a b s t r a c t

Introduction: End stage heart failure is associated with high mortality. However, recent developments such as the ventricular assist device (VAD) have improved patient outcomes, with left ventricular assist devices (LVAD) most commonly implanted.

Objective: This narrative review evaluates LVAD epidemiology, indications, normal function and components, and the assessment and management of complications in the emergency department (ED).

Discussion: The LVAD is a life-saving device in patients with severe heart failure. While first generation devices provided pulsatile flow, current LVAD devices produce continuous flow. Normal components include the pump, inflow and outflow cannulas, driveline, and external controller. Complications related to the LVAD can be divided into those that are LVAD-specific and LVAD-associated, and many of these complications can result in severe patient morbidity and mortality. LVAD-specific complications include device malfunction/failure, pump thrombosis, and suction event, while LVAD-associated complications include bleeding, cerebrovascular event, infection, right ventricular failure, dysrhythmia, and aortic regurgitation. Assessment of LVAD function, pa- tient perfusion, and mean arterial pressure is needed upon presentation. Electrocardiogram and bedside ultra- sound are key evaluations in the ED. LVAD evaluation and management require a team-based approach, and consultation with the LVAD specialist is recommended.

Conclusion: Emergency clinician knowledge of LVAD function, components, and complications is integral in opti- mizing care of these patients.

1. Introduction

Heart failure is increasingly common in the United States, affecting over 6.5 million patients in the United States [1,2]. This disease is asso- ciated with significant morbidity and mortality, with mortality at 5 years approaching over 50% [1-3]. However, recent developments have improved survival, specifically Ventricular assist devices in patients with advanced heart failure. The number of patients with VAD will continue to increase. Newer FDA approved devices include the axial-flow HeartMate II (HMII) and centrifugal-flow HeartMate III (HMIII) LVADs (Abbott Laboratories, Lake Bluff, IL), and HeartWare (HVAD) (Medtronic, Minneapolis, MN) [4-6]. These devices, as well as improved patient selection, are associated with significantly improved

* Corresponding author at: 3841 Roger Brooke Dr., San Antonio, TX 78234, United States.

E-mail addresses: [email protected] (B. Long), [email protected] (W. Brady).

survival, ranging from 76 to 83% at 2 years, compared to a survival rate of 54% with first generation devices [4,5,7].

Most patients with VADs undergo significant education concerning

the device, including the components and means of self-management. These patients also receive significant outpatient care and follow up with specialists. However, LVAD patients will likely present to the ED with increasing frequency. Approximately half of patients with a newly placed LVAD present to the ED within the first month after im- plantation, and patients present on average 7 times to the ED within the first year postimplantation [8,9]. Emergency clinicians must under- stand the associated anatomy and physiology with the device present, the device components, and complications.

1. Methods

Authors searched PubMed and Google Scholar for articles using the keywords “ventricular assist device” OR “left ventricular assist device” OR “VAD” OR “LVAD” AND “emergency” for production of this narrative review. Authors included case reports and series, retrospective and

https://doi.org/10.1016/j.ajem.2019.04.050 0735-6757/

history and examination for the LVA”>prospective studies, systematic reviews and meta-analyses, clinical guidelines, and other narrative reviews. The literature search was re- stricted to studies published in English. Initial literature search revealed over 600 articles. Authors reviewed all relevant articles and decided which studies to include for the review by consensus, with focus on emergency medicine-relevant articles, including guidelines. A total of 97 resources were selected for inclusion in this review.

1. Discussion
   1. VAD function and components

A VAD can be placed into either or both ventricles; in other words, the patient can have a right ventricular assist device, left ventricular as- sist device, or biventricular assist device. The anatomic location of inser- tion obviously is heavily dependent upon the patient’s clinical syndrome, strategic goals, and body habitus. In particular, the strategic goals are quite important in the placement consideration. These goals include three different strategies: bridge to recovery, bridge to trans- plantation, or Destination therapy (i.e., the patient is unlikely to recover and not a candidate for cardiac transplant) [10-14]. Contraindications to placement include metastatic cancer, irreversible renal/hepatic failure, and cerebral accident with severe neurologic deficits [12-14].

The most commonly placed device is the left ventricular assist de-

vice, or LVAD. The emergency physician is most likely to see patients with an LVAD, and therefore, this review will discuss LVAD structure and placement.

The LVAD has two basic designs which produce different patterns of perfusion, including the pulsatile and Continuous-flow devices. The pul- satile pump, found in b10% of patients with LVADs, attempts to mimic natural perfusion [9]. First generation devices include pulsatile positive displacement pumps, but these devices have significant limitations in- cluding limited durability, extensive surgery for implantation, large ex- ternal lead, and audible pump [4-6,9]. Second generation devices include continuous flow devices, such as the HMII. Third generation de- vices use centrifugal pumps, with longer lifespans. These include the HVAD and HMIII devices. Continuous-flow devices are present in over 90% of patients with an LVAD. These devices provide constant perfusion. This is in contrast to cardiac-mediated perfusion with pulsatile pumps. Continuous flow devices deliver superior organ perfusion compared to the more “natural” pulsatile pump design [4-6,19]. In addition to the more effective perfusion, continuous-flow devices are both more dura- ble and more compact [4-6].

The continuous-flow LVAD has several basic parts, including the in- ternal pump, an external power source, and a control unit; specific com- ponents of the LVAD include the inflow cannula, pumping chamber, outflow cannula, percutaneous driveline, controller, and power source. The inflow cannula, usually placed in the apex of the Left ventricle , provides the route for blood flow from the native LV cavity to the LVAD pumping chamber. The pumping chamber, the component of the circuit which provides perfusion, is located in different positions depending upon the LVAD model type: the LV apex for the HMIII and HVAD devices and the subdiaphragmatic space adjacent to the heart for the HMII device. The pumping chamber contains the impeller, a near-friction-less rotor with rotation speeds ranging from 2500 to 9800 rpm; these types of impeller designs can generate blood flow up to 10 L per minute. The outflow cannula provides the conduit back to the patient’s native cardiovascular system and connects the pumping chamber to the Ascending aorta [4-6,9]. Fig. 1 details LVAD components, Fig. 2 depicts an LVAD appearance on a patient, and Table 1 presents normal LVAD parameters. Fig 3 demonstrates the controller panel of the HMIII device.

The percutaneous driveline provides a conduit for the electrical wir- ing, connecting the pump to the system controller. These wires not only connect the power source to the pump, but they also provide controlling and sensing functions for the LVAD. The driveline is tunneled

subcutaneously from the pump and exits the skin in the anterior ab- dominal area to connect to the controller. Thus, it is a frequent source of infection in the LVAD patient. The controller performs multiple func- tions and contains several important components. It controls LVAD functioning, including power source monitoring and regulation, overall system monitoring, data collection, and alarm system function. The con- troller has a panel which demonstrates important functions, status, and warnings regarding system operation. Lastly, the power source is usu- ally composed of rechargeable batteries. Most systems have the capabil- ity to have two batteries.

History and examination for the LVAD patient

Initial evaluation of patients with an LVAD is similar to most critical patients, though it differs in several aspects. Patients who are hemody- namically stable with an LVAD should be evaluated in the same manner as other patients, with the exception that the LVAD team or coordinator should be consulted. History, examination, and device evaluation are recommended for Hemodynamically stable patients. Heart rate is de- pendent on the patient’s rate and rhythm, though many patients with an LVAD may have a pacemaker or implantable cardioverter defibrilla- tor (ICD). blood pressure measurement depends on whether a palpable pulse is present [4-6,9,13]. A continuous flow LVAD will not typically produce a palpable pulse on its own, but patients may have enough ven- tricular function to produce pulsatile flow and a pulse [4-6,9,13]. A pal- pable pressure may be due to pump thrombosis, and thus, it is important to determine if the patient has a palpable pulse at baseline [4,9]. If a pulse is palpable, a standard sphygmomanometer may detect a blood pressure, which reflects a systolic blood pressure, rather than mean arterial pressure (MAP) [15,16]. However, a continuous flow LVAD with low Pulse pressures may not allow measurement of blood pressure by this method. If the pulse is not palpable, a pencil Doppler probe should be placed over the radial or Brachial artery. The point at which Doppler signal returns corresponds to the MAP for continuous flow devices [4-6,9]. If this is unobtainable, an Arterial line may be re- quired, which is the most accurate device for monitoring MAP. Invasive arterial monitoring will demonstrate minimal pulse pressure or flat ar- terial waveform [4-6,9,13,14]. Caution is recommended in using pulse oximetry, as a low reading commonly reflects a lack of pulsatile flow. However, a normal value may be accurate [17].

LVADs, especially those with continuous-flow, are sensitive to afterload and preload. Guidelines recommend maintaining a MAP of 70-90 mm Hg [18,19]. Elevated MAPs, corresponding to increased afterload, may cause decreased pump flow, which may result in wors- ening symptoms of heart failure. This may also cause subendocardial is- chemia and ventricular dysrhythmias. Acute hypertensive adverse event is associated with MAP N110 mm Hg in patients with continuous flow pumps [6,18,19].

Physical examination should otherwise evaluate the primary sys- tems involved with the chief complaint, as well as inspection of the de- vice components [4-6,9,13,14]. heart sounds are typically difficult to ascertain in patients with an LVAD due to the device’s mechanical hum that often obscures other sounds. The mechanical hum indicates device power and function. Signs of volume overload (extremity edema, ascites, elevated jugular venous pressure) can be due to sub- acute or chronic right ventricular failure. However, acute dyspnea, pul- monary edema, or hypotension are more commonly due to acute malfunction of the device, such as cannula obstruction or pump throm- bosis [4-6]. Clinicians must also assess the extremities for capillary refill and temperature. Altered mental status, focal neurologic deficit, or new headache are concerning for neurologic pathology such as intracranial hemorrhage. The device exit site, which is normally covered with a ster- ile dressing, and line should be examined with sterile gloves and mask for warmth, erythema, and discharge, which suggest infection. Clini- cians should evaluate the controller, current settings, pump parameters,

Fig. 1. LVAD components.

and alarms. Finally, the patient should be asked if he/she brought the back-up battery and back-up controller.

Recommended emergency department evaluation

Fig. 2. LVAD example. From https://commons.wikimedia.org/wiki/File:Left_ventricular_ assist_device_hannover.PNG

Electrocardiogram (ECG) is a vital component of the assessment to evaluate for dysrhythmia. ECG findings are often non-specific but can demonstrate low voltage, electrical artifact, and splintering of the QRS interval [4,20]. Patients with ventricular dysrhythmias most commonly present within the first month of LVAD implantation, but the LVAD may allow for adequate perfusion despite the dysrhythmia. Sustained ven- tricular dysrhythmias may be due to underlying cardiomyopathy or de- compressed left ventricle due to elevated pump speed or right ventricular failure [19,20]. Patients with an LVAD will typically demon- strate normal sinus rhythm.

Chest radiograph provides important diagnostic information includ- ing position and the type of LVAD, as well as the presence or absence of an ICD or pacemaker (Fig. 4). Deep space infection of the LVAD compo- nents requires assessment with computed tomography (CT). If concern for an acute intracerebral event is present, neuroimaging including head CT without contrast and head and neck CT angiography (CTA) is needed in the evaluation of acute ischemic stroke and intracranial hemorrhage [6,19]. Magnetic resonance imaging (MRI) is contraindicated.

Echocardiogram is the imaging modality of choice for most LVAD pa- tients presenting to the ED. Echocardiogram can evaluate cardiac func- tion and assess for complications such as regurgitation, right ventricular failure, and thrombus formation, though thrombi can be dif- ficult to detect on ultrasound alone [4-6,9,13]. Key components of the assessment include valvular function, inflow/outflow abnormalities, ventricular size and function, and septal position.

Laboratory assessment includes hemoglobin/hematocrit, lactate de- hydrogenase (LDH), haptoglobin, free hemoglobin, and coagulation panel. Hemoglobin and hematocrit with type and screen/cross are needed if concern of bleeding is present. Patients with LVADs are anticoagulated with a vitamin K antagonist, with a goal INR of 2-3, as

Table 1

LVAD parameters.

Parameter	Device
	HeartWare	HeartMate II	HeartMate III
Flow (L/min) Speed (RPM) Power (W) Pulsatility	4-7 2500-3000 3-7 2-4 L/min flow/time waveform pulsatility from peak to trough	4-8 8600-9800 6-7 4-6	3-6 5000-6000 3-7 1-4

Abbreviations: L/min - liters per minute, RPM - rotations per minute, W - watts.

well as aspirin [19]. Free hemoglobin and haptoglobin can assess for he- molysis. elevated LDH N2.5 times the Upper limit of normal suggests he- molysis, which is most commonly due to pump thrombosis in an LVAD patient [21-23]. Troponin is recommended in patients with new ECG findings, chest pain, or dyspnea. BNP is a sensitive indicator of volume overload in patients with an LVAD and may be elevated in those with new Right heart failure or pump thrombosis or malfunction [4-6,13,14]. Patients should have a controller tag around their waist indicating the type of device, the institution that placed it, and a phone number. Alarms and functional parameters are shown on the external system controller [4-6,9,19]. Pump speed controls flow. Pump power, flow, and speed should be noted, with assessment of alarms and battery. RPMs and pulsatility index must also be evaluated. The pulsatility index depends on the individual patient and device, with an average of flow pulses over 15 s. Hazard alarms indicate poor circulatory sup- port: low flow, pump turn-off or disconnection, low voltage requiring immediate battery replacement or alternate power source, or power

loss [9,19].

Complications

LVAD complications can be categorized via several means. This re- view will divide complications into those specific to the LVAD and those associated with the LVAD (Table 2).

LVAD-specific complications

LVAD-specific complications center on parameters reported on the controller. These parameters provide important information on the po- tential underlying conditions, such as a suction event.

A suction event is a common LVAD complication and is associated with low flow events, including dysrhythmia, hemorrhage, and other hypovolemic states such as diarrhea or vomiting [24,25]. Reduced LV preload results in collapse of the LV and decreased inflow into the LVAD. Low flow, speed, and power will be present on the controller [4-6,19]. While bedside US can demonstrate decreased LV volume, this is often difficult in LVAD patients due to poor acoustic windows, and as- sessment of the LV diameter may assist in evaluating volume status. Treatment requires fluid resuscitation and managing the underlying eti- ology. With improved preload and intravascular volume, pump speed and flow will improve [19].

Continuous-flow LVADs place patients at high risk of thrombosis, which may originate in the pump or the components such as the inflow or outflow cannula [26-28]. However, current generation continuous flow devices are at much lower risk of thrombus formation [26-28]. Risks of thrombus formation include inadequate anticoagulation, infec- tion, atrial fibrillation, and Hypercoagulable states [27,28]. These pa- tients are on chronic anticoagulation, typically with a vitamin K antagonist such as warfarin, and aspirin [9,19]. LVAD thrombosis in the circuit and/or pump may result in increased afterload and low flow and high power alarms on the system controller [4-6]. Types of pump thrombi include acute catastrophic red thrombi entrapped within a fibrin mesh and white thrombi rich in platelets [28]. Red thrombi form at the inlet and outlet areas due to blood stasis, while white thrombi typically form on the pump surface and are associated with turbulent flow [28]. Thrombosis can result in pump dysfunction, hemolysis, em- boli, stroke, and death [26-28], but patients with thrombosis present with a variety of symptoms due to these potential complications, rang- ing from no symptoms to cardiac arrest and death [13,21-23]. Patient

Fig. 3. LVAD controller components (HMIII).

Fig. 4. Chest radiograph of LVAD with ICD. From https://commons.wikimedia.org/wiki/File:Left_ventricular_assist_device_-_56jm_-_Roe_-_001.jpg

presentation may resemble that of massive pulmonary embolism. On examination, evidence of hemolysis may be present with scleral icterus, dark urine, and fatigue. Serum LDH is typically N2.5 times normal. Uri- nalysis may demonstrate hematuria. Other important laboratory assess- ments include hemoglobin, free hemoglobin, haptoglobin, and coagulation panel [21-23,29]. Chest radiograph is needed to assess de- vice location and evaluate for any evidence of pump displacement. Other imaging tests include US and computed tomography (CT) in sta- ble patients [30,31]. US may demonstrate inappropriate unloading, while CT may visualize thrombi [6,22]. The controller will demonstrate high power consumption and increased pump speed, but decreased pump flow [6,21-23]. Emergent consultation is recommended with the LVAD specialist, as anticoagulation with heparin and temporary cir- culatory support should be considered and discussed with the LVAD specialist. Inflow or outflow thrombosis may benefit from endovascular stenting [32-34]. However, severe thrombosis can result in full stoppage of the pump, and stoppage duration that is unknown or lasting over sev- eral minutes requires emergent therapy. Full pump stoppage can also occur during a controller exchange or internal wire short. Thrombolysis may be required if patients are hemodynamically unstable [32,35,36]. Emergent surgical pump exchange may be needed if the pump stops, the patient is unstable, or if alarms are present.

Mechanical failure is the second most common cause of death in LVAD patients and may result from several different issues [4,11,32]. Pump failure is the most important Life-threatening complication re- quiring immediate care. The controller may demonstrate low flow, low voltage, and power loss. A low flow alarm should always be evalu- ated by first checking the power [4-6]. Physicians should auscultate over the LVAD and evaluate for disconnected leads and cannula issues such as kinking or obstruction. A disconnected lead should be reconnected. However, if auscultation reveals no pump activity but all leads are in place, the clinician must assess power and power leads. Complete loss

Table 2

LVAD complications.

LVAD-specific complications LVAD-associated complications

of power should result in the sounding of an alarm, and the physician will be unable to auscultate the motor, blood pressure will be undetect- able, and the power light will be absent. If this occurs or if the low volt- age alarm is present, a substitute power source or replacement battery should be used. Specific alarms can assist the physician in determining the cause of pump failure. For example, a red heart icon may appear on the HMII/HMIII controller with pump stoppage. If all leads are con- nected, the pump can be reset. If a power lead is not connected to the batteries or unit cable, the cable disconnect advisory will alarm and demonstrate a flashing symbol [14,37,38]. Power lead connection will result in discontinuation of the alarm. Clinicians must consider that even a short time of noncirculating flow within the LVAD drastically in- creases the risk of thrombus formation and potential emboli [4-6,14]. If the patient is stable and the device has been off for only several minutes, immediately restarting the device is recommended. However, if the de- vice has been off for over an hour and the patient is stable, consultation with the LVAD specialist is required, as the device should not be imme- diately restarted due to high risk of thromboembolic evets. In the setting of hemodynamic instability, the device should be restarted immediately no matter the duration of stoppage, with continuous anticoagulation. If the clinician and/or LVAD specialist cannot restart the LVAD, pump ex- change is needed, which requires discussion with the LVAD specialist and surgeon. For patients with inadequate perfusion and hemodynamic instability without an alarm activated, resuscitation with IV fluids and standard ACLS protocol is needed.

LVAD-associated complications

Patients with LVAD are at elevated bleeding risk, with one study finding rates of bleeding requiring transfusion to be 1.66 and 1.13 events per patient year in early and mid-trial groups, respectively [39]. Bleeding can occur from several sources: pump connections, grafts in the conduits, and most commonly, mucosal surfaces such as the gastro- intestinal (GI) tract. GI bleeding affects 15-30% of patients with an LVAD [40,41]. Bleeding in the immediate postoperative period is often due to hepatic congestion associated with severe heart failure and the effects of extracorporeal circulation of the bypass machine [40,41]. After the first post-operative week, several different factors contribute to bleeding.

Suction event Pump thrombosis

Pump complications: failure, stoppage, driveline damage

Bleeding

Cerebrovascular pathology: Ischemic or hemorrhagic stroke

Infection: device-related, device-specific, non-LVAD

Right ventricular failure Dysrhythmia

Aortic regurgitation

First, patients are on lifelong anticoagulation using a vitamin K antago- nist with goal INR of 2.0-3.0 as well as aspirin, though patients with prior thrombosis may have a higher goal INR [19,42,43]. Patients also develop the acquired form of von Willebrand factor (vWF) disease due to the high shear stress associated with LVAD circulation resulting in cleavage and deficiency of vWF [43-50]. Bleeding in elderly patients with acquired vWF is more severe [43,50,51]. The continuous device

Table 3

LVAD conditions and complications

Physiological problem

Considerations and differential Evaluation Management

Decreased Preload

Increased Afterload

Hypovolemia (bleeding, dehydration, septic shock), RV failure, device failure (inflow cannula or mechanical obstruction)

- Suction event can occur in this setting

Inability to empty the LVAD chamber: hypertensive event, outflow cannula obstruction (thrombosis/mechanical kink)

US to evaluate RV function and IVC

• Small RV suggests low preload
• Small LV suggests suction event
• Large RV and small LV suggest RV failure
• Large RV and LV suggest pump thrombosis/obstruction

Evaluate with US to evaluate ventricular size and IVC

MAP N90 mmHg impairs the LVAD’s

flow ability

Hypovolemia - Provide IV fluid or blood products if bleeding

RV failure - Provide vasopressors/inotropes, Pulmonary vasodilators

Inflow/mechanical obstruction due to thrombosis - anticoagulate

Reduce blood pressure with vasodilators to MAP b80 mmHg

VAD complications Alarm/notification Considerations Management

Pump failure HMII/III: “Low flow - call hospital contact”;

Red visual signal

HVAD: No auditory or visual alarm Power disruption HMII/III: “Connect power immediately”;

Yellow/red battery icon

HVAD: “Controller fault/failed”, “Change controller”, with loud continuous alarm; Yellow flashing signal

Evaluate connections to battery and the battery itself for appropriate insertion

Evaluate all connections, including

controller-driveline, controller-power supply, and evaluate connections

Emergent LVAD consultation; Reconnect any disconnections and ensure battery is inserted

Emergent LVAD consultation; if connections are intact with charged device, exchange of the device may be required

Driveline damage/electrical fault

HMII/III: “Connect driveline”; Red visual signal

HVAD: “VAD stopped”, “Connect driveline”; No visual alarm

Driveline contains 6 separate wires with redundancy; evaluate all lines for damage

Patient may present in cardiogenic shock

Emergent LVAD specialist consultation; patients with cardiogenic shock require resuscitation with vasopressors and/or inotropes

High flow High flow alarm High flow and normal watts suggest infection/sepsis due to peripheral vasodilation

Closely evaluate for sepsis: Treat with antibiotics, may require surgery consultation

Low flow Low flow alarm: Assess clinical stability and

perfusion status

Evaluate pump function and components; examine for hypovolemia, thrombosis, dysrhythmia (VT/VF)

Evaluate pump and connections Obtain emergent ECG and US

US - Collapsible IVC suggests decreased preload; high RV: LV ratio suggests RV dysfunction

Laboratory assessment with hemoglobin, free hemoglobin, haptoglobin, lactate dehydrogenase, urinalysis

Obtain IV access bilaterally Thrombus may cause low flow alarm

Treat as pump malfunction if mechanical complication associated with LVAD is found

Anticoagulate for thrombosis

Vasopressors and/or inotropes may be needed

Collapsible IVC on US suggests decreased preload and need for IV fluid resuscitation

RV dysfunction may require vasopressors/inotropes, pulmonary vasodilators, and IV fluid resuscitation

Cardiovert for unstable dysrhythmia

Table 3 Abbreviations: LVAD - left ventricular assist device, US - ultrasound, LV - left ventricle, RV - right ventricle, IV - intravenous, ECG - electrocardiogram, VT - ventricular tachycardia, VF - ventricular fibrillation, IVC - inferior vena cava, MAP - mean arterial pressure.

flow and decreased pulse pressure also result in formation of arteriove- nous malformations, especially in the GI tract [40,41].

Resuscitation of patients with significant hemorrhage with LVAD in- cludes product replacement and reversal agent administration. How- ever, reversing anticoagulation should be weighed with the risk of thrombotic complications, and consultation with the LVAD specialist is recommended. Reversal agents include vitamin K, fresh frozen plasma, and prothrombin complex concentrates. A patient with significant GI bleeding typically requires endoscopy to determine the source and pro- vide control of any lesions, and gastroenterology consultation is recom- mended [40,41]. bleeding rates are higher in the upper GI tract, compared to the lower GI tract [51,52]. If Upper endoscopy does not re- veal a source of hemorrhage, colonoscopy is conducted [40,41]. Lesions are typically treated with coagulation or clips. Due to the risk of sensiti- zation and reducing the success of heart transplant, blood product transfusion should not be reflexive in patients who are hemodynami- cally stable [40,41,50-52]. Significant transfusion can also increase afterload and exacerbate underlying heart failure. However,

hemodynamically unstable patients due to bleeding require resuscita- tion with blood products. Leukoreduced and irradiated blood products are recommended if available [50]. Octreotide has demonstrated effi- cacy in LVAD-related GI bleeding in several studies [53-56]. Desmopressin can be provided, which is a Synthetic analogue of vaso- pressin, or infusion of vWF concentrates [50,57]. Discussion of platelet transfusion is needed with the LVAD specialist if the patient is thrombo- cytopenic and bleeding, as well as those with severe hemorrhage.

Ischemic and hemorrhagic stroke can result in poor outcomes and demonstrate a prevalence of 6.8% and 8.4%, respectively [42,58]. The in- cidence in the first several months after placement approximates 8-25% [59-61]. While some of these events are clinically silent and discovered on imaging, Neurologic events can drastically affect quality of life, with increased debility, loss of independence, further requirements for sup- port, and even compromised candidacy for Heart transplantation [61,62]. Stroke is also associated with a 4-18 fold increase in mortality in patients with an LVAD [63]. Patients are at high risk due to thrombus formation with severe heart failure, the greater incidence of atrial

fibrillation, and the presence of a foreign mechanical device [60-63]. High systolic blood pressure, prior stroke, and postoperative infection are the greatest risk factors for a neurologic event [64,65]. A systolic blood pressure N100 mm Hg is associated with over a 2.5-fold higher risk of stroke, with a 19% increase in stroke risk with every 5 mm Hg in- crease in systolic blood pressure [66]. The ENDURANCE trial found a lower stroke rate with MAP b90 mm Hg, with patients receiving close blood pressure control demonstrating a 24.7% reduction in total neuro- logic events and 50% decrease in hemorrhagic stroke rate [67]. Acute is- chemic stroke more commonly affects the right cerebral hemisphere in patients with an LVAD [64,65]. Stroke risk is decreased by targeting a MAP b90 mm Hg, prophylactic daily aspirin 81 mg, and ensuring INR levels remain within 2.0-3.0 [58,68]. Acute hemorrhagic stroke was the leading cause of death in one study, but this is decreasing [6,7,39]. Cerebral hemorrhage requires immediate blood pressure control with avoidance of hypertension; consultation with the LVAD specialist, neu- rology, and neurosurgery; and consideration of reversal of anticoagulation. Surgical intervention may be required. For ischemic stroke, thrombolytic therapy has not been widely studied in LVAD pa- tients, and these patients are at high risk for Hemorrhagic conversion. A multidisciplinary approach with consideration of endovascular ther- apy is recommended [69,70].

Patients with an LVAD are at high risk of sepsis, with rates of infec- tion approaching over 42% in the first year post-implant, usually 2 weeks to 2 months [8,11,19,71]. Infection is the third most common cause of death in patients with LVAD within the first year, and infections also increase the risk of thrombosis, stroke, intracerebral hemorrhage, and GI bleeding [42,71]. First generation pulsatile devices had signifi- cant rates of bacterial and fungal infection, though continuous flow de- vices and improved surgical techniques have decreased the infection rate. LVAD infections include those specific to the device, related to the device, and non-LVAD infections [72]. Device-specific infections are those associated with the device components. The driveline and VAD pump pocket are the most common infectious sites, with 80% of driveline infections occurring in the first 30 days of transplant [71-76]. The exit site is an entry site for bacteria. Infection along this site can range from superficial, involving the exit site only, or involve deeper structures within the pump pocket or pump [71,77]. The system con- troller may demonstrate a high-flow alarm with distributive shock due to loss of vascular tone [78]. LVAD-related infections include those that may occur in patients without an LVAD, but occur with greater fre- quency in LVAD patients such as mediastinitis, endocarditis, and bacter- emia [71]. Non-LVAD infections include pneumonia, Clostridium Difficile infection, and urinary tract infection . Within the first 3 months post implantation, the most common sources of infection typically in- clude catheters, pneumonia, and C. difficile, while later sources of infec- tion are more commonly related to the device [73,78,79]. Only half of patients will demonstrate fever, leukocytosis, or meet criteria for sys- temic inflammatory response syndrome [73]. Some patients will dem- onstrate malaise, pain over the infected site, fever, warmth of the exit site, or drainage from the wound [73,80]. Though a variety of organisms may result in device infection including Gram-negative bacteria and Pseudomonas, staphylococcal species are the most common organisms found on culture [72,75,80-83]. Candidal infection is associated with mortality reaching 90% [83]. Patients may present with systemic symp- toms and severe infection, requiring fluid resuscitation and rapid ad- ministration of broad-spectrum antimicrobials [71,72,80-82]. Laboratory assessment includes blood cultures, complete blood cell count, lactic acid, and inflammatory markers, as well as driveline sam- ples (including bacterial and fungal cultures, Gram stain, potassium hy- droxide) in those with suspected driveline infection. Chest radiograph is also recommended, but Definitive imaging includes CT with contrast to evaluate for deep space infection. central venous access may be re- quired. Fluid resuscitation is needed in patients with severe toxicity due to sepsis, and except for those with severe right ventricular failure, volume overloading is unlikely. Antibiotics should include coverage for

gram-positive and gram-negative species, as well as methicillin- resistant S. aureus. Discussion with the LVAD specialist and cardiotho- racic surgery is recommended [71-74,80]. Deep infections typically re- quire Surgical debridement, while persistent bacteremia may require removal and implantation of a new device [71-74,80].

RV failure is a major cause of morbidity and mortality, occurring in 15-40% of patients [4-6,19]. Late onset right heart failure is increasingly being reported with RV dysfunction, ventricular dysrhythmias, pulmo- nary hypertension, tricuspid regurgitation, and device thrombosis or malfunction [84]. This can result in reduced preload to the LV, decreas- ing LVAD flows and triggering a low-flow alarm. RV failure may result in elevated liver function tests, creatinine, and lactic acid. RV failure re- quires inotropes and/or vasopressors, pulmonary vasodilators, and LVAD specialist consultation [6]. Patients may require careful fluid re- suscitation, with 250 mL boluses.

Dysrhythmia can be a significant cause of morbidity and mortality, with 10 episodes for every 100 LVAD patient months in the first 3 months after placement, though this deceases after this period [19]. Patients may tolerate severe ventricular dysrhythmias with minimal symptoms due to the LVAD producing adequate cardiac output to meet end organ perfusion [13,85-90]. Etiologies for dysrhythmia in- clude ischemia, RV failure, electrolyte abnormalities, and electrophysio- logic changes after implantation [5,6,85-87]. The greatest risk of ventricular dysrhythmia after LVAD implantation is ventricular dys- rhythmia before device placement. Primary dysrhythmias are due to pa- tient intrinsic cardiac physiology, while secondary dysrhythmias are associated with the LVAD [85-87]. The most common secondary causes of dysrhythmia are hypovolemia and poor venous return. Patients often have an ICD prior to LVAD placement. Dysrhythmias may eventually re- sult in compromised blood flow and can also contribute to RV dysfunc- tion, suction events, thrombus formation, and poor perfusion [14,87,91- 93]. The controller will demonstrate low flow in patients with hypoten- sion due to the dysrhythmia [14,87,91-93]. If an ICD is not in place, ad- vanced cardiac lifesaving interventions are required with electrical and/ or chemical therapy. Consultation with the LVAD specialist is also im- perative. With this risk of dysrhythmia, ECG is an integral component of ED evaluation, as well as electrolyte assessment. If hemodynamically unstable, electrical cardioversion is recommended. If the patient is sta- ble with dysrhythmia, fluid resuscitation is recommended with bedside US. Primary dysrhythmias can be managed with antiarrhythmics, though this should be discussed with the LVAD specialist. Patients with an ICD may have received a shock [14,87,91-93]. Physicians should determine if this shock was appropriate or inappropriate [14,87,91]. If the shock was appropriate, evaluation for ischemia and RV dysfunction is needed.

Aortic regurgitation (AR) may develop de novo in up to 25% of pa-

tients after LVAD placement [84,94-96]. AR more commonly occurs in patients with a closed aortic valve compared to patients in whom the valve frequently opens [84,94-96]. AR results in decreased LVAD efficacy and may require modifications in pump speed, managed by the LVAD specialist. Patients may require aortic valve replacement.

Resuscitation

Standard procedures for resuscitation are recommended as needed. Hypotension in LVAD patients is defined by MAP b60 mm Hg [4- 6,13,14]. Patients who are conscious should be assessed with history and examination, with close assessment of volume and perfusion status. ECG and bedside echocardiogram are vital components of the assess- ment, with analysis of LVAD components.

Patients who are unresponsive and hypotensive require external chest compressions. Prior recommendations discouraged chest com- pressions due to fear of dislodging the LVAD. However, literature sug- gests no cases of dislodgement during cardiopulmonary resuscitation (CPR) [17,18,97]. If the patient has a MAP N50 mm Hg or end tidal CO2 N20 mm Hg with a device possessing an audible hum, perfusion is likely adequate, and compressions are not necessary [17,18,97]. A

MAP b50 mm Hg without an audible hum in the unresponsive patient is associated with compromised perfusion and requires chest compres- sions at the same depth and frequency as in those without an LVAD [4-6,13,14]. Defibrillation should be performed for unstable ventricular dysrhythmia. The pads should be placed distant from the pump, and if an ICD is present, the pads should not be placed directly over the ICD [4-6,13,14]. In patients with adequate perfusion and respiration but who remain unconscious, evaluate for hypoglycemia, stroke, hypoxia, sedation, and coma.

Chest thoracostomy with chest tube placement in the setting of trauma with pneumothorax and/or hemothorax is recommended, but clinicians must avoid the driveline [4,5]. Arterial line placement can be beneficial, and US guidance is recommended. Pericardiocentesis should be avoided due to risk of serious device complications, but it is recom- mended in the case of Pericardial tamponade with hemodynamic com- promise [4-6].

1. Conclusions

An LVAD is a potentially life-saving device in patients with end stage heart failure. Most current LVAD devices provide continuous flow. While LVAD patients may present to the ED with complaints unrelated to their devices, there are many complications that are related to the LVAD, and emergency physicians should be familiar with these compli- cations. These include LVAD-associated complications and LVAD- specific complications. Assessment of LVAD function, patient perfusion, and MAP is needed upon presentation. LVAD evaluation and manage- ment require a team-based approach, and consultation with the LVAD specialist is recommended.

Conflicts of interest

None.

Acknowledgements

This manuscript did not utilize any grants, did not use funding, and has not been presented in abstract form. This clinical review has not been published, it is not under consideration for publication elsewhere, its publication is approved by all authors and tacitly or explicitly by the responsible authorities where the work was carried out, and that, if ac- cepted, it will not be published elsewhere in the same form, in English or in any other language, including electronically without the written consent of the copyright-holder. This review does not reflect the views or opinions of the U.S. government, Department of Defense, Brooke Army Medical Center, U.S. Army, U.S. Air Force, or SAUSHEC EM Resi- dency Program.

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