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      Associations of arterial carbon dioxide and arterial oxygen concentrations with hospital mortality after resuscitation from cardiac arrest

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          Abstract

          Introduction

          Arterial concentrations of carbon dioxide (PaCO 2) and oxygen (PaO 2) during admission to the intensive care unit (ICU) may substantially affect organ perfusion and outcome after cardiac arrest. Our aim was to investigate the independent and synergistic effects of both parameters on hospital mortality.

          Methods

          This was a cohort study using data from mechanically ventilated cardiac arrest patients in the Dutch National Intensive Care Evaluation (NICE) registry between 2007 and 2012. PaCO 2 and PaO 2 levels from arterial blood gas analyses corresponding to the worst oxygenation in the first 24 h of ICU stay were retrieved for analyses. Logistic regression analyses were performed to assess the relationship between hospital mortality and both categorized groups and a spline-based transformation of the continuous values of PaCO 2 and PaO 2.

          Results

          In total, 5,258 cardiac arrest patients admitted to 82 ICUs in the Netherlands were included. In the first 24 h of ICU admission, hypocapnia was encountered in 22 %, and hypercapnia in 35 % of included cases. Hypoxia and hyperoxia were observed in 8 % and 3 % of the patients, respectively. Both PaCO 2 and PaO 2 had an independent U-shaped relationship with hospital mortality and after adjustment for confounders, hypocapnia and hypoxia were significant predictors of hospital mortality: OR 1.37 (95 % CI 1.17–1.61) and OR 1.34 (95 % CI 1.08–1.66). A synergistic effect of concurrent derangements of PaCO 2 and PaO 2 was not observed (P = 0.75).

          Conclusions

          The effects of aberrant arterial carbon dioxide and arterial oxygen concentrations were independently but not synergistically associated with hospital mortality after cardiac arrest.

          Electronic supplementary material

          The online version of this article (doi:10.1186/s13054-015-1067-6) contains supplementary material, which is available to authorized users.

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          Most cited references35

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          Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality.

          J Hope Kilgannon, Alan Jones, Nathan I. Shapiro … (2010)
          Laboratory investigations suggest that exposure to hyperoxia after resuscitation from cardiac arrest may worsen anoxic brain injury; however, clinical data are lacking. To test the hypothesis that postresuscitation hyperoxia is associated with increased mortality. Multicenter cohort study using the Project IMPACT critical care database of intensive care units (ICUs) at 120 US hospitals between 2001 and 2005. Patient 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. Patients were divided into 3 groups defined a priori based on PaO(2) on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO(2) of 300 mm Hg or greater; hypoxia, PaO(2) of less than 60 mm Hg (or ratio of PaO(2) to fraction of inspired oxygen <300); and normoxia, not classified as hyperoxia or hypoxia. In-hospital mortality. Of 6326 patients, 1156 had hyperoxia (18%), 3999 had hypoxia (63%), and 1171 had normoxia (19%). The hyperoxia group had significantly higher in-hospital mortality (732/1156 [63%; 95% confidence interval {CI}, 60%-66%]) compared with the normoxia group (532/1171 [45%; 95% CI, 43%-48%]; proportion difference, 18% [95% CI, 14%-22%]) and the hypoxia group (2297/3999 [57%; 95% CI, 56%-59%]; proportion difference, 6% [95% CI, 3%-9%]). In a model controlling for potential confounders (eg, age, preadmission functional status, comorbid conditions, vital signs, and other physiological indices), hyperoxia exposure had an odds ratio for death of 1.8 (95% CI, 1.5-2.2). Among patients admitted to the ICU following resuscitation from cardiac arrest, arterial hyperoxia was independently associated with increased in-hospital mortality compared with either hypoxia or normoxia.
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            Death by hyperventilation: a common and life-threatening problem during cardiopulmonary resuscitation.

            Tom Aufderheide, Keith G Lurie (2004)
            This translational research initiative focused on the physiology of cardiopulmonary resuscitation (CPR) initiated by a clinical observation of consistent hyperventilation by professional rescuers in out-of-hospital cardiac arrest. This observation generated scientific hypotheses that could only ethically be tested in the animal laboratory. To examine the hypothesis that excessive ventilation rates during performance of CPR by overzealous but well-trained rescue personnel causes a significant decrease in coronary perfusion pressure and an increased likelihood of death. In the in vivo human aspect of the study, we set out to objectively and electronically record rate and duration of ventilation during performance of CPR by trained professional rescue personnel in a prospective clinical trial in intubated, adult patients with out-of-hospital cardiac arrest. In the in vivo animal aspect of the study, to simulate the clinically observed hyperventilation, nine pigs in cardiac arrest were ventilated in a random order with 12, 20, or 30 breaths/min, and physiologic variables were assessed. Next, three groups of seven pigs in cardiac arrest were ventilated at 12 breaths/min with 100% oxygen, 30 breaths/min with 100% oxygen, or 30 breaths/min with 5% CO2/95% oxygen, and survival was assessed. Ventilation rate and duration in humans; mean intratracheal pressure, coronary perfusion pressure, and survival rates in animals. In 13 consecutive adults (average age, 63 +/- 5.8 yrs) receiving CPR (seven men) the average ventilation rate was 30 +/- 3.2 breaths/min (range, 15 to 49 breaths/min) and the average duration of each breath was 1.0 +/- 0.07 sec. The average percentage of time in which a positive pressure was recorded in the lungs was 47.3 +/- 4.3%. No patient survived. In animals treated with 12, 20, and 30 breaths/min, the mean intratracheal pressures and coronary perfusion pressures were 7.1 +/- 0.7, 11.6 +/- 0.7, 17.5 +/- 1.0 mm Hg/min (p < .0001) and 23.4 +/- 1.0, 19.5 +/- 1.8, 16.9 +/- 1.8 mm Hg (p = .03) with each of the different ventilation rates, respectively (p = comparison of 12 breaths/min vs. 30 breaths/min for mean intratracheal pressure and coronary perfusion pressure). Survival rates were six of seven, one of seven, and one of seven with 12, 30, and 30 + CO2 breaths/min, respectively (p = .006). Despite seemingly adequate training, professional rescuers consistently hyperventilated patients during out-of-hospital CPR. Subsequent hemodynamic and survival studies in pigs demonstrated that excessive ventilation rates significantly decreased coronary perfusion pressures and survival rates, despite supplemental CO2 to prevent hypocapnia. This translational research initiative demonstrates an inversely proportional relationship between mean intratracheal pressure and coronary perfusion pressure during CPR. Additional education of CPR providers is urgently needed to reduce these newly identified and deadly consequences of hyperventilation during CPR. These findings also have significant implications for interpretation and design of resuscitation research, CPR guidelines, education, the development of biomedical devices, emergency medical services quality assurance, and clinical practice.
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              Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest

              Rinaldo Bellomo, Michael Bailey, Glenn Eastwood … (2011)
              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 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 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). 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 FiO2 in these patients.
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                Author and article information

                Contributors
                Hendrik J. F. Helmerhorst: 0031715266087 , H.J.F.Helmerhorst@lumc.nl
                Marie-José Roos-Blom: m.blom@amc.uva.nl
                David J. van Westerloo: D.J.van_Westerloo@lumc.nl
                Ameen Abu-Hanna: a.abu-hanna@amc.uva.nl
                Nicolette F. de Keizer: n.f.keizer@amc.uva.nl
                Evert de Jonge: E.de_Jonge@lumc.nl
                Journal
                Journal ID (nlm-ta): Crit Care
                Title: Critical Care
                Publisher: BioMed Central (London )
                ISSN (Print): 1364-8535
                ISSN (Electronic): 1466-609X
                Publication date (Electronic): 29 September 2015
                Publication date PMC-release: 29 September 2015
                Publication date (Print): 2015
                Volume: 19
                Electronic Location Identifier: 348
                Affiliations
                [ ]Department of Intensive Care Medicine, Leiden University Medical Center, Post Box 9600, Leiden, 2300 RC The Netherlands
                [ ]Laboratory of Experimental Intensive Care and Anesthesiology, Academic Medical Center, Meibergdreef 9, Amsterdam, 1105 AZ The Netherlands
                [ ]Department of Medical Informatics, Academic Medical Center, Meibergdreef 9, Amsterdam, 1105 AZ The Netherlands
                [ ]National Intensive Care Evaluation (NICE) foundation, Meibergdreef 9, Amsterdam, 1105 AZ The Netherlands
                Article
                Publisher ID: 1067
                DOI: 10.1186/s13054-015-1067-6
                PMC ID: 4587673
                PubMed ID: 26415731
                SO-VID: fb612cb6-59dc-4f50-8a68-f5806cf3bfcf
                Copyright © © Helmerhorst et al. 2015
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 12 August 2015
                Date accepted : 12 September 2015
                Categories
                Subject: Research
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                issue-copyright-statement © The Author(s) 2015

                ScienceOpen disciplines: Emergency medicine & Trauma
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                ScienceOpen disciplines: Emergency medicine & Trauma

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