Background: 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-of-hospital cardiac arrest (OHCA) was associated with increased mortality rate after correction for prehospital variables.
Methods: 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.
Results: 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).
Conclusions: 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.