GLOBAL ENERGETIC FAILURE IN BRAIN-DEAD PATIENTS

The objective of this prospective, clinical study of consecutive patie nts was to test the hypothesis of a global energetic failure in brain- dead patients by analyzing indices of peripheral oxygenation during br ain-dead resuscitation. Subjects comprised 24 subjects with brain deat h criteria from a multidisciplinary intensive care unit, The causes of brain death were multiple: severe traumatic head injury, cerebrovascu lar event, cerebral anoxia, primary brain tumor, and gunshot wound to the head, Interventions used were radial and pulmonary artery catheter ization, Hemodynamic and gasometric parameters and blood lactate level s were measured immediately after the diagnosis of brain death (T-0) a nd 4 hr later (T-4), while patients were receiving a therapeutic proto col (fluids, vasopressive drugs) adjusted to reach a mean arterial pre ssure of 75 mmHg. In 18 of our 24 patients, a blood lactate level grea ter than or equal to 2 mmol/L (mean +/- SD: 4+/-2 mmol/L) associated w ith an increased mean lactate to pyruvate ratio (14.4+/-3.2) was obser ved at T-0, while oxygen delivery (DO2) was high (533+/-208 ml/min/m(2 )) and mean arterial pressure was 76+/-21 mmHg, Patients were subdivid ed into two groups according to changes in DO2 from T-0 to T-4: group D comprised 14 patients (10 with hyperlactatemia and 4 with normal lac tate) in whom DO2 and oxygen consumption (VO2) simultaneously decrease d from T-0 to T-4 without significant change in lactate level; group I comprised 10 patients (8 with hyperlactatemia and 2 with normal lacta te) in whom DO2 and VO2 simultaneously increased, while the blood lact ate level decreased significantly from 3.5+/-2.5 mmol/L at T-0 to 2.1/-1.0 mmol/L at T-4 (P<0.05). Our results indicate that the brain-dead state was frequently associated with a global energetic failure proba bly due to a cellular oxygen deficit, despite blood pressure within th e normal range, This energetic failure, because it is associated with high levels of DO2, could result from a defect in peripheral oxygen ex traction, Aggressive therapy, achieved by producing a further increase in DO2, may reduce this global tissue oxygen deficit.