Effect of hypocapnea on CBF and extracellular intermediates of secondary brain injury

We examined the metabolic response of the brain underlying subdural hematomas or surrounding contusions to hyperventilation and looked for evidence of ischemia. Twelve consecutive patients with severe traumatic brain injury (TBI) (GCS < 8) who required surgery for evacuation of subdural hematoma or hemorrhagic contusion were studied. At surgery, a microdialysis catheter was placed into the cortex in a gyrus adjacent to the contusion or underlying the subdural hematoma. A thermal diffusion flow probe was placed on the cortex directly above the dialysis catheter. On days 1 and 3 post injury, two trials of hyperventilation were performed which dropped the patients' pCO2 10 mm Hg for 30 minutes. Monitoring of CBF and collection of dialysis fluid continued throughout each hyperventilation trial. Data was analyzed for a three hour window surrounding each hyperventilation. Brief periods of hyperventilation did not cause a significant elevation of the extracellular lactate/pyruvate ratio or glutamate level in areas of the brain likely to be the most vulnerable to secondary injury. In spite of hyperventilation leading to a significant decline in local CBF in 20% of the trials, there was no evidence of ischemia or excitatory amino acid release associated with hyperventilation.