Cerebral Tissue Oxygenation During the Initiation of Venovenous ECMO

Abstract

In an acute respiratory distress syndrome, venovenous extracorporeal membrane oxygenation (vvECMO) can rapidly normalize arterial hypoxemia and carbon dioxide tension (PaCO2). Considering the positive relationship between PaCO2 and cerebral blood flow, the aim of the current study was to evaluate cerebral regional tissue oxygen saturation (rSO2) during the implementation of vvECMO. Fifteen acute respiratory distress syndrome patients with recordings of cerebral rSO2 by near-infrared spectroscopy before vvECMO implementation until the optimization of the ECMO/ventilator settings were retrospectively studied. median (interquartile range). The cerebral rSO2 increased significantly (p < 0.05) from 69(61-74) to 75(60-80)% after ECMO was started, concomitant to the arterial oxygenation. Until the end of the observation period after 83(44-132) minutes, cerebral rSO2 decreased significantly to 61(52-71)%. PaCO2 decreased from 70(61-87) to 43(38-54) mm Hg and the pH increased from 7.23(7.14-7.29) to 7.39(7.34-7.43). The baseline arterial oxygen saturation and tension as well as the actual bicarbonate concentration were negatively correlated with the absolute change in cerebral rSO2 (ΔrSO2). In the 11 nonhypoxemic patients (arterial oxygen saturation ≥90%) ΔPaCO2 was significantly correlated with ΔrSO2. Patients receiving vvECMO treatment are at risk for a decrease in cerebral rSO2. This decrease is more distinct in patients with normal baseline arterial oxygenation and high actual bicarbonate.