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Perioperative Echocardiographic Examination for Ventricular Assist Device Implantation

Chumnanvej, Siriluk MD*; Wood, Malissa J. MD; MacGillivray, Thomas E. MD; Melo, Marcos F. Vidal MD, PhD*

doi: 10.1213/01.ane.0000278088.22952.82
Cardiovascular Anesthesia: Review Article
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Ventricular assist devices (VADs) are systems for mechanical circulatory support of the patient with severe heart failure. Perioperative transesophageal echocardiography is a major component of patient management, and important for surgical and anesthetic decision making. In this review we present the rationale and available data for a comprehensive echocardiographic assessment of patients receiving a VAD. In addition to the standard examination, device-specific pre-, intra-, and postoperative considerations are essential to the echocardiographic evaluation. These include: (a) the pre-VAD insertion examination of the heart and large vessels to exclude significant aortic regurgitation, tricuspid regurgitation, mitral stenosis, patent foramen ovale, or other cardiac abnormality that could lead to right-to-left shunt after left VAD placement, intracardiac thrombi, ventricular scars, pulmonic regurgitation, pulmonary hypertension, pulmonary embolism, and atherosclerotic disease in the ascending aorta; and to assess right ventricular function; and (b) the post-VAD insertion examination of the device and reassessment of the heart and large vessels. The examination of the device aims to confirm completeness of device and heart deairing, cannulas alignment and patency, and competency of device valves using two-dimensional, and color, continuous and pulsed wave Doppler modalities. The goal for the heart examination after implantation should be to exclude aortic regurgitation, or an uncovered right-to-left shunt; and to assess right ventricular function, left ventricular unloading, and the effect of device settings on global heart function. The variety of VAD models with different basic and operation principles requires specific echocardiographic assessment targeted to the characteristics of the implanted device.

From the *Department of Anesthesia and Critical Care; †Division of Cardiology, Department of Medicine; and ‡Cardiac Surgical Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.

Accepted for publication May 24, 2007.

Supported, in part, by the Department of Anesthesia and Critical Care, MA General Hospital and Harvard Medical School. Dr. Chumnanvej was supported by a scholarship of the Phramongkutklao Hospital, Bangkok, Thailand.

Address correspondence and reprint requests to Marcos F. Vidal Melo MD, PhD, Department of Anesthesia and Critical Care, MA General Hospital, 55 Fruit St., Boston, MA 02114. Address e-mail to mvidalmelo@partners.org.

This article has supplementary material on the Web site: www.anesthesia-analgesia.org.

Since their first clinical use in the 1980s, ventricular assist devices (VADs) have benefited thousands of patients suffering from end-stage heart failure. Current devices provide a broad spectrum of support, ranging from short-term to intermediate- and long-term duration (1,2), as a bridge to cardiac transplantation (3) or recovery, or as destination therapy (4,5). The Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure trial demonstrated that the use of a left VAD (LVAD) resulted in a clinically meaningful survival benefit and improved quality of life for patients with symptoms of New York Heart Association class IV heart failure despite optimal medical management (5). This positioned LVADs as an alternative therapy for congestive heart failure in selected patients who are not candidates for cardiac transplantation. Improvements in preoperative selection, perioperative techniques, and postoperative care, resulted in the reduction of mortality and morbidity after device implantation. With these advances, the number of patients undergoing cardiothoracic surgery for device implantation and noncardiac surgery for post-device insertion events is expected to increase.

Transesophageal echocardiography (TEE) is an important tool in the perioperative management of patients undergoing VAD implantation. TEE has been shown to provide critical information on the diagnosis of preinsertion abnormalities, and the evaluation of postinsertion function (6,7). In this review we will present the rationale for a comprehensive assessment of the patient undergoing VAD implantation focusing on perioperative considerations for TEE examination. To further illustrate this manuscript, a collection of representative TEE images on several topics discussed is accessible as digital clips on the website of Anesthesia & Analgesia (www.anesthesia-analgesia.org).

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OVERVIEW OF THE FUNCTION OF VADs

VADs are electromechanical pumps used for circulatory support of patients with severe heart failure. They are usually positioned in parallel with the circulation and comprise the following essential components: 1) an inflow cannula that brings the blood from one of the heart chambers to the device, 2) a pump for propulsion of blood, 3) an outflow cannula that returns the blood to the patient, and 4) a controller, which receives and processes information from the pump and returns information for pump operation. Typically, for a LVAD, the inflow cannula originates in the left atrium (LA) or left ventricle (LV) and the outflow cannula is anastomosed to the ascending aorta. Anastomosis to the descending aorta has been used in some new devices (8) and alternative surgical approaches (9). This approach is uncommon, and has generally been done with axial flow devices, particularly the Jarvik. For a right VAD (RVAD), the inflow cannula originates in the right atrium (RA) or right ventricle (RV) and the outflow cannula is anastomosed to the main pulmonary artery (PA). Mechanical or bioprosthetic valves in the inflow and outflow circuit provide directionality of flow in pulsatile devices. Different devices and controllers range from paracorporeal VADs with transcutaneous inflow and outflow cannulas or intracorporeal VADs with transcutaneous drivelines, to completely implantable intra- or extraventricular systems. The blood propulsion mechanism also ranges from traditional roller pumps (e.g., Stöckert) to pulsatile pumps (e.g., ABIOMED BVS5000, HeartMate I, Novacor, Thoratec), and up to recent axial-flow devices (e.g., HeartMate II, Jarvik2000, MicroMed DeBakey) (10–12) and centrifugal pumps (Biomedicus and TandemHeart) devices (13,14).

The VAD performance characteristics produce distinctive relationships between pressure and flow in the circulation. These will determine measured echocardiographic data, such as the continuous (CW) and pulsed wave (PW) Doppler signals (6,15). In pneumatic or electric pulsatile pumps, “fill to empty” is used to describe the method of operation by passive draining or active suctioning of blood from the atrium or ventricle across an inflow valve, and, once the device chamber is filled, active blood pumping through an outflow valve into the outflow path (aorta or PA). This defines the automatic mode of operation, which typically produces higher pressures at lower flows when compared to axial flow pumps. These devices totally depend on the patient’s preload status for adequate pump output to support systemic circulation, and will increase or decrease their pumping frequency according to the rate of device filling. For this reason, the patient’s cardiac cycle and the pulsatile VAD cycle are not usually in synchrony when run in this mode (16). In contrast, in the fixed mode of operation, the VAD is set to pump at a fixed rate regardless of VAD volume. This mode is used temporarily in the operating room for initial hemodynamic adjustments and in patients receiving a VAD as destination therapy. Because of the larger size, requirement of unidirectional valves in the VAD inflow and outflow cannulas, and complicated control mechanism of these pulsatile VADs, axial flow pumps have been gaining popularity (12). In nonpulsatile axial-flow pumps, the operation is based on a rotating impeller pump, which propels blood to the systemic circulation at a fixed rate depending on pump speed and inflow–outflow pressure gradient. The advantages of these systems are that they are smaller, they do not require unidirectional valves, they are more durable, and they typically generate higher flows at lower pressures.

Overall, given the several different models of VADs presently available, it is essential that the echocardiographer have a clear understanding of the specific device at hand to perform a suitable postinsertion examination.

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ECHOCARDIOGRAPHIC EXAMINATION

Echocardiographic assessment of the patient undergoing VAD insertion involves aspects pertaining both to a general echocardiographic examination and to the specific considerations associated with the VAD (Table 1). As in most echocardiographic assessments, a comprehensive examination is required (17–20). TEE is ideal for defining LVAD dysfunction in the perioperative setting. Transthoracic echocardiography (TTE) is less invasive and simple to use, although it may be technically difficult in the presence of postsurgical changes, respiratory disease, obesity, and chest wall deformities (6,7,21). Consequently, combined information from both TTE and TEE is used postoperatively (22). In each of the following sections, we will first discuss the pre-VAD insertion examination and then the post-VAD insertion examination with specific considerations regarding type of VAD being assessed.

Table 1

Table 1

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DEFECTS CREATING INTRACARDIAC SHUNTS

Patent Foramen Ovale

Investigation of a Patent Foramen Ovale (PFO) should always be performed before and after cardiopulmonary bypass (CPB) for implantation of a VAD. Because a PFO is common [27.3% in one study (23)], meticulous care should be taken to identify its presence. Contrast (agitated saline or bubble study) and color Doppler TEE are highly sensitive and specific methods for diagnosis of a PFO and for estimating the degree of shunt flow (24).

In the pre-CPB period, examination of the interatrial septum of the patient with LV failure will often show a rightward deviation (25) indicative of increased LA pressure surpassing the RA pressure. Because of this factor, investigation of a PFO with color Doppler echocardiography may clearly show a left-to-right shunt. In contrast, a bubble study may not reveal a PFO due to the difficulty in producing a transient reversal of the left-to-right pressure gradient in the presence of left heart failure, even when a Valsalva maneuver release is correctly applied. Additionally, hemodynamic instability may occur with the Valsalva maneuver, preventing its use. Clinical judgment should be exercised when using that maneuver in the patient with heart failure. In the case of biventricular failure, increased RA and LA pressures reduce the interatrial pressure gradient, hindering PFO detection by both agitated saline and color Doppler. After insertion of a LVAD, there is LV unloading with decrease of the LA pressure. This hemodynamic change, in association with maintained or increased right heart pressures, may uncover an unsealed PFO, as reported in 3 of 14 patients without a PFO in the pre-CPB examination who presented with a PFO after LVAD activation (26). Those hemodynamic conditions can also favor a paradoxical embolism. One of the serious consequences of this sequence of events is the development of severe hypoxemia in the presence of pulmonary hypertension. Significant right-to-left shunting can be visualized with TEE and present as severe hypoxemia acutely upon activation of the LVAD, resolving with interruption of LVAD function (27,28), or months after LVAD support from a previously unrecognized PFO (29). TEE assessment for PFO after VAD insertion can be started early, while weaning from CPB, and a PFO can be potentially detected even before complete separation. Early detection is important, because the presence of a PFO requires return to CPB for closure.

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Other Septal Abnormalities

Traumatic atrial septal defects (fossa ovalis) can occur intraoperatively and, as discussed above, also produce profound hypoxemia in the setting of increased right-to-left atrial pressure gradient with LVAD support (30). The degree of shunting across an interatrial septal defect may be aggravated by chest closure, which results in RA pressure increases due to: direct transmission of increased pleural pressure to the RA, decrease in the effective compliance of the RV (30), and reduction in LV filling due to ventricular interdependence in the presence of negative intrathoracic pressure from chest tube suction (31).

Finally, ventricular septal defects, particularly postinfarct, are a potential cause of significant shunting before and after VAD placement.

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VALVULAR AND ASCENDING AORTIC DEFECTS

Aortic Valve

Normal function of the LVAD during full support usually prevents systolic opening of the native or prosthetic aortic valve, given the increase in the aortic-to-LV pressure gradient due to the suction of the blood from the LV through the inflow cannula and its propulsion into the aorta though the outflow cannula. This is typically the case with pulsatile VADs generating full cardiac output. In contrast, VADs that provide partial [e.g., Jarvik 2000 (32)] or variable (e.g., HeartMate II) support will be associated with intermittent opening of the aortic valve. M-mode imaging can be used in these cases to assess the duration of aortic valve opening (15). In some axial flow devices, such as the Impella, TEE examination of the aortic valve includes device positioning.

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Aortic Insufficiency

Diagnosis of significant pre- and postoperative Aortic Insufficiency (AI) is crucial in the patient receiving a LVAD. The presence of AI reduces the forward flow produced by the LVAD due to the regurgitation of LVAD-supported flow into the LV cavity.

Echocardiographic evaluation of AI pre-LVAD insertion can be difficult, because the degree of AI may be underestimated in heart failure patients (33). This is due to increased LV end-diastolic pressure and low aortic diastolic pressure resulting in diminished transvalvular gradients. For this reason, aortic competence should also be assessed during CPB by intraoperative TEE before the insertion of the LVAD (33) (Fig. 1A) when transvalvular gradients are closer to those to be observed after LVAD insertion. Identification of severe and, possibly, moderate AI should indicate the need for surgical correction (34). Of additional significance for patient management, severe AI may be associated with RV diastolic dysfunction due to remodeling of the RA, RV, and LV (35). This could affect optimal RV performance after LVAD implantation.

Figure 1

Figure 1

There is considerable controversy regarding the surgical intervention to be performed, and evaluated echocardiographically, once AI is diagnosed. In patients who require long-term support as a bridge to transplant, closure of the leaflets with pledgeted and commissural sutures, or over-sewing of an incompetent aortic valve with pericardial patch, may provide a safeguard against peripheral embolization and regurgitation (33,36) (Figs. 1B–D). On the other hand, in LVAD patients who receive short-term support as a bridge to recovery, the incompetent aortic valve may be repaired or replaced at the time of LVAD placement (33,37).

The risk for the development of significant AI is increased during LVAD support because the closed native valve is exposed to systolic pressure rather than diastolic pressure levels (38). The presence of the VAD cannula in the ascending aorta can also lead to valvular distortion and alteration in the aortic flow pattern conducive to insufficiency. Despite this, the incidence of AI after LVAD insertion in patients without previous aortic insufficiency is low (7) and may present months later (39,40). Mechanisms producing post-LVAD AI include endocarditis (41), aortic dissection (42,43), and aortic leaflet prolapse or perforation. Development of AI in previously competent native aortic valves requiring reoperation may become more prevalent as the use of LVAD for destination therapy increases (33). In our institution, we did not observe a significant change in the degree of AI quantified by echocardiography (trace = 19, mild = 10, moderate = 2) between pre- and early (10 wk) post-LVAD placement in 31 patients. One of our patients developed AI 20 mo after LVAD insertion due to thickening of multiple aortic leaflets and ascending aortic dilation.

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Aortic Stenosis

Preoperative Aortic Stenosis (AS) is usually not critical to the LVAD recipient because pulsatile devices typically generate full cardiac output and, thus, systemic blood flow does not depend on antegrade flow through the aortic valve (33). In VADs that provide partial or variable support, such as axial flow devices, intermittent opening of the aortic valve occurs and contributes to global cardiac output. Consequently, patients with severe AS may not be good candidates for such devices. AS can occur during LVAD support due to progressive thrombosis of the aortic valve (44) and commissural fusion (45). In a retrospective study, 7 of 33 hearts were found to have varying degrees of aortic valve cusp fusion after chronic LVAD support (46). Thrombosis is due to blood stasis, low level of anticoagulation, and limited or absent aortic valve movement during LVAD function. This can be a significant problem, particularly for patients in whom the device is being used as a bridge to recovery (44,45,47,48). It has been recommended that a bioprosthetic valve be used when aortic valve replacement is performed in the presence of a LVAD (33,36). Thrombotic complications may be less frequent with the new axial propulsion VADs, because intermittent opening of the aortic valve is a target for device setting (e.g., opening of the aortic valve documented echocardiographically once every three cardiac cycles for a HeartMate II and reduction of pump output in the Jarvik 2000 to allow for ventricular ejection through the aortic valve) (15).

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Prosthetic Aortic Valves

The main issue due to the presence of an aortic valve prosthesis is the risk of valve thrombosis and subsequent systemic thromboembolism. For this reason, there is current agreement that mechanical valves should not be used intraoperatively and, if present preoperatively, they should be substituted by a bioprosthesis or a patch closure. Even tissue valves may require over-sewing to prevent thromboembolism (33,36,47).

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Ascending Aorta

The ascending aorta should be examined to detect abnormalities before performing the end-to-side anastomosis of the outflow cannula. A mid-esophageal (ME) ascending aortic long-axis view should be used to locate and classify structural abnormalities in the ascending aorta. The aortic arch and descending aorta should be assessed with the same goal. Atheromata with thickness ≥5 mm and/or protruding and/or mobile components are associated with increased risk of cerebral embolic events during cardiac surgery (49–51). Epiaortic echocardiography can be alternatively used for better assessment of the ascending aorta, particularly when high grade lesions are found in the descending aorta (52). The presence of an ascending aortic aneurysm should lead to aneurysm repair. In this case, during VAD implantation, the LVAD outflow cannula is anastomosed to the ascending aortic graft.

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Tricuspid Regurgitation

Functional Tricuspid Regurgitation (TR) is a common finding in the patient with heart failure (53). Adequate RV function is essential after LVAD insertion to optimize LVAD filling. The presence of significant postoperative TR can significantly contribute to RV dysfunction and the development of a low output state.

The assessment of the tricuspid valve (TV) by echocardiography is dependent upon the preload and afterload conditions of the RA and RV, and the RV contractility (54). Increased RV preload and afterload lead to RV enlargement and subsequent incompetence of the tricuspid apparatus (tricuspid annulus dilation and chordal tension) (38,55). Given that LVAD insertion produces unloading of the LV and a decrease in PA pressure, it could be expected that TR would be reduced postinsertion. This has been found by some authors (6,33), but not by others (38) who reported an acute worsening in TR after LVAD insertion. The fact that isolated implantation of an LVAD does not produce a consistent change in the degree of perioperative TR (33) is likely associated with a combination of factors, including the leftward shift of the interventricular septum produced by the LVAD; an increase in PA pressure and RV dysfunction due to the inflammatory response to surgery, CPB and blood transfusion; and the increase in preload to the RV due to an increased left-sided output delivered by a functioning LVAD in lieu of the previous failing left heart. Leftward interventricular septal shift is more pronounced in LVAD patients who are hypovolemic and who have higher VADs flows. The appreciable influence of LVAD settings on the degree of TR by shifting the interventricular septum with the unloading of the LV can be observed in devices such as the HeartMate II, which generates flow through a turbine mechanism. Excessively high flow settings (LV output flow through the pump) in these devices can exacerbate TR, presumably by mechanisms such as distraction of the septal papillary muscle with systolic restriction of septal leaflet motion and distortion of the tricuspid annulus. Relative RV overload and increased PA pressures can further contribute to worsened TR. Once identified echocardiographically, the effect of those mechanisms is minimized by adjusting pump flow (decreasing pump speed) (Fig. 2). Such adjustment leads not only to the reduction of the TR, but can also result in improved RV function. Finally, it has been suggested that the absence of significant TR does not imply that the tricuspid orifice is free from abnormality, with significant tricuspid annular dilation representing a particularly important risk for postoperative TR (54). All these factors indicate the importance of a meticulous examination of the TV pre-LVAD insertion, not only in the diagnosis of TR but also in the definition of its mechanism.

Figure 2

Figure 2

The detailed analysis of the TV and definition of the mechanism of TR have important consequences for the planning of the surgery. Surgical techniques are available to reduce the degree of TR in the setting of device implantation, and may result in significant improvement in RV function and remodeling of the RV, with reduction in size and enhanced ejection fraction (56). Our experience in the analysis of 36 cases of LVAD insertion showed that the performance of a tricuspid annuloplasty in 11 of those patients provided a consistent reduction in TR, as assessed by TEE or TTE, with grading of TR reduced from moderate–severe to no–mild TR (57). In contrast, LVAD insertion per se, without tricuspid intervention, produced no uniform change in the degree of TR. This is in line with Rao et al. (33) who recommended an annuloplasty ring in the presence of moderate or greater TR. Prophylactic tricuspid repair, however, is discouraged, given the trivial improvement on RV performance and the risk of complications such as pulmonary embolism (33). Overall, these studies suggest that a tricuspid intervention should be considered when significant TR is present and reliable improvement in TR would represent a significant factor for optimization of RV performance after LVAD insertion, as in the presence of RV dysfunction pre-CPB, or when significant structural tricuspid abnormalities are present.

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Mitral Valve

Mitral Regurgitation

Functional Mitral Regurgitation (MR) is a significant and common complication of end-stage heart failure and cardiomyopathy (53,58). This form of MR is characterized by a central jet on the color Doppler image, which has been reported to be of at least moderate severity in 39% of the patients in a retrospective study of patients with advanced systolic heart failure (59). Incomplete leaflet coaptation secondary to remodeling of both the mitral annulus (increased anteroposterior diameter and intertrigonal distance) and the LV produces the MR. LV shape changes include increased sphericity and generalized dilation of the chamber. Individuals with ischemic cardiomyopathies often exhibit focal apical displacement of the papillary muscles with characteristic valve tethering (60,61). LV sphericity seems to be the primary determinant of functional MR during congestive heart failure (60,62) whereas the other factors contribute to the worsening of MR (59,62).

Insertion of a LVAD leads to reduced LV size, improved coaptation of the mitral valve leaflets and, ultimately, decreased preexisting MR (38). Persistence of significant MR post-LVAD insertion may indicate inadequate LV decompression. Results in our institution are in line with these findings, with data from 29 patients who received LVADs showing that the degree of MR was reduced from moderate–severe to trace–mild without any additional intervention. There has been concern about the contribution of MR to symptoms experienced by patients post-LVAD and the need for mitral valve intervention during surgery (33). Such concern derived from the dissociation between ventricular contraction and device pulsation, with consequent mitral regurgitation when LV contraction would occur against a closed aortic and VAD valve. However, the reduction in MR usually observed after LVAD (6,38) indicates that the finding of MR pre-VAD rarely requires intervention for surgical success. Any surgical intervention would likely be minimal, such as the use of an Alfieri stitch.

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Mitral Stenosis

Mitral Stenosis (MS) is a rare finding in patients scheduled for LVAD insertion. In our institution, MS was present before LVAD insertion in only 1 of 105 cases. Significant MS restricts the filling of the LVAD and leads to low device output and, consequently, low cardiac output. RV failure can also occur due to increased pulmonary vascular resistance (PVR). Thorough imaging of the mitral valve includes an evaluation for the presence of stenosis. If significant MS is found, surgical intervention with either a mitral commissurotomy or mitral valve replacement is required (33).

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Pulmonic Valve

Pulmonic valve lesions are relatively rare in the patient receiving a VAD. Pulmonic insufficiency more than moderate would be an important finding in those patients. In patients receiving only a LVAD, it would compromise RV function through volume overload. In those receiving RVADs, it would reduce forward flow and require surgical intervention, with considerations similar to those discussed for AI in LVAD insertion. Significant pulmonic valve stenosis would be a relevant finding in patients receiving LVADs, given the RV pressure overload and limitation of RV output.

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VENTRICULAR ASSESSMENT

Right Ventricle

RV dysfunction is a well-recognized and serious condition that may occur in LVAD recipients (63). Because the output of the native RV determines the preload of the LVAD (59), a decrease in RV function will translate into a reduction in the LVAD output. Reports suggest that at least 9%–33% of patients have severe RV failure after LVAD insertion (63–68) and may require an RVAD. This decision is often needed when CPB is discontinued, because the RVAD insertion should be performed early after the development of severe RV failure following LVAD implantation (69,70). In fact, most patients requiring RVAD support after LVAD insertion receive the RVAD just after LVAD implant or on the same day of surgery (67,70). A LVAD can have a beneficial effect on the RV by reducing afterload (71), or a detrimental effect by increasing preload to an already compromised RV (72) and by impairing RV contractility through leftward septal shift during LVAD support (63,73). Two methods are usually applied to evaluate RV function. First, two-dimensional images at the ME RV inflow–outflow and four-chamber views and transgastric level allow for the semiquantitative assessment of RV function and dilation. This assessment is based on the visual appreciation of both the longitudinal function; RV base (TV annulus) to apex motion, and free-wall motion (74). Quantitative analysis is also desirable in the clinical setting. Measurements such as the global RV fractional area change (6,75), the regional fractional area change (73), and the maximum derivative of the RV pressure (dP/dt max), have been used to quantify systolic function (76,77). Of these, the global RV fractional area change is most often used, and in patients undergoing LVAD implantation it is usually between 20% and 30% (6). The TV inflow velocity profile has been used as a measure of RV diastolic function. There is no clear evidence that mechanical LV support affects RV diastolic performance (78).

Because of its multifactorial nature, RV dysfunction after CPB remains difficult to predict in the individual patient (67,69). Preoperative identification of risk factors for RV dysfunction aids in optimal device selection by detecting patients who would benefit from biventricular assistance, and may improve clinical outcome by preventing end-organ failure due to a period of low output from RV failure (67). A strong association between low preoperative RV performance, based on low PA pressure and RV stroke work index, and RVAD requirement has been demonstrated (67,69,79), indicating that preoperative identification of RV dysfunction assists in the prediction of post-CPB RV failure. A preoperatively dilated RV with increased RV preload and afterload predisposes to RV dysfunction after LVAD implantation (79,80), and patients with a RV fractional area change <20% may suffer RV failure after LVAD insertion (6). Detection of a moderately depressed RV is also important for the anesthesiologist involved in anticipated LVAD-only placement, because it will guide towards aggressive inodilator therapy for decreasing pulmonary hypertension and increasing RV contractility and strict volume management to minimize volume overload to the right heart after separation from CPB. Finally, early identification of primary RV failure after cardiotomy following other cardiac surgical procedures, before significant end-organ damage occurs, is also essential, because early temporary RVAD can usually bridge some patients to recovery in less than 1 wk (81). In a study of patients with isolated RV failure that required postcardiotomy RVAD support, the perioperative echocardiographic sign of RV failure consisted of a hypokinetic RV free-wall motion associated with a normal underfilled LV (81).

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Left Ventricle

Evaluation of the LV function pre-LVAD insertion will show depressed function with either a dilated or normal size ventricle, depending on the cause of heart failure (82). The LV ejection fraction (LVEF) for LVAD insertion is typically <25%–30% (83). Significant diastolic dysfunction is also usually present and diagnosed with PW Doppler of the transmitral inflow combined with PW Doppler of the pulmonary veins (84,85) or with tissue Doppler (86–88). The presence of a restrictive LV diastolic physiology reflects increased LV and LA pressures and, when severe, supports the indication of a heart transplant (89). Severe LV dysfunction increases the risk of apical thrombus formation. Apical thrombus, when present, is often located near the inflow cannula insertion site. Thus, preoperative interrogation of the LV for the presence of thrombus is an essential part of the echocardiographic examination. IV echocardiographic contrast injection can help increase the sensitivity of detecting LV apical thrombus (90).

After LVAD activation, the LV is unloaded with a reduction in its size to approximately normal (1,7). On TEE examination, reduced LV volume, also called LV decompression or unloading, with persistent closure of the aortic valve should be seen, along with adequate cardiac output through the LVAD, indicating normal device function. Neutral interventricular septum position indicates adequate LV filling. If the LV is not decompressed after LVAD implantation, a rightward septum shift can be seen, and a suspicion of insufficient device ejection or cannula obstruction should be immediately raised. In contrast, a leftward septal shift may indicate excessive decompression due to high pump speed in an axial VAD, or RV dysfunction. Spontaneous echocardiographic contrast in the LA or LV is also a sign of LVAD malfunction (19).

Because LVADs promote LV unloading, LV function is usually not accurately assessed during LVAD function. When this evaluation is desired, usually because LVAD explantation is considered, several echocardiographic indices have been used during temporary VAD interruption, such as LVEF, fractional shortening and preejection period divided by ejection time (91,92), LV diameter in end-diastole (93), the heart rate-corrected ejection time divided by the LA pressure (94), and the end systolic elastance (95). An interesting finding is that the fractional shortening of the LV, obtained during LVAD function when LV systole coincides with LVAD filling, was similar to the fractional shortening of the LV when the LVAD function was interrupted (92). This suggests the possibility of obtaining representative information on intrinsic LV performance during LVAD support.

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ASSESSMENT OF VAD COMPONENTS

Mechanical dysfunction is occasionally observed after VAD insertion (96,97), with a cumulative probability of device failure increasing from 6% at 6 mo to 64% at 2 yr (96). Device dysfunctions can be due either to failure of the VAD system components themselves (97–99) or to pathophysiological changes that interfere with the VAD function (99). The usefulness of echocardiography has been stressed by the use of a protocol based on TTE, which could accurately identify common malfunctions of patients on chronic LVAD support (7).

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VAD Cannulas

The inflow and outflow cannulas for conventional pulsatile and axial flow devices typically have a diameter of 16–25 mm (15). They are made of woven polyester fabric, which has hyperechoic density in the echocardiographic image. Alternative cannulation methods have been increasingly used and lead to distinct echocardiographic images and considerations (Fig. 3 and Table 2).

Figure 3

Figure 3

Table 2

Table 2

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Cannula Position

Inflow cannula.

The inflow cannulas and their orientation within the RA or LA or ventricles can be visualized on two-dimension imaging. The inflow cannula to a LVAD may originate from the LA or LV. The most common origin is the apex of the LV (Fig. 3A) and, in this case, the cannula should be aligned with the LV inflow tract, i.e., with the mitral valve opening, and not abutting any wall. To obtain an adequate assessment of the three-dimensional alignment of the cannula, its position should be evaluated in at least two views. We use a ME four-chamber view to evaluate deviations towards the interventricular septum and a ME two-chamber long-axis view to evaluate the anterior–posterior direction (Fig. 4).

Figure 4

Figure 4

Color Doppler is an important component of the examination. A properly aligned inflow cannula should have a laminar and unidirectional flow from the ventricle to the device. Abnormally high velocity, turbulent flow suggests obstruction of the inflow cannula, e.g., due to thrombus or partial obstruction of the cannula by the ventricular wall (100). PW Doppler allows for computation of device stroke volume and output both in the inflow and outflow cannulas (Fig. 5). PW Doppler of the RV and LV outflow tracts can be used to indirectly calculate device flow in LVADs providing partial circulatory support (15). CW Doppler is used for quantification of the flow along the inflow pathway from the atrium or ventricle to the VAD (Fig. 5). Particularly important are high velocities produced by cannula obstruction (Fig. 6). The measurement axis is aligned with the central axis of the cannula in a four-chamber or long axis view. The flow pattern will depend on the device used. Pulsatile devices such as the HeartMate I, Novacor, and Thoratec will show a pattern of pulsatile flow. Axial flow devices such as the HeartMate II will show a pulsatile pattern, synchronous with the patient’s electrocardiogram, superimposed to a continuous pattern of flow throughout the device cycle (Fig. 5B). This pattern is present even when the aortic valve does not open due to ventricular contraction. Normal flow into the LV cannula during LVAD filling for pulsatile devices was suggested as having a peak velocity below 2.3 m/s (6). This is compatible with a cannula diameter of 16 mm and a stroke volume of 65 mL. Axial flow devices show peak filling velocity between 1.0 and 2.0 m/s according to preload and to the remaining pumping action of the patient’s heart. Given the limited information on pressure gradients and velocities in VAD cannulas, and the variety of device models and flow patterns, it is helpful to use the continuity equation relating the cardiac output, cannula diameter, and mean velocity as a gauge to interpret the results and estimate mean velocities.

Figure 5

Figure 5

Figure 6

Figure 6

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Outflow cannula.

The outflow cannula for a LVAD or RVAD (Fig. 3A) is visualized with two-dimensional imaging. A long axis view of the ascending aorta at the level of the right PA will usually show the outflow cannula anastomosis to the ascending aorta. The ascending aorta should also be interrogated for the presence of calcification, plaque, or dilation, which could modify the placement of the cannula. The LVAD outflow cannula for most devices (Thoratec, HeartMate, ABIOMED) will be localized at the right anterolateral aspect of the ascending aorta (101), consistent with the surgical performance of an end-to-side anastomosis. More recent devices, which provide partial support and aim for smaller device size and surgery (e.g., Jarvik 2000), can have their outflow cannula connected as an end-to-side anastomosis to the descending thoracic aorta (lower one-third) (102).

The RVAD outflow cannula (Fig. 3A) can be anastomosed to the main trunk of the PA, to the right PA between the ascending aorta and the superior vena cava (103), or be inserted with a purse-string suture in the RV and through the pulmonic valve into the main PA. The RVAD outflow cannula will be visualized in a ME 20–70° view (Fig. 7). In heart-transplanted patients, the outflow cannulas are sewn into the great vessels (aorta and/or PA) of the donor heart and placed just distal to the aortic or pulmonic valves and just proximal to the transplant anastomoses (104).

Figure 7

Figure 7

Color flow, PW, and CW Doppler are used to evaluate flow patterns of the outflow cannula (Fig. 5). To measure flow velocity in the outflow graft, the PW sample volume should be 1 cm proximal to the aortic anastomosis. The peak velocity in the outflow graft in axial flow pumps usually ranges from 1.0 to 2.0 m/s, with unidirectional and slightly pulsatile flow (Fig. 5D) (105), and it is about 2.1 m/s in a normally functioning pulsatile LVAD (7). Outflow valve regurgitation is defined as retrograde flow seen within the outflow graft occurring during LVAD diastole.

Simulation studies showed that flow patterns of the aortic outflow cannula are significantly affected by the angle of insertion of the LVAD outflow cannula into the native aorta (106). Zones of flow recirculation and high shear stress on the aortic wall can be observed when the cannula is at a 90° angle with the ascending aorta, gradually decreasing in size with decreasing angle. Connecting the LVAD outflow conduit at a shallower angle to the proximal aorta produces fewer secondary flows. However, this inhibits the washing of the aortic valve, which helps to reduce thrombus formation in the proximal aorta.

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Cannula Obstruction

Inflow cannula obstruction.

Inflow cannula obstruction is defined as interrupted flow at the mouth of the inflow cannula occurring during LVAD or RVAD diastole (7). It can be caused by hypovolemia (107), intracardiac clot or thrombus (105,108) (Fig. 6A), misalignment or compression of the interventricular septum (7), and, in RVADs, by the anterior leaflet of the TV, the tricuspid subvalvular apparatus, or an aneurysmal interatrial septum (109,110). Diagnosis can be performed using TTE, TEE, or epicardial echocardiography. Intermittent inflow cannula obstruction was reported in 2 of a 32-patient series studied with a protocol based on TTE (7). The true incidence of cannula obstruction is likely more frequent considering its causative factors, and may well be unrecognized and under-reported. The presence of turbulent flow in color Doppler images is a criterion for an obstructed cannula. PW and CW Doppler can be used for further quantification by measuring velocities in the inflow cannula (Fig. 6B). Intermittent interruptions of the usually continuous laminar diastolic flow into the inflow cannula (7) or a peak velocity greater than 2.3 m/s (6) can be used as indicative of inflow cannula obstruction.

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Outflow cannula obstruction.

Outflow graft distortion results in acceleration of Doppler velocities proximal in the graft compared with the values measured more distally (7,111). Color Doppler is characterized by a turbulent high-velocity flow at the cannula orifice with a clear flow convergence area. Cannula obstruction can be caused by cannula orifice obstruction (105) or intrinsic obstructing lesions (112). Patient position can worsen graft distortion and the produced obstruction. These result in increased CW and PW velocities at the site of obstruction (7). Complete cannula obstruction will cause the loss of Doppler flow signal in any echocardiographic view (105).

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Cannula perforation.

Cannula perforation is an unusual event. One inflow cannula perforation and one outflow cannula perforation were reported in a series of 68 LVAD patients (97). In our series, there is one inflow cannula perforation in 95 patients. Perforation can be suspected if air bubbles are observed in the outflow cannula or aorta using two-dimension echocardiography. If the perforation occurs intraoperatively, air bubbles will persist in the perforated cannula even after thorough deairing and separation from CPB.

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VAD Valves

Inflow Valve Regurgitation

Inflow valve regurgitation is the most common cause of LVAD dysfunction in long-term LVAD support (7,113). The incidence of inflow valve dysfunction after 1-yr implantation of a HeartMate LVAD has been reported to be 2.4%–5.3% (112,114) and 2% for the Thoratec/TCI HeartMate and the Thoratec paracorporeal VAD devices (96). Inflow valve incompetence in LVADs that use tissue valves can be due to a torn cusp, dehisced commissures or endocarditis (7,111,115). Hypertension and outflow graft twisting increase afterload to the LVAD and may lead to high pump chamber pressure and inflow valve regurgitation (115).

The normal PW Doppler flow into the apical cannula during LVAD filling is unidirectional and laminar (6) (Fig. 5B). Inflow valve regurgitation is indicated by the presence of biphasic inlet conduit flow pattern in color Doppler images and turbulent flow at the inflow cannula during LVAD ejection (7). PW Doppler shows flow reversal in the inflow cannula during device ejection (6). In patients with inflow valve regurgitation, TEE may demonstrate a nondecompressed or dilated LV, frequent opening of the aortic valve, and reduction of the outflow graft velocity time integral and peak velocities (6,7). Regurgitant flow can be estimated from the product of the graft area by the regurgitant flow velocity–time integral.

A mismatch between Doppler-derived cardiac output at the pulmonic valve and device output, i.e., between LVAD output and forward cardiac output, will be observed in the case of inflow valve regurgitation. Such mismatch can also be found in other conditions, such as during outflow valve regurgitation, native or prosthetic valve regurgitation, and incomplete filling of the VAD chamber. Consequently, the finding of that mismatch should always alert to the presence of device malfunction (116) or of a potentially serious condition.

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Outflow Valve Regurgitation

Outflow valve regurgitation has been reported in 3% of patients receiving LVADs within 547 days after insertion (97). The presence of retrograde flow within the outflow graft during LVAD diastole in color Doppler images is indicative of outflow valve regurgitation (7,40). This finding will be associated with a mismatch between the high LVAD output and the effective forward cardiac output due to the increased number of LVAD beats caused by the regurgitation.

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Impeller Dysfunction in Axial Flow Pumps

Thrombotic complications can occur in these pumps, and protocols for fast evaluation of axial pump LVADs have been developed (105). Because of the devices’ echogenicity, it is not possible to visualize thrombi within the pump. Thromboembolic material can develop and be detected in the LA appendage or the LV apex and impair forward flow. Thrombi have been also found in the small pocket next to the LVAD inflow cannula orifice and interventricular septum-inferior wall, frequently associated with low regional flow assessed by PW Doppler (105). It is also essential to exclude, with TEE, the presence of obstruction of the inflow and outflow cannula and other sources of thromboemboli (Fig. 6).

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Devices with Alternative Principles and Implantation Methods

A variety of new devices with alternative principles and cannulation methods have been introduced. Besides the general considerations after VAD placement, as discussed above, such as LV unloading, RV function, deairing, and PFO detection, they also require specific echocardiographic considerations (Table 2). We will describe three devices to exemplify some of the alternative methods.

The Jarvik 2000 is an axial flow-based device implanted in the apex of the LV (Fig. 3B). This requires particular attention to exclusion of intracardiac thrombus, particularly in the LV apex. Correct alignment of the device with the mitral valve opening is evaluated similarly to that of the inflow cannulas of conventional cannulation (15,32). The outflow cannula is anastomosed to the descending aorta (Fig. 3B). Thus, disease of the descending aorta should be excluded. The outflow cannula-descending aorta anastomoses should be evaluated post-VAD insertion, and flows in the distal and proximal descending aorta evaluated. Aortic valve opening as a function of pump flows should be verified, usually at 1000 rpm step changes in pump rotation. Spontaneous echocardiographic contrast in the aortic root can occur at high device flows. This prothrombotic condition is eliminated by reducing the device output, allowing for partial ventricular ejection through the aortic valve (15).

The Impella series (Fig. 3C) are miniaturized axial pump catheter devices implanted either surgically by sewing a graft to the ascending aorta or percutaneously through the femoral artery (12). The device aspirates blood through a caged blood flow inlet positioned in the LV in a retrograde fashion from the aorta, across the aortic valve, and ejects the blood past the impeller into the ascending aorta (Fig. 8). The correct position is monitored intraoperatively with TEE, which will confirm that the tip of the device is 3–4 cm from the aortic valve annulus, reaching the anterior mitral leaflet edge. Occlusion of the inlet by ventricular walls should be excluded and the cause determined, usually contact with septum or free wall versus low LV volume. The outflow port is visualized in 2D and color Doppler and should be positioned 1.5–2 cm distally to the sinuses of Valsalva (117).

Figure 8

Figure 8

The TandemHeart (Fig. 3D) is a continuous-flow percutaneously or surgically implanted LVAD for short-term support. The inflow cannula is inserted through the femoral vein, up the inferior vena cava (IVC) to the RA and trans-septally at the fossa ovalis (ME aortic valve short axis view) into the LA. This implies the need to exclude intraatrial thrombi and to assess the IVC, RA, LA, and the interatrial septum for other structural abnormalities. Monitoring of the needle tip used for septal perforation with TEE is essential to prevent puncture of the aorta or atrial wall (118). In addition, a ME four-chamber view is used to visualize the position of the wire, sheath, and dilator used for ultimate inflow cannula positioning towards the pulmonary veins (118). The position of the inflow orifices entirely in the LA should be confirmed. Evaluation of adequate flow into the trans-septal cannula is done with color Doppler, with exclusion of flow from the RA. The outflow cannula is inserted through the femoral artery and positioned in the lower abdominal aorta. The potential for low flow conditions in the descending and ascending aorta is present. These structures should be interrogated for signs of spontaneous echocardiographic contrast. PW Doppler of the LV outflow tract at different device speeds allows for estimation of reduction of ventricular workload according to device settings.

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DEVICE-ASSOCIATED COMPLICATIONS

Bleeding

The incidence of excessive bleeding after LVAD insertion has been reported with high variability, ranging from 11% to 48%, (99,119–121) and 0.6 non-neurological bleeding events/patient/year in the REMATCH experience (97). This variability is due to factors such as device characteristics, surgical and anesthetic management, and definition of bleeding. More recently, it seems that the incidence of bleeding is decreasing, a fact that can be assigned to improved experience with devices and perioperative patient management, use of antifibrinolytics, and advances in surgical techniques. Two-dimensional TEE for assessment of bleeding after implantation of a device allows for determination of the site and estimation of the volume of pericardial effusion (122), hemopericardium, and distortion, partial displacement and compression of one or more cardiac chambers, despite the limitations of echocardiography for diagnosis of tamponade (123,124). Cardiac tamponade is one of the most common reasons for hemodynamic instability after VAD insertion. Findings compatible with tamponade are RA systolic collapse, RV diastolic collapse, reciprocal respiratory changes in RV and LV volume, swinging heart and IVC plethora (reduction in dilated IVC diameter ≤50% during inspiration), and respiratory flow variation of mitral and tricuspid inflow velocities (123,124). Regional tamponade may be associated with LA compression and LV diastolic compression without collapse of the RA or RV (123). Isolated tamponade due to anterior mediastinal clot can be somewhat difficult to visualize echocardiographically. Tamponade should be suspected when a decline in cardiac output is observed in a small or nondistended ventricle on reduced or partial mechanical support (125).

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Thromboemboli

The presence of intracavitary thrombi requires extra care during cannulation because of the risk of embolism (126). The incidence of thromboembolic complications after LVAD support varies significantly in different reports from 5% to 47% (98,99,127,128). This wide range reflects the variability in device thrombogenicity, patient characteristics and anticoagulation management principles in different studies. LV thrombus has been reported to occur in 9% and 16% of patients receiving VADs (6,126). LA cannulation was found to be an independent risk factor for LVAD-associated LV thrombus (126). In this study, 7 of 13 patients with LA cannulation presented LV thrombus in contrast to 1 of 44 for LV cannulation. The two-dimensional TEE examination for assessment of emboli or thrombus after implantation of a device will include all cardiac chambers, particularly the LA, LA appendage, and apex of the LV, which is the insertion site of the inflow cannula. Use of TEE allows for identification of mobile LV thrombi adjacent to the LVAD inflow cannula (129) (Fig. 6), and the LV outflow tract (41).

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Aortic Dissection

TEE is a sensitive and specific technique for diagnosis of aortic dissection (21,130), allowing for visualization of intimal flaps and tears, identification of true and false lumens, and documentation of complications such as aortic regurgitation or pericardial effusion. Aortic dissection can be caused by a LVAD through increased shear stress on the aortic intima secondary to the blood injected at high velocity against the aortic wall. Accordingly, there are reports of LVAD patients who suffered fatal aortic dissection detected by echocardiography (42,131). TEE can also be used to exclude the presence of aortic dissection. The presence of competing flow in the ascending aorta from anterograde transaortic output and retrograde VAD pump flow, particularly in patients with the outflow cannula anastomosed to the descending aorta, can lead to the suspicion of dissection by computed tomography (132). TEE can be used in these cases to evaluate the lumen for the presence of intimal tear and, using Doppler, to examine the characteristics of flow in the ascending aorta (132).

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VAD Endocarditis

Infection is an important cause of morbidity and mortality after LVAD implantation (127,133,134). VAD endocarditis is established when the inner components of the VAD are infected (135). This will often be associated with mechanical complications of the VAD (127). TEE is recommended to evaluate endocarditis (136). Echocardiographic findings suggestive of VAD endocarditis are: 1) visualization of echodense structures compatible with vegetations on the inflow or outflow conduits, as well as in native or prosthetic valves (136,137); 2) LVAD inlet obstruction (127); 3) Inflow and outflow valve malfunction (138); 4) LVAD outflow rupture (127).

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DEAIRING

Echocardiography is very useful for detection and management of micro- or macro-bubbles, observed in the echocardiographic image as white reflections (139–141). The VAD and its cannulas may harbor a significant amount of air. This adds to the general common sites of intracardiac air after open-heart surgery such as the right and left upper pulmonary veins, LV apex, LA, right coronary sinus of Valsalva, LA appendage, and PA (140,141). Reestablishment of pulmonary perfusion after CPB will result in the transport of the air bubbles to the heart and systemic circulation. The most common locations to which air will migrate are the right coronary artery and the innominate artery (142). This may produce right coronary ischemia and RV dysfunction or contribute to postoperative neurocognitive impairment.

Three distinct perioperative periods are relevant to air detection: from the conclusion of device anastomoses to release of the aortic cross-clamp, from release of the aortic cross-clamp to termination of CPB, and from the end of CPB to the end of operation (141). The first two periods are the most critical, because they will correspond to the removal of the largest amount of intravascular and intracavitary air and, consequently, reduce the likelihood of subsequent complications.

Careful deairing is performed before the device is fully activated. To observe signs of air entrapment in the device, structures distal to the outflow cannula should be inspected. These include the ascending and descending aorta using the ME aortic valve long-axis view, ME ascending aorta long-axis view and descending aorta short- and long-axis view. The ME aortic valve long-axis view will allow for observation of both air from the outflow cannula and air present in ventral regions of the heart chambers, where bubbles would most likely collect. Finally, anastomotic sites, such as at the ascending aorta, descending aorta, pulmonary trunk, RA or LV apex, can be a source of air entrance. This is particularly important in the case of an air entry port in the circuit upstream to the device (i.e., inflow cannula and respective anastomosis), due to the negative pressures generated by several devices during filling (e.g., ABIOMED AB5000, Thoratec, HeartMate I). Air entrapment due to this mechanism can also occur postoperatively and result in air embolism with RV failure and neurological complications (142,143).

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RECOVERY AND WEANING

LV and RV recovery can occur after VAD implantation. Several studies have reported recovery and weaning strategies based on cardiopulmonary testing, and hemodynamic and echocardiographic variables (144–146). Echocardiographic variables indicative of left myocardial recovery are LVEF >45% (147), LV internal diameter in diastole (LVIDd) <45 mm (142), fractional area change >40% (148), and improved myocardial ventricular contractility (2). The largest series of weaning and removal from chronic LVAD support used a LVEF ≥40% and LVIDd <60 mm as echocardiographic criteria for myocardial recovery (93). Dobutamine stress echocardiography, combined with invasive hemodynamic monitoring, has been proposed to assess the ability of LV response to the increased load and to consider device explantation (149). This test is performed with an infusion at 5 μg · kg−1 · min−1 titrated every 5 min up to 40 μg · kg−1 · min−1 and simultaneous assessment of cardiac index, LVEF, LVIDd, and dP/dt. The test is halted if the patient demonstrates symptoms of heart failure or unacceptable hemodynamics. The favorable test is defined as the improvement of cardiac index and LVEF without symptoms of heart failure, and pulmonary capillary wedge pressure ≤15 mm Hg.

Less quantitative data are available for weaning from a RVAD. The PVR is a crucial variable in this case, and most patients can be weaned once the PVR is optimized (150). Patients with malignant arrhythmias or fixed PVR will need additional management to allow for weaning. During the weaning process, the RVAD flows are decreased, e.g., by setting a pulsatile RVAD to the asynchronous mode and progressively reducing the pumping rate and vacuum (151). The central venous pressure, PVR, RV, and LV function are assessed throughout the process (150). If the left and right components of the circulation continue to fill and function without excessive elevation of the central venous pressure, the RVAD can be further weaned and ultimately removed.

It is important to recognize that identification of the patient ready for successful LVAD and RVAD weaning is still a topic of current study and depends on integration of clinical and echocardiographic factors (98,152).

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CONCLUSIONS

LVAD implantation has been increasingly used in patients with terminal heart failure as a bridge to transplant or recovery, and as destination therapy. Echocardiography plays a fundamental role in evaluating perioperative structure and function related both to the patient’s heart and large vessels and to the implanted device. This evaluation is essential for anesthetic and surgical planning and intervention success. A comprehensive echocardiographic examination includes a pre- and a post-VAD assessment phases. The pre-VAD insertion examination of the heart and large vessels addresses the structural and functional factors relevant to anesthetic and surgical management: aortic regurgitation, tricuspid regurgitation, mitral stenosis, patent foramen ovale or other cardiac abnormalities that could lead to right-to-left shunt after LVAD placement, intracardiac thrombi, ventricular scars, pulmonic regurgitation, pulmonary hypertension, pulmonary embolism, and atherosclerotic disease in the ascending aorta, and RV function. The post-VAD insertion examination addresses device function and reassessment of the heart and large vessels. The examination of the device aims to confirm completeness of device and heart deairing, cannula alignment and patency, and competency of device valves using two-dimensional, and color, CW, and PW Doppler modalities. The examination of the heart targets to exclude aortic regurgitation, or an uncovered right-to-left shunt; and to assess RV function, LV unloading, and the effect of device settings on global heart function. Specific echocardiographic considerations should be taken into account according to the VAD model used. Performance of an echocardiographic assessment firmly based on the principles detailed in this review can optimize perioperative clinical management and provide data for objective decision-making in patients receiving VADs.

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ACKNOWLEDGMENTS

The authors would like to thank the members of the Cardiac Anesthesia Group who contributed with the acquisition of the images: Drs. Edwin Avery, Michael D’Ambra, Dwight Geha, Fumito Ichinose, Carolyn Mehaffey, Vipin Mehta, Robert Schneider, Scott Streckenbach, Jason Qu, and Xiping Zhang; Mark Handschumacher for the preparation of images for the website supplement; Mark S. Adams, BS, RDCS, FASE, for his helpful suggestions on the manuscript; and O.H. Frazier, MD, and C. J. Genmato, BS, for the web supplement images on the Jarvik 2000 and TandemHeart.

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