Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest

Abstract

Introduction: Hyperoxia has recently been reported as an independent risk factor for mortality in patients resuscitated from cardiac arrest. We examined the independent relationship between hyperoxia and outcomes in such patients. Methods: We divided patients resuscitated from nontraumatic cardiac arrest from 125 intensive care units (ICUs) into three groups according to worst PaO 2 level or alveolar-arterial O 2 gradient in the first 24 hours after admission. We defined 'hyperoxia' as PaO 2 of 300 mmHg or greater, 'hypoxia/poor O 2 transfer' as either PaO 2 < 60 mmHg or ratio of PaO 2 to fraction of inspired oxygen (FiO 2 ) < 300, 'normoxia' as any value between hypoxia and hyperoxia and 'isolated hypoxemia' as PaO 2 < 60 mmHg regardless of FiO 2. Mortality at hospital discharge was the main outcome measure. Results: Of 12,108 total patients, 1,285 (10.6%) had hyperoxia, 8,904 (73.5%) had hypoxia/poor O 2 transfer, 1,919 (15.9%) had normoxia and 1,168 (9.7%) had isolated hypoxemia (PaO 2 < 60 mmHg). The hyperoxia group had higher mortality (754 (59%) of 1,285 patients; 95% confidence interval (95% CI), 56% to 61%) than the normoxia group (911 (47%) of 1,919 patients; 95% CI, 45% to 50%) with a proportional difference of 11% (95% CI, 8% to 15%), but not higher than the hypoxia group (5,303 (60%) of 8,904 patients; 95% CI, 59% to 61%). In a multivariable model controlling for some potential confounders, including illness severity, hyperoxia had an odds ratio for hospital death of 1.2 (95% CI, 1.1 to 1.6). However, once we applied Cox proportional hazards modelling of survival, sensitivity analyses using deciles of hypoxemia, time period matching and hyperoxia defined as PaO 2 > 400 mmHg, hyperoxia had no independent association with mortality. Importantly, after adjustment for FiO 2 and the relevant covariates, PaO 2 was no longer predictive of hospital mortality (P = 0.21). Conclusions: Among patients admitted to the ICU after cardiac arrest, hyperoxia did not have a robust or consistently reproducible association with mortality. We urge caution in implementing policies of deliberate decreases in FiO 2 in these patients.