Small amplitude electrical activity has been recorded from the myocardium during cardioplegic arrest in the absence of electromechanical activity. The presence of persistent electrical activity has been associated with impaired myocardial metabolic and functional recovery. To determine whether or not oxygenated cardioplegia would provide sufficient oxygen to support the increased metabolic activity associated with persistent electrical activity during cardioplegic arrest, we randomized 14 adult mongrel dogs to receive either non-oxygenated or oxygenated cardioplegia during 90 min of ischaemia. Cardiac index (CI), left ventricular stroke work index (LVSWI) and dp/dt were measured before bypass and after 90 min of ischaemia and 45 min of reperfusion. Myocardial oxygen consumption (MVO2) and lactate extraction were measured before and after bypass. Intramyocardial voltage was monitored during cardioplegic arrest, and MVO2 was measured during cardioplegia infusion. The onset of small amplitude electrical activity was associated with a rise in intramyocardial voltage and an increase in MVO2. CI, LVSWI and dp/dt were better preserved in those animals receiving oxygenated cardioplegia. MVO2 and lactate consumption following cardioplegia arrest were also higher in this group. CONCLUSIONS (1) small amplitude electrical activity during cardioplegic arrest is associated with a rise in MVO2. (2) Oxygenated cardioplegia increases myocardial protection by providing oxygen for the increased metabolic activity associated with the presence of this small amplitude electrical activity.