Association Between Early Hyperoxia Exposure After Resuscitation from Cardiac Arrest and Neurologica
Roberts, Brian, et al. “Association Between Early Hyperoxia Exposure After Resuscitation from Cardiac Arrest and Neurological Disability: A Prospective Multi-Center Protocol-Directed Cohort Study.” Circulation (2018).
Cardiac arrest occurs in over 400,000 people in the US each year. In-hospital mortality in post-cardiac arrest patients is >50% many survivors have severe neurologic disability. Exposure to hyperoxia is shown to increase free radicals causing neuronal injury and death. A prior retrospective study by this group showed an association between exposure to PaO2>300 and in-hospital mortality.
In contrast to prior studies, this was a prospective, multi-center study that used ABG measurements in the early hours after resuscitation. The main objective of this study was to look at the association between exposure to hyperoxia after cardiac arrest and neurologic outcomes.
The study was a prospective cohort study conducted at 6 hospitals. They enrolled post-cardiac arrest adult patients who were comatose after ROSC over the course of nearly 4 years. The inclusion criteria were: 1) age ≥ 18 years; 2) cardiac arrest, defined as a documented absence of pulse and cardiopulmonary resuscitation (CPR) initiated; 3) ROSC > 20 min; 4) mechanically ventilated after ROSC; and 5) clinician intent to perform targeted temperature management. They included patients with in- and out-of-hospital arrest. ABGs were obtained one and six hours after ROSC. The SaO2 and FiO2 were recorded every 15 minutes over this time. The primary outcome was poor neurologic function or death at hospital discharge. Secondary outcomes were in-hospital mortality and early neurologic injury.
They included 280 of 2084 screened patients. 105 patients were exposed to hyperoxia and 175 were not exposed to hyperoxia in the first 6 hours after ROSC. PEA/asystole out-of-hospital cardiac arrest was the most common initial rhythm (39%), second was out-of-hospital Vfib/Vtach (31%). They found a poor correlation between PaO2 and SaO2 as well as PaO2 and FiO2. The SaO2 could not rule out hyperoxia. A PaO2 as high as 295 occurred with an FiO2 of 0.4. Study subjects with exposure to hyperoxia had a higher incidence of poor neurological function at hospital discharge than patients with no exposure (77% vs. 65%). The in-hospital mortality for the entire cohort was 55%. The mortality rate was 59% for hyperoxia and 52% without (p= 0.251). 41% of patients with hyperoxia had neurologic injury at 72 hours vs 35% without hyperoxia. Hyperoxia was an independent predictor of poor neurologic outcome. Only PaO2 of 300 or greater was associated with poor neurologic outcome. One hour longer of hyperoxia is associated with 3% increased risk of poor neurologic outcome.
Early exposure to hyperoxia (PaO2>300) after ROSC was an independent predictor of poor neurologic function.
SaO2 and FiO2 levels cannot reliably rule out hyperoxia- we need to get frequent ABGs to prevent hyperoxia.