No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury

Object. Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hy perventilation could lead to cerebral ischemia; these concerns have been ma gnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induc ed early after TBI would not produce a reduction in CBF severe enough to ca use cerebral energy failure (CBF that is insufficient to meet metabolic nee ds). Methods. Nine patients were studied a mean of 11.2 +/- 1.6 hours (range 8-1 4 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score wa s 5.6 +/- 1.8 and their mean age 27 +/- 9 years; eight of the patients were male. Intracranial pressure (ICP), mean arterial blood pressure, and jugul ar venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when need ed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic ra te for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venou s oxygen content (CvO(2)) were made before and after 30 minutes of hyperven tilation to a PaCO2 of 30 +/- 2 mm Hg. Ten age-matched healthy volunteers w ere used as normocapnic controls. Global CBF, CBV, and CvO(2) did not differ between the two groups, but in t he TBI patients CMRO2 and OEF were reduced (1.59 +/- 0.44 ml/100 g/minute [ p < 0.01] and 0.31 +/- 0.06 [p < 0.0001], respectively). During hyperventil ation, global CBF decreased to 25.5 +/- 8.7 ml/100 g/minute (p < 0.0009), C BV fell to 2.8 +/- 0.56 ml/100 g (p < 0.001), OEF rose to 0.45 +/- 0.13 (p < 0.02), and CvO(2) fell to 8.3 +/- 3 vol% (p < 0.02); CMRO2 remained uncha nged. Conclusions. The authors conclude that early, brief, moderate hyperventilat ion does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional stu dies are needed to assess focal changes, the effects of more severe hyperve ntilation, and the effects of hyperventilation in the setting of increased ICP.