The effects of induced ventricular fibrillation on ventricular performance and cardiac metabolism were studied in dogs. When ventricular fibrillation was induced by a brief 7.5-v a-c stimulus and allowed to persist spontaneously for one hour, no significant effects on subsequent cardiac function were apparent. An increase in myocardial oxygen consumption and a decrease in coronary vascular resistance occurred during the period of fibrillation. When ventricular fibrillation was maintained by constant a-c stimulation, however, immediate and significantly deleterious effects on cardiac performance resulted. Coronary vascular resistance rose; myocardial oxygen consumption increased, but the increase was significantly less than in animals in which fibrillation persisted without electrical stimulation. Anerobic glycolysis ensued, leading to lactate accumulation in coronary venous blood. The small a-c current used to maintain ventricular fibrillation impairs oxygen utilization, interferes with oxygen availability, and has a markedly deleterious effect on cardiac performance. A more satisfactory method of dependably maintaining the heart in ventricular fibrillation is needed before induced ventricular fibrillation can be safely employed to arrest cardiac contraction for prolonged periods during open cardiac operations.