing oscillations in membrane voltage. They can arise before the repolarization of an action potential is completed (early aftwdt. pOlaV-iuttwns m EADs) or following its complete repolarization (hhyed afterdepolar-izations m DADS). EADs occur only at low stimulation frequencies, and are abolished at higher stimulation frequencies, whereas the opposite is true of DADS. EADs have been most closely identified as the cause of torsades de pointes occurring with long syndrome. EADs are postulated to be one proarrhythmic mechanism of some antiarrhythmic drugs. DADS are thought to underlie some tachyarrhythmias of digitalis intoxication. Both EADs and DADS occur in experimental models of myocardd ischemia and/or repehsion. The cellular mechanism for Ca2+ overload postulated to underlie DADS has been reviewed elsewhere. a Supported by National Heart, Lung, and Blood Institute Grants HL 20592, HL 38927, and