Abstract The metabolism of the artificially arrested and the gas-perfused heart is reviewed. Various factors influence the oxygen uptake of the potassium chloride-arrested heart perfused under aerobic conditions (time after arrest, decrease in temperature, oxygen consumption of the heart prior to the arrest and the perfusion pressure in the coronary vascular bed). Potassium lowers the oxygen uptake of the arrested heart. The contents of creatine phosphate (CrP), adenosine triphosphate (ATP) and lactic acid of the arrested perfused heart are normal, thereby suggesting that the production of energy in the arrested heart is not disturbed. Under anaerobic conditions, lactic acid production and the uptake of glucose by the arrested heart are increased; however, energy production is not limited by the capacity for glycolysis. The myocardial oxygen uptake and the capacity of the heart to be revived depend upon the type of arrest. The potassium chloride-arrested heart can be resuscitated after an anoxic period of 90 minutes. During potassium chloride-induced cardiac arrest, the oxygen supply of the isolated heart is sufficient. This fact is borne out by morphologic studies on mitochondria. During gas perfusion of the coronary arteries, there is a fall in left ventricular peak systolic pressure. The first derivative of the left ventricular pressure and the isovolumetric work decrease. These findings are reflected in high tissue content of creatine phosphate.