The conditions of postcardioplegia reperfusion that influence cardiac electrophysiologic recovery have not yet been fully elucidated. Studies of postcardioplegia electrophysiologic recovery and reperfusion-induced arrhythmias, particularly reperfusion-induced ventricular fibrillation, are useful for improving our understanding of reperfusion injury since reperfusion-induced arrhythmias are sensitive indicators for reperfusion injury. The purpose of this study was to determine the effects of asystolic reperfusion and reperfusate electrolyte composition on postcardioplegia electrophysiologic recovery of the heart. The hypothesis tested is that the duration of asystolic reperfusion produced by a hyperkalemic reperfusate is a primary determinant for the return of cardiac electrical activity without reperfusion-induced ventricular fibrillation and that reperfusion with a hypocalcemic-hyperkalemic solution further reduces the prevalence of reperfusion-induced ventricular fibrillation by limiting myocyte calcium exposure during initial postischemic recovery. Fifty-six pigs were supported by cardiopulmonary bypass and subjected to identical conditions of hypothermic cardioplegic arrest. Reperfusion was initiated with unmodified pump blood, a hypocalcemic-normokalemic cardioplegic solution, a hyperkalemic-normocalcemic cardioplegic solution, or a hyperkalemic- hypocalcemic cardioplegic solution. The hyperkalemic-normocalcemic solution was administered at a dose of 500 ml/m2 or 1500 ml/m2. The hyperkalemic- hypocalcemic and hypocalcemic-normokalemic solutions were given only at a dose of 500 ml/m2. All cardioplegic reperfusion solutions were followed by infusion of unmodified pump blood for the remainder of the 15-minute period of controlled reperfusion. Reperfusion-induced ventricular fibrillation was less prevalent in the high-dose hyperkalemic solution group (4/12) than in the low-dose hyperkalemic solution (9/10) or unmodified pump blood (12/12) groups (p < 0.05). The transmyocardial lactate gradient at the time of initial postreperfusion electrical activity was positive (0.21 ± 0.04 mmol/L) in the high-dose hyperkalemic group and negative (-0.05 ± 0.09 mmol/L) in the low-dose hyperkalemic group (p < 0.05). Fibrillation was less prevalent in the hypocalcemic-hyperkalemic group (8/12) than in the other groups reperfused with cardioplegic solution at a dose of 500 ml/m2 (hypocalcemic-normokalemic, 10/10; hyperkalemic-normocalcemic, 9/10) or in the group reperfused with unmodified pump blood (12/12) (p < 0.05, hypocalcemic-hyperkalemic group versus other reperfusate groups). Reperfusion-induced ventricular fibrillation is an indicator of reperfusion injury, and in this study the conditions of reperfusion influenced the prevalence of reperfusion-induced ventricular fibrillation. Recovery of aerobic metabolism during hyperkalemia-induced asystolic reperfusion was associated with a lower prevalence of reperfusion-induced ventricular fibrillation. Combining hypocalcemia with hyperkalemia decreased the prevalence of reperfusion-induced ventricular fibrillation.