This is a nice little review by Dr. Long in Dallas entitled:
B. Long, J. Robertson, A. Koyfman, et al., Left ventricular assist devices and their complications: A review for emergency clinicians, American Journal of Emergency Medicine, https://doi.org/10.1016/j.ajem.2019.04.050
A ventricular assist device (VAD) can be placed into the right, left, or both ventricles thus the patient can have a right ventricular assist device, left ventricular assist device, or biventricular assist device. The goals of these devices include three different strategies: bridge to recovery, bridge to transplantation, or destination therapy (i.e., the patient is unlikely to recover and not a candidate for cardiac transplant). Contraindications to placement include metastatic cancer, irreversible renal/hepatic failure, and CVA with severe neurologic deﬁcits. The LVAD has two basic designs which produce different patterns of perfusion, including the pulsatile and continuous-ﬂow devices. More commonly these days are the non-pulsatile continuous flow devices.
The continuous-ﬂow LVAD has several basic parts including: the internal pump an external power source, and a control unit.The speciﬁc components 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 (LV), 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 (HeartMate) 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,
The percutaneous driveline provides a conduit for the electrical wiring, 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 abdominal area to connect to the controller. Thus, it is a frequent source of infection in the LVAD patient. The controller performs multiple functions and contains several important components. It controls LVAD functioning, including power source monitoring and regulation, overall system monitoring, data collection, and alarm system function. subcutaneously from the pump and exits the skin in the anterior abdominal area to connect to the controller. Thus, it is a frequent source of infection in the LVAD patient.
HISTORY AND EXAM:
A continuous ﬂow LVAD will not typically produce a palpable pulse on its own, but patients may have enough native ventricular function to produce pulsatile ﬂow and a pulse. A palpable pressure may also be due to pump thrombosis, and thus, it is important to determine if the patient has a palpable pulse at baseline. 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). 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. If this is unobtainable, an arterial line may be required, which is the most accurate device for monitoring MAP. Invasive arterial monitoring will demonstrate minimal pulse pressure or ﬂat arterial waveform. 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.
LVADs, especially those with continuous-ﬂow, are sensitive to afterload and preload. Guidelines recommend maintaining a MAP of 70–90 mm Hg. Acute hypertensive adverse event is associated with MAP N110 mm Hg in patients with continuous ﬂow pumps. The mechanical hum indicates device power and function. Signs of volume overload (extremity edema, ascites, elevated jugular venous pressure) can be due to subacute or chronic right ventricular failure. However, acute dyspnea, pulmonary edema, or hypotension are more commonly due to acute malfunction of the device, such as cannula obstruction or pump thrombosis. The device exit site, which is normally covered with a sterile dressing, and line should be examined with sterile gloves and mask for warmth, erythema, and discharge, which suggest infection. Finally, the patient should be asked if he/she brought the back-up battery and back-up controller. Sustained ventricular dysrhythmias may be due to underlying cardiomyopathy or decompressed left ventricle due to elevated pump speed or right ventricular failure. Patients with an LVAD will typically demonstrate normal sinus rhythm.
Chest radiograph provides important diagnostic information including position and the type of LVAD, as well as the presence or absence of an ICD or pacemaker. Deep space infection of the LVAD components requires assessment with computed tomography (CT). Sustained ventricular dysrhythmias may be due to underlying cardiomyopathy or decompressed left ventricle due to elevated pump speed or right ventricular failure. Patients with an LVAD will typically demonstrate normal sinus rhythm.
Echocardiogram can evaluate cardiac function and assess for complications such as regurgitation, right ventricular failure, and thrombus formation, though thrombi can be difﬁcult to detect on ultrasound alone. Key components of the assessment include valvular function, inﬂow/outﬂow abnormalities, ventricular size and function, and septal position.
Laboratory assessment includes hemoglobin/hematocrit, lactate dehydrogenase (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 well as aspirin. Free hemoglobin and haptoglobin can assess for hemolysis. Elevated LDH >2.5 times the upper limit of normal suggests hemolysis, which is most commonly due to pump thrombosis in an LVAD patient. 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.
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. 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.
LVAD specific complications:
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. 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. While bedside US can demonstrate decreased LV volume, this is often difﬁcult in LVAD patients due to poor acoustic windows, and assessment of the LV diameter may assist in evaluating volume status. Treatment requires ﬂuid resuscitation and managing the underlying etiology. With improved preload and intravascular volume, pump speed and ﬂow will improve.
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. Types of pump thrombi include acute catastrophic red thrombi entrapped within a ﬁbrin mesh and white thrombi rich in platelets. 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. Thrombosis can result in pump dysfunction, hemolysis, emboli, stroke, and death, but patients with thrombosis present with a variety of symptoms due to these potential complications, ranging from no symptoms to cardiac arrest and death. On examination, evidence of hemolysis may be present with scleral icterus, dark urine, and fatigue. Serum LDH is typically >2.5 times normal. Urinalysis may demonstrate hematuria. Other important laboratory assessments include hemoglobin, free hemoglobin, haptoglobin, and coagulation panel. Thrombolysis may be required if patients are hemodynamically unstable. 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. Pump failure is the most important life-threatening complication requiring immediate care. The controller may demonstrate low ﬂow, low voltage, and power loss. A low ﬂow alarm should always be evaluated by ﬁrst checking the power. 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. If all leads are connected, 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. However, if the device 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 immediately restarted due to high risk of thromboembolic events. 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 exchange 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.
Patients with LVAD are at elevated bleeding risk. Bleeding can occur from several sources: pump connections, grafts in the conduits, and most commonly, mucosal surfaces such as the gastrointestinal (GI) tract. GI bleeding affects 15–30% of patients with an LVAD. 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. Patients may also develop an 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. Bleeding in elderly patients with acquired vWF is more severe. Resuscitation of patients with signiﬁcant hemorrhage with LVAD includes product replacement and reversal agent administration. However, reversing anticoagulation should be weighed with the risk of thrombotic complications, and consultation with the LVAD. Lesions are typically treated with coagulation or clips. Due to the risk of sensitization and reducing the success of heart transplant, blood product transfusion should not be reﬂexive in patients who are hemodynamically hemodynamically stable. Leukoreduced and irradiated blood products are recommended if available. Octreotide has demonstrated efﬁcacy in LVAD-related GI bleeding in several studies. Desmopressin can be provided, which is a synthetic analogue of vasopressin, or infusion of vWF concentrates. Discussion of platelet transfusion is needed with the LVAD specialist if the patient is thrombocytopenic 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. There is an increased risk with every 5 mm Hg increase in systolic blood pressure. The ENDURANCE trial found a lower stroke rate with MAP 90 mm Hg, with patients receiving close blood pressure control demonstrating a 24.7% reduction in total neurologic events and 50% decrease in hemorrhagic stroke rate. Acute ischemic stroke more commonly affects the right cerebral hemisphere in patients with an LVAD.
Patients with an LVAD are at high risk of sepsis, with rates of infection approaching over 42% in the ﬁrst year post-implant, usually 2 weeks to 2 months. 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. The system controller may demonstrate a high-ﬂow alarm with distributive shock due to loss of vascular tone. LVAD-related infections include those that may occur in patients without an LVAD, but occur with greater frequency in LVAD patients such as mediastinitis, endocarditis, and bacteremia. Non-LVAD infections include pneumonia, Clostridium difﬁcile infection, and urinary tract infection (UTI). Within the ﬁrst 3 months post implantation, the most common sources of infection typically include catheters, pneumonia, and C. difﬁcile, while later sources of infection are more commonly related to the device. Only half of patients will demonstrate fever, leukocytosis, or meet criteria for systemic inﬂammatory response syndrome. Discussion with the LVAD specialist and cardiothoracic surgery is recommended. Deep infections typically require surgical debridement, while persistent bacteremia may require removal and implantation of a new device.
RV failure is a major cause of morbidity and mortality, occurring in 15–40% of patients. Late onset right heart failure is increasingly being reported with RV dysfunction, ventricular dysrhythmias, pulmonary hypertension, tricuspid regurgitation, and device thrombosis or malfunction. This can result in reduced preload to the LV, decreasing LVAD ﬂows and triggering a low-ﬂow alarm. RV failure may result in elevated liver function tests, creatinine, and lactic acid. RV failure requires inotropes and/or vasopressors, pulmonary vasodilators, and LVAD specialist consultation. Patients may require careful ﬂuid resuscitation, with 250 mL boluses.
Patients may tolerate severe ventricular dysrhythmias with minimal symptoms due to the LVAD producing adequate cardiac output to meet end organ perfusion despite poor venous return. Patients often have an ICD prior to LVAD placement. Dysrhythmias may eventually result in compromised blood ﬂow and can also contribute to RV dysfunction, suction events, thrombus formation, and poor perfusion. The controller will demonstrate low ﬂow in patients with hypotension due to the dysrhythmia.
Aortic regurgitation (AR) may develop de novo in up to 25% of patients after LVAD placement. AR more commonly occurs in patients with a closed aortic valve compared to patients in whom the valve frequently opens. AR results in decreased LVAD efﬁcacy and may require modiﬁcations in pump speed, managed by the LVAD specialist. Patients may require aortic valve replacement.
Standard procedures for resuscitation are recommended as needed. Hypotension in LVAD patients is deﬁned by MAP <60 mm Hg. 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 assessment, with analysis of LVAD components. Patients who are unresponsive and hypotensive require external chest compressions. Literature suggests no cases of dislodgement during cardiopulmonary resuscitation (CPR). If the patient has a MAP N<50 mm Hg or end tidal CO2 <20 mm Hg with a device possessing an audible hum, perfusion is likely adequate, and compressions are not necessary MAP <50 mm Hg without an audible hum in the unresponsive patient is associated with compromised perfusion and requires chest compressions at the same depth and frequency as in those without an LVAD. 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. 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. 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 recommended in the case of pericardial tamponade with hemodynamic compromise.