Effect of Peripheral VA-ECMO Flow Variations on the Pulmonary Arterial Occlusion Pressure (PAPO) in Patients With Refractory Cardiogenic Shock: the PAPO-Flow Study

Cardiogenic shock is the most severe form of heart failure. It is characterized by acute and profound myocardial contractile dysfunction, leading to a severe decrease in cardiac index (<2.2 L/min) associated with signs of peripheral hypoperfusion. In its most severe forms, the impairment of cardiac contractile function is associated with an intense systemic inflammatory response syndrome (SIRS), leading to multiorgan failure and patient death. The mortality rate for patients in this situation is very high, approaching 50%.

Over the last decades, mechanical circulatory support techniques have gained interest, and their use in patients with cardiogenic shock refractory to medical treatments has significantly increased worldwide. Peripheral Veno-Arterial Extracorporeal Membrane Oxygenation (VA-ECMO) is the main temporary cardiac support technique used to maintain sufficient blood perfusion to the organs while awaiting myocardial recovery or heart transplantation. Its principle involves draining venous blood near the right atrium through a cannula inserted percutaneously or surgically into the patient's femoral vein. The venous blood is then reinfused after extracorporeal oxygenation into the descending aorta, countering the natural blood flow, via another cannula inserted into the femoral artery.

It has been postulated that the retrograde blood reinfusion by ECMO could increase cardiac afterload, enhance cardiac workload, and consequently reduce its own perfusion and recovery capabilities. Additionally, it has been suggested that, through this same effect, Pulmonary Artery Occlusion Pressure (PAOP) could rise, leading to acute pulmonary edema (APE), found in 30% of patients under peripheral ECMO. This, in turn, worsens the patient's tissue oxygenation and, ultimately, prognosis. According to this principle, this effect would amplify as the ECMO flow, set by the clinician, increases.

Several authors have written about this phenomenon, considering these hypothetical physiological considerations. However, to date, no prospective study has confirmed that the sequential increase in ECMO flow leads to a correlated elevation in PAOP in patients placed under peripheral VA-ECMO for refractory cardiogenic shock. Moreover, several factors may oppose this principle.

Firstly, as VA-ECMO retrogradely injects blood into the aorta via the arterial route, it simultaneously unloads the right cardiac chambers by an equivalent amount (in liters/minute) and reduces cardiac preload. Consequently, the filling of the left cardiac chambers and the left ventricular end-diastolic volume, both determinants of PAOP, are diminished. Secondly, arterial reinfusion by peripheral ECMO occurs more than 30 cm from the aortic valve, and its effect on cardiac afterload may be minimal, especially in patients with residual cardiac ejection. Finally, patients in cardiogenic shock under ECMO often present severe circulatory insufficiency, leading to significant volume expansion. They may have a markedly positive sodium-water balance, which alone could explain the elevation of PAOP and the occurrence of APE independently of the ECMO effect.