The objective of this prospective, clinical study of consecutive patients was to test the hypothesis of a global energetic failure in brain-dead patients by analyzing indices of peripheral oxygenation during brain-dead resuscitation. Subjects comprised 24 subjects with brain death criteria from a multidisciplinary intensive care unit. The causes of brain death were multiple: severe traumatic head injury, cerebrovascular event, cerebral anoxia, primary brain tumor, and gunshot wound to the head. Interventions used were radial and pulmonary artery catheterization. Hemodynamic and gasometric parameters and blood lactate levels were measured immediately after the diagnosis of brain death (T0) and 4 hr later (T4), while patients were receiving a therapeutic protocol (fluids, vasopressive drugs) adjusted to reach a mean arterial pressure of 75 mmHg. In 18 of our 24 patients, a blood lactate level > or = 2 mmol/L (mean +/- SD: 4 +/- 2 mmol/L) associated with an increased mean lactate to pyruvate ratio (14.4 +/- 3.2) was observed at T0, while oxygen delivery (DO2) was high (533 +/- 208 ml/min/m2) and mean arterial pressure was 76 +/- 21 mmHg. Patients were subdivided into two groups according to changes in DO2 from T0 to T4: group D comprised 14 patients (10 with hyperlactatemia and 4 with normal lactate) in whom DO2 and oxygen consumption (VO2) simultaneously decreased from T0 to T4 without significant change in lactate level; group I comprised 10 patients (8 with hyperlactatemia and 2 with normal lactate) in whom DO2 and VO2 simultaneously increased, while the blood lactate level decreased significantly from 3.5 +/- 2.5 mmol/L at T0 to 2.1 +/- 1.0 mmol/L at T4 (P < 0.05). Our results indicate that the brain-dead state was frequently associated with a global energetic failure probably due to a cellular oxygen deficit, despite blood pressure within the normal range. This energetic failure, because it is associated with high levels of DO2, could result from a defect in peripheral oxygen extraction. Aggressive therapy, achieved by producing a further increase in DO2, may reduce this global tissue oxygen deficit.