• D W Marion, A Firlik, and M R McLaughlin.
• Brain Trauma Research Center, University of Pittsburgh Medical Center, PA., USA.
• New Horiz. 1995 Aug 1;3(3):439-47.

AbstractThe management of brain swelling that frequently occurs following severe traumatic brain injury (TBI) presents a difficult challenge for physicians treating these patients. A traditional cornerstone for the treatment of post-traumatic brain swelling has been prophylactic hyperventilation to reach PaCO2 levels of 25 to 28 torr. While there are anecdotal reports of improvement in intracranial pressure (ICP) and neurologic functioning following institution of this therapy, the only prospective, randomized trial of its use has found worse outcomes in those treated with prophylactic hyperventilation therapy for 5 days. That hyperventilation therapy might exacerbate secondary brain injury seems likely based on abnormalities in cerebral blood flow (CBF) and metabolism which result from TBI, and the potential for hyperventilation to worsen those abnormalities. Both global and regional CBF are critically reduced, and metabolism increased, during the first several hours and days after injury. As a result, focal ischemia is common following severe TBI. Hyperventilation causes a further decrease in CBF, often without a concomitant reduction in ICP. In some cases, TBI also causes an increase in cerebral vascular responsivity to hypocapnia, increasing the drop in regional CBF that occurs with hyperventilation. Thus, there is a well defined physiologic basis for expecting hyperventilation to cause worsened clinical outcomes following TBI. While this therapy clearly is indicated for the management of acute neurologic deterioration or intracranial hypertension refractory to all other forms of medical therapy, hyperventilation is no longer recommended as a first-line therapy for intracranial hypertension or as prophylactic therapy following severe TBI.

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