Accepted Manuscript Anesthetic Management of the Patient with a Ventricular Assist Device Marie-Louise Meng, MD, Jessica Spellman, MD
PII:
S1521-6896(17)30040-X
DOI:
10.1016/j.bpa.2017.06.004
Reference:
YBEAN 947
To appear in:
Best Practice & Research Clinical Anaesthesiology
Received Date: 25 April 2017 Revised Date:
12 June 2017
Accepted Date: 19 June 2017
Please cite this article as: Meng M-L, Spellman J, Anesthetic Management of the Patient with a Ventricular Assist Device, Best Practice & Research Clinical Anaesthesiology (2017), doi: 10.1016/ j.bpa.2017.06.004. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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Jessica Spellman, MD Columbia University Medical Center 622 W 168th Street, PH5 New York, NY 10032 Email:
[email protected] Phone (212) 342-2210 Fax (212) 342-2211
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Marie-Louise Meng, MD (Corresponding Author) Columbia University Medical Center 622 W 168th Street, PH5 New York, NY 10032 Email:
[email protected] Phone (212) 342-2210 Fax(212) 342-2211
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Anesthetic Management of the Patient with a Ventricular Assist Device
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Abstract: The use of long-term and short-term mechanical circulatory support in the form of ventricular assist device (VAD) has increased over the last decade. While
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cardiothoracic anesthesiologists care for these patients during device placement, increasingly higher numbers of general anesthesiologists are involved in the
management of VAD patients during non-cardiac surgery and procedures. An
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understanding of devices, their indications and complications is essential to the
anesthesiologist caring for these patients. We review the anesthetic considerations
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for the implantation of these devices, as well as concerns when caring for patients with durable and short-term devices already in place.
Keywords:
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Left ventricular assist device, heart failure, anesthetic care, non-cardiac surgery, transesophageal echocardiography, mechanical circulatory support, right
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Words: 6735
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ventricular assist device
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Ventricular Assist Devices 1. Indications for ventricular assist devices Mechanical circulatory support (MCS) in the form of ventricular assist devices
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(VAD) can be employed for cases of acute or chronic cardiopulmonary failure.
Conditions where MCS is employed include: cardiomyopathies, post-myocardial
graft failure following heart transplantation.
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infarction cardiogenic shock, myocarditis, post-cardiotomy stunning, and primary
The Interagency Registry for Mechanical Circulatory Support (INTERMACS) is a
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collaboration between hospitals, industry and the National Heart, Lung and Blood Institute that collects data on over 15,000 patients who have undergone long term Federal Drug Administration (FDA) approved continuous flow ventricular assist device placement. INTERMACS defines seven profiles for acute and chronic heart
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failure for MCS insertion, ranging from acute critical shock to stable New York Heart Association (NYHA) III heart failure, and timeline for insertion (Table 1). [1, 2]
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Table 1: Interagency Registry for Mechanically Assisted Circulatory Support
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(INTERMACS) Levels [1-3]
Use of MCS can be described in terms of bridge or destination therapy. Bridge therapy includes: bridge to recovery (BTR) if the myocardium is expected to recover, a bridge to a bridge (BTB) or bridge to a decision (BTD) in cases where extracorporeal support is placed as a rescue or more time is needed to decide
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definitive therapy, a bridge to transplant (BTT) or bridge to improve candidacy [1] for transplantation, or as destination therapy (DT). [4] Destination therapy is permanent therapy for individuals not considered candidates for heart
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transplantation and is progressively increasing as a designation for VAD
implantation, now representing over 38% of implants in the most recent
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INTERMACS report. [1, 4]
2. Device classification
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VADs can be categorized by duration of intended support (short-term or long-term), pump flow type (pulsatile or continuous), engineering design (first, second, or third generation), which ventricle the device can support (left, right or biventricular support), and FDA approved indications. Table 2 outlines established and
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investigational devices that, in the experience of the authors and based on literature reviews [5-12], are currently being implanted in larger numbers. Only the most
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salient points about the design and function of these devices are noted in the table.
Pulsatile VADs are first-generation and use volume displacement. First generation LVADs are loud, large, and require placement in a subdiaphragmatic pocket. This pocket can be a nidus for infection and bleeding after implantation. Second generation devices were developed addressing these issues, offering simpler, smaller, quieter designs that are associated with fewer cerebral vascular events and
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less device malfunction than pulsatile flow devices. Hence, first generation devices are no longer in use. [4, 13]
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Continuous flow devices are either second or third generation as distinguished by bearing design, which can be contact or noncontact. This determines the device
support, movement, friction and heat created. Second generation devices employ
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contact-bearing design and axial pattern of blood flow. [13]
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Sometimes referred to as “bearing-less,” third generation devices employ noncontact-bearing design, which utilizes magnetic and hydrodynamic levitation to suspend the device impeller and a centrifugal flow path of blood, with the exception of the Incor (Berlin Heart GmbH, Berlin, Germany), which employs axial blood flow
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design. Perceived benefits of centrifugal pumps include greater sensitivity of pressure-flow relationship, resulting in greater changes in pump flow for changes in
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pressure across the pump, and increased reliability of estimated flow. [13]
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3. Anesthetic Management of Long-Term Device Placement A. Preoperative assessment Pre-operative evaluation of all organ systems should be performed. The extent of ischemia, valvular abnormalities, arrhythmias and right heart function should be noted. Right heart catheterization data should be reviewed. Neurological deficits should be noted. Pulmonary function tests, if available, and chest radiography should be reviewed. Electrolyte abnormalities secondary to renal dysfunction and
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use of diuretics should be corrected pre-operatively. Coagulation laboratories should be evaluated in light of intentional medical anticoagulation and hepatic dysfunction from congestive hepatopathy. Patients should be screened for absolute
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and relative contraindications to intraoperative use of transesophageal echocardiography (TEE). [14]
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B. Induction
Prior to induction of anesthesia, routine noninvasive monitoring and invasive
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arterial blood pressure monitoring should be established to allow for beat-to-beat blood pressure monitoring. External defibrillator pads should be placed on the patient. Slow induction of anesthesia should be performed with agents that are
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routinely used for inducing patients in heart failure.
C. Anesthetic considerations in heart failure pre-device implantation The heart failure patient will have alterations in neuroendocrine systems (renin–
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angiotensin–aldosterone system, natriuretic system, and sympathetic nervous
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system) and may be on agents to compensate for these alterations. Heart failure patients may present to the operating room grossly volume overloaded or adequately diuresed and perhaps hypovolemic. Trendelenburg position can be utilized for a gross assessment of volume responsiveness, keeping in mind that a failing heart may not tolerate an acute increase in preload.
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Medical management including inotropic and hemodynamic support may already be initiated in patients with heart failure. Milrinone is often used in patients with nonischemic cardiomyopathy to improve systolic function, decrease afterload and
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improve diuresis. [15, 16] Hypotension and arrhythmias can occur with milrinone. [17] The anesthesiologist should continue this support in the operating room,
monitor and be prepared to increase or add additional agents as some patients may
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not be able to tolerate the decrease in systemic vascular resistance (SVR) that
accompanies many anesthetic agents. Careful titration of anesthetic agents, or
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consideration of use of anesthetic agents with greater hemodynamic stability is advised.
Patients in heart failure are on the plateau portion of the Frank-Starling preload-
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cardiac output curve and may not be able to mount an increase in stroke volume in response to increased preload. Therefore, if an increase in cardiac output is desired, consider increasing the heart rate. Increases in heart rate come at the cost of
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decreased time in diastole for ventricular relaxation, coronary perfusion, and
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ventricular filling. If high dose opioid techniques are used, the resulting bradycardia may need to be counteracted by positive chronotropic medications to maintain cardiac output.
Patients may not tolerate further increase in pulmonary vascular resistance (PVR) that may accompany periods of hypoventilation. PVR may already be increased due to elevated pressures from a failing left heart, and further increase in PVR may cause
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acute or worsened right heart failure. Ventilation is therefore recommended throughout induction. Should aspiration be a concern, a modified rapid sequence
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with intermittent ventilation and cricoid pressure may be considered. [18]
D. Invasive Monitoring
Following induction of anesthesia, central venous access should be established.
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Pulmonary artery catheters may be useful in the post-operative period to monitor both left and right heart pressures, cardiac output, and allow mixed-venous
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saturation sampling. It is prudent to replace existing catheters with new catheters so as to minimize sources of infection during new device placement.
E. Antibiotic prophylaxis
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Prior to surgical incision, prophylactic antibiotics should be administered. The choice of antibiotics will vary between institutions. Staphylococci and Pseudomonas species are the main bacteria implicated in VAD infections. [19] Evidence supports
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the use of a beta-lactam first generation cephalosporin and vancomycin in hospitals
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where Methicillin-resistant Staohyoccoccus aureus (MRSA) rates are high. Some centers include Fluoroquinolones for additional gram-positive coverage. Anti-fungal prophylaxis can be used in patients at risk of fungal infections or in patients where the closure of the chest following VAD insertion is temporarily deferred. [19]
F. Autologous blood
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Sequestration of autologous blood in patient-labeled citrate-phosphate-dextrose (CPD) bags for re-infusion after cardiopulmonary bypass (CPB) can be considered if preoperative hematocrit is at an appropriate level. This process is similar to acute
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normovolemic hemodilution, which is used by some centers in cardiac surgery, without the infusion of crystalloid to maintain normovolemia. In the severely volume overloaded heart failure patient, this approach may help resolve
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hypervolemia and re-establish euvolemia. [20] Removal of autologous blood (500 ml - 1 liter) is usually well tolerated or may improve hemodynamics pre-bypass.
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Autologous blood can be kept at room temperature (22-25C) and periodically agitated to prevent platelet aggregation and preserve platelet function. Autologous blood should be re-infused into the patient within 4-8 hours of removal. After 8 hours the blood should be stored at 1-6° Celsius for up to 24 hours, and re-infused.
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It is not recommended to store autologous blood longer due to the risk of infection. Although perceived benefits of improved volume state and possible reduction of allogenic red blood cell and blood factor transfusion, this practice has not been
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formally studied VAD populations.
G. Pre-implantation TEE exam A comprehensive perioperative TEE exam should be performed pre and post VAD insertion. Inspection for intracardiac shunts, specifically patent foramen ovale (PFO), should be performed, because once the device is in place and left sided heart pressures are reduced, right to left shunting can result in systemic delivery of hypoxic blood and paradoxical emboli. If identified, shunts may be closed at the time
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of device insertion. It may be challenging to identify a PFO in the setting of elevated left heart pressures. Saline contrast study with a ventilator induced Valsalva maneuver is recommended. The examiner should look for thrombus in the cardiac
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chambers, particularly the left ventricular (LV) apex. Native and prosthetic valvular function should be assessed. Mitral stenosis is of particular concern as it may
prevent LV and device filling. Aortic insufficiency (AI) will result in recirculation of
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flow through the device and decreased flow to the systemic circulation. Both a failing LV, with increased end-diastolic pressure, and decreased SVR under
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anesthesia, may mask the severity of AI, resulting in higher degrees of AI once the device is activated. The aortic valve may be sutured closed should severe AI be present. The ascending aorta should be examined for significant calcification at the intended site of VAD outflow cannula placement. The right ventricle (RV) function
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and tricuspid regurgitation must be assessed, as patients with borderline RV function are at a high risk of RV failure post-implantation. [21, 22] (Table 3).
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Table 3: TEE Checklist for LVAD insertion
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This is a checklist for the echocardiographer performing the pre and post device implantation TEE. [21]
H. Device implantation Implantation of durable LVADs is most often performed utilizing median sternotomy and CPB. If no valvular, septal or other anatomic abnormalities require repair, LVADs can usually be placed without arresting the heart. As technology has
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evolved and some devices have become smaller, experience has been gained with minimally invasive surgical approaches, avoiding sternotomy, utilizing peripheral CPB or avoiding CPB altogether. It is desirable to avoid sternotomy in patients with
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adhesions from previous surgery or in patients likely to have re-operations. [23] Theoretical benefits of performing an implantation without CBP include less
vasodilation, infection, coagulopathy and RV failure after separation from bypass.
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[24, 25] Minimally invasive approaches capitalize on anastomosing the VAD outflow cannula to the innominate artery, the subclavian artery, or the descending aorta, via
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left or right clavicular incisions, left or bilateral anterior thoracotomies, or ministernotomy approaches. [23, 26] Pump pockets can be created through anterolateral thoracotomy, left lateral mini-thoracotomy, bilateral thoracotomy incisions, or left subcostal incision. [23] If a minimally invasive strategy is employed, lung isolation
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may be required for surgical access. [24]
Heparinization and antifibrinolytic agents for the device insertion will vary
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depending on whether CBP is used. When CPB is not used, partial heparinization for
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device placement can be employed, with a goal activated clotting time (ACT) of 250 seconds to prevent thrombosis during clamping of access vessels.
To place the LVAD inflow cannula or device, the surgeons locate the LV apex by palpation. The midesophageal 4-chamber or 2-chamber views can be used for TEE confirmation during minimally invasive approaches. When the inflow cannula is inserted the patient should be placed in the Trendelenburg position to prevent air
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entrainment and rapid ventricular pacing via epicardial leads to 180 beats/minute can be used to decompress the LV. Hypotension and ventricular fibrillation can persist after rapid pacing and may need to be treated. The outflow graft can be
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placed via a side-binding clamp on the target vessel. The echocardiographer should ensure that the heart is free of air as the surgeon completes the de-airing process of the device with progressive clamping of the device from inflow to outflow. [27] Air
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usually collects along the atrial or ventricular septum, LV apex and in the pulmonary
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veins but the aorta and the inflow and outflow grafts should be checked for air. [21]
To initiate the device, revolutions per minute (RPM) are increased gradually while myocardial function, hemodynamics and echocardiographic parameters (discussed below) are followed closely. If RV failure is expected to occur, the device can be
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initiated while on CPB to support the RV. In order to allow full flow through the device, CPB must be fully weaned. Temporary hemodynamic support may be
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transition.
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required in the form of bolus vasopressor or inotrope agents to allow for this
I. Post-implantation assessment of RV function Careful attention should be placed on assessing the RV function during weaning, which includes TEE (See Table 3) and hemodynamic monitoring as well as visual inspection in the surgical field. The function of the RV is dependent on preload, afterload and contractility, all of which can be altered by device placement. With initiation of the device, RV preload will be increased and afterload may be reduced
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or remain the same. A dysfunctional RV may not be able to compensate for these changes and failure may occur. The interventricular septum may bow to the left, impairing the septal contribution to RV contractility requiring the RV free wall to
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compensate in function, which can result in RV exhaustion. [28] The function of an already incompetent tricuspid valve can be worsened if the tricuspid annulus dilates with increase in preload or if the septal leaflet of the tricuspid valve becomes
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tethered by changes in interventricular septal architecture post LVAD implantation. [28] Despite mixed outcomes; a severely incompetent tricuspid valve can be
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augmented with a ring, or replaced. [29]
The RV can be supported with inotrope infusions such as milrinone, afterload reduction in the form inhaled pulmonary dilators such as nitric oxide or iloprost (a
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synthetic PGI2 analog), and preload optimization. To minimize PVR, hypoxia, hypercarbia and acidosis should be avoided. [28] An RV may be able to compensate for a brief period of time in the operating room after device insertion, and fail
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several hours later in the intensive care unit (ICU). If supportive measures do not
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improve RV function, ECMO or a RV assist device may be inserted. [30]
J. Post-implantation coagulopathy Once the device is in place and the patient has been separated from CPB, protamine is given to reverse the effects of heparin. Transfusion of fresh frozen plasma, cryoprecipitate and platelets may be needed to reverse coagulopathy. Bearing in mind the risk of thrombotic complications, the safe use of prothombin complex
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concentrate, which can replace clotting factors in a smaller volume than FFP, has been reported. [31] Thromboelastography (TEG), or rotational thromboelastometry
K. Post-implantation intraoperative TEE
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(ROTEM) can be used for real time assessment of coagulation deficits.
The echocardiographer should examine blood flow at the inflow and outflow
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cannulas using spectral and color Doppler to verify laminar low velocity flow (flow should be <2.0 m/s, ideally <1.5 m/s). Examination of the aorta for dissection at the
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site of cannulation is imperative. Aortic valve function, frequency of opening and insufficiency should be assessed. It is possible that AI can be unmasked after the device decompresses the LV, creating a pressure gradient favorable to reveal AI. [21] Adequate decompression of the LV and septal wall position should be noted. A
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midline septum indicates optimal device and myocardial function. A septum shifted to the left could be a sign of excessive LV decompression due to high device speed or RV failure leading to incomplete filling of the LV. Septal shift to the right signifies
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incomplete LV emptying which may be due to inflow cannula obstruction or
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inadequate device function. RV function should be examined. [22] TEE should again verify absence of intracardiac shunts and thrombus. (See Table 3)
L. Post-device implantation Transportation of patients with devices to and from the operating room requires multiple team members. Pulse oximetry, ECG, arterial pressure monitoring and backup power supply should be available on transport. Care should be taken to
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prevent device dislodgement if there are any external components (peripherally inserted RV support, ECMO, or as in the case with short term devices).
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Patients with newly implanted LVADs should be transferred to an ICU intubated and sedated. Once hemodynamic, pulmonary and coagulation parameters have
stabilized, sedation can be weaned and patients extubated. ICU length of stays can
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be shorter in patients with well functioning RVs, and those who did not require CPB
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for VAD implantation.
4. Understanding VAD parameters
Speed, power, flow and pulsatility are parameters that vary between devices. Though every patient's clinical situation must be evaluated individually, key VAD
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concepts help the anesthesiologist to understand acute events. Echocardiography can be invaluable in the diagnosis of device dysfunction. [21]
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Pump speed is the revolutions per minute (RPM) of the impeller and is a parameter
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that is set. At low pump speeds, there is a low flow state and an increased risk of thrombosis. At high pump speeds, suction events may occur (see below). Power is directly measured as the watts needed to drive the pump at a set speed. There is a direct relationship between power and flow. An increase or decrease in one results in a proportional change in the other. Sustained elevations in power can be seen when device thrombosis develops. Low power can be due to occlusion of either the device inflow or outflow, or low device preload.
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Device flow does not equal cardiac output as it does not take into account any native output of the ventricles or any regurgitant flow. Flow in two commonly inserted
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devices, HeartMate II and HeartWare, is preload and afterload dependent. Low flows may be due to low LV preload to the device (hypovolemia, bleeding, RV dysfunction, tamponade, arrhythmias or a suction event). Typically high flow may be the result of
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sepsis or vasodilation, or it may be erroneously high if there is a device thrombosis. Increases in SVR increase the pressure differential across the HeartMate II or
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HeartWare pumps, and, consequently, decrease flow.
Pulsatility or pulsatility index (PI) is a unitless measure that reflects the stroke volume added by the native ventricle to flow through the device. PI depends on
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ventricular preload, myocardial function, afterload and device output. PI can increase with high preload, recovery of myocardial function and increased afterload, and can decrease with inadequate LV preload and increased device output. PI for
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the HeartMate II ideally should be 4.0-6.0, and serves as an indirect indicator of
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ventricular volume. For the HeartWare, pulsatility is visually assessed by the peaks and nadirs of the flow waveforms on the display.
A ‘suction event’ occurs when a portion of the LV myocardium contacts and obstructs VAD inflow, resulting in decreased flow, and is associated with low pulsatility. The LVAD pump will detect a sudden decrease in flow and alarm. Echocardiographic evaluation during a suction event will reveal decreased LV
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chamber size. Depending on the cause and severity, it may show right-to-left interventricular septal shift, inflow cannula abutting the endocardium and with offaxis appearance, or increased inflow peak velocity if partial obstruction is present.
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[21] Due to the negative pressure gradient created between the LV and the left
atrium, the mitral valve leaflets may be in a fixed open position. [32] Suction events can result from high pumps speeds reducing LV chamber dimensions, and
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presenting increased preload to a tenuous RV. After device implantation, a suction
event that occurs despite low pump flows may represent a failing RV that is unable
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to pump preload forward to the LV. [33] Treatment would be decreasing pump speed, supporting a failing RV, or addressing the primary reason for decreased preload to the device.
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The monitor of the CentriMag displays the pump speed and flow that is directly measured from a flow probe on the cannula. Flow in the CentriMag is affected by pump speed, differential pressure across the pump, afterload and preload.
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Inadequate preload, excessive pump speed, or return of ventricular activity
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reducing preload to the device, will result in "chattering", which is a low frequency jerking movement of the cannulas. Chattering can usually be treated by correcting hypovolemia or decreasing pump speed. The pulmonary or systemic arterial tracing pulsatility, respectively, can be used to determine if RV or LV function is improving.
5. Following Device Insertion
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Life expectancy in patients with continuous flow devices has improved over the last 5 years with 1 and 2-year life expectancy now being 80% and 70%, respectively. [1] Causes of mortality in the first months after device implantation are multisystem
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organ failure, neurologic injury and right heart failure. The causes of late mortality include multisystem organ failure, neurologic injury and infection. [1]
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Neurologic injury in VAD patients is a concern. A prospective study of 402 LVAD
patients (HeartMate II and HeartWare) demonstrated a stroke rate of approximately
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17%, with equal prevalence of ischemic and hemorrhagic strokes. Modifiable risk factors identified were tobacco use, pump thrombosis, pump infection, bacteremia and hypertension. [34] The ENDURANCE and MOMENTUM 3 trials did not reveal a statistically significant difference in stroke rates between LVAD types. [11, 35] Post
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hoc analysis of the ENDURACE trial data suggested that MAP greater than 90mmHg in the HeartWare population was associated with more hemorrhagic strokes. [35]
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Right heart failure can occur in 10-50% of LVAD recipients. [36] RV failure in LVAD
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population is defined by INTERMACS as CVP greater than 18 mmHg with a cardiac index less than 2.0 L/min/m2 without increased left heart filling pressure, or a patient requiring an RVAD, inotropic agents, or nitric oxide for more than 14 days post LVAD implantation. [37] Models utilizing clinical, hemodynamic and echocardiographic markers have been developed to predict which patients are at risk of early and late onset RV failure post-LVAD implantation. [38-41] One such model is the CRITT score, which assigns a point to the following 5 variables: ‘C’ -
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CVP >15 mmHg, ‘R’ - severe RV dysfunction, ‘I’ - preoperative mechanical ventilation/intubation, ‘T’ - severe TR, and ‘T’ - tachycardia (>100 bpm). In the CRITT score study, 93% of patients with a score of 0 or 1 did not require RVAD
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support, but 80% of patients with a score 4 or 5 required RVAD in addition to LVAD support. [42] Patients who require unplanned RVAD insertion have higher
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mortality, post-operative complications, renal failure and recurrent RV failure. [43]
LVAD patients require anticoagulation to prevent thrombosis, which may require
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device exchange and is a significant cause of morbidity in long-term support. Thrombosis risk results from factors associated with the pump itself (sheer stress, blood surface contact, heat, device malposition, platelet activation) and from underlying patient pathology (current thrombus, atrial fibrillation,
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hypercoagulability, surgical inflammatory state, Virchow’s triad). Risk factors associated with pump thrombosis in HeartMate II patients are female sex, white race, younger age, increased BMI, CHA2DS2-VASc score of >3, increased creatinine,
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LVEF >20%, higher LDH at 1 month post-implantation, history of treatment non-
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adherence, and RV failure. [44] Recent efforts to decreased morbidity in HeartMate II patients have centered around preventing pump thrombosis by adhering to the guidelines suggested by the PREVENT investigators: optimizing anticoagulation (warfarin and antiplatelet), positioning of inflow and outflow cannulas, and appropriate VAD flow >9,000 rpm. [45] The MOMENTUM 3 trial found HeartMate II axial flow devices had a statistically significant greater rate of suspected or confirmed pump thrombosis leading to device replacement or urgent transplant
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(10.1%) than the HeartMate III group, which had no cases of pump thrombosis during the trial. [11] Risk factors associated with pump thrombosis in the HeartWare population are: MAP >90 mmHg, ASA dose <81 mg, INR <2 and
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INTERMACS >3. [44]
Bleeding complications are often the result of supratherapeutic anticoagulation,
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mechanical or enzymatic coagulation factor deficits or dysfunctions, mucosal bleeding, and arteriovenous malformations (AVM). [46-48] Patients with
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continuous flow VADs are at risk of an acquired form of Type 2A von Willebrand disease: a qualitative defect with inability to form the large von Willebrand factor (VWF) multimers required for clot formation. [46, 48] Sheer stress from the mechanical device likely results in VWF unfolding, which leaves the large multimers
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open to proteolytic cleaving. [49] While it has been observed that patients with centrifugal flow VADs (designed to have less sheer stress on blood) have preservation of large VWF multimers as compared to axial continuous flow devices,
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the MOMENTUM 3 trial did not find a statistically significant difference in bleeding
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complications between HeartMate II and HeartMate III patients both maintained on antiplatelet and warfarin regimens. [11, 50] Lower PI is associated with a greater risk of non-surgical bleeding (gastrointestinal, epistaxis, genitourinary, and intracranial), supporting the notion that the absence of or a decrease in pulsatility may lead to the formation of AVMs by way of dilation of mucosal veins and relaxation of arterial smooth muscle. [51]
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Infection is a cause of readmission for LVAD patients. A younger, more active LVAD patient may be at a higher risk of driveline infection. [52] Sterile dressing changes at driveline sites are an important mainstay of VAD care. The treatment for infections
or deep driveline infections, pump pocket infections). [53]
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can be medical and or surgical depending on the extent of the infection (superficial
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6. Anesthetic Management of Patients with Existing LVAD Undergoing Non-
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Cardiac Surgery
LVAD patients may present for non-cardiac surgery (NCS) or, with increasing frequency, procedures outside of the operating room (endoscopy, cystoscopy suites, interventional radiology, catheterization laboratory). [54] Institutions are reporting
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a trend toward providing anesthetic care to these patients by non-cardiac trained anesthesiologists. [54-56] Stone et al reported that 88% LVAD patients presenting for NCS had anesthetic care provided by non-cardiac anesthesiologists. Aiding in
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this trend is the availability of LVAD nurses or technicians familiar with the patient
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and device, who can assist the anesthesiology team in connecting the patient to the external console so that device parameters (speed, power, pump flow, and pulsatility index) can be monitored throughout NCS procedures. [56, 57] In preparing patients with LVAD for NCS, it is important to evaluate patients with a multidisciplinary approach including heart failure cardiologists to optimize their clinical condition, hematologists to guide perioperative coagulation management, and intensivists for postoperative care, if indicated. Cardiac surgical resources and
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postoperative recovery units or ICUs experienced in LVAD care should be available. [56]
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Standard ASA monitors are sufficient for LVAD patients having non-major NCS. [5457] A noninvasive blood pressure cuff often provides adequate mean pressure readings in patients with continuous flow devices. However, in LVAD patients
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requiring general anesthesia, invasive blood pressure monitoring may be more
reliable than oscillometric measurements, especially if rapid or marked changes in
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preload or afterload are expected. [56] Central venous access is indicated if vasopressors are expected to be required. In the series reported by Degnan et al, of 74 NCS procedures performed on 31 LVAD patients, 88% did not require vasopressor doses, and only one patient who was on an inotropic infusion
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preoperatively had the inotrope continued intraoperatively. [55] It should be noted, however, that 65% of these NCS procedures were upper and lower endoscopies and 81% of the procedures were performed under MAC anesthesia. [55] Stone reports
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similar vasopressor use in his reported series of 241 patients from 2003-2013, with
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vasopressor or inotrope bolus use in 24%, infusion use in 22%, and both bolus and infusion in only 7.5% of cases, all described as either “major” cases or having significant comorbidities. [54] TEE or TTE can be used to assess right heart function. Cerebral oximetry can be used in lieu of pulse oximetry should lack of pulsatility preclude pulse oximetry measurement. [54]
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It is usually not necessary to alter the device settings in otherwise stable patients, provided that hemodynamics and volume status are maintained throughout the case. Hemodynamic derangements and resulting VAD parameter changes are
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described above. In general, if a patient with a VAD becomes hypotensive the VAD flows should be checked. If the flows are high, vasodilation due to medications or
infection are most common and should be suspected. If hypotension occurs with low
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flows, the differential diagnosis includes RV failure, cannula obstruction,
tamponade, hypovolemia, arrhythmia and suction event. For this, the clinical
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scenario, filling pressures, ECG and echocardiogram can aid in the diagnosis and selection of focused treatment maneuvers.
Decisions regarding anticoagulation management for NCS should be made in
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conjunction with the surgeon, heart failure cardiologist and hematologist. [56] Consideration should be given to the patient's history of thrombotic events and the nature of the procedure. Anticoagulation reversal may be considered in urgent
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surgery where anticoagulation has not been held, or in neurosurgery or
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ophthalmologic surgery. [54] Blood product transfusion is as per usual expectations of surgical blood loss and coagulation status.
Patients having minimally invasive procedures can usually recover in postanesthesia care units, but hospitals should have ICU availability should higher levels of care be required.
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Summary VADs are inserted for a variety of indications and clinical situations, ranging from “crash and burn” to advanced heart failure, and are used as bridging or destination
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therapies. A variety of devices are available, with the most commonly inserted
being second generation axial continuous flow devices and the newest being third generation, centrifugal continuous flow devices in which there is the hope of
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offering improved flow dynamics and fewer device complications. Anesthetic care for VAD patients requires an understanding of heart failure physiology and VAD
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parameters. Increasingly, the care of VAD patients undergoing non-cardiac surgery
Practice points
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is provided by non-cardiac anesthesiologists.
•
INTERMACS defines seven profiles of patients for VAD insertion.
•
VADs can be classified in a variety of ways including duration of support,
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engineering design, and the supported ventricle. First, second or third
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generation refers to pulsatile, axial continuous, or centrifugal “bearing-less” continuous flows.
•
Preoperative assessment of patients undergoing LVAD insertion should include evaluation of all systems affected by heart failure.
•
Anesthetic care in patients with LVADs undergoing non-cardiac surgery is increasingly provided by non-cardiac anesthesiologists.
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Research agenda •
Best practices in determining patients at risk for, and management of, RV failure after LVAD insertion are still to be determined. Although perceived benefits of improved volume state and possible reduction of
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•
allogenic red blood cell and blood factor transfusion, formal evaluation of the
requires study in VAD populations.
Optimal strategies for perioperative care for VAD patients undergoing non-
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•
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practice of removing autologous blood for re-infusion after device implantation
cardiac surgery, including management of perioperative anticoagulation, need to
Conflict of Interest: None
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References
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be studied further vis-a-vis the risks of device thrombosis and bleeding.
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1. Kirklin JK, Naftel DC, Pagani FD, et al. Seventh INTERMACS annual report: 15,000 patients and counting. J Heart Lung Transplant. 2015;34(12):1495-504. 2. Stevenson LW, Pagani FD, Young JB, et al. INTERMACS profiles of advanced heart failure: the current picture. J Heart Lung Transplant. 2009;28(6):535-41. 3. Boyle AJ, Ascheim DD, Russo MJ, et al. Clinical outcomes for continuous-flow left ventricular assist device patients stratified by pre-operative INTERMACS classification. J Heart Lung Transplant. 2011;30(4):402-7. 4. Sladen RN. New Innovations in Circulatory Support With Ventricular Assist Device and Extracorporeal Membrane Oxygenation Therapy. Anesth Analg. 2017;124(4):1071-86. 5. Timms D. A review of clinical ventricular assist devices. Med Eng Phys. 2011;33(9):1041-7.
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6. Frazier OH, Myers TJ, Jarvik RK, et al. Research and development of an implantable, axial-flow left ventricular assist device: the Jarvik 2000 Heart. Ann Thorac Surg. 2001;71(3 Suppl):S125-32; discussion S44-6. 7. Noon GP, Loebe M. Current status of the MicroMed DeBakey Noon Ventricular Assist Device. Tex Heart Inst J. 2010;37(6):652-3. 8. Griffith K, Jenkins E, Pagani FD. First American experience with the Terumo DuraHeart left ventricular assist system. Perfusion. 2009;24(2):83-9. 9. Cheung A, Chorpenning K, Tamez D, et al. Design Concepts and Preclinical Results of a Miniaturized HeartWare Platform: The MVAD System. Innovations (Phila). 2015;10(3):151-6. 10. Esmore D, Spratt P, Larbalestier R, et al. VentrAssist left ventricular assist device: clinical trial results and Clinical Development Plan update. Eur J Cardiothorac Surg. 2007;32(5):735-44. 11. Mehra MR, Naka Y, Uriel N, et al. A Fully Magnetically Levitated Circulatory Pump for Advanced Heart Failure. N Engl J Med. 2017;376(5):440-50. 12. Nagpal AD, Singal RK, Arora RC, et al. Temporary Mechanical Circulatory Support in Cardiac Critical Care: A State of the Art Review and Algorithm for Device Selection. Can J Cardiol. 2017;33(1):110-8. 13. Nguyen DQ, Thourani VH. Third-generation continuous flow left ventricular assist devices. Innovations (Phila). 2010;5(4):250-8. 14. Hahn RT, Abraham T, Adams MS, et al. Guidelines for performing a comprehensive transesophageal echocardiographic examination: recommendations from the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr. 2013;26(9):921-64. 15. Young JB, Moen EK. Outpatient parenteral inotropic therapy for advanced heart failure. J Heart Lung Transplant. 2000;19(8 Suppl):S49-57. 16. Felker GM, Benza RL, Chandler AB, et al. Heart failure etiology and response to milrinone in decompensated heart failure: results from the OPTIME-CHF study. J Am Coll Cardiol. 2003;41(6):997-1003. 17. Benza RL, Tallaj JA, Felker GM, et al. The impact of arrhythmias in acute heart failure. J Card Fail. 2004;10(4):279-84. 18. Heath MJ, Dickstein ML. Perioperative management of the left ventricular assist device recipient. Prog Cardiovasc Dis. 2000;43(1):47-54. 19. Acharya MN, Som R, Tsui S. What is the optimum antibiotic prophylaxis in patients undergoing implantation of a left ventricular assist device? Interact Cardiovasc Thorac Surg. 2012;14(2):209-14. 20. Barile L, Fominskiy E, Di Tomasso N, et al. Acute Normovolemic Hemodilution Reduces Allogeneic Red Blood Cell Transfusion in Cardiac Surgery: A Systematic Review and Meta-analysis of Randomized Trials. Anesth Analg. 2017;124(3):743-52. 21. Stainback RF, Estep JD, Agler DA, et al. Echocardiography in the Management of Patients with Left Ventricular Assist Devices: Recommendations from the American Society of Echocardiography. J Am Soc Echocardiogr. 2015;28(8):853-909. 22. Patangi SO, George A, Pauli H, et al. Management issues during HeartWare left ventricular assist device implantation and the role of transesophageal echocardiography. Ann Card Anaesth. 2013;16(4):259-67.
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23. Hanke JS, Rojas SV, Avsar M, et al. Minimally-invasive LVAD Implantation: State of the Art. Curr Cardiol Rev. 2015;11(3):246-51. 24. Karaca N, Sahutoglu C, Kocabas S, et al. Anesthetic Management for Left Ventricular Assist Device Implantation Without Using Cardiopulmonary Bypass: Case Series. Transplant Proc. 2015;47(5):1503-6. 25. Selzman CH, Sheridan BC. Off-pump insertion of continuous flow left ventricular assist devices. J Card Surg. 2007;22(4):320-2. 26. Hanke JS, Rojas SV, Martens A, et al. Minimally invasive left ventricular assist device implantation with outflow graft anastomosis to the innominate artery. J Thorac Cardiovasc Surg. 2015;149(4):e69-70. 27. Bienia S, Feider A, Griauzde R, et al. CASE 13-2016 Minimally Invasive Left Ventricular Assist Device Insertion Without Cardiopulmonary Bypass. J Cardiothorac Vasc Anesth. 2016;30(6):1716-26. 28. Kimmaliardjuk DM, Ruel M. Cardiac passive-aggressive behavior? The right ventricle in patients with a left ventricular assist device. Expert Rev Cardiovasc Ther. 2017. 29. Han J, Takeda K, Takayama H, et al. Durability and clinical impact of tricuspid valve procedures in patients receiving a continuous-flow left ventricular assist device. J Thorac Cardiovasc Surg. 2016;151(2):520-7 e1. 30. Deschka H, Holthaus AJ, Sindermann JR, et al. Can Perioperative Right Ventricular Support Prevent Postoperative Right Heart Failure in Patients With Biventricular Dysfunction Undergoing Left Ventricular Assist Device Implantation? J Cardiothorac Vasc Anesth. 2016;30(3):619-26. 31. Bradford CD, Stahovich MJ, Dembitsky WP, et al. Safety of Prothombin Complex Concentrate to Control Excess Bleeding During Continuous Flow LVAD Insertion. ASAIO J. 2015;61(5):509-13. 32. Yoon AJ, Sohn J, Grazette L, et al. Pan-Cardiac Cycle Fixed Mitral Valve Opening in an LVAD Patient Presenting with Hemorrhagic Shock. Echocardiography. 2016;33(4):644-6. 33. Steinberg MH. Go with the Flow. N Engl J Med. 2017;376(5):485-7. 34. Frontera JA, Starling R, Cho SM, et al. Risk factors, mortality, and timing of ischemic and hemorrhagic stroke with left ventricular assist devices. J Heart Lung Transplant. 2016. 35. Rogers JG, Pagani FD, Tatooles AJ, et al. Intrapericardial Left Ventricular Assist Device for Advanced Heart Failure. N Engl J Med. 2017;376(5):451-60. 36. Meineri M, Van Rensburg AE, Vegas A. Right ventricular failure after LVAD implantation: prevention and treatment. Best Pract Res Clin Anaesthesiol. 2012;26(2):217-29. 37. Karimov JH, Sunagawa G, Horvath D, et al. Limitations to Chronic Right Ventricular Assist Device Support. Ann Thorac Surg. 2016;102(2):651-8. 38. Matthews JC, Koelling TM, Pagani FD, et al. The right ventricular failure risk score a pre-operative tool for assessing the risk of right ventricular failure in left ventricular assist device candidates. J Am Coll Cardiol. 2008;51(22):2163-72. 39. Fitzpatrick JR, 3rd, Frederick JR, Hsu VM, et al. Risk score derived from preoperative data analysis predicts the need for biventricular mechanical circulatory support. J Heart Lung Transplant. 2008;27(12):1286-92.
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40. Drakos SG, Janicki L, Horne BD, et al. Risk factors predictive of right ventricular failure after left ventricular assist device implantation. Am J Cardiol. 2010;105(7):1030-5. 41. Wang Y, Simon MA, Bonde P, et al. Decision tree for adjuvant right ventricular support in patients receiving a left ventricular assist device. J Heart Lung Transplant. 2012;31(2):140-9. 42. Atluri P, Goldstone AB, Fairman AS, et al. Predicting right ventricular failure in the modern, continuous flow left ventricular assist device era. Ann Thorac Surg. 2013;96(3):857-63; discussion 63-4. 43. Yoshioka D, Takayama H, Garan RA, et al. Contemporary outcome of unplanned right ventricular assist device for severe right heart failure after continuous-flow left ventricular assist device insertion. Interact Cardiovasc Thorac Surg. 2017. 44. Nguyen AB, Uriel N, Adatya S. New Challenges in the Treatment of Patients With Left Ventricular Support: LVAD Thrombosis. Curr Heart Fail Rep. 2016;13(6):302-9. 45. Maltais S, Kilic A, Nathan S, et al. PREVENtion of HeartMate II Pump Thrombosis Through Clinical Management: The PREVENT multi-center study. J Heart Lung Transplant. 2017;36(1):1-12. 46. Uriel N, Pak SW, Jorde UP, et al. Acquired von Willebrand syndrome after continuous-flow mechanical device support contributes to a high prevalence of bleeding during long-term support and at the time of transplantation. J Am Coll Cardiol. 2010;56(15):1207-13. 47. Uriel N, Adatya S, Maly J, et al. Clinical hemodynamic evaluation of patients implanted with a fully magnetically levitated left ventricular assist device (HeartMate 3). J Heart Lung Transplant. 2017;36(1):28-35. 48. Bartoli CR, Restle DJ, Zhang DM, et al. Pathologic von Willebrand factor degradation with a left ventricular assist device occurs via two distinct mechanisms: mechanical demolition and enzymatic cleavage. J Thorac Cardiovasc Surg. 2015;149(1):281-9. 49. Adatya S, Bennett MK. Anticoagulation management in mechanical circulatory support. J Thorac Dis. 2015;7(12):2129-38. 50. Netuka I, Kvasnicka T, Kvasnicka J, et al. Evaluation of von Willebrand factor with a fully magnetically levitated centrifugal continuous-flow left ventricular assist device in advanced heart failure. J Heart Lung Transplant. 2016;35(7):860-7. 51. Wever-Pinzon O, Selzman CH, Drakos SG, et al. Pulsatility and the risk of nonsurgical bleeding in patients supported with the continuous-flow left ventricular assist device HeartMate II. Circ Heart Fail. 2013;6(3):517-26. 52. Goldstein DJ, Naftel D, Holman W, et al. Continuous-flow devices and percutaneous site infections: clinical outcomes. J Heart Lung Transplant. 2012;31(11):1151-7. 53. Leuck AM. Left ventricular assist device driveline infections: recent advances and future goals. J Thorac Dis. 2015;7(12):2151-7. 54. Stone M, Hinchey J, Sattler C, et al. Trends in the Management of Patients With Left Ventricular Assist Devices Presenting for Noncardiac Surgery: A 10-Year Institutional Experience. Semin Cardiothorac Vasc Anesth. 2016;20(3):197-204.
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55. Degnan M, Brodt J, Rodriguez-Blanco Y. Perioperative management of patients with left ventricular assist devices undergoing noncardiac surgery. Ann Card Anaesth. 2016;19(4):676-86. 56. Barbara DW, Wetzel DR, Pulido JN, et al. The perioperative management of patients with left ventricular assist devices undergoing noncardiac surgery. Mayo Clin Proc. 2013;88(7):674-82. 57. Nelson EW, Heinke T, Finley A, et al. Management of LVAD Patients for Noncardiac Surgery: A Single-Institution Study. J Cardiothorac Vasc Anesth. 2015;29(4):898-900.
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Table 1: Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) Levels
Short Hand
Description
Time Frame for Intervention
5
“House bound”
Critical cardiogenic shock Progressive decline on inotropic support Stable but inotrope dependent Resting symptoms home on oral therapy Exertion intolerant
Definitive intervention needed within hours.
4
“Crash and burn.” “Sliding on inotropes.” “Dependent stability.” “Frequent flyer”
6
“Walking wounded.” “Place holder”
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Definitive intervention needed within few days. Definitive intervention elective over a period of weeks to few months. Definitive intervention elective over period of weeks to few months. Variable urgency, depends upon maintenance of nutrition, organ function, and activity. Variable, depends upon maintenance of nutrition, organ function, and activity level. Transplantation or circulatory support may not currently be indicated.
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7
Exertion limited
Advanced NYHA Class III symptoms
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3
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2
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Risk Level 1
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Summary of INTERMACS profiles for acute and chronic heart failure for MCS insertion.
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Table 2: Summary of commonly inserted VAD Devices and Classifications. Legacy pulsatile flow devices are not listed. All long-term devices use LV apex to ascending aorta inflow/outflow configuration, except the Jarvik 2000, where
Location
Flow Type
Duration of support
Thoratec HeartMate II Thoratec HeartMate III
Subdiaphragmatic
Axial
Long-term
Intrapericardial
Centrifugal
Long-term
Jarvik 2000 HeartWare HVAD HeartWare MVAD Reliant HeartAssist 5 Thoratec CentriMag
Intrapericardial Intrapericardial
Axial Centrifugal
Intrapericardial
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Impella P (2.5, 4.0/CP, 5.0)
= percutaneous placement
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P
Investigational
Long-term Long-term
Flow calculated based on power and speed, and may be inaccurate 7 10
Axial/ Centrifugal Axial
Long-term
7
BTT
Long-term
10
Investigational
Centrifugal
Short-term
6
6 hours (LVAD) 30 days (RVAD)
Centrifugal
Short-term
4.5
Axial
Short-term
2.5, 4.0, 5.0, respectively
6 hours but in practice used for up to 1 week Cardiogenic shock: 2.5/CP: <4 days 5.0: <6 days High-risk PCI: ≤ 6 hours
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Left atrium to aorta (LVAD) Right atrium to pulmonary artery (RVAD) Femoral vein transseptally to LV Retrograde from femoral artery and across aortic valve
FDA-approved Indications
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TandemHeart P
Subdiaphragmatic
Maximum Flow In Liters Per Minute 10
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Device
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outflow connection to the ascending or descending aorta is possible.
BTT, DT
Investigational BTT
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Table 3: TEE Checklist for LVAD insertion. A comprehensive TEE examination should be performed pre and post device
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implantation, with special attention and comment on the highlighted items
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(adapted from the American Society of Echocardiography Guidelines). [21]
Post-implantation TEE Exam
Left ventricle size and systolic function
Left ventricle size
Right ventricle size and systolic function Evaluate for septal defects, including PFO Evaluate all chambers for thrombus
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Pre-implantation TEE Exam
Right ventricle size and systolic function Evaluate for tricuspid regurgitation Re-evaluate for septal defects, including PFO Evaluate aortic valve opening and aortic insufficiency
Evaluate mitral valve (is there greater than moderate mitral stenosis?)
Evaluate inflow cannula position, color Doppler, flow velocities
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Evaluate aortic valve (is there greater than mild aortic insufficiency?)
Outflow cannula position, color flow Doppler, flow velocities
Evaluate the aorta
Evaluate the aorta to exclude dissection
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Evaluate the function of the tricuspid valve
Document changes in pump speed during assessment