Right ventricular failure (RVF) occurs at a rate of approximately 20 % with continuous-flow LVADs [17] and may eventually occur in up to 25 % of supported patients [22]. Patients with early post-LVAD RVF have higher mortality at 1 year [19] and impaired exercise tolerance [23], although the impact of RVF on overall quality of life is not well-described. These patients manifest predominantly ‘right-sided’ symptoms of heart failure with abdominal fullness, anorexia, and peripheral edema with relatively little orthopnea unless ascites or pleural fluid accumulations cause a reduction in lung capacity. In the perioperative period, right-ventricular assist device implantation may be required, prolonging the hospital course [19]. For those with symptomatic congestion, diuretics are the mainstay of therapy. In patients with concomitant pulmonary hypertension, oral pulmonary vasodilators, such as sildenafil, may have a role in unloading the right ventricle and reducing central venous pressures [24]. Digoxin may improve acute hemodynamics in pulmonary hypertension [25], but there are no data to support its use in the management of RV failure associated with LVADs. If symptoms are refractory to oral therapies, intravenous inotropes may be required. Pump speed may be reduced to decrease RV workload. Patients who are awaiting heart transplant on mechanical right ventricular support or inotropic support generally require hospitalization for medical management and physical therapy in order to maintain adequate conditioning. Patients ineligible for heart transplant may benefit symptomatically from continuous intravenous inotropic support and palliative care consultation should be considered.

Bleeding complications occur frequently on LVAD support, and the most common types of bleeding are gastrointestinal (GI) hemorrhage and epistaxis. Single-center data suggest that GI bleeding occurs in about 20 % of LVAD patients [26]. While some GI bleeding is due to gastritis or hemorrhoids, patients with continuous flow LVADs are subject to GI bleeding related to the formation of superficial arterio-venous malformations in the intestinal mucosa. Additionally, these patients develop an acquired von-Willebrand syndrome due to lysis of von-Willebrand factor multimers, resulting in an impairment of primary hemostasis [27, 28]. LVAD patients presenting with significant GI bleeding generally have anticoagulation held or reversed and often undergo extensive evaluation to determine the source of bleeding. This may include upper GI endoscopy, colonoscopy, capsule endoscopy or, in the case of brisk bleeding, tagged red blood cell nuclear scan or angiography. Hospitalizations are often protracted as anticoagulation is resumed and the patient observed for recurrence of bleeding. In patients who have had more than one bleeding episode, anticoagulation is generally reduced, with a lower dose of aspirin and/or lower target INR. While this may decrease the likelihood of further bleeding, it may also increase the likelihood of pump thrombosis, resulting in pump dysfunction or embolic complications. Occasionally GI bleeding is refractory and anticoagulation must be discontinued altogether. Patients may also be placed on adjunctive therapies such as thalidomide (which reduces vascular endothelial growth factor expression), subcutaneous octreotide (which reduces gastric acidity and induces portal and splanchnic vasoconstriction), or oral estrogen (which is prothrombotic). Data supporting these adjuvant strategies are limited and further investigation is needed. Despite these measures, some patients have low-grade chronic or intermittent GI blood loss and require periodic transfusions to maintain control of symptoms. Because less pulsatile flow is associated with greater degrees of GI bleeding [29] and discontinuation of continuous flow may ‘cure’ GI bleeding, patients may be managed with reduced LVAD support at lower pump speed.

Epistaxis is another potential complication of LVAD support and may share some of the same causal mechanisms as GI bleeding. Severe bleeding may require hospitalization with blood transfusion and nasal packing. Patients should be instructed to keep the nares moist with nasal saline or lubricant gel and to use oxymetazoline at the onset of bleeding episodes. Antiplatelet and anticoagulant management strategies are similar to those employed for GI bleeding.

Device malfunction or pump failure occurs in approximately 10 % of patients during the first 2 years of support with continuous flow pumps, leading to pump exchange or death [17]. Clinically, pump dysfunction is usually discovered after the emergence of heart failure symptoms and/or intravascular hemolysis, which is caused by shearing of red blood cells as they traverse a region of pump thrombosis. Pump replacement surgery may be performed with moderate morbidity and a 1-year survival rate post-exchange of 70 % [30]. The alternative to pump exchange for those patients unwilling to undergo further surgery is inotropic therapy and supportive care. These patients may require blood transfusions to maintain acceptable hemoglobin concentrations and severe hemolysis may induce arterial vasospasm through a mechanism of nitric oxide depletion resulting in visceral pain. For acute pump dysfunction, a strategy of thrombolysis or augmented anticoagulation (e.g. glycoprotein IIb/IIIa inhibitors) has been employed in an attempt to resolve thrombosis. Despite some reported successes [31, 32], it is our experience that the risk for major bleeding is high and likely prohibitive. As patients weigh the uncertainty of further surgery against mortality and impaired quality of life, palliative care consultation is particularly helpful for clarifying patient and family goals.