Cerebral oxygenation in mechanically ventilated early cardiac arrest survivors: The impact of hypercapnia

Background: Optimal cerebral oxygenation is considered fundamental to cerebral protection in cardiac arrest (CA) patients. Hypercapnia increases cerebral blood flow and may also improve cerebral oxygenation. It is uncertain, however, whether this effect occurs in mechanically ventilated early survivors of CA. Methods: We enrolled mechanically ventilated resuscitated patients within 36 h of their cardiac arrest. We performed a prospective double cross-over physiological study comparing the impact of normocapnia (PaCO₂ 35-45 mmHg) vs. mild hypercapnia (PaCO₂ 45-55 mmHg) on regional cerebral tissue oxygen saturation (SctO₂) assessed by near infrared spectroscopy (NIRS). Results: We studied seven adult CA patients with a median time to return of spontaneous circulation of 28 min at a median of 26 h and 30 min after CA. During normocapnia (median EtCO₂ of 32 mmHg [30-41 mmHg] and PaCO₂ of 37 mmHg [32-45 mmHg]) the median NIRS-derived left frontal SctO₂ was 61% [52-65%] and the right frontal SctO₂ was 61% [54-68%]. However, during mild hypercapnia (median EtCO₂ of 49 mmHg [40-57 mmHg] and PaCO₂ of 52 mmHg [43-55 mmHg) the median left frontal SctO₂ increased to 69% [59-78%] and the right frontal SctO₂ increased to 73% [61-76%])(p = 0.001, for all comparisons). Conclusion: During the early post-resuscitation period, in mechanically ventilated CA patients, mild hypercapnia increases cerebral oxygenation as assessed by NIRS. Further investigations of the effect of prolonged mild hypercapnia on cerebral oxygenation and patient outcomes appear justified.