Hyperoxia and Hypoxia in Children Resuscitated From Cardiac Arrest

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Abstract

Background:

Ischemia depletes antioxidant reserves and impairs mitochondrial electron transport. Oxygen within blood reperfusing ischemic tissue can form free radicals, worsen oxidative stress, and exacerbate tissue injury (reperfusion injury). One strategy for limiting reperfusion injury is to limit delivery of “luxuriant” oxygen during or after reperfusion. Resuscitation guidelines for children with cardiac arrest recommend early weaning of supplemental oxygen as tolerated. There are currently no studies demonstrating the frequency and outcomes of hyperoxia and hypoxia after pediatric cardiac arrest.

Objective:

To determine the frequency and outcomes of hyperoxia and hypoxia in patients following resuscitation from pediatric cardiac arrest admitted to a tertiary care center.

Design and Methods:

This is a retrospective observational cohort study. Charts of children resuscitated from cardiac arrest and admitted to our hospital from 2004 to 2008 were reviewed. Partial pressures of oxygen (PaO2) obtained within the first 24 hours following return of spontaneous circulation and mortality at 6 months was recorded. Children who did not survive the initial 48 hours, patients having undergone extracorporeal oxygenation or had congenital heart disease, and those in whom arterial blood gases were not obtained were excluded.

Results:

Seventy-four patients met inclusion criteria. Of these, 38 (51%) had at least one arterial blood gases with a PaO2 > 300 mm Hg and 10 (14%) had a PaO2 < 60 mm Hg in the first 24 hours. Neither hyperoxia nor hypoxia on initial arterial blood gases (p = 0.912 and p = 0.384) nor any arterial blood gases within the first 24 hours after cardiac arrest (p = 0.325 and p = 0.553) was associated with 6-month mortality.

Conclusions:

Hyperoxia occurs commonly within the first 24 hours of management in children resuscitated from cardiac arrest.

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