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DP35: UNLOADING THE FAILING HEART: COORDINATING ECMO AND IMPELLA SUPPORT IN A HIGH-RISK CARDIAC TRAUMA CASE
Gabriel Flambert, BS1; Arthur C De Souza1; Yong G Peng, MD, PhD, FASE, FASA2
1University of Florida College of Medicine; 2University of Florida Department of Anesthesiology
Introduction: Managing concurrent cardiogenic and distributive shock presents significant hemodynamic challenges, especially when mechanical circulatory support modalities are required. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) provides emergent circulatory support in refractory cardiogenic shock. However, its retrograde aortic flow increases left ventricular (LV) afterload, potentially precipitating LV distension, pulmonary edema, arrhythmias, and impaired coronary perfusion. Growing evidence supports using Impella devices during ECMO to actively unload the LV, lower LV end-diastolic pressure (LVEDP), and improve myocardial oxygen balance. We present a case of refractory cardiogenic shock and mesenteric ischemia requiring sequential veno-arterial (VA), veno-veno-arterial (V-VA), and veno-venous ECMO (VV-ECMO) support with Impella 5.5 for LV unloading.
Case Report: A 75-year-old male with coronary artery disease (Coronary Artery Bypass Graft ×4, drug-eluting stents ×7), ischemic cardiomyopathy (Ejection Fraction 40%), COPD, and obstructive sleep apnea, presented after a fall with GCS 15, severe hypertension, and right clavicle and rib fractures. Early labs showed mildly elevated troponin,?B-type natriuretic peptide (BNP), and C-reactive protein (CRP). By day 3, he developed abdominal pain, hypotension, rising troponins, and occult GI bleeding. CT angiography revealed an active gastric bleed and chronic superior mesenteric artery (SMA) occlusion. After intubation and initiation of vasopressors, esophagogastroduodenoscopy (EGD), exploratory laparotomy, and sigmoidoscopy on day 4 revealed no source of bleeding. During SMA revascularization on day 5, he suffered cardiac arrest requiring 60 minutes of ACLS. VA-ECMO was initiated intraoperatively and subsequently escalated to V-VA ECMO for differential hypoxemia. On day 8, an Impella 5.5 was placed for LV unloading, enabling conversion to VV-ECMO. He was weaned from VV-ECMO on day 10. During left heart catheterization on day 14, he experienced ventricular fibrillation arrest; ROSC was not achieved.
Discussion: This case highlights the physiologic interplay between ECMO support and LV loading. Although VA-ECMO restored systemic perfusion, the retrograde aortic flow it created caused increased LV afterload. This in turn limited aortic valve opening, promoting LV distension, a complication know to impair myocardial recovery. The Impella 5.5 provided active forward-flow LV unloading, reducing LVEDP, decreasing myocardial oxygen demand, and improving coronary perfusion. This facilitated transition from V-VA to VV-ECMO, demonstrating the complementary nature of Impella + ECMO support. Early LV unloading during ECMO has been associated with improved hemodynamics and improved survival.
Conclusion: This case demonstrates the value of LV unloading during VA-ECMO in managing severe cardiogenic shock. The Impella 5.5 effectively mitigated ECMO-induced LV afterload and supported myocardial decompression. Timely recognition of LV distension and early incorporation of unloading strategies may enhance myocardial recovery and reduce ECMO-related complications. The combined use of ECMO and Impella offers a synergistic, physiology-driven approach to managing complex shock states.