Abstract
BACKGROUND: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) has been used increasingly to support patients with cardiogenic shock (CS). There has been growing recognition of the favorable and unfavorable hemodynamic effects of this therapy and recent interest in the use of other percutaneous circulatory support devices to offset some of the potentially harmful hemodynamic effects. Herein, we provide visual evidence of the effects of intra-aortic balloon pump (IABP) counterpulsation for a patient with peripheral VA-ECMO cannulation. CASE PRESENTATION: A 68 year old man who had undergone orthotopic heart transplantation presented with 2 days of fatigue, orthopnea, and paroxysmal nocturnal dyspnea. On examination, he was tachycardic, hypotensive and hypoxic with cool extremities, consistent with CS. Transthoracic echocardiogram (TTE) showed new severe biventricular dysfunction with a left ventricular ejection fraction of 15%, right heart catheterization demonstrated elevated filling pressures and low output. An IABP was inserted via the left femoral artery with minimal improvement in hemodynamics. He was escalated to VA-ECMO. Repeat TTE demonstrated aortic valve (AV) opening with each cardiac cycle and mild MR. With placement of the IABP on standby Additional file 1: Video 1 (video 0:03), the AV no longer opened. Re-initiation of balloon counterpulsation resulted in resumed AV opening with each beat Additional file 1: Video 1 (video 0:17). He was treated for presumed acute allograft rejection with methylprednisolone, thymoglobulin, intravenous immunoglobulin and plasmapheresis with improvement in allograft function. However, he developed an Enterobacter aerogenes pneumonia and rapidly fatal septic shock. CONCLUSIONS: This case visually demonstrates effective LV decompression by IABP counterpulsation in VA-ECMO support. While the overall effects of LV decompression in patients on VA-ECMO with IABP are still unclear, this report demonstrates one potential mechanism of benefit in the prevention of stagnation of blood flow that may lead to intra-cardiac or aortic root thrombus formation.