Title:
Acute RV Failure post LVAD: The Forgotten Ventricle
Introduction:
Cardiogenic shock (CS) from decompensated cardiomyopathy varies from patients with acute myocardial infarction related CS. We present a case of CS from decompensated non-ischemic cardiomyopathy (NICM) who ultimately underwent successful left ventricular assist device (LVAD) placement followed by acute right ventricular failure requiring temporary right ventricular mechanical circulatory support.
Clinical Case:
67-year-old male with history of heart failure with reduced ejection fraction (HFrEF), diabetes mellitus, hypertension presented to our facility with lower extremity edema, dyspnea on exertion. Left ventricular ejection fraction (LVEF) from years prior was 10-15% and was not on comprehensive medical therapy for advanced heart failure. On arrival, blood pressure was 122/100 mmHg, heart rate 127 bpm with normal oxygen saturation. Physical examination revealed elevated jugular venous pressure, pitting lower extremity edema with cool extremities. Laboratory values revealed creatinine 2.06mg/dl (baseline 1.3), sodium 139 mmol/dl, normal AST/ALT, high sensitivity troponin I of 32 ng/L, NT pro-brain natriuretic peptide (NT-proBNP) 52000 pg/ml, lactate 2 mmol/L. Clinical presentation with exam findings were consistent for cardiogenic shock with biventricular congestion, therefore intravenous Milrinone with high dose intravenous loop diuretic was initiated. Urgent right heart catheterization revealed right atrial (RA) pressure of 15 mmHg, pulmonary artery (PA) pressure of 40/20 with mean of 27 mmHg, pulmonary capillary wedge pressure (PCWP) of 20. Thermodilution cardiac index was 2.1 L/min. Transthoracic echocardiography (TTE) revealed LV dilatation, biventricular failure with LVEF 10-15% and severe LV global hypokinesis without valvular abnormalities. Left heart catheterization revealed non-obstructive coronary artery disease. Despite medical treatment he remained symptomatic with evidence of end-organ dysfunction, therefore a shock team discussion was conducted to decide next therapies. Given the degree of cardiomyopathy, a temporary axillary microaxial continuous flow transvalvular pump (Impella 5.5) was implanted as a bridge to decision for durable LVAD. Subsequently, his renal function normalized and PCWP decreased to 10. RA pressure was 5 with pulmonary artery pulsatility index (PAPi) above 1.5. Prior to implanting durable LVAD- a repeat TTE was performed to assess the right ventricle (RV) which had normalized on the Impella. Successful LVAD was performed with removal of the Impella. In the OR, he had significant blood loss with concomitant hypotension requiring multiple vasopressors. Hemodynamics revealed RA pressure of 15, PAPi 0.7 despite inotrope. Therefore, urgently a percutaneous temporary mechanical RV circulatory support device (Protek duo) was implanted to treat acute RV failure post LVAD. Given the significant hypotension, he developed acute kidney injury from acute tubular necrosis requiring dialysis. Using hemodynamics, serial TTE, we were able to wean down Protek duo and eventually decannulate. He was successfully weaned off all vasopressors and inotropic support. He continued to require renal replacement therapy and was discharged to inpatient rehabilitation center in a medically stable condition.
Discussion
:
5-year survival with durable LVAD is 50% which can be further decreased by RV Failure. Predicting RV failure post LVAD remains challenging despite many novel hemodynamic and imaging tools. Early and possibly pre-emptive temporary mechanical RV support post LVAD appears to improve outcomes.