A major objective of cardioplegic arrest for protection of the heart during cardiac operations is total electromechanical quiescence. Recent studies from our laboratory in which we used multiple bipolar intracardiac and unipolar intramural electrodes have detected the presence of electrical activity in the lower atrial septum, the atrioventricular node-His bundle complex, and in ventricular myocardium during elective cardioplegic arrest that cannot be detected on the limb-lead electrocardiogram. Moreover, this low-amplitude electrical activity is not associated with visible mechanical activity of the heart and occurs at ventricular septal temperatures previously thought to be adequate for myocardial protection. The present study was designed to determine the effect of cardioplegic solution potassium concentration and myocardial temperature on the occurrence and duration of low-amplitude electrical activity during elective cardioplegic arrest. Fifty adult mongrel dogs were subjected to two consecutive 20 minute periods of cardioplegic arrest. The animals were divided into six groups, depending upon the cardioplegic solution potassium concentration they received and on whether or not topical cooling techniques were employed. The probability of occurrence of low-amplitude electrical activity during the arrest interval was significantly decreased by (1) application of topical hypothermic techniques and (2) reinfusion of hyperkalemic, as compared to normokalemic, cardioplegic solution. These effects of hyperkalemic cardioplegic solution and myocardial hypothermia acted synergistically, but independently, to decrease the likelihood of low-amplitude electrical activity occurring during the period of cardioplegic arrest. Nevertheless, low-amplitude electrical activity did occur in all groups after each cardioplegic solution administration and was not detected by routine monitoring techniques. This suggests that low-amplitude electrical activity may represent a fundamental type of metabolic activity that can be recorded from the heart during arrest and may be responsible for the temporary depression in ventricular function that frequently follows a period of elective cardioplegic arrest.