Hyperoxia during extracorporeal cardiopulmonary resuscitation for refractory cardiac arrest is associated with severe circulatory failure and increased mortality

Abstract

Background High levels of arterial oxygen pressures (PaO2) have been associated with increased mortality in extracorporeal cardiopulmonary resuscitation (ECPR), but there is limited information regarding possible mechanisms linking hyperoxia and death in this setting, notably with respect to its hemodynamic consequences. We aimed therefore at evaluating a possible association between PaO2, circulatory failure and death during ECPR. Methods We retrospectively analyzed 44 consecutive cardiac arrest (CA) patients treated with ECPR to determine the association between the mean PaO2 over the first 24 h, arterial blood pressure, vasopressor and intravenous fluid therapies, mortality, and cause of deaths. Results Eleven patients (25%) survived to hospital discharge. The main causes of death were refractory circulatory shock (46%) and neurological damage (24%). Compared to survivors, non survivors had significantly higher mean 24 h PaO2 (306 ± 121 mmHg vs 164 ± 53 mmHg, p < 0.001), lower mean blood pressure and higher requirements in vasopressors and fluids, but displayed similar pulse pressure during the first 24 h (an index of native cardiac recovery). The mean 24 h PaO2 was significantly and positively correlated with the severity of hypotension and the intensity of vasoactive therapies. Patients dying from circulatory failure died after a median of 17 h, compared to a median of 58 h for patients dying from a neurological cause. Patients dying from neurological cause had better preserved blood pressure and lower vasopressor requirements. Conclusion In conclusion, hyperoxia is associated with increased mortality during ECPR, possibly by promoting circulatory collapse or delayed neurological damage.

EISOR Delivery: Regional experience with sharing equipe, equipment & expertise to increase cDCD donor pool in time of pandemic

“…The fraction of oxygen in the FGF to the device (FdO 2 ) is set to 50% at initiation, and adapted to target normoxemia (P POST-ML O 2 80 to 100 mmHg). Hyperoxemia, thus excessive FdO 2 and P POST-ML O 2 and their potential impact on ischemia-reperfusion injury and vascular tone 17 , 18 are avoided, even if, to date, no diriment data exist.…”

Optimizing PO2 during peripheral veno-arterial ECMO: a narrative review

“…However, studies describing general oxygenation in VA-ECMO patients could provide some information. Using a threshold of PaO 2 ≥ 300 mmHg, the reported prevalence of severe hyperoxemia in the first 24 h ranged from 12 to 89% [ 13 – 15 , 17 – 19 , 29 ] (Table 1 ). In the study of Justus et al, the mean right radial P a O 2 was higher than 250 mmHg at day 1 and decreased between day 3 and day 10, ranging from 100 to 150 mmHg [ 20 ].…”

“…In a retrospective study of 79 ECPR patients, the mean right radial P a O 2 over the 8 first days was 211 ± 58 mmHg [ 15 ]. Based on a study on ECPR, the median value of mean P a O 2 in the non-cannulated femoral artery during the first day was 328 mmHg (IQR 228–524) [ 19 ].…”

“…Based on a study on ECPR, the median value of mean P a O 2 in the non-cannulated femoral artery during the first day was 328 mmHg (IQR 228–524) [ 19 ].…”

“…The target of 150 mmHg for P POST O 2 does not rely on randomized data. However, several observational and preclinical data support this recommendation [ 14 , 17 – 19 , 29 , 30 ]. It might correspond to a safety zone, avoiding both hypoxemia and severe hyperoxemia.…”