SUMMARY To assess the effects of moderate potassium cardioplegia (37 mEq/l KCI) on the severity of myocardial ischemia during arrest and on post arrest ventricular function, 32 isolated, isovolumic feline hearts were studied before, during and I hour after ischemic arrest. Normothermia (37°C) was maintained in 16 hearts, eight without KCI and eight with KCI. Hypothermia (27°C) was maintained in the remaining 16 hearts, eight with KCI and eight without KCI. Myocardial oxygen (PmO,) and carbon dioxide tensions (PmCO,) were measured by mass spectrometry. Maximum developed intraventricular pressure (max DP) and max dP/dt were used as indices of performance. Compared with normothermic or hypothermic arrest alone, the addition of potassium cardioplegia resulted in a significant reduction in the peak PmCO2 measured during the arrest period. Hypothermia alone resulted in morphologic evidence of improved myocardial preservation and a significant reduction in peak PmCO, compared with normothermia. Post arrest ventricular function was best with the combination of hypothermic arrest and potassium cardioplegia (max DP = 96 ± 6% of control and max dP/dt = 99 ± 5% of control). These data suggest that the beneficial effects of potassium cardioplegia and 27°hypothermia are additive, and that reduction in myocardial ischemia as evidenced by a reduction in peak PmCO, correlated with improvement in ventricular performance in the post arrest period and with preservation of myocardial structure.ISCHEMIC CARDIAC ARREST during open heart surgery provides a tranquil operative field and thereby facilitates valve replacement, direct coronary artery revascularization procedures and the definitive correction of complex congenital anomalies. Once cardiopulmonary bypass is instituted, aortic cross-clamping totally interrupts coronary flow, resulting in fibrillation. Although observable mechanical activity soon stops, electrocardiographic evidence of energyconsuming fibrillation continues until energy substrates are depleted. By reducing metabolic activity, myocardial cooling can prolong the safe period of ischemia. [1][2][3] In addition, various studies suggest that hyperkalemic arrest at the time of aortic crossclamping preserves myocardial function after the ischemic period by quickly inducing electromechanical arrest and thereby reducing substrate utilization.2' 4-7 Early experience with hypertonic potassium citrate arrest was unfavorable due to structural evidence of myocardial damage directly related to the cardioplegic solution.8' 9More recent reports have advocated use of a moderately hyperkalemic, isosmotic solution as an adjunct to hypothermia during ischemic arrest.10 Utilizing such a solution, this study was designed to determine the effect of potassium cardioplegia on development of myocardial ischemia during cardiac arrest at normothermia and at 270 C hypothermia. Furthermore, the protocol allowed for examination of the relationship between severity of ischemia as assessed by myocardial gas tension changes during the arrest peri...