Neurological and respiratory effects of lung protective ventilation in acute brain injury patients without lung injury: brain vent, a single centre randomized interventional study.
Acknowledgements: We acknowledge the medical doctors Christian Holgersen and Krister Ekeroth and the medical student Lisa Jakobsen who participated in part of the data collection. We acknowledge statistician, Professor of Medical epidemiology at UiT the Arctic University of Norway, Dr. Tom Wilsgaard...
| Main Authors: | , , , , , , |
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| Format: | Article in Journal/Newspaper |
| Language: | English |
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Springer Science and Business Media LLC
2023
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| Subjects: | |
| Online Access: | https://www.repository.cam.ac.uk/handle/1810/347748 https://doi.org/10.17863/CAM.95167 |
| Summary: | Acknowledgements: We acknowledge the medical doctors Christian Holgersen and Krister Ekeroth and the medical student Lisa Jakobsen who participated in part of the data collection. We acknowledge statistician, Professor of Medical epidemiology at UiT the Arctic University of Norway, Dr. Tom Wilsgaard for assistance with sample size calculation. Funder: UiT The Arctic University of Norway (incl University Hospital of North Norway) INTRODUCTION: Lung protective ventilation (LPV) comprising low tidal volume (VT) and high positive end-expiratory pressure (PEEP) may compromise cerebral perfusion in acute brain injury (ABI). In patients with ABI, we investigated whether LPV is associated with increased intracranial pressure (ICP) and/or deranged cerebral autoregulation (CA), brain compensatory reserve and oxygenation. METHODS: In a prospective, crossover study, 30 intubated ABI patients with normal ICP and no lung injury were randomly assigned to receive low VT [6 ml/kg/predicted (pbw)]/at either low (5 cmH2O) or high PEEP (12 cmH2O). Between each intervention, baseline ventilation (VT 9 ml/kg/pbw and PEEP 5 cmH2O) were resumed. The safety limit for interruption of the intervention was ICP above 22 mmHg for more than 5 min. Airway and transpulmonary pressures were continuously monitored to assess respiratory mechanics. We recorded ICP by using external ventricular drainage or a parenchymal probe. CA and brain compensatory reserve were derived from ICP waveform analysis. RESULTS: We included 27 patients (intracerebral haemorrhage, traumatic brain injury, subarachnoid haemorrhage), of whom 6 reached the safety limit, which required interruption of at least one intervention. For those without intervention interruption, the ICP change from baseline to "low VT/low PEEP" and "low VT/high PEEP" were 2.2 mmHg and 2.3 mmHg, respectively, and considered clinically non-relevant. None of the interventions affected CA or oxygenation significantly. Interrupted events were associated with high baseline ICP (p < 0.001), low ... |
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