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

Aim: Improving 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 (SctO(2)) in patients with coma after CA monitored with near-infrared spectroscopy (NIRS) during therapeutic hypothermia (TH). Methods: Prospective pilot study including comatose patients successfully resuscitated from out-of-hospital CA treated with TH, monitored with NIRS. Dynamic changes of SctO(2) upon HV and IH were analyzed during the stable TH maintenance phase. HV was induced by decreasing PaCO2 from similar to 40 to similar to 30 mmHg, at stable mean arterial blood pressure (MAP similar to 70 mmHg). IH was obtained by increasing MAP from similar to 70 to similar to 90 mmHg with noradrenaline. Results: Ten patients (mean age 69 years; mean time to ROSC 19 min) were studied. Following HV, a significant reduction of SctO(2) 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 SctO(2) (baseline 73.6 +/- 3.5% vs. 74.1 +/- 3.8% at the end of IH test, p = 0.24). Conclusions: Moderate hyperventilation was associated with a significant reduction in SctO(2), 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. (C) 2013 Elsevier Ireland Ltd. All rights reserved.