Hyperoxia in the intensive care unit and outcome after out-of-hospital ventricular fibrillation cardiac arrest.
ABSTRACT Laboratory and clinical studies have suggested that hyperoxia early after resuscitation from cardiac arrest may increase neurological injury and worsen outcome. Previous clinical studies have been small or have not included relevant prehospital data. We aimed to determine in a larger cohort of patients whether hyperoxia in the intensive care unit in patients admitted after out-ofhospital cardiac arrest (OHCA) was associated with increased mortality rate after correction for prehospital variables.
Data from the Victorian Ambulance Cardiac Arrest Registry (VACAR) of patients transported to hospital after resuscitation from OHCA and an initial cardiac rhythm of ventricular fibrillation between January 2007 and December 2011 were linked to the Australian and New Zealand Intensive Care Society Adult Patient Database (ANZICS-APD). Patients were allocated into three groups (hypoxia [PaO2<60mmHg], normoxia [PaO2,60-299mmHg] or hyperoxia [PaO2≥300mmHg]) according to their most abnormal PaO2 level in the first 24 hours of ICU stay. The relationship between PaO2 and hospital mortality was investigated using multivariate logistic regression analysis to adjust for confounding prehospital and ICU factors.
There were 957 patients identified on the VACAR database who met inclusion criteria. Of these, 584 (61%) were matched to the ANZICS-APD and had hospital mortality and oxygen data available. The unadjusted hospital mortality was 51% in the hypoxia patients, 41% in the normoxia patients and 47% in the hyperoxia patients (P=0.28). After adjustment for cardiopulmonary resuscitation by a bystander, patient age and cardiac arrest duration, hyperoxia in the ICU was not associated with increased hospital mortality (OR, 1.2; 95% CI, 0.51-2.82; P=0.83).
Hyperoxia within the first 24 hours was not associated with increased hospital mortality in patients admitted to ICU following out-of-hospital ventricular fibrillation cardiac arrest.
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ABSTRACT: IntroductionThe safety of arterial hyperoxia is under increasing scrutiny. We performed a systematic review of the literature to determine whether any association exists between arterial hyperoxia and mortality in critically ill patient subsets.Methods Medline, Thomson Reuters Web of Science and Scopus databases were searched from inception to June 2014. Observational or interventional studies evaluating the relationship between hyperoxia (defined as a supranormal arterial O2 tension) and mortality in adult intensive care unit (ICU) patients were included. Studies primarily involving patients with exacerbations of chronic pulmonary disease, acute lung injury and perioperative administration were excluded. Adjusted odds ratio (OR) of patients exposed versus those non-exposed to hyperoxia were extracted, if available. Alternatively, unadjusted outcome data were recorded. Data on patients, study characteristics and the criteria used for defining hyperoxia exposure were also extracted. Random-effects models were used for quantitative synthesis of the data, with a primary outcome of hospital mortality.ResultsIn total 17 studies (16 observational, 1 prospective before-after) were identified in different patient categories: mechanically ventilated ICU (number of studies (k)¿=¿4, number of participants (n)¿=¿189,143), post-cardiac arrest (k¿=¿6, n¿=¿19,144), stroke (k¿=¿2, n¿=¿5,537), and traumatic brain injury (k¿=¿5, n¿=¿7,488). Different criteria were used to define hyperoxia in terms of PaO2 value (first, highest, worst, mean), time of assessment and pre-determined cut-offs. Data from studies on ICU patients were not pooled because of extreme heterogeneity (Inconsistency (I2) 96.73%). Hyperoxia was associated with increased mortality in post-cardiac arrest patients (OR¿=¿1.42 (1.04 to 1.92) I2 67.73%) stroke (OR¿=¿1.23 (1.06 to 1.43) I2 0%) and traumatic brain injury (OR¿=¿1.41 (1.03 to 1.94) I2 64.54%). However, these results are limited by significant heterogeneity between studies.Conclusions Hyperoxia may be associated with increased mortality in patients with stroke, traumatic brain injury and those resuscitated from cardiac arrest. However, these results are limited by the high heterogeneity of the included studies.Critical care (London, England) 12/2014; 18(6):711. DOI:10.1186/s13054-014-0711-x
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ABSTRACT: High inspiratory oxygen concentrations are frequently administered in ventilated patients in the intensive care unit (ICU) but may induce lung injury and systemic toxicity. We compared beliefs and actual clinical practice regarding oxygen therapy in critically ill patients. In three large teaching hospitals in the Netherlands, ICU physicians and nurses were invited to complete a questionnaire about oxygen therapy. Furthermore, arterial blood gas (ABG) analysis data and ventilator settings were retrieved to assess actual oxygen practice in the same hospitals 1 year prior to the survey. In total, 59% of the 215 respondents believed that oxygen-induced lung injury is a concern. The majority of physicians and nurses stated that minimal acceptable oxygen saturation and partial arterial oxygen pressure (PaO2) ranges were 85% to 95% and 7 to 10 kPa (52.5 to 75 mmHg), respectively. Analysis of 107,888 ABG results with concurrent ventilator settings, derived from 5,565 patient admissions, showed a median (interquartile range (IQR)) PaO2 of 11.7 kPa (9.9 to 14.3) [87.8 mmHg], median fractions of inspired oxygen (FiO2) of 0.4 (0.4 to 0.5), and median positive end-expiratory pressure (PEEP) of 5 (5 to 8) cm H2O. Of all PaO2 values, 73% were higher than the upper limit of the commonly self-reported acceptable range, and in 58% of these cases, neither FiO2 nor PEEP levels were lowered until the next ABG sample was taken. Most ICU clinicians acknowledge the potential adverse effects of prolonged exposure to hyperoxia and report a low tolerance for high oxygen levels. However, in actual clinical practice, a large proportion of their ICU patients was exposed to higher arterial oxygen levels than self-reported target ranges.01/2014; 4(1):23. DOI:10.1186/s13613-014-0023-y
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ABSTRACT: Post-cardiac arrest patients 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. We 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. We 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). Higher 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.Critical care (London, England) 12/2015; 19(1):824. DOI:10.1186/s13054-015-0824-x