Abstract

Background: Brain death is a major cause of death among refractory ventricular tachycardia/ventricular fibrillation (VT/VF) out-of-hospital cardiac arrest (OHCA) who are treated with extracorporeal cardiopulmonary resuscitation (ECPR). Studies regarding the clinical consequences of hyperoxemia in this population are lacking. We aimed to determine whether hyperoxemia (PaO 2 >300mmHg) is associated with brain death in patients treated with an established ECPR protocol. Methodology: This single-center retrospective study included consecutive patients presenting to the University of Minnesota between 2015-2021 with refractory VT/VF OHCA. All patients were treated with an ECPR protocol including VA-ECMO. All blood gases collected within the first 48 hours were reviewed and the highest and lowest values for PaO2, PaCO2, and lactate were recorded. The primary outcome was brain death. This was defined as a lack of brainstem reflexes on physical examination and herniation on CT imaging or lack of blood flow on a brain perfusion scan. Results: One-hundred and eighty-two patients met inclusion criteria and 141/182 (77.5%) had hyperoxemia. Presenting characteristics were comparable in both groups aside from higher initial PaCO 2 in patients who developed hyperoxemia ( Figure ). Brain death occurred in 42/141 (29.8%) of the hyperoxemia group vs 3/41 (7.3%) in the non-hyperoxemia group. After adjustment for age, CPR time, initial PaCO 2 and lactate, hyperoxemia was significantly associated with brain death (OR 5.2, 95% CI 1.4-19.0, p=0.014). The risk was independent of the number of hours spent with hyperoxemia ( Figure ). Overall survival was comparable between groups. Hypoxemia (PaO2 <60mmHg) occurred in 76/182 (41.8%) and was not associated with survival or brain death. Conclusion: Among refractory VT/VF OHCA patients treated with ECPR, hyperoxemia after the cardiac arrest is associated with brain death independent of the number of hours spent with hyperoxemia.

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