How much oxygen should we give patients after successful cardiac arrest resuscitation? Too little oxygen may potentiate anoxic injury. Too much oxygen may increase oxygen free radical production, possibly triggering cellular injury and apoptosis. A multicentre ICU database of over 6300 post-arrest patients was analysed and demonstrated an association between ‘hyperoxia’ and in-hospital mortality.
Adult patients who sustained nontraumatic cardiac arrest and were admitted to the ICU at a participating center between 2001 and 2005 were included. Specifically, inclusion criteria were age older than 17 years, nontraumatic cardiac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following ICU arrival.
The cohort was divided into 3 exposure groups defined a priori based on PaO2 on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO2 of 300 mm Hg (39.5 kPa) or greater; hypoxia, PaO2 of less than 60 mm Hg (7.9 kPa) (or ratio of PaO2 to fraction of inspired oxygen [FIO2] <300); and normoxia, cases not classified as hyperoxia or hypoxia.
Exposure to hyperoxia was found to be a significant predictor of in-hospital death (OR, 1.8 [95% CI, 1.5-2.2]; this was an independent effect that persisted after adjusting for all other significant risk factors
The authors acknowledge that association does not necessarily imply causation, but add that these data support the hypothesis that high oxygen delivery in the postcardiac arrest setting may have adverse effects.
Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality