Pathophysiological consequences of brain death

Hemodynamic instability after brain death is an universal clinical problem with effects on potential donor organs. Actual shortage of potential donor hearts continues to raise controversial discussion about adequate donor management with regard to graft quality. From the mid eighties numerous studies investigated the effects of brain death on the cardiocirculatory system and other organs. It could be shown that brain death induction leads to 1) an initial hyperdynamic Cushing-type reaction, followed by 2) loss of neural control and hormone depletion, 3) marked alteration of loading conditions and coronary perfusion and 4) cardiac and peripheral organ dysfunction. The causal relationship between these phenomena, however, could not be proven accurately. Studies using ex vivo evaluation of the hearts or applying load-independent indices of myocardial function suggested that brain death does not lead to an irreversible myocardial damage but only a reversible dysfunction or even more accurately a downregulation of myocardial contractility. These results may also be of a clinical importance: based on the knowledge of the physiologic regulatory mechanisms, it is possible to conclude that hemodynamic instability in the potential organ donor should not necessarily indicate primary cardiac dysfunction. Therefore, donor hearts, especially from marginal donors, should be carefully evaluated by load-independent indices of cardiac function. Furthermore, the normalization of loading conditions in the brain dead donor may lead to an improvement of cardiac performance. In fact, an increasing number of clinical studies demonstrate that cardiac dysfunction can be reversed in potential organ donors, and the clinical outcome of transplant patients receiving hearts from primarily marginal donors is comparable to those of normal donors.