Protection from ischemic cardiac arrest by coronary perfusion with cold Ringer’s lactate solution

Abstract

Cardiac output, peak systolic pressure, and heart rate were reduced and left ventricular end-diastolic pressure was increased in 10 animals following 1 hour of normothermic aortic cross-clamping. Although no cardiotonic drugs were required for resuscitation, the central venous pressure had to be doubled to achieve preoperative levels of cardiac output and peak systolic pressure. Histologic and hislochemical studies revealed irregular, diffuse damage of 50 per cent of the myocardium. While it is usually assumed that the dog tolerates ischemic cardiac arrest very poorly, this study would indicate that the canine and human hearts do not differ significantly in their tolerance to ischemia, with over 90 per cent of either species surviving 1 hour of normothermic ischemic arrest in spite of serious myocardial damage. On the other hand, in 10 animals whose hearts were cooled by a single aortic root infusion of 4° C. Ringer’s lactate, there was no drop in cardiac output, peak systolic pressure, and heart rate following recovery from 1 hour of ischemic arrest. Histologic and histochemical studies revealed only minimal changes. Profound myocardial hypothermia is easy to achieve by perfusion and protects the myocardium from ischemic damage while providing operating conditions equally as good as with normothermic arrest. To extend the period of ischemic arrest during which no diminution of cardiac function occurs and to reduce myocardial irritability, studies of metabolic inhibitors and hypothermic perfusion solutions without lactate are now in progress.