The role of coronary perfusion changes in cardiac dysfunction associated with brain death.

Abstract

Previous studies described a hemodynamic instability in the potential organ donor which has clinical relevance for cardiac transplantation. The possible pathophysiological link between altered loading conditions, coronary perfusion, and cardiac function after brain death has not been investigated yet. Therefore this study was undertaken to investigate the role of coronary perfusion changes during brain death in cardiac dysfunction. Dogs on cardiopulmonary bypass provided iso-volumetric left-ventricular (LV) contractions. By protocol, coronary perfusion pressure was kept at the level of mean aortic pressure. LV pressure, LV dP/dt, the slope of end-systolic pressure-volume relationship (Emax), coronary blood flow (CBF), and myocardial oxygen consumption (MVO2) were measured. Brain death was induced by a subdurally placed balloon-catheter. Induction of brain death led to a transient hyperdynamic response with a significant increase of aortic and LV pressure, dP/dt, Emax, CBF, and MVO2. Thereafter, aortic pressure and, parallelly, LV pressure, dP/dt, Emax, CBF, and MVO2 decreased significantly. However, if coronary perfusion pressure was decoupled from aortic pressure and elevated to pre-brain death level, CBF and myocardial contractility were restored to baseline level. The impairment of coronary blood flow may contribute to decreased contractility after brain death.