Elevated intracranial pressure is a dangerous and potentially fatal complication after traumatic brain injury. Hyperventilation is a medical intervention to reduce elevated intracranial pressure by inducing cerebral vasoconstriction, which might be associated to cerebral ischemia and hypoxia.

The main hypothesis is that a moderate degree of hyperventilation is sufficient to reduce the intracranial pressure without inducing cerebral ischemia.

In patients with severe traumatic brain injury (TBI), and with intracranial pressure-monitoring, brain tissue oxygen tension and/or microdialysis probes hyperventilation-tests are performed in the acute phase after trauma. Data are collected and TCCD measurements are performed at baseline, at the beginning of moderate hyperventilation, after prolonged moderate hyperventilation (for 50 minutes) and after return to baseline.

The present study aims to quantify potential adverse effects of moderate short-term hyperventilation during the acute phase of the severe TBI on cerebral hemodynamics, oxygenation, and metabolism.

Inclusion Criteria:

• nonpenetrating traumatic brain injury
• Glasgow coma scale <9 at presentation
• Intracranial pressure monitoring
• brain tissue oxygen tension monitoring and/or microdialysis monitoring
• invasive mechanical ventilation with FIO2 <60% and PEEP <15 mbar

Exclusion Criteria:

• decompressive craniectomy
• pregnancy
• pre-existing neurological disease
• previous traumatic brain injury
• acute cardiovascular disease
• severe respiratory failure
• acute on chronic liver disease
• sepsis
• failure to obtain satisfactory bilateral TCCD signals
• persisting hypovolemia or hemodynamic instability