No abstract

The hemodynamic and metabolic effects of combined extracorporeal circulation and hypothermia induced by veno-arterial shunting were determined in 32 dogs following the production of acute myocardial infarction with shock by plastic sphere coronary embolization. Cardiac output, central aortic pressure, left ventricular work, systemic vascular resistance, left ventricular contractile force, right atrial and left ventricular pressures, arterial pH, CO 2 , potassium, plasma hemoglobin, and hematocrit were determined in dogs brought to the level of ventricular fibrillation or arrest or to profoundly hypothermic levels of 5 to 10 C. esophageal temperature for four to six hours and then rewarmed; in those maintained at 28 to 30 C. esophageal temperature for four to six hours and then rewarmed; and in those remaining normothermic for four to six hours following coronary embolization. The average esophageal temperature at the time of ventricular fibrillation was 19.3 C., and at the time of complete asystole was 12.0 C., figures comparable to results in normal animals. It is concluded that an animal with acute myocardial infarction and shock is not more susceptible to fatal hypothermic arrhythmia than is a normal animal. It was also demonstrated that there was relatively little irreversible deleterious hemodynamic effect after five to six hours of profound or moderate hypothermia combined with low-flow extracorporeal circulation, although the more profoundly cooled animals did demonstrate a metabolic acidosis and less return to precooling levels of cardiac output and aortic pressure following rewarming than did those maintained at 28 to 30 C. Both the profoundly and moderately cooled animals demonstrated, following rewarming, more adequate recovery of cardiac output, aortic pressure, and systemic vascular resistance than did animals which remained normothermic for similar periods after coronary embolization, suggesting that hypothermia affords a "protective" effect in recent myocardial infarction.