Refractory Pulmonary Edema and Upper Body Hypoxemia During Veno‐Arterial Extracorporeal Membrane Oxygenation—A Case for Atrial Septostomy

Abstract

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) provides mechanical circulatory support for patients with advanced cardiogenic shock, facilitating myocardial recovery and limiting multi-organ failure. In patients with severely limited left ventricular ejection, peripheral VA-ECMO can further increase left ventricular and left atrial pressures (LAP). Failure to decompress the left heart under these circumstances can result in pulmonary edema and upper body hypoxemia, that is, myocardial and cerebral ischemia. Atrial septostomy can decrease LAP in these situations. However, the effects of atrial septostomy on upper body oxygenation remain unknown. After IRB approval, we identified 9 out of 242 adult VA-ECMO patients between January 2011 and June 2016 who also underwent atrial septostomy for refractory pulmonary edema/upper body hypoxemia. We analyzed LAP/pulmonary capillary wedge pressure (PCWP), right atrial pressures (RAPs), P O /F O ratios (blood samples from right radial artery), intrathoracic volume status, and resolution of pulmonary edema before and up to 48 h after septostomy. There were no procedure-related complications. Thirty-day survival was 44%. LAP/PCWP decreased by approximately 40% immediately following septostomy and remained so for at least 24 h. P O /F O ratios significantly increased from 0.49 (0.38-2.12) before to 5.35 (3.01-7.69) immediately after septostomy and continued so for 24 h, 6.6 (4.49-10.93). Radiographic measurements also indicated a significant improvement in thoracic intravascular volume status after atrial septostomy. Atrial septostomy reduces LAP and improves upper body oxygenation and intrathoracic vascular volume status in patients developing severe refractory pulmonary edema while undergoing peripheral VA-ECMO. Atrial septostomy therefore appears safe and suitable to reduce the risk of upper body ischemia under these circumstances.

Early prediction of transition to durable mechanical circulatory support in patients undergoing peripheral veno‐arterial extracorporeal membrane oxygenation for critical cardiogenic shock

“…We analyzed a retrospective cohort of 70 patients surviving pVA‐ECMO for cCS. Our clinical management protocol targeted LV pressure unloading, that is, PCWP ≤18 mm Hg, by means of pharmacological support and additional interventions if necessary …”

“…Our clinical management protocol targeted LV pressure unloading, that is, PCWP ≤18 mm Hg, by means of pharmacological support and additional interventions if necessary. 9,13 F I G U R E 2 LV pressure unloading, fluid balance, and LVSWT in pVA-ECMO patients with and without transition to dMCS. A, No significant differences in PCWP MIN between patients transitioned to dMCS than those not transitioned to dMCS, suggesting a comparable degree of LV pressure unloading in both groups.…”

“…Treatment options involved diuretic therapy, renal replacement therapy in cases of failed diuretic therapy, and titration of inotropic drugs. If patients developed signs of clinically relevant LV overload, that is, refractory pulmonary edema, despite maximal medical management, patients would undergo mechanical LV decompression by means of either atrial septostomy (preferred) or placement of an Impella device.…”

“…pVA‐ECMO can contribute to acute cardiac unloading by replacing cardiac output, thereby uncoupling arterial blood flow and perfusion pressure from (left) ventricular function. However, pVA‐ECMO can increase left ventricular (LV) afterload because of its retrograde flow, leading to LV distention or even pulmonary edema with upper body hypoxemia . LV afterload is defined as LV wall tension during systole.…”

“…However, pVA-ECMO can increase left ventricular (LV) afterload because of its retrograde flow, leading to LV distention or even pulmonary edema with upper body hypoxemia. 9 LV afterload is defined as LV wall tension during systole. Systolic wall tension in turn correlates very well with myocardial oxygen consumption.…”