Physiological hemodynamic impact of veno-arterial ECMO

Abstract

Veno-arterial ECMO (VA-ECMO) is increasingly used to rescue most severe forms of cardiogenic shock. Although it restores blood circulation, it induces major disturbances of hemodynamic physiology, both regarding macro- and microcirculation. Effects on the macrocirculation are dominated by the decrease of right ventricular preload, and on the contrary the increase of left ventricular afterload. Although the consequences of these two effects vary largely from one patient to the other, they trigger two major complications: 1) ECMO-induced pulmonary edema. Affecting more than 50% of ECMO-assisted patients, it is associated with increased morbidity, 20 to 30% of them needing the use of another invasive therapeutic to treat it. 2) the decrease in the spontaneous ejection of the native heart, which increases the risk of thrombus in cardiac cavities. Harlequin syndrome, which might occur during peripheral VA-ECMO, reflects a conflict in the aorta between the ECMO flow and the native cardiac output of the patient. Lastly, severe forms of cardiogenic shock trigger an intense systemic inflammation, responsible for vasoplegia, vascular leakage, and finally pronounced microcirculation disorders. Although ECMO effects on these inflammation-induced hemodynamic disorders remains poorly characterized to date, their management is a major area of improvements for ECMO-assisted patients.