Abstract Sun1407: Inhaled Nitric Oxide Facilitates VA-ECMO Weaning in ECPELLA-Supported Patients with Precapillary Pulmonary Hypertension

Abstract

Background: Combined support with a micro-axial flow pump (mAFP) and venoarterial extracorporeal membrane oxygenation (VA-ECMO) (ECPELLA) is effective for refractory biventricular failure after cardiac arrest. However, VA-ECMO weaning can be challenging in patients with right ventricular (RV) failure or pulmonary hypertension. Inhaled nitric oxide (iNO) selectively dilates the pulmonary arteries, reducing RV afterload and potentially facilitating ECPELLA weaning. We report a case in which iNO enabled successful VA-ECMO removal in a patient with precapillary pulmonary hypertension. Case Presentation: An 83-year-old woman with hypertension, diabetes mellitus, chronic kidney disease, and peripheral artery disease (PAD) was admitted for heart failure exacerbation. After stabilization with medical therapy, she was transferred to a rehabilitation hospital. However, during rehabilitation she developed ventricular tachycardia. After successful resuscitation, she was readmitted to our center. Electrocardiography and echocardiography diagnosed anteroseptal acute coronary syndrome with cardiogenic shock. Emergent coronary angiography revealed critical stenosis of the left anterior descending artery. Percutaneous coronary intervention under mAFP support was performed, but systemic hypoperfusion persisted, prompting initiation of VA-ECMO to establish ECPELLA. Treatment and Outcome: Right heart catheterization under ECPELLA support demonstrated a mean pulmonary artery pressure of 27 mmHg, a pulmonary capillary wedge pressure of 6 mmHg, a pulmonary vascular resistance of 11.7 Wood units, and a pulmonary artery pulsatility index (PAPi) of 3.0—findings consistent with precapillary pulmonary hypertension and markedly reduced native cardiac output (CO) that precluded VA-ECMO weaning. Concomitant limb ischemia from PAD prompted initiation of iNO at 20 ppm. Following iNO, pulmonary vascular resistance decreased and both PAPi and native CO improved, allowing stepwise VA-ECMO weaning. VA-ECMO was removed on hospital day 2 and mAFP on day 3. Despite initial hemodynamic stabilization, worsening limb ischemia led to uncontrollable renal dysfunction and acidosis, and the patient died on day 4. Teaching Point: Early iNO may lower pulmonary vascular resistance, improve PAPi and native CO, and enable VA-ECMO weaning in ECPELLA patients with precapillary pulmonary hypertension.