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

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Object. Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hyperventilation could lead to cerebral ischemia; these concerns have been magnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induced early after TBI would not produce a reduction in CBF severe enough to cause cerebral energy failure (CBF that is insufficient to meet metabolic needs).

Methods. Nine patients were studied a mean of 11.2 ± 1.6 hours (range 8–14 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score was 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 jugular venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when needed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venous oxygen content (CvO2) were made before and after 30 minutes of hyperventilation to a PaCO2 of 30 ± 2 mm Hg. Ten age-matched healthy volunteers were used as normocapnic controls.

Global CBF, CBV, and CvO2 did not differ between the two groups, but in the 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 hyperventilation, global CBF decreased to 25.5 ± 8.7 ml/100 g/minute (p < 0.0009), CBV fell to 2.8 ± 0.56 ml/100 g (p < 0.001), OEF rose to 0.45 ± 0.13 (p < 0.02), and CvO2 fell to 8.3 ± 3 vol% (p < 0.02); CMRO2 remained unchanged.

Conclusions. The authors conclude that early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional studies are needed to assess focal changes, the effects of more severe hyperventilation, and the effects of hyperventilation in the setting of increased ICP.

Article Information

Address reprint requests to: Michael Diringer, M.D., Department of Neurology, Box 8111, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, Missouri 63110. email: diringerm@neuro.wustl.edu.

© AANS, except where prohibited by US copyright law.

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Figures

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    Bar graph depicting cerebrovascular hemodynamics in patients with TBI compared with age-matched healthy controls.

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    Bar graph showing arterial and jugular venous blood gas levels before and during hyperventilation (HV) to 30 ± 2 mm Hg.

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    Bar graph depicting cerebrovascular hemodynamics in patients with TBI before and during hyperventilation at a PaCO2 of 30 ± 2 mm Hg.

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    Graph showing changes in OEF and CMRO2 for individual patients before and during hyperventilation to a PaCO2 of 30 ± 2 mm Hg.

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    Scatterplots illustrating the correlation of CBF and CMRO2 before (left) and during (right) hyperventilation.

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    Schematic representation of the relationship between CBF, OEF, and CMRO2 during primary changes in CMRO2 (upper) or CBF (lower). Upper: Under normal circumstances CBF and CMRO2 are matched and the OEF is normal. If there is a primary reduction in CMRO2, as observed in hypothermia or after administration of barbiturate medications, there is a secondary passive fall in CBF and again OEF remains normal. Lower: Situations in which there is a primary alteration in CBF. When there is a moderate reduction in CBF, the OEF rises and CMRO2 remains constant. This is referred to as “misery perfusion.” If the CBF is reduced further, the OEF becomes maximal. Any further reduction in CBF results in a fall in CMRO2 or ischemia, which can lead to permanent injury. When CBF exceeds the metabolic needs, the OEF is low, a situation referred to as “luxury perfusion.”

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