Purpose Previous observational studies have inconsistently associated early hyperoxia with worse outcomes after cardiac arrest and have methodological limitations. We tested this association using a high-resolution database controlling for multiple disease-specific markers of severity of illness and care processes. Methods This was a retrospective analysis of a single-center, prospective registry of consecutive cardiac arrest patients. We included patients who survived and were mechanically ventilated ≥24h after arrest. Our main exposure was arterial oxygen tension (PaO2), which we categorized hourly for 24 hours as severe hyperoxia (>300mmHg), moderate or probable hyperoxia (101-299mmHg), normoxia (60-100mmHg) or hypoxia (<60mmHg). We controlled for Utstein-style covariates, markers of disease severity and markers of care responsiveness. We performed unadjusted and multiple logistic regression to test the association between oxygen exposure and survival to discharge, and used ordered logistic regression to test the association of oxygen exposure with neurological outcome and Sequential Organ Failure Assessment (SOFA) score at 24h. Results Of 184 patients, 36% were exposed to severe hyperoxia and overall mortality was 54%. Severe hyperoxia, but not moderate or probable hyperoxia, was associated with decreased survival in both unadjusted and adjusted analysis (adjusted odds ratio (OR) for survival 0.83 per hour exposure, P=0.04). Moderate or probable hyperoxia was not associated with survival but was associated with improved SOFA score 24h (OR 0.92, P<0.01). Conclusion Severe hyperoxia was independently associated with decreased survival to hospital discharge. Moderate or probable hyperoxia was not associated with decreased survival and was associated with improved organ function at 24h.
IntroductionPost-cardiac arrest patients are often exposed to 100% oxygen during cardiopulmonary resuscitation and the early post-arrest period. It is unclear whether this contributes to development of pulmonary dysfunction or other patient outcomes.MethodsWe performed a retrospective cohort study including post-arrest patients who survived and were mechanically ventilated at least 24 hours after return of spontaneous circulation. Our primary exposure of interest was inspired oxygen, which we operationalized by calculating the area under the curve of the fraction of inspired oxygen (FiO2AUC) for each patient over 24 hours. We collected baseline demographic, cardiovascular, pulmonary and cardiac arrest-specific covariates. Our main outcomes were change in the respiratory subscale of the Sequential Organ Failure Assessment score (SOFA-R) and change in dynamic pulmonary compliance from baseline to 48 hours. Secondary outcomes were survival to hospital discharge and Cerebral Performance Category at discharge.ResultsWe included 170 patients. The first partial pressure of arterial oxygen (PaO2):FiO2 ratio was 241 ± 137, and 85% of patients had pulmonary failure and 55% had cardiovascular failure at presentation. Higher FiO2AUC was not associated with change in SOFA-R score or dynamic pulmonary compliance from baseline to 48 hours. However, higher FiO2AUC was associated with decreased survival to hospital discharge and worse neurological outcomes. This was driven by a 50% decrease in survival in the highest quartile of FiO2AUC compared to other quartiles (odds ratio for survival in the highest quartile compared to the lowest three quartiles 0.32 (95% confidence interval 0.13 to 0.79), P = 0.003).ConclusionsHigher exposure to inhaled oxygen in the first 24 hours after cardiac arrest was not associated with deterioration in gas exchange or pulmonary compliance after cardiac arrest, but was associated with decreased survival and worse neurological outcomes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-015-0824-x) contains supplementary material, which is available to authorized users.
Introduction: Prior studies inconsistently report an association between hyperoxemia and worse outcomes after cardiac arrest (CA), but are methodologically limited. We used a high-resolution CA-specific database to control for cumulative early oxygen exposure, disease-specific covariates and care processes to test if rigorous adjustment would eliminate any association between hyperoxemia and outcomes. We also tested if exposure to higher inspired oxygen (FiO2) was associated with development of lung dysfunction. Methods: We included patients surviving and ventilated for >24 hours after ROSC. To test the association between hyperoxemia and outcomes, we categorized PaO2 hourly for 24h as severe hyperoxemia (>300mmHg), moderate hyperoxemia (101-299mmHg), normoxia (60-100mmHg) or hypoxia (<60mmHg). We controlled for CA-specific covariates and markers of potentially less attentive care (time to first FiO2 wean, number of weans, etc). We used multiple logistic regression to test the association between PaO2 and survival and discharge CPC. To test for development of lung dysfunction, we calculated oxygen exposure as the area under the curve of the FiO2 x hour (FiO2AUC) for each patient over 24h. Our main outcomes in this analysis were change in the respiratory SOFA score (SOFA-R) and change in dynamic lung compliance from baseline to 48h. Results: Of 184 patients overall mortality was 54% and 36% had severe hyperoxemia. The first PaO2:FiO2 ratio was 241±137, and at baseline 85% had pulmonary failure and 55% had cardiovascular failure as assessed by SOFA. Only severe hyperoxemia was independently associated with decreased survival to hospital discharge (adjusted OR 0.83 per hour, P=0.04) and worse discharge CPC. Higher FiO2AUC was not associated with worsened SOFA-R or lung compliance over 48h but was associated with decreased survival to discharge and worse discharge CPC. This was driven by 50% decreased survival in the highest quartile of FiO2AUC (FIO2>80%/24h) compared to other quartiles. Conclusion: Despite rigorous adjustment, severe hyperoxemia was independently associated with decreased survival to hospital discharge and discharge CPC. We did not observe toxicity at lower levels. High FiO2 was not associated with pulmonary toxicity.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.