Left Ventricular Assist Device Management in the Emergency Department

Paul Trinquero, MD; Andrew Pirotte, MD; Lauren P. Gallagher, MD, MA; Kimberly M. Iwaki, MD; Christopher Beach, MD; Jane E. Wilcox, MD


Western J Emerg Med. 2018;19(5):834-841. 

In This Article

Specific Complications in VAD Patients

Complications unique to VAD patients can be classified as "VAD-specific" and "VAD-associated." VAD-specific complications include 1) pump failure/malfunction, and 2) pump thrombus. These will be discussed in detail in the next section. VAD-associated complications include the following: 1) gastrointestinal (GI) bleeding, specifically related to the presence of arteriovenous malformations (AVM); 2) cerebrovascular accidents (CVA), either embolic or hemorrhagic in etiology; 3) VAD driveline infections, which may be localized to the percutaneous exit site or deeper within the pump or pump pocket;[13] and additionally, 4) right ventricular (RV) failure occurs in 15–20% of VAD patients and can lead to persistent HF symptoms and/or pump dysfunction (e.g. low flows).[14]

GI bleeding in VAD patients is multifactorial. Patients are maintained on lifelong therapeutic anticoagulation. Additionally, continuous-flow VAD patients will usually develop acquired von Willebrand factor (vWF) disease.[14,15] The relatively higher shear stress brought on by non-physiologic circulation distorts the vWF multimers and leads to increased systemic cleavage and subsequent deficiency.[15] Furthermore, VAD patients are susceptible to GI vascular malformations secondary to the decreased pulse pressure from continuous flow. A retrospective analysis of patients implanted with a HMII device found that 43% had a major bleeding episode requiring blood transfusion, the majority of which were localized to the GI tract.[14] Management of GI bleeding often requires examination via endoscopy and colonoscopy for source control of AVM lesions. Blood transfusion should not be reflexive for the stable patient with GI bleeding, especially in BTT patients, as blood products are sensitizing and may reduce the chance of successful heart transplantation. In addition, robust transfusion of blood products will increase afterload and may lead to HF exacerbation. However, for larger GI bleeds or bleeding resulting in hemodynamic instability, blood transfusion is crucial. Because blood transfusion may lead to an increase in circulating antibodies and make it more difficult to find a donor match, transfuse with leukoreduced and irradiated blood products if available to decrease sensitization.[16] Multidisciplinary consultation with VAD and transplant teams is essential in the management of GI bleeding.

CVA, either embolic or hemorrhagic, is often a devastating VAD-associated complication. In addition to the pro-thrombotic milieu of a failing heart, the implantation of a mechanical assist device creates a nidus for the formation of clots. Development of atrial fibrillation after VAD implantation is common, and increases risk of embolic CVA.[17] Blood pressure control with a MAP <90, daily 81mg aspirin, and avoidance of supratherapeutic INR levels (>3.0) have shown to be effective at reducing stroke risk.[18] Data from the ADVANCE trial estimates prevalence of ischemic CVA at 6.8% and hemorrhagic CVA at 8.4%.[14,18] In the event of a CVA, early coordination with the VAD team and neurology/neurosurgery team is necessary to discuss reversal of anticoagulation and surgical options.

The driveline exit site provides a conduit for bacterial entry, making infection a relatively common VAD-associated complication affecting nearly 20% of patients within the first year of implantation.[19] Infections may be superficial and localized to the percutaneous exit site or deeper within the pump pocket or pump itself.[13] Blood cultures and driveline cultures should be obtained in any patient with suspected infection.[20] Staphylococci are the most commonly isolated organism, but pseudomonas and other gram-negative bacteria are common culprits as well.[21] Empiric antibiotics should be tailored to each individual patient. An abdominal CT is often helpful to evaluate for an associated fluid collection.[20] In the event of systemic spread, management of sepsis mirrors that of non-VAD patients: aggressive fluid resuscitation; early delivery of antimicrobials; and central/arterial line placement as indicated. Central catheterization can be achieved from any of the routine sites. Unless patients have residual RV failure, the risk of "volume overloading" a VAD patient is generally low. Vasopressors may be appropriate after adequate volume resuscitation.

While the VAD provides circulatory support to the failing LV, RV failure is a common problem, occurring in 15–20% of VAD patients.[22,23] Reduced preload to the LV leads to low VAD flows. "Low- flow alarms" on the VAD may be related to reduced preload from RV failure, but also may be secondary to hypovolemia or inflow cannula obstruction (less common, but a known complication). Laboratory markers of end organ dysfunction can aid in the diagnosis of RV failure. Elevated creatinine, liver transaminases, and the presence of lactic acidosis can indicate cardiogenic shock. If a shock state is suspected due to RV failure, inotropes (e.g. milrinone or dobutamine) should be used.