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.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
TREATMENT
Masking
NONE
Enrollment
11
Increase of the alveolar ventilation by a stepwise increase in tidal volumes and respiratory rate until a reduction of end-tidal CO2 of 0.7 kPa is achieved
University Hospital Zurich
Zurich, Switzerland
intracranial pressure
Change of intracranial pressure during moderate hyperventilation
Time frame: 10, 20, 50, 60 minutes after begin of the hyperventilation test
cerebral flow velocity in the middle cerebral artery
Change of cerebral flow velocity during moderate hyperventilation
Time frame: 20, 50, 60 minutes after begin of the hyperventilation test
brain tissue oxygenation (PbrO2)
no changes
Time frame: 10, 20, 50, 60 minutes after begin of the hyperventilation test
cerebral Lactate/ Pyruvate ratio
no changes
Time frame: 1 hour before initiation of the hyperventilation test, and 1 and 2 hours after begin of the hyperventilation test
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