Henry E Wang1, David K Prince2, Ian R Drennan3, Brian Grunau4, David J Carlbom5, Nicholas Johnson6, Matthew Hansen7, Jonathan Elmer8, Jim Christenson4, Peter Kudenchuk9, Tom Aufderheide10, Myron Weisfeldt11, Ahamed Idris12, Stephen Trzeciak13, Michael Kurz14, Jon C Rittenberger8, Denise Griffiths7, Jamie Jasti10, Susanne May2. 1. Department of Emergency Medicine, University of Alabama at Birmingham, Birmingham, AL, United States; Department of Emergency Medicine, University of Texas Health Science Center at Houston, Houston, TX, United States. Electronic address: henry.e.wang@uth.tmc.edu. 2. The Clinical Trials Center, Department of Biostatistics, University of Washington, Seattle, WA, United States. 3. Rescu, Li Ka Shing Knowledge Institute, St Michael's Hospital, Institute of Medical Science, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada. 4. Department of Emergency Medicine, University of British Columbia, Vancouver, British Columbia, Canada. 5. Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, Seattle, WA, United States. 6. Division of Emergency Medicine, Department of Medicine, University of Washington, Seattle, WA, United States. 7. Department of Emergency Medicine, Oregon Health & Science University, Portland, OR, United States. 8. Department of Emergency Medicine, University of Pittsburgh, Pittsburgh, PA, United States. 9. Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA, United States. 10. Department of Emergency Medicine, Medical College of Wisconsin, Milwaukee, WI, United States. 11. Department of Medicine, Johns Hopkins University, Baltimore, MD, United States. 12. Department of Emergency Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States. 13. Division of Critical Care Medicine, Department of Medicine, United States; Department of Emergency Medicine, Cooper Medical School of Rowan University, Camden, NJ, United States. 14. Department of Emergency Medicine, University of Alabama at Birmingham, Birmingham, AL, United States.
Abstract
OBJECTIVE: To determine if arterial oxygen and carbon dioxide abnormalities in the first 24h after return of spontaneous circulation (ROSC) are associated with increased mortality in adult out-of-hospital cardiac arrest (OHCA). METHODS: We used data from the Resuscitation Outcomes Consortium (ROC), including adult OHCA with sustained ROSC ≥1h after Emergency Department arrival and at least one arterial blood gas (ABG) measurement. Among ABGs measured during the first 24h of hospitalization, we identified the presence of hyperoxemia (PaO2≥300mmHg), hypoxemia (PaO2<60mmHg), hypercarbia (PaCO2>50mmHg) and hypocarbia (PaCO2<30mmHg). We evaluated the associations between oxygen and carbon dioxide abnormalities and hospital mortality, adjusting for confounders. RESULTS: Among 9186 OHCA included in the analysis, hospital mortality was 67.3%. Hyperoxemia, hypoxemia, hypercarbia, and hypocarbia occurred in 26.5%, 19.0%, 51.0% and 30.6%, respectively. Initial hyperoxemia only was not associated with hospital mortality (adjusted OR 1.10; 95% CI: 0.97-1.26). However, final and any hyperoxemia (1.25; 1.11-1.41) were associated with increased hospital mortality. Initial (1.58; 1.30-1.92), final (3.06; 2.42-3.86) and any (1.76; 1.54-2.02) hypoxemia (PaO2<60mmHg) were associated with increased hospital mortality. Initial (1.89; 1.70-2.10); final (2.57; 2.18-3.04) and any (1.85; 1.67-2.05) hypercarbia (PaCO2>50mmHg) were associated with increased hospital mortality. Initial (1.13; 0.90-1.41), final (1.19; 1.04-1.37) and any (1.01; 0.91-1.12) hypocarbia (PaCO2<30mmHg) were not associated with hospital mortality. CONCLUSIONS: In the first 24h after ROSC, abnormal post-arrest oxygen and carbon dioxide tensions are associated with increased out of-hospital cardiac arrest mortality.
OBJECTIVE: To determine if arterial oxygen and carbon dioxide abnormalities in the first 24h after return of spontaneous circulation (ROSC) are associated with increased mortality in adult out-of-hospital cardiac arrest (OHCA). METHODS: We used data from the Resuscitation Outcomes Consortium (ROC), including adult OHCA with sustained ROSC ≥1h after Emergency Department arrival and at least one arterial blood gas (ABG) measurement. Among ABGs measured during the first 24h of hospitalization, we identified the presence of hyperoxemia (PaO2≥300mmHg), hypoxemia (PaO2<60mmHg), hypercarbia (PaCO2>50mmHg) and hypocarbia (PaCO2<30mmHg). We evaluated the associations between oxygen and carbon dioxide abnormalities and hospital mortality, adjusting for confounders. RESULTS: Among 9186 OHCA included in the analysis, hospital mortality was 67.3%. Hyperoxemia, hypoxemia, hypercarbia, and hypocarbia occurred in 26.5%, 19.0%, 51.0% and 30.6%, respectively. Initial hyperoxemia only was not associated with hospital mortality (adjusted OR 1.10; 95% CI: 0.97-1.26). However, final and any hyperoxemia (1.25; 1.11-1.41) were associated with increased hospital mortality. Initial (1.58; 1.30-1.92), final (3.06; 2.42-3.86) and any (1.76; 1.54-2.02) hypoxemia (PaO2<60mmHg) were associated with increased hospital mortality. Initial (1.89; 1.70-2.10); final (2.57; 2.18-3.04) and any (1.85; 1.67-2.05) hypercarbia (PaCO2>50mmHg) were associated with increased hospital mortality. Initial (1.13; 0.90-1.41), final (1.19; 1.04-1.37) and any (1.01; 0.91-1.12) hypocarbia (PaCO2<30mmHg) were not associated with hospital mortality. CONCLUSIONS: In the first 24h after ROSC, abnormal post-arrest oxygen and carbon dioxide tensions are associated with increased out of-hospital cardiac arrest mortality.
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