Cardiac function and microsphere blood flow distribution in the brain-dead dog

Abstract

The mechanisms for the deterioration of the brain-dead organ donor are not clearly defined. We measured myocardial blood flow and function during the 4 hours after the induction of brain death in dogs. Brain death was induced by elevating and maintaining intracranial pressure above systolic arterial pressure and effectively stopping central nervous system blood flow. Multiorgan blood flow and systemic arteriovenous shunting were measured using radioactive microspheres. The mean arterial pressure was found to decrease markedly with the induction of brain death. The initial changes in mean arterial pressure were attributed to a decrease of systemic vascular resistance, with the more terminal changes due to a decrease in cardiac index. There was a marked decrease of left ventricular dP/dt with the induction of brain death and a gradual decrease of stroke volume despite no change in pulmonary capillary wedge pressure. The microsphere calculated blood flows to the left ventricle and septum of the myocardium were significantly lower at the 1- and 4-hour time points relative to control. However, the coronary sinus oxygen extraction ratio was not statistically different from control at 4 hours. Systemic arteriovenous shunts increased after the induction of brain death but remained below 10%. We conclude that despite brain death-induced hypotension, there is little evidence to suggest that marked myocardial hypoxic ischemic changes initiated the deterioration in this model.