Poster 016: Veno-Pulmonary Artery (V-PA) ECMO as Salvage Therapy in Isolated Right Ventricular Infarction Post-Cardiotomy

Background: Veno-pulmonary artery (V-PA) ECMO is a configuration that drains deoxygenated blood and returns oxygenated blood directly into the pulmonary artery, effectively bypassing the right ventricle (RV). Although most commonly used as bridge to lung transplantation, its role as rescue therapy for isolated RV infarction in postcardiotomy cardiogenic shock remains limited.

Methods: A 67-year-old man with type 2 diabetes mellitus and hypertension, previously treated with percutaneous balloon valvuloplasty for severe mitral stenosis, presented with progressive dyspnoea. Transthoracic echocardiography revealed moderate aortic stenosis with regurgitation and recurrent severe mitral stenosis. He underwent double valve replacement (mitral and aortic), with cardiopulmonary bypass time and aortic cross-clamp of 261 and 223 minutes, respectively. The early postoperative course was complicated by vasoplegia, which resolved within 48 hours. Subsequently, the patient developed sudden haemodynamic collapse with complete AV block and respiratory failure. We initiated epicardial pacing and prompt bedside assessment with point-of-care ultrasound demonstrated a severely akinetic RV, triggering immediate shock team activation. He was classified as SCAI stage D cardiogenic shock, and veno-arterial (VA) ECMO was initiated for mechanical circulatory support (MCS). Coronary angiography revealed thrombotic occlusion of the right coronary artery ostium. Percutaneous coronary intervention with biodegradable polymer drug-eluting stent implantation restored TIMI 3 flow.
Right heart catheterization revealed severe RV dysfunction with biventricular congestion: right atrial pressure 17 mmHg, mean pulmonary artery pressure 20 mmHg, pulmonary capillary wedge pressure 19 mmHg, cardiac output 5.2 L/min (on ECMO), pulmonary artery pulsatility index (PAPi) 0.59, and cardiac power output (CPO) 1.15 W.

Outcome: Despite early reperfusion and one week of VA-ECMO support, repeat haemodynamics demonstrated persistent RV failure (RA 11 mmHg, mPAP 18 mmHg, PCWP 17 mmHg, PAPi 0.82, CPO 1.6 W). Given the lack of RV recovery, the shock team elected to promptly transition to a V-PA ECMO configuration to provide selective right-sided support. Following 10 days of V-PA ECMO, progressive haemodynamic and echocardiographic recovery was observed, with TAPSE 14 mm, LVEF 61%, and PAPi 1.0, allowing successful weaning. The patient subsequently recovered from acute kidney injury and nosocomial pneumonia, achieving sustained clinical stability.
Postcardiotomy isolated RV infarction is a rare but catastrophic cause of cardiogenic shock, requiring rapid diagnosis and phenotype-directed therapy. This case underscores the importance of early shock team involvement to guide timely escalation and adjustment of MCS. While VA-ECMO provides immediate haemodynamic support, it may be suboptimal for isolated RV failure due to increased left ventricular afterload and lack of targeted RV unloading. Early recognition of persistent RV dysfunction using invasive haemodynamics enabled prompt conversion to V-PA ECMO, resulting in improved PAPi and CPO and facilitating myocardial recovery.

Conclusion: This case highlights the critical role of early identification of cardiogenic shock, rapid shock team activation, and timely initiation of appropriate MCS. V-PA ECMO represents an effective, physiology-driven strategy for isolated RV failure when early recovery is not achieved with VA-ECMO, offering potential to improve outcomes in postcardiotomy cardiogenic shock.