Kilgannon JH, Jones AE, Shapiro NI, et al
Cardiac arrest is a devastating clinical situation, and the causes of out-of-hospital arrests often differ from those of in-hospital arrests.[1,2] Furthermore, survival after cardiac arrest is not improving. Laboratory investigations suggest that exposure to hyperoxia after resuscitation from cardiac arrest can worsen anoxic brain injury.[4-6]
June 2, 2010 (Camden, New Jersey) — Hyperoxia in patients recovering in the intensive care unit (ICU) after cardiac arrest increases the risk of in-hospital death, a study from the Project IMPACT database shows .
Dr J Hope Kilgannon (Cooper University Hospital, Camden, NJ) and colleagues analyzed the outcomes of patients in ICUs following cardiopulmonary resuscitation after cardiac arrest at 120 centers. Results of the study, supported by the National Institutes of Health and the Emergency Medicine Foundation, appear in the June 2, 2010 issue of the Journal of the American Medical Association. It is the first large multicenter study documenting the association between postresuscitation hyperoxia and poor clinical outcome, according to the authors.
Of the 6326 patients in the study, 1156 were hyperoxic–defined as arterial blood pressure (PaO2) >300 mm Hg within 24 hours after arriving in the ICU; 3999 were hypoxic (PaO2 <60 mm Hg); and 1171 were normoxic.
In-hospital mortality was 63% in the hyperoxic group, significantly higher than the 57% mortality in the hypoxic group and 45% mortality in the normoxic group (p<0.001). Hyperoxia was also associated with a lower likelihood of independent functional status at hospital discharge.
Kilgannon created a statistical model controlling for potential cofounders such as age, preadmission functional status, comorbid conditions, vital signs, and other factors and found that hyperoxia was associated with almost twice the risk of in-hospital mortality as normoxia (odds ratio 1.8; 95% CI 1.5–2.2).
“Reperfusion after an ischemic insult is associated with a surge of reactive oxygen species, which may overwhelm host natural antioxidant defenses,” the Kilgannon et al suggest. “The oxidative stress from the reactive oxygen species formed after reperfusion may lead to increased cellular death by diminishing mitochondrial oxidative metabolism, disrupting normal enzymatic activities, and damaging membrane lipids through peroxidation.”
In an accompanying editorial , Drs Patrick Kochanek and Hulya Bayir (University of Pittsburgh, PA) point out that the study also found a link between hypoxia and mortality after cardiopulmonary arrest. “This complicates the ability to make sweeping recommendations against the use of 100% oxygen early in resuscitation.” They suggest that measuring brain oxygen pressure may help optimize oxygen levels in postresuscitation patients but note that this approach is untested.
Study coauthor Dr Stephen Trzeciak (Cooper University Hospital) reported that he receives material support for research from Ikaria and consults for Spectral Diagnostics but receives no remuneration from any commercial interest. None of the other authors reported disclosures.