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Anesthesia for placement of ventricular assist devices

Anesthesia for placement of ventricular assist devices
Literature review current through: Aug 2023.
This topic last updated: Jun 13, 2022.

INTRODUCTION — Mechanical circulatory support (MCS) is increasingly used in the management of patients with end stage heart failure, most commonly to support the left ventricle (LV) as a bridge to cardiac transplantation or as destination therapy.

This topic will discuss the anesthetic management of patients undergoing ventricular assist device (VAD) implantation, including preoperative assessment, intraoperative management, and postoperative considerations. A separate topic addresses anesthetic management during noncardiac surgery for patients with a functioning previously implanted VAD. (See "Anesthesia for noncardiac surgery in adults with a durable ventricular assist device".)

Other topics discuss intermediate- and long-term VADs in detail, including the indications, implantation procedures, medical management, and emergency care for patients with such devices:

(See "Treatment of advanced heart failure with a durable mechanical circulatory support device".)

(See "Management of long-term mechanical circulatory support devices".)

(See "Emergency care of adults with mechanical circulatory support devices".)

TYPES OF VENTRICULAR ASSIST DEVICES

Short-term devices — Temporary mechanical circulatory support (MCS) devices are available for rapid implantation when acutely needed for survival (ie, bridge to recovery) (table 1). Short-term left ventricular (LV) devices can be placed peripherally (via a percutaneous approach or surgical incision) or centrally (via a sternotomy or mini-thoracotomy approach) to provide adequate cardiac output to support coronary, cerebral, and systemic perfusion as well as to reduce LV filling pressure. In some cases, temporary mechanical support with a right ventricular assist device (RVAD) may be necessary to provide adequate preload to the LV.

The role of transesophageal echocardiography (TEE) to guide insertion and positioning of MCS device cannulae in these settings, and initial assessment of device function and patient response are discussed in a separate topic. (See "Short-term left ventricular mechanical circulatory support: Use of echocardiography during initiation and management".)

Long-term devices — Several intermediate- and long-term durable VADs have been approved by the US Food and Drug Administration (FDA) as bridge to transplant and destination therapy devices. More than 90 percent of the VADs entered in the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) database are continuous flow devices that employ either a centrifugal or axial flow pump [1]. Older pulsatile flow devices are no longer used.

The table summarizes key characteristics of devices used for long-term VADs including (table 2):

Ventricular assist devices – The HeartMate 3 (picture 1) is a centrifugal-flow device available in the United States and Europe [2-8]. This pump has a spinning bladed disc levitated within an electromagnetic housing unit. Potential advantages of this design include long durability, optimization of blood flow through the device to minimize risk of thrombus formation and hemolysis, compact size, and simplified surgical implantation. (See "Treatment of advanced heart failure with a durable mechanical circulatory support device", section on 'Types of durable MCS devices'.)

Total artificial heart (TAH) – For patients who require long-term biventricular support, options include the SynCardia Total Artificial Heart. Patient support with a TAH prior to heart transplantation has been successful for as long as four years. Also, temporary off-label use of two centrifugal-flow VADs as a TAH has been described in case reports [9-12]. (See "Treatment of advanced heart failure with a durable mechanical circulatory support device", section on 'Types of durable MCS devices'.)

PREANESTHETIC ASSESSMENT — Preoperative discussions with the cardiology team managing the patient's end-stage heart failure and the cardiac surgical team performing implantation of the specific VAD are extremely useful. These discussions ensure awareness of heart failure severity and preoperative management of sequelae of end-organ hypoperfusion due to low cardiac output (CO), such as renal insufficiency, pulmonary insufficiency, hepatic dysfunction, and coagulopathy. Preoperative discussion includes information regarding whether the patient has already developed hemodynamic instability necessitating urgent VAD implantation and the type of VAD to be implanted in order to facilitate management of device-specific intraoperative problems. Finally, team-based planning for postoperative care is important.

Cardiovascular evaluation — Patients who present for left ventricular assist device (LVAD) implantation have end-stage heart failure and/or cardiogenic shock.

Assessment of urgency — The Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) group employs a patient profile classification to stratify risk according to clinical severity (table 3). Patients who fall into the INTERMACS profile 1 are in critical cardiogenic shock and are candidates for immediate emergency LVAD implantation. Conversely, patients who meet criteria for INTERMACS profile 4 typically undergo elective LVAD implantation after stabilization of underlying cardiac and other major end-organ dysfunction. In some instances, delaying LVAD implantation to achieve optimal overall preoperative status may increase the likelihood of survival since restoration of normal CO may improve or reverse manifestations of end-organ dysfunction. Also, preoperative nutritional status is a potentially modifiable risk factor, and cachexia (ie, body mass index [BMI] <20 kg/m2) or malnutrition (ie, albumin <3 g/dL) increase postoperative mortality and morbidity, such as prolonged mechanical ventilation, infection, and delayed wound healing [13,14]. However, decisions to delay VAD implantation are carefully weighed against risks for development of irreversible end-organ dysfunction [15,16].

If urgent or emergency surgery is necessary, opportunities to establish optimal preoperative cardiovascular status are limited. However, attempts to improve hemodynamic status before VAD implantation in a hypotensive patient may include initiation of inotropic agents, vasopressors, inhaled pulmonary vasodilators, or temporary mechanical circulatory support (MCS) with an intra-aortic balloon pump (IABP). (See "Management of refractory heart failure with reduced ejection fraction" and "Treatment of acute decompensated heart failure: Specific therapies", section on 'Management of hypotensive patients'.)

Preoperative echocardiography and cardiac catheterization — Completed cardiac imaging and hemodynamic studies are evaluated to assess the patient's baseline status and determine whether any identified lesions require concurrent intervention during LVAD implantation or increase the risk of complications.

Echocardiography – Prior transthoracic echocardiography (TTE) and/or transesophageal echocardiography (TEE) studies provide valuable information, although TEE examination is repeated in the operating room after anesthetic induction (see 'Role of TEE in the prebypass period' below). Preoperative and prebypass examinations include assessment of the following features and conditions:

Ventricular size and function – Chamber size and regional and global function for the left ventricle (LV) and right ventricle (RV) are evaluated. LVAD candidates generally have severe LV systolic function which may be accompanied by RV systolic dysfunction. LVAD implantation supports CO and unloads the LV. In some patients, LVAD support may also enhance RV performance by decreasing pulmonary artery pressure (PAP) and RV afterload. However, exacerbation of RV dysfunction may occur after LVAD implantation [17-21], owing to decreases in LV pressure and size, leading to interventricular septal bowing and distortion of RV geometry and function. The development of RV failure in LVAD recipients is associated with significantly worse outcomes since optimal LVAD performance depends on adequate RV function to provide effective preload to the pump. Risk scores have been developed to predict severe right-sided heart failure after LVAD implantation (table 4) [18,22]. (See 'Role of TEE at the end of CPB' below and 'Right heart failure' below.)

Valve disease – The presence and severity of existing cardiac valve pathology is assessed in the preoperative period. Decisions regarding interventions on cardiac valves should be based on studies obtained while the patient is in an optimal hemodynamic state, and not during periods of hemodynamic instability. There is consensus regarding the approach to aortic valve disease for patients undergoing LVAD placement, but lack of consensus on the approach to mitral or tricuspid valve disease.

-Aortic regurgitation (AR) – The presence and severity of AR is assessed preoperatively, prebypass, as well as shortly after institution of cardiopulmonary bypass (CPB) as the severity of AR may be underestimated with high LV diastolic pressures. Uncorrected AR can result in reduced CO after LVAD implantation due to recirculation of VAD output in a retrograde fashion through the incompetent aortic valve [23]. The 2013 International Society of Heart Lung Transplantation (ISHLT) guidelines recommend intervention for more than mild degrees of pre-existing AR at time of LVAD placement [24]. Between 25 and 40 percent of LVAD recipients develop mild or moderate AR within one year of implantation due to lack of aortic valve opening, leaflet fibrosis and fusion, and retraction of the leaflets tips [25,26]. Thus, preexisting AR is likely to progress after LVAD implantation and may impact device durability.

For patients with greater than mild AR with a central jet, partial oversewing (with a "Park stitch") is often employed. However, if the aortic valve is sewn completely closed, the patient becomes fully dependent on LVAD flow; thus, device malfunction would likely be fatal [27,28]. If there is mild AR with an eccentric jet, surgical aortic valve replacement is performed; in this setting, most surgeons recommend a bioprosthetic valve because mechanical valves have a greater risk of thromboembolic complications and need for a higher level of anticoagulation. An observational study of patients undergoing LVAD implantation found that aortic valve closure was associated with lower actuarial survival rate (63.2 percent) compared with aortic valve repair (76.8 percent) or aortic valve replacement (71.8 percent) at one year [29].

-Aortic stenosis (AS) – For most patients with AS (of any degree) and more than mild AR, the ISHLT guidelines recommend a bioprosthetic aortic valve replacement during LVAD implantation [24]. For most patients with severe AS (regardless of degree of any AR), the ISHLT guidelines recommend aortic valve replacement, typically with a bioprosthetic valve [24].

-Aortic prosthetic valve – For patients with a pre-existing aortic mechanical valve, the ISHLT guidelines recommend either bioprosthetic valve replacement or oversewing the mechanical valve at the time of LVAD placement [24]. For patients with a functioning aortic bioprosthetic valve, no aortic valve intervention is required [24].

-Mitral stenosis (MS) – For most patients with moderate or worse MS, the 2013 ISHLT guidelines recommend a bioprosthetic mitral valve replacement at the time of LVAD implantation [24]. There is lack of consensus on the mitral valve area threshold for this recommendation. Many surgeons replace the mitral valve if its area is ≤1.5 cm2; this was the threshold for moderate to severe MS in the 2008 American College of Cardiology (ACC)/American Heart Association (AHA) valve guidelines [30]. Some surgeons replace the mitral valve at a larger mitral valve area limit, in keeping with the 2014 AHA/ACC valve guidelines which defined a mitral valve area of ≤1.5 cm2 as severe; however, these 2014 guidelines lack a definition for moderate MS [31].

A mitral valve area ≤1.5 cm2 is usually associated with a transmitral mean gradient of 5 to 10 mmHg at normal heart rates. However, the transmitral gradient may overestimate the severity of MS if mitral regurgitation (MR) is present, or may underestimate the severity of MS if there is low CO with low flow across the mitral valve. Thus, multiple methods to measure the severity of MS (including the standard method of using the pressure half-time to estimated mitral valve area as well as measurement of mitral valve area by planimetry using multiplanar reconstruction of a three-dimensional dataset [32]) may be helpful during the decision-making process. (See "Echocardiographic evaluation of the mitral valve", section on 'Mitral stenosis'.)

The presence of MS impedes optimal LVAD filling, which is needed to generate appropriate systemic CO and may lead to postoperative persistence of elevated pulmonary venous pressure and heart failure symptoms. Also, the elevated left atrial (LA) pressures in patients with MS may exacerbate pulmonary hypertension and further impair RV function. (See "Rheumatic mitral stenosis: Clinical manifestations and diagnosis".)

-Mitral regurgitation (MR) – Many patients requiring LVAD support have secondary (functional) MR, but consensus is lacking regarding an optimal approach for such patients. Since the severity of functional MR is significantly reduced in most patients after LVAD implantation due to reverse remodeling and improved leaflet coaptation, surgical intervention is not typically recommended for those with moderate or severe MR [24]. However, in selected patients, such as those expected to have adequate myocardial recovery allowing eventual LVAD removal, mitral valve repair or replacement with a bioprosthetic valve may be performed [33,34]. An observational study of patients with moderate to severe MR found that neither mitral valve repair nor replacement at the time of LVAD implantation was associated with significant improvement in survival at two postoperative years, although quality of life was improved and hospital readmissions were reduced [35]. (See "Chronic secondary mitral regurgitation: General management and prognosis".)

-Tricuspid regurgitation (TR) – Approximately 50 percent of patients considered for LVAD implantation have significant TR, likely as a result of pulmonary hypertension and structural changes in the RV. Consensus is lacking on the approach to functional TR in patients undergoing LVAD placement. Earlier studies suggested that concurrent tricuspid procedures reduce postoperative right-sided heart failure, renal dysfunction, and need for rehospitalization [36,37], and the 2013 ISHLT guidelines recommended surgical repair if moderate or greater TR was present [24]. However, subsequent analysis of INTERMACS data noted that concurrent tricuspid valve procedures confer no survival benefit in patients with moderate or severe TR [38].

Evaluation of the tricuspid valve for TR is complex and should include not only color flow and spectral Doppler interrogation of the regurgitant jet, but also assessment of tricuspid annulus dimensions, tricuspid leaflet tethering, size of the right atrium (RA), RV, and inferior vena cava, and position and motion of the interventricular septum. Of note, severe TR is often associated with a low peak Doppler jet velocity as there is near equalization of RV and RA pressures [23,39]. Further discussion of evaluation of TR is available in a separate topic. (See "Echocardiographic evaluation of the tricuspid valve", section on 'Tricuspid regurgitation'.)

Intracardiac shunts – Intracardiac shunts are identified and repaired prior to LVAD placement. With unloading of the LV by a functioning LVAD, LV and LA pressures decrease while the RA pressure may remain elevated or increase as a result of increased venous return from an augmented systemic CO. Thus, right-to-left shunting may occur after LVAD implantation if an intracardiac shunt is present, leading to hypoxemia or paradoxical embolism. The 2013 ISHLT guidelines recommend closure of atrial septal defects and patent foramen ovale (PFO), at the time of LVAD implantation [24]. Generally, congenital or post-myocardial infarction ventricular septal defects are also closed.

TEE examination for the most common causes of intracardiac shunting includes two-dimensional imaging with color flow Doppler optimized for detection of low velocity flow across a PFO or atrial septal defect. Agitated saline injections along with maneuvers (cough and Valsalva release in conscious patients; positive pressure release in intubated patients) are also employed to provoke transient right-to-left shunting. However, in the presence of severe LV dysfunction and very elevated LA pressure, it may be difficult to raise the RA pressure above the LA pressure even with such respiratory maneuvers, leading to a false negative bubble study [40]. Special attention is warranted in patients with an atrial septal aneurysm or a Chiari network since these anatomical findings are commonly associated with a PFO. (See "Patent foramen ovale".)

Intracardiac thrombus – Intracardiac thrombi are often present in candidates for LVAD implantation and should be identified and removed (figure 1). Echocardiographic microbubble contrast agents that traverse the pulmonary circulation can aid in identifying ventricular and atrial thrombi if image quality is adequate. Thrombi in the LA are often associated with atrial fibrillation, and are best identified with TEE rather than TTE. Thrombi in the LV are most commonly seen in areas with akinesis or aneurysm, and are generally best evaluated by employing TTE with contrast. However, thrombus may be missed unless all LV segments are well visualized. For example, the true LV apex is often missed during TEE examination, with consequent failure to identify apical thrombus. (See "Left ventricular thrombus after acute myocardial infarction", section on 'Diagnosis' and "Contrast echocardiography: Clinical applications", section on 'Clinical applications for microbubble contrast agents'.)

The limited sensitivity of echocardiography for identification of LV thrombus in this setting was illustrated in a retrospective study in 99 patients undergoing 107 LVAD implantation [41]. The results of preoperative TTE and TEE (performed twice approximately 23 days before and 4 days before implantation) were compared with intraoperative direct LV inspection for thrombus. Intraoperative direct inspection revealed LV thrombus in 14 cases. For preoperative TTE with contrast, a sensitivity of 16.7 percent and a specificity of 100 percent were noted for thrombus detection [41]. For preoperative TEE (without contrast), sensitivity was 0 percent and specificity was 93.8 percent. For intraoperative TEE (see 'Role of TEE in the prebypass period' below), sensitivity was 0 percent and specificity was 98.9 percent. While this was a small retrospective study, it suggests the limitations of echocardiographic thrombus detection in both the preoperative and intraoperative periods.

Cardiac catheterization – Right heart catheterization studies are reviewed. These provide important data regarding baseline central venous pressures (CVP), PAP, pulmonary vascular resistance (PVR), and cardiac index. These studies also confirm a diagnosis of pulmonary hypertension and determine whether this results from left heart disease or other causes [42,43].

Evaluation of other organ systems

Pulmonary evaluation – Review of chest radiographs may reveal cardiogenic pulmonary edema caused by chronically increased intrapulmonary hydrostatic pressures with increased fluid filtration into the alveolar space. These changes are typically reversed after the institution of LVAD flow. Persistent pulmonary abnormalities in the immediate post-implantation period are usually multifactorial (eg, acute respiratory distress syndrome, transfusion-related acute lung injury, cardiogenic pulmonary edema etc).

Patients presenting for LVAD implantation may have pulmonary hypertension due to left heart disease, often accompanied by significant concurrent pulmonary disease. Before elective LVAD implantation, patients are screened for pulmonary comorbidities such as pulmonary hypertension, preexisting chronic obstructive pulmonary disease (COPD), pneumonia, recent changes in oxygen requirements, or decreased activity, so that opportunities to treat acute events or exacerbations of chronic disease processes may be identified. Pulmonary function tests should be examined since severe COPD has been associated with worse late survival after VAD implantation [44]. (See "Pulmonary hypertension due to left heart disease (group 2 pulmonary hypertension) in adults" and "Evaluation of perioperative pulmonary risk" and "Strategies to reduce postoperative pulmonary complications in adults".)

Renal evaluation – Renal comorbidity (eg, chronic renal insufficiency, requirement for dialysis) is common in patients with end-stage heart failure, and is a predictor of poor outcomes after LVAD implantation [44]. Preoperative efforts to optimize renal function and volume status may include diuretics, inotropic agents, MCS with an IABP, and avoidance of nephrotoxins. (See "Cardiorenal syndrome: Definition, prevalence, diagnosis, and pathophysiology" and "Cardiorenal syndrome: Prognosis and treatment", section on 'Management'.)

Also, electrolyte disturbances such as hypokalemia, hyperkalemia, and hypomagnesemia are corrected to avoid precipitation of cardiac arrhythmias that can lead to hemodynamic instability during anesthesia and surgery.

Hepatic evaluation – Chronically elevated right-sided filling pressures can lead to variable degrees of hepatic congestion and dysfunction. Laboratory evaluation of hepatic synthetic and metabolic function typically includes prothrombin time, international normalized ratio, partial thromboplastin time, total bilirubin, aspartate aminotransferase, alanine aminotransferase, and albumin.

Hematologic evaluation – Hematologic abnormalities leading to perioperative thrombosis or bleeding are common in patients with end-stage heart failure. Thromboembolism remains one of the most serious complications of VADs, and may be present in patients with previous VAD implantation [5,7,15]. Chronic administration of anticoagulants and history of thromboembolism are noted in the history. Perioperative management of anticoagulation balances thromboembolic risk and bleeding risk to determine the optimum timing of anticoagulant interruption. At our institution patients receiving chronic anticoagulation are transitioned to intravenous heparin infusions as bridge therapy. (See "Perioperative management of patients receiving anticoagulants".)

Patients that have been previously exposed to preoperative intravenous heparin (typically heparin infusion) are prone to develop heparin-induced decreases in circulating antithrombin III (AT-III) levels with consequent heparin resistance [45]. We typically order anti-thrombin levels in these patients [46]. (See 'Management of anticoagulation and bleeding' below and "Blood management and anticoagulation for cardiopulmonary bypass", section on 'Heparin resistance'.)

Anemia should be noted on preoperative laboratory tests and treated before elective surgery. Patients with iron-deficiency (with or without anemia) should be treated with iron replacement, along with evaluation for the underlying cause of the deficiency. Iron replacement in this setting is commonly performed with intravenous iron given limitations of oral iron (slow time course, limited evidence in heart failure and possible reduced absorption in heart failure) (see "Evaluation and management of anemia and iron deficiency in adults with heart failure"). The use of erythropoietin is avoided since it has been associated with increased risk of venous thromboembolism in patients with heart failure and higher risks of pump thrombosis in these patients [47,48]. (See "Evaluation and management of anemia and iron deficiency in adults with heart failure", section on 'ESAs (not recommended)' and "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Anemia'.)

Presence of infection – The presence of an active systemic infection generally precludes VAD implantation. An exception is LVAD exchange (eg, replacement of a HeartMate II device with an intrapericardial HVAD device) performed to replace an infected device as an attempt to eradicate the infection. (See "Overview of control measures for prevention of surgical site infection in adults".)

Prior sternotomy or VAD implantation — Patients with previous sternotomy are at risk during redo sternotomy for injury to the cardiac chambers, great vessels, internal mammary artery graft if present, or previously implanted VAD cannulae. Review of chest computed tomographic scans determines proximity of cardiac structures to the sternum. Removal of a previously implanted VAD typically results in significant blood loss even if sternotomy is uneventful.

Anesthetic preparation for such patients includes ensuring that sufficient cross-matched blood products are available prior to sternotomy. For example, our protocol includes six units of packed red blood cells (RBCs) and six units of Fresh Frozen Plasma (FFP) for VAD implantation, with two units of RBCs pre-checked and immediately available in case emergency transfusion is needed during sternotomy.

Preoperative medication and device management

Preoperative medications – Chronically administered preoperative cardiovascular medications in patients with end-stage heart failure are generally continued as tolerated, including the following agents (see "Perioperative management of heart failure in patients undergoing noncardiac surgery", section on 'Preoperative management'):

Heart failure therapy including (see "Primary pharmacologic therapy for heart failure with reduced ejection fraction" and "Secondary pharmacologic therapy for heart failure with reduced ejection fraction"):

-Diuretics as needed for volume control

-Angiotensin system blockers (angiotensin receptor-neprilysin inhibitors [ARNIs], angiotensin converting enzyme [ACE] inhibitors, or single agent angiotensin-receptor blockers [ARBs])

-Beta blockers

-Mineralocorticoid receptor antagonist

Digoxin (for control of ventricular response in patients with atrial fibrillation and/or as a component of heart failure therapy)

Antiarrhythmic agents (eg, amiodarone)

Notably, some of these medications may be associated with profound and refractory hypotension during administration of anesthetic agents or a vasoplegic syndrome during or after CPB (eg, ACE inhibitors, amiodarone).

Implantable cardioverter-defibrillators and pacemakers – Patients with end-stage heart failure frequently have an implantable cardioverter defibrillator (ICD) and/or a biventricular pacemaker inserted to provide cardiac resynchronization therapy [49]. Reprogramming of an ICD is necessary to suspend anti-tachyarrhythmia therapy (ie, delivery of shocks or antitachycardia pacing) during the surgical procedure. Also, we routinely reprogram the pacemaker to a higher pacing rate to avoid the need to surgically place epicardial leads that can be a source of bleeding in the postoperative period.

Other aspects of perioperative management of ICDs and pacemakers are discussed elsewhere [50,51]. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator".)

CARDIOVASCULAR MONITORING — In addition to standard anesthesia monitors (eg, pulse oximetry, electrocardiography, non-invasive blood pressure, end-tidal carbon dioxide monitoring, temperature), invasive hemodynamic monitors and transesophageal echocardiography (TEE) are employed. Close attention to noninvasive and invasive monitors is necessary to maintain hemodynamic stability, with an emphasis on support of right ventricular (RV) function.

Invasive hemodynamic monitoring

Intra-arterial catheter – Prior to anesthetic induction, an intra-arterial catheter is inserted for continuous blood pressure monitoring and frequent blood sampling.

Central venous catheter and pulmonary artery catheter – Either before or shortly after anesthetic induction, a large-bore central venous catheter (CVC) is inserted. We routinely use ultrasound to assess vein patency and guide CVC placement.

In addition, a pulmonary artery catheter (PAC) with continuous cardiac output (CO) monitoring capability is inserted to continually assess central venous pressure (CVP), pulmonary artery pressure (PAP), and mixed venous oxygen saturation. We preferably insert CVCs or PACs in the right internal jugular vein, since patients often have a left-sided implantable cardioverter-defibrillator device (ICD) that may complicate PAC insertion.

Transesophageal monitoring – We routinely use TEE during VAD implantation, as discussed below:

(See 'Role of TEE in the prebypass period' below.)

(See 'Role of TEE at the end of CPB' below.)

(See 'Role of TEE in the postbypass period' below.)

INTRAOPERATIVE ANESTHETIC MANAGEMENT

Management before cardiopulmonary bypass

Surgical approaches — Left ventricular assist device (LVAD) implantation has been most commonly performed via a median sternotomy approach. However, the smaller profiles of newer devices allow "minimally invasive," approaches that include hemisternotomy for central aortic cannulation or left thoracotomy (for LVAD inflow graft placement). Possible advantages of a minimally invasive approach include less intraoperative bleeding, less allogenic transfusions of blood product, shorter length of hospital stay, avoidance of potential future redo sternotomy risk, improved postoperative right ventricular (RV) function, and improved postoperative renal function [52,53]. In addition, minimally invasive approaches provide opportunities for enhanced recovery after cardiac surgery (ERACS). (See "Anesthetic management for enhanced recovery after cardiac surgery (ERACS)".)

In general, intraoperative anesthetic management such as invasive monitoring, hemodynamic management, and coagulation management is similar for open versus minimally invasive surgical approaches. However, one lung ventilation may be necessary to achieve better surgical exposure during a minimally invasive approach. (See "One lung ventilation: General principles" and "Lung isolation techniques".)

Prebypass maintenance of hemodynamic stability — Strategies to maintain hemodynamic stability during the prebypass period include:

Placement of defibrillator/pacing pads before induction of anesthesia whether or not the patient has an implantable cardioverter-defibrillator (ICD) or pacemaker. Thus, rapid cardioversion, defibrillation, or pacing can be accomplished if necessary. (See "Perioperative management of patients with a pacemaker or implantable cardioverter-defibrillator", section on 'Placement of transcutaneous pacing/defibrillator pads'.)

Availability of blood products in the operating room with preparations for immediate transfusion if necessary at the time of the surgical incision and sternotomy. Many patients undergoing left ventricular assist device (LVAD) implantation have had at least one prior sternotomy, which increases the likelihood of injury to cardiac or vascular structures during repeat sternotomy. (See 'Prior sternotomy or VAD implantation' above.)

Anesthetic induction in the sitting (ie, upright) position until loss of consciousness is achieved in patients with severe pulmonary venous congestion who cannot tolerate supine positioning.

Careful titration of anesthetic induction agents. We typically employ a combination of intravenous opioid, benzodiazepine, and etomidate or low doses of propofol, followed by slow titration of a volatile anesthetic agent.

Immediate availability of bolus doses and infusions of inotropic or vasopressor agents, which are typically necessary to maintain hemodynamic stability during and after induction of anesthesia (table 5).

Maintenance of general anesthesia with titration of a volatile anesthetic agent, supplemented by small doses of an opioid, and administration of neuromuscular blocking agents as needed. Increased depth of anesthesia may be necessary during painful tunneling of the pump driveline through the abdominal wall in the prebypass period before administration of heparin and onset of cardiopulmonary bypass (CPB).

Preparations for rapid institution of CPB if severe or persistent hemodynamic instability occurs.

Role of TEE in the prebypass period — Transesophageal echocardiography (TEE) in the preimplantation (ie, prebypass) period focuses on identifying or confirming pathophysiologic changes that may require intervention during the LVAD implantation procedure or increase risk for postoperative complications. Reassessment of the features and conditions that were found during preoperative echocardiography studies is important (see 'Preoperative echocardiography and cardiac catheterization' above), but differences in hemodynamic conditions in the prebypass period must be noted as these may impact the findings.

TEE assessments during this prebypass period include:

Ventricular size and function – Preimplantation left ventricular (LV) size and function (including visual estimate of LV ejection fraction) are assessed. RV size and function is also assessed including RV free wall motion, fractional area change (FAC) as a surrogate of RV ejection fraction, and tricuspid annulus plane systolic excursion (TAPSE).

A global RV FAC ≥35 percent is considered normal [54]. However RV FAC is associated with only fair interobserver reproducibility. Patients with a global RV FAC <20 percent are at high risk for RV failure following LVAD support [55].

TAPSE measures the longitudinal lateral annulus displacement, which is the predominant component of the RV ejection, accounting for almost 80 percent of the overall RV function in the normal RV. A TAPSE value <17 mm is the threshold for abnormal RV systolic function [54]. However, TAPSE measurements may be less reliable in assessing RV function in patients who have undergone cardiac surgery because pericardial incision changes the patterns of RV contraction, with relative loss of longitudinal compared with transverse shortening [54-56]. (See "Echocardiographic assessment of the right heart".)

Valve disease – Preimplantation valve disease is assessed (including aortic regurgitation [AR], mitral regurgitation [MR], mitral stenosis [MS], and tricuspid regurgitation [TR]), and implications for perioperative management are considered, as described in detail above. (See 'Preoperative echocardiography and cardiac catheterization' above.)

Of note, underestimation of AR severity is common in patients who are undergoing LVAD placement for advanced heart failure, since the diastolic pressure gradient across the aortic valve is reduced secondary to elevated LV diastolic pressures. For this reason, evaluation for AR should be repeated shortly after institution of CPB when the LV is decompressed and there is direct flow into the ascending aorta through the aortic cannula, which mimics the hemodynamic conditions present during LVAD support. (See "Echocardiographic evaluation of the aortic valve" and "Echocardiographic evaluation of the aortic valve", section on 'Aortic regurgitation'.)

Intracardiac shunts – As discussed above, intracardiac shunts are identified so these can be repaired prior to LVAD placement. (See 'Preoperative echocardiography and cardiac catheterization' above.)

Presence of intracardiac thrombus – The presence of intracardiac thrombus is reassessed prior to CPB since new thrombi may have formed since the most recent preoperative transthoracic echocardiography (TTE) or TEE examination. However, as noted above, the sensitivity of intraoperative TEE for detection of LV thrombus may be limited. (See 'Preoperative echocardiography and cardiac catheterization' above.)

Management of anticoagulation and bleeding — Patients exposed to preoperative intravenous heparin may have decreased circulating antithrombin III (AT-III) levels with consequent heparin resistance such that larger heparin doses may be required to achieve anticoagulation [45]. For those with documented heparin resistance associated with AT-III deficiency, we agree with the Society of Thoracic Surgeons (STS)/Society of Cardiovascular Anesthesiologists (SCA) guidelines for blood conservation that AT-III concentrate (typically 500 to 1000 units is the preferred treatment rather than Fresh Frozen Plasma [FFP]) (algorithm 1) [47]. In particular, AT-III is preferred in patients receiving a VAD as a bridge to heart transplantation since avoiding transfusion of FFP and other blood products minimizes risks of allosensitization. Details regarding management of heparin resistance are described separately. (See "Blood management and anticoagulation for cardiopulmonary bypass", section on 'Heparin resistance'.)

We administer prophylactic antifibrinolytic therapy using a lysine analog (eg, epsilon-aminocaproic acid [EACA] or tranexamic acid [TXA]) to decrease microvascular bleeding in the postbypass period and risk for postoperative mediastinal re-exploration for bleeding. The selected antifibrinolytic agent is typically administered shortly after systemic heparinization, as described in detail separately. (See "Blood management and anticoagulation for cardiopulmonary bypass", section on 'Antifibrinolytic administration'.)

Management during cardiopulmonary bypass

Overview of the implantation procedure — Implantation of an LVAD does not require cross-clamping of the ascending aorta and cardioplegia administration to achieve cardiac arrest. In most patients, implantation can be performed on a beating heart even in those with significant TR requiring surgical intervention. However, if the patient requires surgical aortic valve repair or replacement, mitral valve repair or replacement, or closure of a patent foramen ovale (PFO), then the aorta must be cross-clamped and cardiac arrest is achieved by administration of cardioplegia.

After institution of CPB, the inflow cannula to the LVAD is surgically placed on the anterior surface of the LV apex, lateral to the left anterior descending artery, and pointing toward the mitral valve. The outflow graft is then anastomosed to the ascending aorta using a side-biting clamp. Finally, the LVAD driveline is attached to the external monitor and battery pack.

When the anastomoses are complete, de-airing is performed using a needle in the outflow graft and the aortic root vent (if present). Finally, LVAD pumping is initiated at a low speed (rotations per minute [RPMs]).

Role of TEE at the end of CPB — Before weaning from cardiopulmonary bypass (CPB), transesophageal echocardiography (TEE) is used to assess:

Adequacy of de-airing – Air bubbles in the cardiac chambers appear as highly echogenic mobile targets during TEE examination. These must be removed prior to activation of the LVAD pump to decrease the risk of air embolism and consequent adverse events, particularly embolization into the right coronary artery causing RV ischemia. Since an LVAD can generate negative intraventricular pressure and a suction effect, attention should be paid not only to removing intracardiac air, but also to avoiding entrainment and reintroduction of air by the pump.

Appropriate positioning of the inflow cannula – Ideal LVAD inflow cannula position is in the LV apex aligned with the mitral valve opening and not too close to the interventricular or lateral walls [23]. Cannula position should be routinely evaluated in two-dimensional and three-dimensional TEE imaging in the mid-esophageal long axis views of the LV with color flow and spectral Doppler interrogation (figure 2). Color flow Doppler interrogation at the inflow cannula opening should demonstrate unidirectional and nonturbulent low velocity flow [23]. In addition, continuous or pulse wave Doppler interrogation should demonstrate unobstructed flow from the inflow cannula with peak velocities of 1 to 2 m/second [23,57].

Appropriate positioning of the outflow cannula – Ideal outflow cannula position is in the ascending aorta. It is evaluated in the mid-esophageal ascending aorta short-axis or long-axis views at the level of the right pulmonary artery. Continuous wave Doppler interrogation should demonstrate velocities ≤2 m/second (figure 3) [23,57]. Higher velocities typically indicate obstruction at the anastomotic site that requires surgical intervention. However, if the site of obstruction is remote from the anastomotic site, velocities may be low with a faint Doppler signal that has less systolic/diastolic variability [23,57]. These latter findings should raise suspicion that there may be obstruction or kinking that is between the LVAD pump and the anastomotic site. While the diagnosis of such proximal obstruction cannot be made echocardiographically, discussion of potential causes with the surgical team at the time of LVAD implantation is appropriate.

Weaning from cardiopulmonary bypass — Inotropic and/or vasopressor support is typically necessary to wean from CPB (table 5). Weaning to full LVAD support is gradually achieved by lowering CPB flows with incremental increases in VAD flow by increasing pump speed (RPMs) with continuous TEE and hemodynamic monitoring to ensure that the following conditions are present (see 'Role of TEE at the end of CPB' above):

Appropriate LV decompression without suctioning on the wall of the LV (which would cause leftward interventricular septum shift and may provoke LV collapse) [23].

Interventricular septum that is in a normal midline position [23]. A leftward shift of the septum suggests volume depletion or excessive pump speed and is treated by administering fluid (if central venous pressures [CVPs] are low), or by reducing pump speed (RPMs). Insufficient unloading of the LV causes a rightward shift of the septum; this is treated by increasing pump speed (RPMs).

Adequacy of RV function, with attention on RV size, contractility, and the severity of TR as a sign of RV failure [23]. Exacerbation of RV failure may occur immediately after LVAD implantation due to the effects of CPB and decreases in LV pressure and size which lead to interventricular septal bowing to the left with distortion of RV geometry and mechanics (figure 4) [4-7,17,19-21].

Appropriate LV unloading after the institution of LVAD flow should produce a reduction in pulmonary artery pressure (PAP) compared with baseline PAP, indicating reduction in LV filling pressures and afterload reduction of the LV [23]. Further LVAD speed adjustments are made as necessary based on mean arterial pressure (MAP) and PAP measurements as well as continuous TEE monitoring.

Problems that may occur due to inappropriate LVAD speed include:

If the LVAD speed is set too low the result may be low flow with insufficient systemic circulatory support.

If the LVAD speed is set too high relative to preload, a suction event may occur with partial occlusion of the LVAD inflow cannula by LV myocardium. A suction event may severely reduce LV flow and provoke arrhythmias. Suction is suggested by the presence of excessive LV decompression with small LV size, and may be a manifestation of severe hypovolemia, severe RV dysfunction, or any other cause of decreased preload to the LV. Treatment includes gradual reduction of pump speed (ie, RPMs), while increasing MAP with a vasopressor infusion and titrated fluid administration. (See "Emergency care of adults with mechanical circulatory support devices", section on 'Approach to the unconscious patient'.)

Management after cardiopulmonary bypass

Postbypass fluid and hemodynamic management — After LVAD implantation, we typically maintain MAP between 70 to 80 mmHg. Continuous TEE monitoring and measurements obtained from the pulmonary artery catheter (PAC), including continuous cardiac output (CO), PAP, CVP, and mixed venous oxygen saturation are all used to guide hemodynamic management in the post-implantation period. Continuing infusion of inotropes and/or vasopressors (eg, epinephrine, milrinone, vasopressin) is typically necessary to support RV contractility and maintain RV coronary perfusion in the postbypass period. LVAD filling may be limited by elevations in transpulmonary gradients and high pulmonary vascular resistance (PVR) resulting in a low flow state. In some cases, direct pulmonary vasodilators (eg, inhaled nitric oxide, epoprostenol) are necessary to reduce PVR. Other strategies to achieve optimal right heart function are described below. (See 'Right heart failure' below.)

With adequate filling and optimal unloading, the LV can be entirely supported by LVAD outflow [23]. Meticulous fluid management is necessary after VAD implantation to maintain adequate cardiac filling while simultaneously avoiding RV volume overload. Fluid management is often challenging, particularly when the patient is coagulopathic and has ongoing bleeding requiring transfusion. (See 'Coagulopathy and bleeding' below.)

Role of TEE in the postbypass period — The role of TEE post-implantation focuses on assessing the results of the surgical procedure and detecting any actual or potential problems that require intervention upon separation from CPB or during the postbypass period before leaving the operating room [23]. All components of the pre-implantation and post-bypass TEE examination are repeated. (See 'Preoperative echocardiography and cardiac catheterization' above and 'Role of TEE in the prebypass period' above.)

TEE provides continuous physiologic information regarding LV unloading, LV filling, and RV function:

As described above, when LV filling is optimal the interventricular septum is positioned midline without leftward or rightward displacement [23]. A leftward shift of the interventricular septum indicates inadequate LV preload or excessive LV unloading, which is treated by administering fluid (if CVPs are low), or by reducing pump speed (RPMs). A rightward shift indicates insufficient unloading of the LV, which is treated by increasing pump speed (RPMs).

Greater than mild functional MR may indicate insufficient unloading of the LV, and may diminish or resolve by increasing the pump speed (RPMs) [23].

If LV and RV cavity sizes are small, then hypovolemia is likely and should be treated with fluid administration.

Decreased size of the LV accompanied by RV dilation and dysfunction suggests decreased preload to the LVAD due to failure of the RV. The presence of an LVAD often transiently worsens RV function and severity of TR due to changes in the geometry of the RV and tricuspid valve apparatus. Furthermore, RV dysfunction is temporarily worsened by the effects of CPB. Treatment options for RV dysfunction are described below. (See 'Right heart failure' below.)

A PFO may be detectable only after LVAD implantation. In one study, detection occurred in 20 percent of patients with a PFO only after implantation of the LVAD [58]. Return to CPB for PFO repair is usually unnecessary unless shunting through the PFO significantly affects LVAD function.

The presence of AR will reduce effective forward LVAD flow; moderate or severe AR can compromise LV unloading and is addressed (surgical repair or replacement) before leaving the operating room [23].

Problems in the post-bypass period

Right heart failure — Significant RV dysfunction occurs in approximately one-third of patients undergoing LVAD implantation and is a predictor of early and late mortality [17-21]. Early failure of RV output in the operating room may be evidenced by a decreased MAP, elevated CVP, low CO, and echocardiographic evidence of RV dysfunction in the presence of an adequately unloaded LV. The result is insufficient delivery of volume to the left heart leading to low LVAD pump output. RV dysfunction may manifest as LVAD suction events with insufficient forward flow, hypotension, as well as an increased CVP. While an increased CVP associated with depressed CO and LVAD output is usually a sign of RV dysfunction, prompt TEE evaluation is indicated to determine if RV dysfunction is present and to rule out cardiac tamponade as a cause of this hemodynamic state.

Strategies to achieve optimal RV performance include:

Meticulous management of fluid and/or blood administration to maintain adequate cardiac filling for RV support, with avoidance of RV volume overload by constantly monitoring CVP and RV size with TEE (and direct visualization while the chest remains open).

Careful unloading of the LV with gradual titration of LVAD speeds as hemodynamic and TEE data are continuously assessed. We adjust LVAD speed to avoid either a leftward or rightward shift of the interventricular septum.

Infusion of inotropes to support RV contractility (eg, epinephrine, milrinone) (table 5).

Infusion of vasopressors (eg, vasopressin) if necessary to maintain adequate MAP and RV perfusion pressure (table 5).

Avoidance of factors that increase PVR and RV afterload (eg, hypoxia, hypercarbia, atelectasis, high positive end-expiratory pressures, respiratory acidosis).

If necessary, use of direct pulmonary vasodilators (eg, inhaled nitric oxide, epoprostenol) to reduce PVR and decrease RV afterload [59]. (See "Anesthesia for noncardiac surgery in patients with pulmonary hypertension or right heart failure", section on 'Hemodynamic management'.)

If RV function deteriorates significantly during attempted sternal closure, delayed closure may be necessary.

In some patients, insertion of a temporary right ventricular assist device (RVAD) is used as a strategy to manage patients with acute severe refractory right ventricular failure after LVAD implantation [17]. Although RVAD placement in the perioperative period is associated with postoperative mortality [44], early institution of mechanical support for the RV results in better survival than delayed conversion to biventricular support [60].

Coagulopathy and bleeding — After neutralization of heparin with protamine administration (see "Achieving hemostasis after cardiac surgery with cardiopulmonary bypass", section on 'Reversal of anticoagulation'), we obtain standard laboratory tests include prothrombin time, activated partial thromboplastin time, international normalized ratio, fibrinogen level, and platelet count. In addition, point-of-care (POC) viscoelastic tests of coagulation are often used to supplement standard laboratory tests of hemostatic function (eg, thromboelastography [TEG] or an adaptation of TEG known as rotational thromboelastometry [ROTEM]) (table 6). Such POC tests allow rapid assessment of causes of coagulopathy and responses to treatment such as transfusion of blood products or administration of a hemostatic agent. (See "Intraoperative transfusion and administration of clotting factors", section on 'Standard tests' and "Intraoperative transfusion and administration of clotting factors", section on 'Point-of-care tests'.)

We use a goal-directed protocol or algorithm, based on measurement of hemoglobin or hematocrit as well as assessment of specific abnormalities of hemostasis, to guide transfusion decisions and avoid unnecessary transfusions of blood products. (See "Achieving hemostasis after cardiac surgery with cardiopulmonary bypass", section on 'Use of transfusion algorithms'.)

In patients with persistent severe bleeding, our algorithm suggests administration of low dose prothrombin complex concentrates (PCCs) [61-63]. Administering a PCC in the setting of low-flow or stasis incurs risk for thrombosis. In one study that included 530 patients undergoing LVAD implantation, 27 patients received low-dose PCC (10 to 15 units/kg) to correct persistent coagulopathy unresponsive to transfusion of appropriate blood products [63]. In this study, the 21 patients receiving intermediate- or long-term VADs had no instances of perioperative pump thrombosis. However, pump thrombosis was noted in one patient with an RVAD, and in three of the six patients who had received a short-term LVAD. (See "Achieving hemostasis after cardiac surgery with cardiopulmonary bypass", section on 'Prothrombin complex concentrate products'.)

In some patients with refractory persistent bleeding, recombinant activated factor VII (rFVIIa) may be administered. However, thromboembolic risk is a particular concern with this agent; thus, it is reserved for use only in patients with intractable, non-surgical bleeding [64,65]. (See "Achieving hemostasis after cardiac surgery with cardiopulmonary bypass", section on 'Recombinant activated factor VII'.)

If bleeding persists after transfer of the patient to the intensive care unit, we typically continue infusion of antifibrinolytic therapy (ie, TXA or EACA). (See "Blood management and anticoagulation for cardiopulmonary bypass", section on 'Antifibrinolytic administration'.)

Vasoplegia — Severe systemic vasodilation (vasoplegia, vasodilatory shock) with markedly decreased systemic vascular resistance is common after CPB. Risk factors for vasoplegia are often present in patients with end-stage heart failure (eg, preoperative use of angiotensin-converting enzyme [ACE] inhibitors, calcium channel blockers, or heparin, as well as prebypass hemodynamic instability) [66-68].

If MAP is low in a patient with adequate preload and RV function after LVAD implantation, vasoplegia should be excluded as the cause of low MAP. Pharmacologic agents used for treatment include norepinephrine and vasopressin; in refractory cases, methylene blue, angiotensin II, vitamin C, or hydroxycobalamin have been administered (table 5) [69-85]. (See "Intraoperative problems after cardiopulmonary bypass", section on 'Vasoplegia'.)

Persistent postoperative vasoplegia has been associated with increased morbidity and mortality rates, length of stay in the intensive care unit and hospital, and costs after VAD implantation [86]. (See "Postoperative complications among patients undergoing cardiac surgery", section on 'Vasodilatory shock'.)

MANAGEMENT OF POSTOPERATIVE PAIN — Patients remain intubated and sedated with controlled mechanical ventilation during the immediate postoperative period. Standard systemic analgesic pain management strategies are employed (see "Pain control in the critically ill adult patient"). Analgesic options after left ventricular assist device (LVAD) implantation include continuous bilateral erector spinae plane blocks [87,88]. Pectoralis I, pectoralis II, or serratus anterior plane blocks have been used for minimally invasive LVAD implantation [89]. (See 'Surgical approaches' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Heart failure in adults".)

SUMMARY AND RECOMMENDATIONS

Preanesthetic assessment – Preoperative discussions with the cardiology team managing the patient's end-stage heart failure and the cardiac surgical team performing implantation of a ventricular assist device (VAD) are important for assessment of urgency and patient-specific management of associated organ dysfunction (eg, renal insufficiency, hepatic dysfunction). (See 'Preanesthetic assessment' above and 'Assessment of urgency' above and 'Evaluation of other organ systems' above.)

Cardiovascular monitors

Invasive hemodynamic monitoring including an intra-arterial catheter and a pulmonary artery catheter (PAC) with continuous cardiac output (CO) monitoring capability are inserted; central venous pressures (CVP), pulmonary artery pressures (PAP), and mixed venous oxygen saturation are also monitored, and TEE is employed. (See 'Cardiovascular monitoring' above.)

Use of echocardiography – We routinely use transesophageal echocardiography (TEE):

-(See 'Role of TEE in the prebypass period' above.)

-(See 'Role of TEE at the end of CPB' above.)

-(See 'Role of TEE in the postbypass period' above.)

Prebypass period – Strategies to maintain hemodynamic stability during the prebypass period include (see 'Prebypass maintenance of hemodynamic stability' above):

Reprogramming of an implantable cardioverter defibrillator (ICD) to suspend anti-tachyarrhythmia therapy and to reset the pacemaker to a higher pacing rate threshold (see 'Preoperative medication and device management' above)

Placement of defibrillator/pacing pads before induction of anesthesia

Availability of blood products in the operating room for immediate transfusion if necessary. In particular, patients with previous sternotomy are at risk of significant blood loss due to injury to the cardiac chambers, great vessels, internal mammary artery graft if present, previously implanted VAD cannulae during redo sternotomy, or during removal of a previously implanted VAD. Thus, adequate cross-matched blood products are immediately available in the operating room prior to sternotomy. (See 'Prior sternotomy or VAD implantation' above.)

Anesthetic induction in the sitting or upright position in patients with severe pulmonary hypertension who cannot tolerate supine positioning

Careful titration of anesthetic induction agents

Immediate availability of bolus doses and infusions of inotropic or vasopressor agents

Titration of anesthetic agents

Preparations for rapid institution of cardiopulmonary bypass (CPB) for severe hemodynamic instability.

Device implantation during CPB – Implantation of a left ventricular assist device (LVAD) is typically performed on a beating heart during CPB without cross-clamping of the ascending aorta or cardioplegia administration. Exceptions include the need for a concomitant surgical procedure (eg, aortic valve repair/replacement, closure of a PFO). (See 'Overview of the implantation procedure' above.)

Weaning from CPB

Before weaning from CPB, TEE is used to assess (see 'Role of TEE in the prebypass period' above):

-Adequacy of de-airing and absence of entrainment of air by the pump

-Appropriate positioning of the inflow cannula in the LV apex aligned with the MV opening and not too close to the interventricular or lateral walls

-Appropriate positioning of the outflow cannula in the ascending aorta

Inotropic and/or vasopressor support is typically necessary to wean from CPB (table 5). Weaning to full LVAD support is gradually achieved by lowering CPB flows with incremental increases in VAD flow by increasing pump speed (rotations per minute [RPMs]) with continuous TEE and hemodynamic monitoring to ensure (see 'Weaning from cardiopulmonary bypass' above):

-Appropriate LV decompression without suctioning on the LV wall or LV collapse

-Midline positioning of the interventricular septum

-Adequacy of RV function, with attention focused on RV size, contractility, and the severity of TR

-Appropriate LV unloading after institution of VAD flow, which should produce lower PAP compared with baseline

-Appropriate adjustment of VAD speed

Postbypass period – After LVAD implantation, we typically maintain mean arterial pressure (MAP) between 70 to 80 mmHg with vasopressor and/or inotropic support and meticulous fluid management to maintain adequate cardiac filling, while simultaneously avoiding RV volume overload (see 'Postbypass fluid and hemodynamic management' above). Problems in the postbypass period may include:

Right heart failure. (See 'Right heart failure' above.)

Coagulopathy and bleeding. We use a goal-directed algorithm based on measurement of hemoglobin as well as assessment of specific abnormalities of hemostasis to guide transfusion decisions. (See 'Coagulopathy and bleeding' above.)

Vasoplegia manifesting as low MAP and leftward shift of the interventricular septum. Treatment typically includes norepinephrine and vasopressin. In refractory cases, methylene blue, angiotensin II, vitamin C, or hydroxycobalamin have been administered. (See 'Vasoplegia' above.)

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References

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