To evaluate rhythm and QRS-T changes after cardioversion of induced ventricular arrhythmias, 56 patients underwent continuous three-lead and serial 12-lead electrocardiographic monitoring for 15 min after 77 cardioversions. Fifty patients were cardioverted externally and nine internally with an implanted automatic cardioverter/defibrillator. Initial energy for external cardioversion was 200 Wsec in 57 of 64 arrhythmia episodes. Two hundred watt-seconds of energy effectively terminated 41 of 44 episodes of ventricular tachycardia and six of 13 episodes of ventricular fibrillation (p < .001). Early bradycardia (mean cycle length 1200 msec during the first 5 sec) occurred after 17 of 64 external and two of 13 internal cardioversions (p = NS) in a total of 16 patients. Bradycardia persisted at 10 sec after cardioversion in nine patients. Early bradycardia was associated with the need for multiple cardioversions to terminate the arrhythmia (six of 10 multiple cardioversions vs 13 of 67 single cardioversions, p < .05) and the presence of inferior myocardial infarction (eight of 16 patients with vs eight of 40 patients without inferior infarction, p < .05). Supraventricular tachycardia (cycle length <500 msec) occurred after 19 of 64 external and six of 13 internal cardioversions (p = NS). Nonsustained ventricular tachycardia (4 to 40 beats) was observed after seven external cardioversions, with three episodes lasting 3 sec or more. Excluding patients with bundle branch block, ST segment elevation ('- 1 mm) occurred after 11 of 58 external cardioversions and after one of 12 internal cardioversions (p = NS) and ST segment depression (−1 mm) was noted after 25 of 58 external and three of 12 internal cardioversions (p = NS). All but one ST segment change resolved by 15 min. Thus, after cardioversion of induced ventricular arrhythmias (1) over 25% of patients develop marked bradycardia and/or supraventricular tachycardia with the development of bradycardia related to the need for multiple cardioversions for arrhythmia termination and previous inferior infarction, (2) ST segment changes are common but short-lived, and (3) the frequency of arrhythmias and ST changes is comparable after external and internal cardioversion. These observations may have implications for backup pacing and triggering rates for automatic cardioverting/defibrillating devices and for the diagnosis of ischemia after termination of induced ventricular arrhythmia.