The epidemic of heart failure is a worldwide problem that is anticipated to increase with both an aging population and the improved survival from cardiac complications producing left ventricular systolic dysfunction (e.g. myocardial infarction). Increasingly, these patients who survive a serious cardiac injury but have persistent ventricular dysfunction precluding normal end-organ function experience a poor quality of life and high rates of morbidity and mortality. At the age of 40, the lifetime risk of developing heart failure is 20%, and the 1-year heart failure mortality rate is 20%.1 The number of hospitalizations for heart failure has tripled between the 1970s and 2004, and contemporary data indicate that heart failure was the primary or secondary cause of 3.8 million annual admissions in the United States.2 It is estimated that the direct and indirect costs of heart failure in the United States will exceed $37 billion in 2009, highlighting the economic importance of this disease.1

While most heart failure patients are managed medically, surgical options for refractory heart failure include orthotopic heart transplantation and mechanical circulatory support. Advances in donor and recipient selection, organ procurement, and immunosuppressant therapy have led to an increase in the survival of grafted organs. Transplant surgery is currently considered the treatment of choice for end-stage heart, lung, and liver diseases, but the predominant limiting factor is a shortage of donors. Mechanical circulatory support has therefore emerged as a valuable and viable adjunct to transplantation in the management of heart failure patients.

Echocardiography plays an essential role in the donor organ selection process and preoperative screening, perioperative management, and post-transplant follow-up of recipients. Similarly, perioperative transesophageal echocardiography (TEE) provides invaluable anatomic and functional information in patients receiving circulatory support devices, which influence not only anesthetic management but also surgical decision making. The following text will first describe the role of TEE in heart transplantation, followed by a discussion of its value in the implantation of mechanical circulatory support devices.

The application of TEE as a diagnostic and monitoring modality in heart transplant surgery can be divided into five categories:

1. 
   

   Cardiac donor screening

   
   
2. 
   

   Intraoperative monitoring in the pretransplant period

   
   
3. 
   

   Intraoperative evaluation of cardiac allograft function and surgical anastomoses in the immediate posttransplantation period

   
   
4. 
   

   Management of early postoperative hemodynamic abnormalities in the intensive care unit

   
   
5. 
   

   Postoperative follow-up studies of cardiac allograft function

Role of TEE in Cardiac Donor Screening

As a result of the shortage of available donor hearts, many institutions are now liberalizing their acceptance criteria to include higher-risk (marginal) donor hearts.3 Table 17–1 presents the conventional cardiac contraindications to the use of a donor heart. Despite the potential risk for transmitting atherosclerotic, hypertensive, and valvular heart diseases, organs from older donors are increasingly being used. This aggressive approach has proved particularly successful when matching for higher-risk recipients (alternate recipient list) with a greater short-term mortality risk or with significant comorbid factors.4

Echocardiography plays an important role in the effort to improve the yield of donor evaluation.5 By ruling out donors with structural abnormalities, severe ventricular dysfunction, or significant wall motion abnormalities (WMAs), the need for costly and time-consuming cardiac catheterization can be circumvented. In potential donors on ventilatory support, TEE has been shown to be particularly useful in providing consistent high-quality imaging when transthoracic echocardiography (TTE) has proved inadequate.

An initial echocardiogram should not be obtained before adequate hemodynamic and metabolic resuscitation. In particular, volume status, acidosis, hypoxemia, hypercarbia, and anemia should be corrected, and inotropic support should be weaned to a minimum compatible with adequate blood pressure and cardiac output (CO). The goals of the echocardiogram are to rule out structural abnormalities and assess regional and global functions. It is unclear if donor hearts with left ventricular (LV) hypertrophy, defined as a wall thicker than 11 mm in the absence of underfilling of the ventricle (pseudohypertrophy), can safely be used for transplantation. One study shows that LV hypertrophy (LVH) may increase the incidence of early graft failure,6 but a more recent study demonstrated that hearts with mild (12 to 13 mm) or moderate (13 to 17 mm) LVH do not increase morbidity.3 Most valvular and congenital abnormalities preclude transplantation, with the possible exception of mild lesions such as mitral valve prolapse in the absence of significant regurgitation, a normal functioning bicuspid aortic valve, or an easily repairable secundum-type atrial septal defect.

Segmental WMAs in donor hearts may be the result of coronary artery disease, myocardial contusion, or ventricular dysfunction after brain injury. Contused myocardial tissue resembles infarcted myocardial tissue histologically and functionally.7 The pattern of ventricular dysfunction after spontaneous intracranial hemorrhage is usually segmental and often spares the apex of the left ventricle.8 This pattern correlates with the sympathetic innervation of the ventricle. In contrast, ventricular dysfunction after traumatic brain injury may be global or regional. For both types of brain injury, there is a poor correlation between the distribution of echocardiographic dysfunction and actual histologic evidence of myocardial injury. Some studies have suggested that WMA and global function improve shortly after heart transplantation, but a recent multi-institutional study identified WMA on the donor echocardiogram as a powerful independent predictor of early graft failure.9 WMA on the donor echocardiogram may be particularly important when associated with a donor age older than 40 years and an ischemic time longer than 4 hours.

The lowest fractional area change in a donor heart permitting safe transplantation is unknown, but it has been suggested that a fractional area change greater than 35%, in the absence of other cardiac abnormalities, could be used as a guide.8

Intraoperative Monitoring in the Pretransplant Period

Idiopathic and ischemic cardiomyopathies are the two most common causes of cardiac failure in the transplant recipient. Regardless of the cause of failure, global cardiac dilatation is a common feature and the term dilated cardiomyopathy has been applied to this end-stage condition. These patients have fixed, low stroke volumes and are very dependent on an adequate preload. Further, even mild increases in afterload may result in a marked reduction in stroke volume. Patients in cardiac failure compensate for their low CO by an increase in sympathetic activity, which leads to generalized vasoconstriction and to sodium and water retention. This delicate balance among preload, contractility, and afterload can be dramatically disturbed after the induction of general anesthesia. TEE is therefore ideally suited to rapidly evaluate and guide intraoperative management in these patients. Several factors commonly seen in recipients, including diastolic dysfunction, regurgitant valvular lesions, and positive pressure ventilation, result in a poor correlation between measured filling pressures and LV volumes. Thus, optimization of LV filling and inotropic support can be more readily and rapidly achieved under TEE guidance. Right ventricular (RV) size and function also should be assessed in these patients. The presence of RV hypertrophy is suggestive of long-standing pulmonary hypertension, which may lead to acute RV dysfunction in the transplanted heart.

TEE is similarly sensitive in detecting intracardiac thrombi, with the possible exception of an apical thrombus. Prethrombotic sluggish blood flow is characterized echocardiographically as spontaneous contrast or “smoke.” Patients with dilated cardiomyopathy, especially in the presence of spontaneous echo contrast, have a high incidence of thrombus formation in the apex of the left ventricle. The left atrial (LA) appendage also should be inspected for possible thrombi, particularly in patients with atrial fibrillation. When thrombi are present in the left heart, manipulation of the heart before cardiopulmonary bypass (CPB) should proceed with great caution in an effort to avoid systemic thromboembolism. Other sources of embolism during the pretransplant period include atheromatous plaque from the ascending aorta during aortic cannulation or air entrainment during the explantation of ventricular assist devices. As in all CPB cases, the aorta (ascending aorta, arch, and descending aorta) should be examined for atherosclerotic plaque before aortic cannulation. TEE is extremely sensitive in the detection of intravascular air and early detection and intervention may potentially limit this complication.

It is common practice to place a pulmonary artery (PA) catheter into the PA only after CPB because it is often difficult to pass these catheters through large dilated ventricles, incompetent tricuspid valves, and in low CO states. PA catheter placement is also more prone to induce arrhythmias. TEE therefore can be used to determine CO and PA pressures during the pre-CPB period (see Chapter 4).

Intraoperative Monitoring in the Posttransplantation Period

TEE imaging of the heart during and after weaning from CPB provides invaluable information with important diagnostic and prognostic implications. Before weaning from CPB, TEE is used to detect retained air and to assist venting and de-airing maneuvers. The most common sites of air retention are the right and left upper pulmonary veins, the LV apex, the left atrium, and the coronary sinus. The right coronary artery is commonly affected by air embolism because of its more superior location in the ascending aorta, resulting in a hypocontractile dilated right ventricle and ST-segment changes in the inferior electrocardiographic leads. After separation from CPB, a detailed examination of the transplanted heart should include the elements listed in Table 17–2.

The function of the newly transplanted heart depends on many factors: baseline function before brain death, degree of myocyte damage before and during harvesting, amount of donor inotropic support, ischemic time, myocardial protection during the ischemic interval, reperfusion injury, cardiac denervation, donor-recipient size mismatch, and degree of pulmonary hypertension in the recipient. To accurately assess cardiac allograft anatomy and physiology, the echocardiographer needs to understand the surgical procedure and appreciate the changes that normally occur in the transplanted heart.

The standard or biatrial technique, originally described by Lower and Shumway, was the primary method for nearly 30 years.10 However, more transplantation centers are now using the bicaval anastomotic technique as the method of choice, except in infants and small children. The advantages of the bicaval technique include preserved geometry and function of the atria, improved CO, and less disruption in the geometry of the atrioventricular valves, resulting in reduced valvular regurgitation, fewer conduction abnormalities, less thrombus formation in the left atrium, and decreased perioperative mortality.11 In the standard technique, most of the native atrial walls and the interatrial septum are left in situ, leaving the inferior vena cava (IVC), superior vena cava, and pulmonary venous inflow tracts undisturbed. In the donor heart, an LA cuff is created by incising through the pulmonary vein orifices, whereas the right atrial (RA) cuff is created by incising through the inferior vena caval orifice and extending the incision up toward the base of the RA appendage. When the bicaval technique is performed, most of the native atrial tissue is excised, thereby creating superior vena cava and IVC cuffs for end-to-end anastomoses with the donor vena cavae. Divisions and end-to-end anastomoses of the great vessels are the same for both techniques.

Intraoperative TEE assessment of allograft LV systolic function early after separation from CPB has been shown to better predict early requirements for inotropic and mechanical support than routinely measured hemodynamic variables, particularly when ischemic times are prolonged.12 In general, allograft LV systolic function after CPB is expected to be normal, and impaired LV systolic function at this stage, usually the result of ischemic injury or early acute rejection, is often transient. It is important to document any intraoperative regional WMAs because coronary atherosclerosis and myocardial infarction, often silent, are major causes of morbidity and mortality after heart transplant surgery.

There are several echocardiographic findings that could be considered abnormal in the general population but are characteristic in the allograft left ventricle. These are listed in Table 17–3. Increases in LV wall thickness and LV mass are thought to represent myocardial edema resulting from manipulation and transport of the heart. Because the donor heart is typically smaller than the original dilated failing heart, it tends to be positioned more medially in the mediastinum and tends to be rotated clockwise. This could result in difficulties in obtaining the standard tomographic planes, and nonstandard TEE probe positions and angles may have to be used.

Diastolic compliance is often decreased in the first few days or weeks after cardiac transplant, but typically improves in the first year.4 This is most likely the result of ischemia or reperfusion injury, a smaller donor heart in a larger recipient, or a larger heart implanted into a restricted pericardial space. Unfortunately, Doppler echocardiographic assessment of LV diastolic function is complicated by a variety of factors, outlined in Table 17–4. When remnant atrial tissues retain mechanical activity, atrial contractions become asynchronous, resulting in beat-to-beat variations in transmitral inflow velocities. Atrial dysfunction can also result in abnormal transmitral and pulmonary venous flow patterns.13 LV diastolic dysfunction therefore is not the sole cause of altered transmitral flow patterns, and atrial dysfunction has to be ruled out. The echocardiographic indicators of atrial dysfunction include a decreased ratio of systolic to diastolic maximum pulmonary venous flow velocity in the presence of normal pulmonary capillary wedge pressures, reduced LA area change, and reduced mitral annulus motion.13

The thin-wall right ventricle is particularly susceptible to injury during the period of ischemia and reperfusion and also compensates poorly for any increase in pulmonary vascular resistance, which often is elevated in patients with end-stage heart failure. Therefore, it is not surprising that acute RV failure is more common than LV failure and accounts for 50% of all cardiac complications and 19% of all early deaths after heart transplantation.14 Once the diagnosis of RV dysfunction is established, stenosis at the PA anastomosis or kinking of the PA should first be ruled out. A systolic gradient higher than 10 mm Hg may indicate the need for surgical revision. TEE should then be used to optimize RV filling to avoid overdistention of the ventricle and to assess the response to inotropic support. In the setting of maximum inotropic support and pulmonary vasodilator therapy, the presence of a small hyperdynamic left ventricle with a dilated right ventricle (Figure 17–1), especially when accompanied by marginal urine output, arrhythmias, or coagulopathy, should prompt the consideration of the implantation of an RV assist device.

The size and geometry of the atria and the atrial anastomoses depend entirely on the transplantation technique employed. In the standard biatrial technique, different-sized portions of the native atria are left in situ (Figure 17–2), resulting in biatrial enlargement, asynchronous contraction, and intraluminal protrusion of the atrial anastomoses. This method also often gives the atria a multichamber configuration on the TEE (Figure 17–3). The anastomotic protrusions appear echo-dense and should not be confused with thrombi, although thrombi may form along the suture line. These protrusions may also occasionally contact the posterior mitral leaflet in systole, or even result in a mild constriction with a step-up of intraatrial Doppler flow velocities. Severe cases of supra-mitral valve obstruction, or acquired cor triatriatum, have been described after heart transplantation and should be suspected intraoperatively when the LA remnant is markedly enlarged and LV volume is reduced. Turbulent flow by color-flow Doppler (CFD), fluttering of the mitral valve leaflets, and elevated blood flow velocities by pulsed-wave Doppler also may aid in the confirmation of the diagnosis.

The integrity of the interatrial septum should be assessed intraoperatively by using color-flow Doppler and contrast echocardiography (agitated saline or saline microcavitation). Shunts can occur at the atrial anastomotic site or through a patent foramen ovale (PFO). Although uncommon, shunting through a PFO that is not apparent preoperatively may become hemodynamically significant postoperatively. As the relative pressure difference between the left and right atria changes as a result of pulmonary hypertension, RV dysfunction, or tricuspid regurgitation (TR), right-to-left shunting can occur and present as refractory postoperative hypoxemia.15 Identification of a left-to-right shunt across the interatrial anastomoses also should prompt surgical repair because it can contribute to progressive RV volume overload and TR.

Spontaneous echo contrast can be detected in up to 55% of heart transplant recipients. This is usually confined to the donor atrial component and is associated with thrombi, usually attached to the LA free wall underneath the protruding suture line. The incidence of thrombus formation in the left atrium is reduced with the bicaval anastomosis technique.

The PA anastomosis should be examined for possible stenosis, and, although rare, kinking or torsion of the donor or recipient pulmonary artery should be ruled out, especially in the setting of RV dysfunction.16 Color-flow Doppler may detect turbulent flow, and the pressure gradient should be measured with continuous-flow Doppler. Pulmonary venous inflow also should be assessed with color-flow and pulsed-wave Doppler.

Mild to moderate degrees of TR and mitral regurgitation (MR) are common after heart transplantation. MR is usually mild, produces an eccentric jet toward the LA free wall, and has a reported incidence of 48% to 87%.16,17 TR, the most common valvular abnormality after heart transplantation with a reported incidence of 85%, is usually mild with an eccentric jet directed toward the interatrial septum.18 TR after heart transplantation is best quantified by using the ratio of the maximum area of the regurgitant jet to the RA area.19 The etiology of atrioventricular valve regurgitation in the transplanted heart is thought to be related to distortion of annular geometry. Annular distortion after the standard biatrial anastomotic technique is predominantly the result of disturbed atrial geometry and function, whereas donor heart and recipient pericardial cavity size mismatch is thought to play an important role after the bicaval anastomotic technique. This hypothesis is supported by the fact that the incidence and severity of TR and MR are reduced after the bicaval technique as compared with the standard biatrial technique.