• Neurocritical care · Apr 2024

    Brain Oxygenation Response to Hypercapnia in Patients with Acute Brain Injury.

    • Marco Anderloni, Sophie Schuind, Michele Salvagno, Katia Donadello, Lorenzo Peluso, Filippo Annoni, Fabio Silvio Taccone, and Gouvea BogossianElisaEDepartment of Intensive Care, Hôpital Universitaire de Bruxelles, Université Libre de Bruxelles, Route de Lennik, 808, Brussels, Belgium. elisa.gouvea.bogossian@ulb.ac.be..
    • Department of Intensive Care, Hôpital Universitaire de Bruxelles, Université Libre de Bruxelles, Route de Lennik, 808, Brussels, Belgium.
    • Neurocrit Care. 2024 Apr 1; 40 (2): 750758750-758.

    BackgroundCerebral hypoxia is a frequent cause of secondary brain damage in patients with acute brain injury. Although hypercapnia can increase intracranial pressure, it may have beneficial effects on tissue oxygenation. We aimed to assess the effects of hypercapnia on brain tissue oxygenation (PbtO2).MethodsThis single-center retrospective study (November 2014 to June 2022) included all patients admitted to the intensive care unit after acute brain injury who required multimodal monitoring, including PbtO2 monitoring, and who underwent induced moderate hypoventilation and hypercapnia according to the decision of the treating physician. Patients with imminent brain death were excluded. Responders to hypercapnia were defined as those with an increase of at least 20% in PbtO2 values when compared to their baseline levels.ResultsOn a total of 163 eligible patients, we identified 23 (14%) patients who underwent moderate hypoventilation (arterial partial pressure of carbon dioxide [PaCO2] from 44 [42-45] to 50 [49-53] mm Hg; p < 0.001) during the study period at a median of 6 (4-10) days following intensive care unit admission; six patients had traumatic brain injury, and 17 had subarachnoid hemorrhage. A significant overall increase in median PbtO2 values from baseline (21 [19-26] to 24 [22-26] mm Hg; p = 0.02) was observed. Eight (35%) patients were considered as responders, with a median increase of 7 (from 4 to 11) mm Hg of PbtO2, whereas nonresponders showed no changes (from - 1 to 2 mm Hg of PbtO2). Because of the small sample size, no variable independently associated with PbtO2 response was identified. No correlation between changes in PaCO2 and in PbtO2 was observed.ConclusionsIn this study, a heterogeneous response of PbtO2 to induced hypercapnia was observed but without any deleterious elevations of intracranial pressure.© 2023. Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society.

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