Early Hyperoxia Exposure Linked to Poor Neurologic Function After Cardiac Arrest Resuscitation

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Hyperoxia exposure was independently associated with poor neurological function at discharge.
Hyperoxia exposure was independently associated with poor neurological function at discharge.

Immediate exposure to hyperoxia at a partial pressure of arterial oxygen (PaO2) ≥300 mmHg following post-cardiac arrest resuscitation is associated with an increased risk for poor neurological function at hospital discharge, according to findings from a multicenter, prospective cohort study published in Circulation.

In the study, investigators assessed 280 adult patients with mechanically ventilated cardiac arrest who received targeted temperature management following the return of spontaneous circulation (ROSC). Investigators measured PaO2 at 1 and 6 hours following ROSC, with hyperoxia defined as PaO2 >300 mmHg during the first 6-hour post-ROSC period. Researchers specifically evaluated patients' neurological function (modified Rankin Scale >3), as well as mortality at hospital discharge.

A total of 105 patients (38%) in this cohort had hyperoxia exposure after resuscitation from cardiac arrest. The majority of the entire cohort experienced poor neurological function at discharge (70%), whereas a significantly greater percentage of patients with early hyperoxia exposure experienced poor neurological function vs patients without exposure (77% vs 65%, respectively; absolute risk difference 12% [95% CI, 1%-23%]; P =.035).

In addition, hyperoxia exposure was independently associated with poor neurological function at discharge (relative risk [RR] 1.23; 95% CI, 1.11-1.35). Investigators found that 1 hour of additional hyperoxia exposure was associated with a 3% increase in poor neurological outcome risk [RR 1.03; 95% CI, 1.02 - 1.05). For exposed patients, PaO2 cut points ≥300 mmHg were associated with poor neurological outcome (RR 1.24; 95% CI, 1.13-1.35; P <.001).

Due to the study's observational nature, the investigators were unable to determine causative factors associated with hyperoxia exposure and the primary outcome. The investigators also noted the potential for unmeasured confounders in this analysis, despite the use of multivariable linear regression.

The study investigators study suggest that the harm of hyperoxia is partly due to “increasing the formation of reactive oxygen species resulting in oxidative impairment of mitochondrial respiration and cerebral energy metabolism.”

Reference

Roberts BW, Kilgannon JH, Hunter BR, et al. Association between early hyperoxia exposure after resuscitation from cardiac arrest and neurological disability: a prospective multi-center protocol-directed cohort study [published online February 1, 2018]. Circulation. doi:10.1161/CIRCULATIONAHA.117.032054

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