Clinicians caring for children with cardiopulmonary failure using extracorporeal membrane oxygenation (ECMO) are refining bedside clinical practices by focusing on minimizing morbidity associated with neurologic complications. Neurologic complications are the main drivers of survival and survivorship (¹). Both enhanced neuromonitoring (^2,3) and neuroimaging (⁴) serve to characterize neurologic morbidity to help the field establish specific objectives for improvement.

In this issue of Pediatric Critical Care Medicine, Shah et al (⁵) investigate potentially modifiable factors known to have a strong physiological foundation. The study investigates the relationship between relative changes in Paco₂ and or mean arterial blood pressure early after starting ECMO and the risk of neurologic complications. The investigators use the registry of the Extracorporeal Life Support Organization (ELSO) and define neurologic complications as any report of seizures, CNS infarction or hemorrhage, or brain death. Among greater than 7,000 ECMO runs, 15% were reported to have neurologic complications. The results suggest an association between a greater magnitude of decrease in Paco₂ and arterial hypertension following ECMO initiation with neurologic complications; in addition, among the group with a greater magnitude change in Paco₂, there was an increased odds of neurologic complication per percentile increase in arterial blood pressure. This analysis of the ELSO registry is very important as it adds epidemiological evidence to previously published reports suggesting an increase in odds of death with decreases in carbon dioxide in children (⁶) and an increase in odds of neurologic adverse events in adults supported with venovenous ECMO (^7,8). The conclusions are consistent with the physiological evidence suggesting alterations in cerebral vascular reactivity and blood flow with changes in blood pressure published in venoarterial animal models of ECMO (^9,10) and in infants with ECMO