Head Injury Trauma, Hyperventilation
Conditions
Keywords
intracranial pressure, cerebral metabolism, cerebral oxygenation
Brief summary
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.
Detailed description
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.
Interventions
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
Sponsors
Study design
Intervention model description
several parameters are collected at different time points: at baseline conditions, during moderate hyperventilation, and after return to baseline
Eligibility
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
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| intracranial pressure | 10, 20, 50, 60 minutes after begin of the hyperventilation test | Change of intracranial pressure during moderate hyperventilation |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| cerebral Lactate/ Pyruvate ratio | 1 hour before initiation of the hyperventilation test, and 1 and 2 hours after begin of the hyperventilation test | no changes |
| cerebral flow velocity in the middle cerebral artery | 20, 50, 60 minutes after begin of the hyperventilation test | Change of cerebral flow velocity during moderate hyperventilation |
| brain tissue oxygenation (PbrO2) | 10, 20, 50, 60 minutes after begin of the hyperventilation test | no changes |
Countries
Switzerland