Factors that influenced resting metabolic expenditure (RME) and the cardiovascular response associated with an elevated RME were examined in 55 patients with penetrating and closed head injuries who were kept normovolemic and hyperalimented during the acute phase of injury. The severity of the neurological injury had a strong effect on the RME; those with a GCS of 4-5 had the highest RME, 168 ± 53% of that expected, whereas those with a GCS of 6-7 had a lower RME, 129 ± 31% of that expected. Increased body temperature was associated with increased RME by 45%/°C in patients with a GCS of 4-5 and by 15%/°C in those with a GCS 6-7. The increase in oxygen utilization was associated with an increase in plasma catecholamines. Sedatives, paralyzing agents, and propranolol all decreased RME. The cardiovascular response associated with increased oxygen utilization was an elevated cardiac output and, when RME was very high, a widened mean arterial-venous oxygen content difference, indicating that the tissues were more fully extracting oxygen. The increased cardiac output was dependent upon the presence of an adequate intravascular volume. During the 2-year period of study, a total of 99 patients with closed head injuries (including 44 patients who underwent studies) were admitted. The mortality rate of this consecutive series of comatose patients was 25%. The incidence of intracranial hypertension (30%) and of death from uncontrolled intracranial hypertension (12%) was not different from that reported in other recent series. There were no deaths from sepsis or with severe electrolyte abnormalities during the first 2 weeks after injury. The data suggest that, in management of the hypermetabolic state that accompanies head injury, supplying adequate nutrients and maintaining an adequate intravascular volume and cardiac output to deliver oxygen and nutrients may reduce deaths due to systemic causes without producing increased intracranial pressure. The practice of dehydration in neurosurgical management is questioned.