ID:167 FC-D07-7 Difference in mechanism of Pulse Pressure reduction during increasing VA-ECMO flow in normal (recovering) hearts and in cardiogenic shock.

Background: Cardiogenic shock is associated with high mortality and morbidity. VA-ECMO is increasingly used for temporary circulatory support to provide time for cardiac recovery and to ensure adequate end-organ perfusion. Increasing VA-ECMO flow reduce native pulsatility while preserving or improving end-organ perfusion. Methods: Animal experiments were conducted at the University of Sydney following Ethics Committee approval. Six crossbreed adult merino sheep underwent left thoracotomy under general anesthesia and mechanical ventilation. Comprehensive Invasive monitoring was established and a pressure-volume conductance catheter placed in the LV cavity. Transit time ultrasonic flow probes were placed around main pulmonary artery and left main coronary artery to monitor cardiac output and coronary flow. Central and peripheral VA-ECMO circuits were established surgically. Randomly assigned ECMO runs were completed in normal conditions and in cardiogenic shock, induced with 15-30 ml of 99% ethanol injected into anterolateral LV wall. PP = SBP – DBP. Mixed effect regression statistical models accounted for individual sheep and ECMO runs. Results: PP reduced similarly in normal (recovering) hearts and in cardiogenic shock. However, the mechanism of this reduction differed. DBP remained unchanged in normal hearts, while SBP reduced, approaching DBP. Conversely, SBP did not change in shock, while DBP increased, approaching SBP. Conclusions: Increasing VA ECMO support similarly decreases PP both normal and shocked hearts, however, the mechanism of such reduction differs.