Acute heart failure (AHF) is present in a substantial proportion of patients after liver transplantation (LT), and is associated with significant morbidity and mortality. 1-4 The pretransplant hemodynamic changes (decreased systemic vascular resistance (SVR), poor ventricular response to stress and increased cardiac output) that occur in patients with end-stage liver disease (ESLD) coupled with the effects of pro-inflammatory cytokines released during reperfusion of the liver during transplantation have been implicated in both systolic and diastolic dysfunction, contributing to AHF. 5 Both ischemic and non-ischemic causes have been implicated. While ischemic heart disease, has well defined risk factors, and may be identified preoperatively, non-ischemic AHF, is a poorly understood entity and can occur in the absence of obvious risk factors. Standard preoperative workup including electrocardiogram (EKG), echocardiography at rest or on stress, or biomarkers has limitations in predicting this risk. Cirrhotic cardiomyopathy, iron overload cardiomyopathy, and stress-induced cardiomyopathy are some of the commonly implicated entities. Distinguishing one etiology from the other is difficult and multiple etiologies may coexist in the same patient. While early recognition of risk factors and diagnosis is difficult, once diagnosed, there are no clear-cut rules for candidacy of transplant in these patients and no guidelines exist to help optimize these patients prior to transplant. These patients are at a high-risk of cardiovascular collapse either during the intraoperative period or in the immediate postoperative period and approaches to mitigate these risks as