Effect of moderate hyperventilation and induced hypertension on cerebral tissue oxygenation after cardiac arrest and therapeutic hypothermia

AimImproving cerebral perfusion is an essential component of post-resuscitation care after cardiac arrest (CA), however precise recommendations in this setting are limited. We aimed to examine the effect of moderate hyperventilation (HV) and induced hypertension (IH) on non-invasive cerebral tissue oxygenation (SctO2) in patients with coma after CA monitored with near-infrared spectroscopy (NIRS) during therapeutic hypothermia (TH).MethodsProspective pilot study including comatose patients successfully resuscitated from out-of-hospital CA treated with TH, monitored with NIRS. Dynamic changes of SctO2 upon HV and IH were analyzed during the stable TH maintenance phase. HV was induced by decreasing PaCO2 from ∼40 to ∼30 mmHg, at stable mean arterial blood pressure (MAP ∼ 70 mmHg). IH was obtained by increasing MAP from ∼70 to ∼90 mmHg with noradrenaline.ResultsTen patients (mean age 69 years; mean time to ROSC 19 min) were studied. Following HV, a significant reduction of SctO2 was observed (baseline 74.7 ± 4.3% vs. 69.0 ± 4.2% at the end of HV test, p < 0.001, paired t-test). In contrast, IH was not associated with changes in SctO2 (baseline 73.6 ± 3.5% vs. 74.1 ± 3.8% at the end of IH test, p = 0.24).ConclusionsModerate hyperventilation was associated with a significant reduction in SctO2, while increasing MAP to supra-normal levels with vasopressors had no effect on cerebral tissue oxygenation. Our study suggests that maintenance of strictly normal PaCO2 levels and MAP targets of 70 mmHg may provide optimal cerebral perfusion during TH in comatose CA patients.