ELECTROPHYSIOLOGIC CONSEQUENCES OF HYPERKALEMIC CARDIOPLEGIA DURING SURGICAL ISCHEMIA

Myocardial protection strategies use cardioplegic solutions to reduce the injury induced by surgical ischemia and reperfusion. However, ther e is a high incidence of electrophysiologic abnormalities after cardio plegic arrest. A computerized epicardial mapping system in a porcine c ardiopulmonary bypass model was used to measure the electrophysiologic consequences of different myocardial protection techniques. Both warm and cold, crystalloid and blood cardioplegic solutions were compared. The effects of hypothermia and prolonged cardiopulmonary bypass were examined in a control group that underwent a 2-hour period of hypother mia without cardioplegia or aortic cross-clamping, followed by 2 hours of normothermic reperfusion. Isochronous activation maps, unipolar el ectrograms, ventricular refractory periods, and pacing thresholds were measured before cardioplegic arrest and during reperfusion. Compared with the control group, crystalloid cardioplegia, but not blood cardio plegia, was accompanied by large changes in the pattern of ventricular activation and by persistent (>2 hours) and significant slowing of th e time required for complete ventricular activation. This was not the result of hypoxia. Moreover, the effective refractory period and the p acing threshold were unchanged by any cardioplegia. Our data suggest t hat crystalloid cardioplegia increases myocardial resistance to curren t flow leading to a derangement of electrical impulse propagation that may underlie arrhythmogenesis.