Purpose of review: Reversal of tissue hypoxia, particularly in the heart and brain, is a fundamental goal of cardiopulmonary resuscitation. However, a growing body of evidence suggests that hyperoxia, especially after return of spontaneous circulation (ROSC), may worsen outcomes. The purpose of this review is to describe the current evidence supporting the concept of controlled oxygenation during and after cardiac arrest.
Recent findings: Animal studies over the last two decades have built a compelling case that arterial hyperoxemia during the first hour after ROSC causes increased oxidative damage, increased neuronal death, and worse neurologic function. However, human data are limited. The only prospective randomized clinical trial comparing different inspired oxygen concentrations in post-cardiac arrest patients was underpowered to detect a difference in survival or neurologic outcome. More recently a retrospective analysis of data from a multicenter registry found that initial arterial hyperoxemia (paO2 ≥ 300 mmHg) was associated with increased mortality and worse functional outcome in patients admitted to the ICU after cardiac arrest. The existing evidence, though limited, has contributed to new guidelines for oxygen therapy in patients resuscitated from cardiac arrest.
Summary: The benefit of supplemental oxygen during cardiopulmonary resuscitation remains uncertain. However, in patients who achieve ROSC after cardiac arrest, available evidence supports adjusting inspired oxygen content to avoid arterial hyperoxemia while providing adequate arterial oxyhemoglobin saturation. This strategy is likely to be most effective when initiated as soon as possible after ROSC and appears to be most important during the first hour. Definitive clinical trials are needed to determine the ultimate impact on outcome.