Brain Oxygenation Response to Hypercapnia in Acute Brain Injured Patients

Abstract Background Cerebral 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 (PbtO 2 ). Methods This single-center retrospective study (November 2014-June 2022) included all patients admitted to the Intensive Care Unit (ICU) after acute brain injury who required multimodal monitoring including PbtO 2 and who underwent induced moderate hypoventilation and increased PaCO 2 , 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 PbtO 2 values when compared to their baseline levels. Results On a total of 163 eligible patients, we identified 23 (14%) patients who underwent moderate hypoventilation (PaCO 2 from 44 [42–45] to 50 [49–53] mmHg; p < 0.001) during the study period at a median of 6 (4–10) days following ICU admission; 6 patients had traumatic brain injury (TBI) and 17 had subarachnoid hemorrhage (SAH). A significant overall increase in median PbtO 2 values from baseline [21 (19–26) to 24 (22–26) mmHg; p = 0.02] was observed. Eight (35%) patients were considered as “responders”, with a median increase of 7 (from 4 to 11) mmHg of PbtO 2 , while non-responders showed no changes (from − 1 to 2 mmHg of PbtO 2 ). Due to the small sample size, no variable independently associated with PbtO 2 response was identified. No correlation between the change in PaCO 2 and in PbtO 2 was observed. Conclusions In this study, a heterogeneous response of brain tissue oxygenation to induced hypercapnia was observed, but without any deleterious elevations of ICP.