Left Ventricular Assist Device (LVAD)
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Case
Mr. S is a 68 year old man who presents to the emergency department with maroon stools and weakness for one day. He appears diffusely weak, diaphoretic, and pale. The tech is struggling to get vital signs while the nurse is working on placing two large bore IVs. After a minute the tech gives up - “I can’t get a heart rate or a blood pressure, doc.” With another quick glance at the (obviously still living) patient, you notice a battery pack at his side. This is followed quickly by the realization that the patient has a Left Ventricular Assist Device (LVAD).
Introduction
Congestive heart failure (CHF) is significant cause of both morbidity and mortality. Patients with advanced disease have few options for definitive therapy aside from heart transplantation. Left ventricular assist devices (LVADs) are increasingly being utilized for both bridge therapy while a patient awaits transplant as well as destination therapy, when it is used as a last resort to support a failing heart. With increased utilization of these complex devices in the already unwell patient, it is unavoidable that this population will present to the emergency department for care. The emergency physician must have a basic understanding of the LVAD and its associated complications.
Mechanism
The modern LVAD has evolved into a very sophisticated devices that augments the function of the failing native heart restoring perfusion and improving blood supply. However they are imperfect at mimicking normal cardiac function, with the continuous nature of the output resulting in non pulsatile flow. Though several different devices are utilized, the basic form and function is consistent.
The LVAD receives blood from an inflow cannula in the left ventricle (LV), and ejects it into an outflow cannula, through the ascending aorta.
A percutaneous driveline connects the internal device to the power source and controller, both external.
Given the complexity of care of these patients, as well as differences between devices, the emergency department physician should contact the appropriate LVAD coordinator as soon as possible within the course of the patients care.
Source: circulation 2013
Initial Assessment
Patient
Initial evaluation of the patient with an LVAD should begin with the same concepts as with a non LVAD patient, though performed differently. The LVAD patient will not have a palpable pulse, nor a blood pressure. The continuous forward propulsion of blood in a non pulsatile manner yields only a mean arterial pressure (MAP), which should be measured with a doppler and a sphygmomanometer.
On auscultation, the physician should be able to hear the hum of the device, which can completely obscure any native heart sounds. Though much of the time no pulse will be felt, it is sometimes possible to feel a peripheral pulse; however if this is a new finding, it can actually be a sign of device thrombosis.
The MAP goal for the majority of LVAD patients is between 70-90mmHg. Assessment of perfusion should additionally include mental state, capillary refill and jugular venous pressure. Patients with LVADs are very sensitive to changes in their perfusion state, thus any change in preload or afterload can significantly affect the function of the device, and thus cardiac output.
Device
The emergency medicine physician should be familiar with the basic evaluation of the LVAD device and its alarms. Listening for the device hum is the first indication of a functional unit, the lack of which indicates pump failure. The physician should make sure all the leads are connected, assure that there is power to the device (never disconnect both batteries simultaneously). Hazard alarms of the device may indicate poor circulatory support, such as can occur with low flow, pump disconnection, low voltage requiring immediate battery replacement, or loss of power. Multiple variables should be able to be obtained from the controlled unit, including:
Pump speed (rpm) - constant variable, intrinsic to device.
Flow (L/min) - determined by pump speed and preload. Decreased flow may indicate decreased preload such as in decreased intravascular volume, RV failure, tamponade, thrombus, or kinking of the cannula.
Power (watts) - sudden increase in power may signal obstruction, such as thrombosis or increase in afterload. As devices do vary, and the systems are quite complex, the emergency medicine physician should contact the LVAD team as soon as possible.
HeartMateIII controller panel
Source W. Brady et al. American Journal of Emergency Medicine 26 (2018) 1295-1999
Complications
Hypovolemia/hypotension
Patients who are reliant on LVADs are very sensitive to changes in preload, thus simple dehydration or hypovolemia can lead to significant decrease in cardiac output and resultant hypotension/hypoperfusion, The pump may signal a “low flow” state, and bedside ultrasound will demonstrate a small RV and LV.
Initial evaluation of these patients must begin with assessment of their perfusion, which can be accomplished by obtaining the MAP and observing capillary refill and level of consciousness. Hypovolemia is a common presentation, and must be treated with preload expansion with crystalloids or blood products, depending on the clinical situation. Right ventricular failure is a significant cause of mortality, as the decreased blood return to the LV in this setting is difficult to treat. In this case, one may consider RV afterload reduction and ionatropic support.
Dysrhythmia
Patients with implanted VADs are prone to ventricular arrhythmia, especially within the first 30 days after device insertion. Due to the fact that much of the cardiac output in patients with LVADs is device dependent, even ventricular arrhythmias can at times be well tolerated. In addition, most patients with LVADs also have AICDs which often terminate arrhythmias prehospital.
Some of the most common causes of arrhythmia are hypovolemia and inadequate venous return (with a corresponding “low flow alarm”), thus patients should be treated with volume replacement. In addition, those rhythms that decrease right ventricular filling can lead to hemodynamic deterioration and even cardiac arrest.
Arrhythmias may be treated with normal ACLS protocols, including pharmacologic and electrical therapy as needed.
Infection/sepsis
Infection is the most common complication in VAD patients, reaching rates as high as 30-50%. These can be broken down into VAD specific infections such as those of hardware and body surfaces that contain them; VAD related infections such as endocarditis or mediastenitis; or non-VAD infections such as pneumonia or urinary tract infections.
The infections affecting the device directly most commonly involve the percutaneous driveline, and can extend into the pump itself. Patients present with local signs of infection at the site of insertion, or with evidence of sepsis and bacteremia. In addition to normal signs of sepsis, the LVAD patient in distributive shock may present with a “high flow” alarm, or even a suction event (see below). The bacteria involved are most commonly those of normal skin flora, as is often the case with endocarditis. When examining the junction of the skin and driveline, the physician should employ the use of sterile gloves and mask. Three blood cultures should be obtained, and the patient should be treated with IV fluids and broad spectrum antibiotics.
Hemorrhage
The incidence of hemorrhage, especially in the GI tract is high in patients with LVADs, reaching up to 40%. The etiology of this is multifactorial, and is likely due to a combination of an acquired von Willibrand factor deficiency, anticoagulated state (goal INR 1.7-2.3), and increased frequency of AV malformations. These malformations seem to be much more common in this patient population, and are thought to be due to alteration in GI perfusion during non pulsatile blood flow. Often these bleeds are slow, leading to anemia that can worsen congestive heart failure.
Patients who present with brisk GI bleeds will demonstrate signs of poor perfusion, and “low flow” alarms secondary to hypovolemia. These patients should be resuscitated similarly to non-LVAD patients; including volume replacement and reversal of anticoagulation. As with other populations of anticoagulated patients, the benefits of anticoagulation reversal must be weighed with the risk of thrombosis. In the case of patients with LVADs, the risk of device thrombosis is substantial, thus this decision is best made in conjunction with the LVAD team.
The risk of both hemorrhagic and ischemic strokes is increased in this patient population, with an incidence of 4-7% per year. A significant neurologic event with resultant obtundation may be difficult to differentiate from cardiac arrest.
Device thrombosis
Despite all patients with LVADs being anticoagulated, thrombosis of the device occurs in approximately 8%, with symptoms at presentation varying widely. Some patients present in cardiogenic shock (dyspnea, tachycardia, hypotension), while others may be completely asymptomatic and come to medical attention only due to an alarming device. The display will demonstrate “high power” and “low flow”. Exam and lab tests will reveal evidence of hemolysis, such myoglobinuria, scleral icterus, and elevated LDH (>600).
This diagnosis is best made via TEE, though CTA can be very diagnostic as well. MRI is contraindicated in patients with VADs.
Treatment of device thrombosis includes IV heparin and admission in the case of a stable patient. In the case of an unstable patient, thrombolytics or emergency pump exchange may be necessary. ECMO may be employed if thrombosis leads to life threatening instability.
In the case of pump stopage of unknown duration (or more than several minutes), thrombosis is a serious concern at time of resumption of flow. In this case it is likely that a formed thrombus will be driven forward, resulting in embolic events. Thus if a patient maintains cardiac output despite a (longer than briefly) stopped pump, emergent consultation with the LVAD team should be pursued prior to restarting the VAD.
Suction event
A suction event may be triggered should preload be reduced, and may occur in setting of hypovolemia or distributive shock. Increased negative pressure in the left ventricle causes the ventricular wall to cover the LVAD inlet cannula, causing the cannula to be partially or completely covered, thus resulting in poor or no forward flow. This can also be quite irritating to the myocardium and can trigger dysrhythmias. In case of a suction event, in addition to treating the underlying cause consideration should be made to slowing the heart rate as this will allow more time for the ventricle to fill.
Hemolysis
When an LVAD device begins to cause hemolysis, as can occur in up to 18% of patients, the one year mortality for this population increases substantially. Increased shear stress on red blood cells as they travel through the device can result in hemolysis, causing patients to present with worsening congestive heart failure and anemia. Laboratory values such as bilirubin and LDH will be elevated. There is no simple treatment for this complication, and device exchange may be required.
Obstruction
As with decreased preload, the LVAD is also sensitive to increased afterload. This can be caused by outflow cannula obstruction or hypertension, with MAP >90 causing significant reductions in cardiac output and forward flow. Thus blood pressure control with a goal MAP of 70-80 mmHg is critical for optimal pump function.
Special considerations
POCUS (point of care ultrasound)
The bedside ultrasound can be a useful tool to assist with diagnosis of the unstable LVAD patient. In conjunction with information provided by the pump mechanism, the knowledge of ventricular size can help the emergency physician in the evaluation of this population. For instance, if a “low flow” alarm is coupled with small ventricular size, the clinician should suspect hypovolemia as the cause of the patients poor perfusion. If the same alarm is present in the setting of a dilated LV, one should suspect device malfunction.
| POCUS Finding | LVAD Pump Display | Potential Causes |
|---|---|---|
| Small LV and RV | Low FLow | Hypovolemia |
| Small LV and Dilated RV | Low flow |
Suction event |
| Large RV and LV | Low flow or no hum |
Pump thrombosis |
CPR (cardiopulmonary resuscitation)
As previously discussed, due to lack of standard measurable blood pressure and pulse in the LVAD patient, it is more difficult to determine when one is, in fact, in cardiac arrest. This determination should be made via evaluation of signs of perfusion, ETCO2, and level of consciousness. Defibrillation of dysrhythmias should be guided by ACLS protocol.
Though LVAD manufacturers do not recommend chest compressions as this can dislodge the VAD; a recent case series of such events have demonstrated the procedure to be likely safe and effective. The American Heart Association (AHA) put out a statement in 2017 that advises the initiation of chest compressions if the patient exhibits signs of non-perfusion, and end tidal CO2 (ETCO2) levels are <20mmHg after intubation.
Case conclusion
Mr. S was found to have a MAP of 55 when his blood pressure was able to be obtained via doppler. His POCUS evaluation demonstrated a small RV and LV, with an inlet cannula visible in the LV. He had a non-tender abdomen and strongly heme-positive maroon stools. He was treated with crystalloids, blood transfusion, and reversal of his anticoagulation. His hemodynamics stabilized and he was transferred to the tertiary health center where his LVAD team is based. An endoscopy/colonoscopy there was a sigmoid AV malformation with evidence of recent bleeding.
References
Robertson et al. The emergency Management of ventricular assist devices. American Journal of Emergency Medicine. 34 (16) 1294-1301
Ornato et al. How to determine whether to perform chest compressions on an unconscious patient with implanted left ventricular assist device. Resuscitation, 2018-08-01. 129. e12-e13
Peberdy et al. Cardiopulmonay resuscitation in adults and children with mechanical circulatory support. A scientific Statement from the American Heart Association. Circulation 2017;135e1115-e1134
Shashima Nakahara, MD et al. Ventricular arrhythmias after left ventricular assist device. Circulation: arrhythmia and electrophysiology 2013;6:648-654
Shinar et al. Chest compressions may be safe in arresting patients with ventricular assist devices (LVADs). Resuscitation 85 (2014( 702-704
William Brady MD, Sabrina Weigand, MD, James Bergin, MD. Ventricular assist device in the emergency department: evaluation and management considerations. American Journal of Emergency Medicine 36(2018)1295-199
Yenisleidy Paez Perez, DO, Terrance McGovern, DO. How to Manage Emergency Department Patients with Left Ventricular Assist Devices. ACEPNOW August 16, 2017