Open Access Highly Accessed Open Badges Research

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

Rinaldo Bellomo1*, Michael Bailey1, Glenn M Eastwood3, Alistair Nichol1, David Pilcher2, Graeme K Hart2, Michael C Reade3, Moritoki Egi4, D James Cooper1 and the Study of Oxygen in Critical Care (SOCC) Group

Author Affiliations

1 Australian and New Zealand Intensive Care Research Centre, School of Public Health and Preventive Medicine, Monash University, 5 Commercial Road, Prahran, Melbourne, Victoria 3181, Australia

2 Australia New Zealand Intensive Care Society (ANZICS) Clinical Outcomes and Resource Evaluation (CORE) Centre, 10 Ievers Terrace, Carlton, Melbourne, Victoria 3053, Australia

3 Department of Intensive Care, Austin Hospital, 145 Studley Road, Heidelberg, Melbourne, Victoria 3084, Australia

4 Department of Anesthesiology and Resuscitology, Okayama University Medical School, 5-1 Shikata-Cho 2-Chome, Okayama 700-8558, Okayama, Japan

For all author emails, please log on.

Critical Care 2011, 15:R90  doi:10.1186/cc10090

See related letter by O’Driscoll and Howard,

Published: 8 March 2011



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.


We divided patients resuscitated from nontraumatic cardiac arrest from 125 intensive care units (ICUs) into three groups according to worst PaO2 level or alveolar-arterial O2 gradient in the first 24 hours after admission. We defined 'hyperoxia' as PaO2 of 300 mmHg or greater, 'hypoxia/poor O2 transfer' as either PaO2 < 60 mmHg or ratio of PaO2 to fraction of inspired oxygen (FiO2 ) < 300, 'normoxia' as any value between hypoxia and hyperoxia and 'isolated hypoxemia' as PaO2 < 60 mmHg regardless of FiO2. Mortality at hospital discharge was the main outcome measure.


Of 12,108 total patients, 1,285 (10.6%) had hyperoxia, 8,904 (73.5%) had hypoxia/poor O2 transfer, 1,919 (15.9%) had normoxia and 1,168 (9.7%) had isolated hypoxemia (PaO2 < 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 PaO2 > 400 mmHg, hyperoxia had no independent association with mortality. Importantly, after adjustment for FiO2 and the relevant covariates, PaO2 was no longer predictive of hospital mortality (P = 0.21).


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 FiO2 in these patients.