Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality

Department of Emergency Medicine, Cooper University Hospital, One Cooper Plaza, Camden, NJ 08103, USA.
JAMA The Journal of the American Medical Association (Impact Factor: 35.29). 06/2010; 303(21):2165-71. DOI: 10.1001/jama.2010.707
Source: PubMed


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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Available from: Nathan I Shapiro, Mar 06, 2014
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    • "Several recent clinical observations have, however, suggested that liberal administration of oxygen can be toxic. In an observational multicenter study concerning patients admitted after resuscitation from cardiac arrest, those exposed to hyperoxemia (PaO2 ≥300 mm Hg) experienced increased mortality compared with both normoxemic and hypoxemic groups (PaO2 <60 mm Hg) [2]. Administering supplemental oxygen to coronary heart disease (CHD) patients with the goal of maintaining 100% saturation might result in vasoconstriction in the coronary circulation and hemodynamic instability [3]. "
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    ABSTRACT: Hypoxemia and high fractions of inspired oxygen (FiO2) are concerns in critically ill patients. An automated FiO2 controller based on continuous oxygen saturation (SpO2) measurement was tested. Two different SpO2-FiO2 feedback open loops designed to react differently based on the level of hypoxemia were compared. The results of the FiO2 controller were also compared to an historical control group. The system measures SpO2, compares to a target range (92% - 96%) and proposes in real time FiO2 settings to maintain SpO2 within target. In 20 patients under mechanical ventilation, two different FiO2-SpO2 open loops were applied by a dedicated research nurse during 3 hours each in random order. The times spent in and outside the target SpO2 were measured. The results of the automatic controller were then compared to a retrospective control group of 30 ICU patients. SpO2-FiO2 values of the control group were collected over 3 different periods of 6 hours. Time in the target range was higher than 95% with the controller. When the 20 patients were separated according to the median PaO2/FiO2 (160(133-176) mmHg vs. 239(201-285)), the loop with the highest slope was slightly better (P = 0.047) for the more hypoxemic patients. Hyperoxemia and hypoxemia durations were significantly shorter with the controller compared to usual care: SpO2 target range was reached 90% versus 24%, 27% and 32% (P < .001) with the controller compared to three historical control group periods. A specific FiO2 controller is able to reliably maintain SpO2 within a predefined target range. Two different feedback loops can be used depending on the initial PaO2/FiO2; with both, the automatic controller showed excellent performance when compared to usual care.
    Full-text · Article · Feb 2014 · Critical care (London, England)
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    • "This was further confirmed by Young et al. studying mechanically ventilated ischemic stroke [46]. Furthermore, studies investigating the relationship between hyperoxemia and outcome in cardiac arrest patients have also yielded controversial results [47,48]. "
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    ABSTRACT: The relationship between hyperoxemia and outcome in patients with traumatic brain injury (TBI) is controversial. We sought to investigate the independent relationship between hyperoxemia and long-term mortality in patients with moderate-to-severe traumatic brain injury. The Finnish Intensive Care Consortium database was screened for mechanically ventilated patients with a moderate-to-severe TBI. Patients were categorized, according to the highest measured alveolar-arterial O2 gradient or the lowest measured PaO2 value during the first 24 hours of ICU admission, to hypoxemia (< 10.0 kPa), normoxemia (10.0-13.3 kPa) and hyperoxemia (> 13.3 kPa). We adjusted for markers of illness severity to evaluate the independent relationship between hyperoxemia and 6-month mortality. A total of 1116 patients were included in the study, of which 16% (N= 174) were hypoxemic, 51% (N= 567) normoxemic and 33% (N= 375) hyperoxemic. The total 6-month mortality was 39% (N= 435). A significant association between hyperoxemia and a decreased risk of mortality was found in univariate analysis (P= 0.012). However, after adjusting for markers of illness severity in a multivariate logistic regression model hyperoxemia showed no independent relationship with 6-month mortality (hyperoxemia vs. normoxemia OR 0.88, 95% CI 0. 63--1.22, P= 0.43; hyperoxemia vs. hypoxemia OR 0.97, 95% CI 0.63-1.50, P= 0.90). Hyperoxemia in the first 24 hours of ICU admission after a moderate-to-severe TBI is not predictive of 6-month mortality.
    Full-text · Article · Aug 2013 · Critical care (London, England)
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    • "This is because even mildly elevated FIO 2 levels have been reported to exacerbate lung injury in an animal study [21], contribute to absorption atelectasis, and increase V/Q mismatch in patients with acute respiratory distress syndrome [22]. Adverse outcomes of hyperoxemia also have been reported in some other settings, such as in patients with acute exacerbations of chronic obstructive pulmonary disease [10], after cardiac arrest [11], and in critical illness [12]. Of even greater concern, a recent follow-up study of a randomized controlled trial revealed that patients randomized to 80% perioperative O 2 administration were more likely to die compared with those randomized to 30% O 2 [23]. "
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    ABSTRACT: Purpose: Oxygen (O2) is the most common therapy in mechanically ventilated patients, but targets and dose are poorly understood. We aimed to describe current O2 administration and titration in such patients in an academic intensive care unit. Materials and methods: In consecutive ventilated (>48 hours) patients we prospectively obtained fraction of inspired O2 (FiO2), pulse oximetry O2 saturation (SpO2) and arterial O2 tension (PaO2) every 6 hours. We calculated the amount of excess O2 delivery and the intensivists' response to hyperoxemia (SpO2>98%). Results: During 358 mechanical ventilation days in 51 critically ill patients, median calculated excess O2 delivery was 3472 L per patient. Patients spent most of their time with their SpO2>98% (59% [29-83]) and PaO2 between 80 and 120 mm Hg (59% [38-72]). In addition, 50% of all observations showed hyperoxemia and 4% severe hyperoxemia (PaO2>202.5 mm Hg). Moreover, 71% of the calculated total excess 263,841 L of O2 was delivered when the Fio2 was 0.3 to 0.5. When hyperoxemia occurred with an Fio2 between 0.3 and 0.4, for 88% of episodes, no Fio2 adjustments were made. Conclusions: Excess O2 delivery and liberal O2 therapy were common in mechanically ventilated patients. Current O2 therapy practice may be suboptimal and further investigations are warranted.
    Full-text · Article · May 2013 · Journal of critical care
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