Respect The Notch: Under-appreciated Pulmonary Vascular Disease and Hemodynamic Collapse Post Left Ventricular Assist Device Placement

Abstract

Introduction Right ventricular (RV) failure occurs in 15-20% of patients post Left ventricular Assist Device (LVAD) implantation and has been associated with increased mortality. Herein we describe a case of severe RV failure post LVAD implantation and how proper identification of the etiology led to a positive outcome. Case description A 58-year-old male with non-ischemic cardiomyopathy is admitted with decompensated heart failure. Right heart catheterization (RHC) showed right atrial pressure (RAP) 5 mmHg, Pulmonary artery pressure (PAP): 45/25, wedge pressure (PCWP) 24 mm Hg, pulmonary vascular resistance (PVR) of 1.4 woods units and cardiac index of 1.7 on inotropes. The patient underwent HMIII LVAD implantation. Immediately postop the patient developed shock. TTE showed an akinetic and dilated RV. He was placed on VA ECMO emergently and then transitioned to a percutaneous right ventricular assist device (RVAD). The patient eventually required dialysis. Decision-making Multiple mechanisms lead to RV failure after LVAD implantation. These include increased RV preload (from increased cardiac output and venous return or blood/fluid administration perioperatively), decreased contractility (LV decompression resulting in intraventricular septal left shift and decreased septal contribution to RV contractility), RV infarct, ventricular arrhythmias, and increased RV afterload (unmasking of pulmonary hypertension or pulmonary embolism). On review of the patient's echocardiogram post RVAD placement, there was RVAD flow dependent notching of the RV outflow tract (RVOT) pulse wave doppler (Figure 1A,B). RVOT notching is a validated sign of high PVR and prompted further review of patient's pre LVAD RHCs and TTEs. Excluding the RHC and TTE immediately pre LVAD implantation, prior RHCs showed RAP:PCWP ratio of 0.7, PAP of 70s/30s and PVR as high as 5.4 with concordant RVOT notching on TTE. The narrower pulmonary pulse pressure on the RHC immediately preceding LVAD implantation suggested a failing RV and was discordant with the lower RAP:PCWP (0.25) and lower PVR. Under-occlusion of the PCWP most likely led to a falsely elevated PCWP and falsely reduced PVR. With aggressive pulmonary vasodilator therapy, hemodynamics improved, the RVAD was explanted and dialysis was successfully discontinued. Figure 1C shows improvement of RVOT notching with this treatment. Conclusion Severe RV failure post LVAD implantation has a significant impact on morbidity/mortality. The echocardiogram provides valuable pathophysiological insights and is an important asset to interpreting invasive hemodynamics, especially pertaining to RV failure.