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      Prevalence and factors correlating with hyperoxia exposure following cardiac arrest – an observational single centre study

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          Abstract

          Purpose of the study

          Arterial hyperoxia during care in the intensive care unit (ICU) has been found to correlate with mortality after cardiac arrest (CA). We examined the prevalence of hyperoxia following CA including pre-ICU values and studied differences between those exposed and those not exposed to define predictors of exposure.

          Materials and methods

          A retrospective analysis of a prospectively collected cohort of cardiac arrest patients treated in an Australian tertiary hospital between August 2008 and July 2010. Arterial blood oxygen values and used fractions of oxygen were recorded during the first 24 hours after the arrest. Hyperoxia was defined as any arterial oxygen value greater than 300 mmHg. Chi-square test was used to compare categorical data and Mann–Whitney U-test to continuous data. Statistical methods were used to identify predictors of hyperoxia exposure.

          Results

          Of 122 patients treated in the ICU following cardiac arrest 119 had one or several arterial blood gases taken and were included in the study. Of these, 49 (41.2%) were exposed to hyperoxia and 70 (58.8%) were not during the first 24 hours after the CA. Those exposed had longer delays to return of spontaneous circulation (26 minutes vs. 10 minutes) and a longer interval to ICU admission after the arrest (4 hours compared to 1 hour). Location of the arrest was an independent predictor of exposure to hyperoxia (P-value = 0,008) with out-of-hospital cardiac arrest patients being more likely to have been exposed (65%), than those with an in-hospital (21%) or ICU (30%) cardiac arrest. Out-of-hospital cardiac arrest patients had higher oxygen concentrations to the fraction of inspired oxygen ratios.

          Conclusions

          Hyperoxia exposure was more common than previously reported and occurred more frequently in association with out-of-hospital cardiac arrest, longer times to ROSC and delays to ICU admission.

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          Most cited references18

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          Cardiopulmonary resuscitation of adults in the hospital: a report of 14720 cardiac arrests from the National Registry of Cardiopulmonary Resuscitation.

          The National Registry of Cardiopulmonary Resuscitation (NRCPR) is an American Heart Association (AHA)-sponsored, prospective, multisite, observational study of in-hospital resuscitation. The NRCPR is currently the largest registry of its kind. The purpose of this article is to describe the NRCPR and to provide the first comprehensive, Utstein-based, standardized characterization of in-hospital resuscitation in the United States. All adult (>/=18 years of age) and pediatric (<18 years of age) patients, visitors, employees, and staff within a facility (including ambulatory care areas) who experience a resuscitation event are eligible for inclusion in the NRCPR database. Between January 1, 2000, and June 30, 2002, 14720 cardiac arrests that met inclusion criteria occurred in adults at the 207 participating hospitals. An organized emergency team is available 24 h a day, 7 days a week in 86% of participating institutions. The three most common reasons for cardiac arrest in adults were (1) cardiac arrhythmia, (2) acute respiratory insufficiency, and (3) hypotension. Overall, 44% of adult in-hospital cardiac arrest victims had a return of spontaneous circulation (ROSC); 17% survived to hospital discharge. Despite the fact that a primary arrhythmia was one of the precipitating events in nearly one half of adult cardiac arrests, ventricular fibrillation (VF) was the initial pulseless rhythm in only 16% of in-hospital cardiac arrest victims. ROSC occurred in 58% of VF cases, yielding a survival-to-hospital discharge rate of 34% in this subset of patients. An automated external defibrillator was used to provide initial defibrillation in only 1.4% of patients whose initial cardiac arrest rhythm was VF. Neurological outcome in discharged survivors was generally good. Eighty-six percent of patients with Cerebral Performance Category-1 (CPC-1) at the time of hospital admission had a postarrest CPC-1 at the time of hospital discharge.
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            Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality.

            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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              Retinopathy of prematurity.

              Retinopathy of prematurity (ROP) is a common blinding disease in children in the developed world despite current treatment, and is becoming increasingly prevalent in the developing world. ROP progresses in two phases. The first phase begins with delayed retinal vascular growth after birth and partial regression of existing vessels, followed by a second phase of hypoxia-induced pathological vessel growth. Two major risk factors of ROP are the use of oxygen and a decreased gestation period. Excessive oxygen contributes to ROP through regulation of vascular endothelial growth factor (VEGF). Suppression of VEGF by oxygen in phase I of ROP inhibits normal vessel growth, whereas elevated levels of VEGF induced by hypoxia in phase II of ROP precipitate pathological vessel proliferation. Insulin-like growth factor 1 (IGF-1) is a critical non-oxygen-regulated factor in ROP. We have found that serum levels of IGF-1 in premature babies directly correlate with the severity of clinical ROP. IGF-1 acts indirectly as a permissive factor by allowing maximal VEGF stimulation of vessel growth. Lack of IGF-1 in preterm infants prevents normal retinal vascular growth in phase I of ROP, despite the presence of VEGF. As infants mature, rising levels of IGF-1 in phase II of ROP allows VEGF stimulated pathological neovascularization. These findings suggest that restoration of IGF-1 to normal levels might be useful in preventing ROP in preterm infants.
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                Author and article information

                Contributors
                Journal
                Scand J Trauma Resusc Emerg Med
                Scand J Trauma Resusc Emerg Med
                Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine
                BioMed Central
                1757-7241
                2013
                2 May 2013
                : 21
                : 35
                Affiliations
                [1 ]Department of Anaesthesiology and Intensive Care, Helsinki University Central Hospital, University of Helsinki, Topeliuksenkatu 5, PL 266, Helsinki, Finland
                [2 ]Intensive Care Unit, Liverpool Hospital, Liverpool Hospital, Elizabeth street, Liverpool, NSW 2170, Australia
                [3 ]University of New South Wales, Sydney, Australia
                Article
                1757-7241-21-35
                10.1186/1757-7241-21-35
                3646691
                23639102
                57a3ba5c-2beb-4e17-aedd-975d0f617c2e
                Copyright © 2013 Nelskylä et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 14 January 2013
                : 25 April 2013
                Categories
                Original Research

                Emergency medicine & Trauma
                cardiac arrest,hyperoxia,mechanical ventilation
                Emergency medicine & Trauma
                cardiac arrest, hyperoxia, mechanical ventilation

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