Intra-aortic Balloon Pumps
Intra-aortic balloon pumps (IABPs) are placed perioperatively in 2% to 12% of cardiac surgical patients, with the majority being placed intraoperatively.5 When IABPs are placed, TEE can be useful in determining the need for the IABP, assessing for contraindications such as aortic insufficiency or severe aortic atherosclerosis, and guiding its placement into the descending aorta. TEE can also rapidly assess the effects of counterpulsation upon LV function and determine if there were any complications such as aortic dissection or aortic valve perforation. Inappropriate placement is the most common complication, and inadvertent passage of the IABP into the aortic arch, left ventricle, subclavian artery, renal artery, contralateral femoral artery, and right atrium have all been reported.23,24
Assessment of IABP placement begins with visualization of the guidewire within the lumen of the descending aorta. This is particularly important in the setting of aortic dissection, when identification of the true aortic lumen may be challenging. Optimal placement of the IABP tip is 3 to 4 cm distal to the origin of the left subclavian artery, or when the tip is seen at the inferior border of the transverse aortic arch.25 To confirm proper placement, the balloon is first identified in the descending aorta short-axis view. Proper placement has been defined by the disappearance of the tip of the IABP from the aortic arch in the upper esophageal aortic arch long-axis view. Placement below the subclavian artery can also be visualized in a descending aorta long-axis view by slowly withdrawing the probe until the subclavian artery is seen at the level of the aortic arch (which is now seen in cross-section). The common carotid artery is sometimes mistaken for the subclavian artery but can be differentiated by its larger diameter and by turning the probe to the left (to visualize subclavian) and then to the right (to visualize the common carotid). The balloon itself typically appears as an echo-dense image when deflated (Figure 17–4) and a scattered echo image when inflated. A side lobe artifact is commonly seen when the tip of the IABP is visualized in the short-axis view.
A midesophageal descending aorta long-axis view demonstrates the aortic lumen and an echo-dense intra-aortic balloon pump (IABP) within the aortic lumen.
Left Ventricular Assist Devices
Transesophageal echocardiography plays a critical role in each step of the management of patients with left ventricular assist devices (LVADs), including the pre-placement evaluation of cardiac structure and function, detection of interatrial shunts, determination of aortic and tricuspid valve pathology, separation from CPB, and assessment of device function in the postoperative period.
A pre-procedure TEE is typically performed in the operating room following induction of general anesthetic and prior to institution of CPB. Determination of the patency of the foramen ovale, aortic valve insufficiency, mitral valve stenosis, tricuspid regurgitation, left heart thrombus, and assessment of right ventricular function are critical to intraoperative planning and management.
Patent Foramen Ovale. While it is important to recognize an atrial or ventricular septal defect, the more common cause of an intracardiac shunt is a patent foramen ovale (PFO). Intracardiac shunts are important to diagnose and repair to reduce the risk of paradoxical embolism or hypoxemia following LVAD placement. An appropriately functioning LVAD will significantly reduce LV diastolic pressures (often to <5 to 10 mm Hg) but right heart filling pressures can remain abnormally elevated, resulting in a right-to-left shunt and hypoxemia. Even small PFOs should be surgically repaired because of the significant incidence of shunting seen in patients with LVADs.
The normal foramen ovale is best seen in a midesophageal (ME) bicaval view; it appears as a thin slice of tissue bound by thicker ridges of tissue, one of which appears as a “flap.” TEE evaluation of the foramen ovale should include two-dimensional (2D) assessment for flap movement and color-flow Doppler assessment, optimized for measurement of lower-velocity flow. Injection of agitated saline (a “bubble study”) along with a Valsalva maneuver is typically used to provoke right-to-left shunting.26 In such a study, the bubbles should be injected after the Valsalva maneuver produces a decrease in RA volume, and the Valsalva should be released (so as to transiently increase RA pressure over LA pressure) when the microbubbles are first seen to enter the RA. Bowing of the septum to the left upon release of Valsalva confirms the transient increase in right atrial pressures. Admixture of agitated saline with small quantities of blood has been reported to improve the acoustic signal of the microbubbles. The bubble study is positive if bubbles appear in the left atrium within five cardiac cycles (Figure 17–5). In patients with severe LV failure, it may be difficult to sufficiently decrease left atrial pressure. In such cases, an alternative method involves partial obstruction of the pulmonary artery by the surgeon after the aortic cannula is placed.27
Mid-esophageal bicaval view with agitated saline contrast injected into the right atrium (RA). A few bubbles are seen simultaneously in the left atrium (arrow). (LA, left atrium.)
Aortic Pathology. The LVAD outflow cannula is typically placed in the ascending aorta (except for the Jarvik 2000, which may be attached to the descending aorta). Thus, a thorough examination of the ascending aorta is an essential component of the intraoperative TEE evaluation. The ascending aorta is optimally viewed in the midesophageal ascending aortic short- and long-axis views. An ascending aortic aneurysm may require repair prior to LVAD placement.26 Protruding atheroma or mobile atheroma increase stroke risk, and their presence must be communicated to the surgeon. These plaques can be difficult to palpate; therefore, an epiaortic image at the site of cannulation for CBP and for the outflow cannula may assist the surgeon with precise placement.28
Aortic Valve Insufficiency. Significant aortic valve regurgitation (AR) results in chronic volume overload of the LV with consequent ventricular dilation and dysfunction. Reduction of the transaortic (valve) pressure gradient secondary to elevated LV end-diastolic pressure and reduced aortic diastolic pressure may confound determination of AR severity and lead to underestimation in a heart failure population.26,29 In LVAD patients with AR, LV volume loading may be more pronounced as blood being returned from the LVAD is delivered to the aorta just above the aortic valve and regurgitant volume is increased because the LV end-diastolic pressure is low relative to the aortic pressure. If the resultant regurgitant volume exceeds 1 to 2 L/min, patients may remain in clinical heart failure despite the LVAD, since this volume is not delivered systemically but remains within a circuit formed by the LV, LVAD, and the ascending aorta. Older, volume displacement LVADs typically eject blood each time the device is full; therefore, AR in these patients increases the pump rate.29
Aortic insufficiency is best assessed in the midesophageal aortic valve short- and long-axis views as discussed in Chapter 9. It has been suggested that patients with worse than mild AR should undergo a concomitant aortic valve repair or replacement.30,31 However, the decision to correct AR is complex since the addition of a valve procedure significantly increases procedural mortality.32 Important considerations include the degree of aortic valve calcification and the characteristics of the regurgitant jet. An eccentric regurgitant jet in a heavily calcified valve may be more likely to worsen with VAD support and usually warrants surgical correction. Another consideration relates to the planned duration of LVAD support. If the LVAD is being used to bridge the patient to transplant and a relatively short period of support is anticipated, then moderate AR may be tolerated, anticipating that LVAD speeds/rates may be higher than normal. On the other hand, if the device is being used as a permanent or “destination” treatment, such aortic regurgitation is likely to progress and may impact the durability of the device.
There are several methods of surgically addressing AR. One option is replacement of the aortic valve. Mechanical valves are not typically used because of the potential for thrombus formation on the valve as a consequence of the immobility of the leaflets during most LVAD cycles. Furthermore, intermittent opening of the aortic valve renders the patient at risk for embolization.29,30 Thus, if the valve requires replacement, most surgeons recommended the use of a bioprosthesis.32 Another alternative to managing AR in the LVAD patient is partial or complete surgical ligation of the aortic valve cusps. This should not be performed if there is a chance of ventricular recovery with subsequent removal of the device.29,30 A third option in patients without the possibility for native heart recovery is placement of an occlusive LV outflow tract patch graft. In this situation, all blood must be delivered from the LV to the LVAD, and pump failure may result in severe hemodynamic instability as the native heart would be required to eject through the LVAD.30,32
Mitral Valve Stenosis. A significant mitral gradient will lead to impairment of LVAD filling, persistent elevation of pulmonary venous pressure, and symptoms of heart failure. While rheumatic mitral stenosis (MS) is rare in this group of patients, previous procedures such as mitral valve repair or replacement are common. TEE should evaluate for the presence of severe MS across repaired mitral valves or prosthetic valves. It is recommended that severe MS be surgically repaired, with a commissurotomy or concomitant replacement of the mitral valve.26,29 Mitral valve stenosis is optimally assessed by TEE in the midesophageal four-chamber view using CFD and spectral Doppler to determine peak and mean transvalvular gradients as described in Chapter 7.
Tricuspid Regurgitation. Careful evaluation of tricuspid regurgitation (TR) is also warranted. Severe TR with hepatic vein flow reversal usually warrants concomitant tricuspid repair, as elimination of severe TR may improve right ventricular function and device filling following LVAD placement. The tricuspid valve is optimally viewed in the midesophageal four-chamber and the midesophageal right ventricular inflow-outflow views (see Chapter 10).
Left Heart Thrombus. Abnormal blood flow patterns in the left atrium and ventricle predispose to thrombus formation. Common sites of left heart thrombus include the left atrial appendage (Figure 17–6) and the left ventricular apex.31,33 In an attempt to reduce the risk for embolization, TEE should be utilized to rule out the presence of LV apical thrombus prior to the ventriculotomy for placement of the LVAD inflow cannula. Epicardial scanning may be helpful when the apex cannot be visualized with TEE.
A midesophageal two-chamber “zoom” view of the left atrial appendage (LAA) demonstrating a thrombus within its cavity. (LA, left atrium; LV, left ventricle.)
Right Ventricular Dysfunction. An LVAD only supports the left heart and is dependent on a functional right ventricle (RV) to provide adequate preload. While the LVAD may enhance RV performance by decreasing its afterload, it may also worsen RV function by increasing its preload.26 When evaluating the RV, it may be helpful to determine the RV fractional area change (RVFAC), defined as:
A normal RVFAC is greater than 40%, while most patients receiving an LVAD have an RVFAC of 20% to 30%.31 An RVFAC less than 20% predicts a high risk for RV failure following LVAD placement.31 Right ventricular dysfunction remains one of the important clinical challenges in left-side mechanical circulatory support. Combinations of inotropic agents, systemic and inhaled vasodilators, and mechanical RV support may be needed to ensure proper function of the LVAD.
Separation From Cardiopulmonary Bypass
The TEE exam must be repeated during separation from CPB initially to assist in the de-airing process. As the pressure gradients within the heart change dramatically with a functional LVAD, it is also important to repeat the assessment for a PFO, AR, and RV dysfunction. Aortic valve opening, placement and orientation of the inflow cannula, flow in the inflow cannula and outflow graft, and assessment of LV size and ventricular septal position are critical in the intraoperative management of these patients.
De-airing. Following open heart surgery, ambient air (Figure 17–7) can be retained in multiple locations of the heart including the right and left upper pulmonary veins, the LV apex, the left atrial appendage, the right coronary sinus of Valsalva, and the pulmonary artery.26,34 In addition, air can be retained in the VAD cannulas and the pump itself.26 The de-airing process is more complicated for this procedure compared to valvular heart procedures. Most LVAD designs are able to generate negative intraventricular pressure or suction, which can lead to entrainment of extracardiac air. This is most commonly seen when device rate or speed is inappropriately increased during a time when the delivery of blood into the LV is reduced. Thus, the complex de-airing process for LVADs includes removal of intracardiac air as well as vigilance to avoid entrainment and reintroduction. A potential negative impact is when entrained air is delivered into the right coronary artery with subsequent RV dysfunction, reduced LV filling, and further entrainment of air by the pump. In this scenario, the TEE will demonstrate a distended RV, a collapsed LV, and significant air in the aorta. Preserving RV function while weaning from CPB so as to maintain LV preload during the period of reduced LVAD flows and until protamine reversal is therefore highly desirable. TEE examination for air should be conducted continually from before initiation of CPB weaning until after protamine reversal.
Midesophageal long-axis view showing a left ventricular assist device cannula (arrow) at the apex of the left ventricle (LV). Air bubbles can be seen as echo-dense spots within the LV cavity, moving with blood flow. (LA, left atrium.)
Patent Foramen Ovale. Although it is optimal to diagnose a PFO prior to CPB, LVAD-induced reductions in LV end-diastolic pressure and left atrial pressure increase the likelihood of right-to-left shunting. Discovery of a previously unrecognized PFO following CPB has been described and may require reinstitution of CPB for repair if there is significant shunt flow.35,36
Aortic Valve. Ideally the severity of AR should be determined preoperatively to allow for correction during LVAD placement. However, the increased transaortic (valve) gradient associated with reduction of the LV end-diastolic pressure and increased flow into the ascending aorta through the outflow graft after CPB is discontinued may worsen preexistent AR. If worse than mild AR is identified, the aortic valve may need to be surgically corrected.37
In addition to examining the aortic valve for severity of AR, the frequency of aortic valve opening should be determined. A functioning LVAD is capable of reducing LV end-diastolic pressure to a level at which the aortic valve does not open during a normal cardiac cycle. However, if the LVAD is only providing partial or variable support, the aortic valve will open intermittently.26
Right Ventricular Dysfunction. As the LVAD provides a normal cardiac output, a commensurate amount of blood is returning to the right heart as preload. Patients with RV dysfunction may be unable to accommodate for this change, and signs of right heart failure may develop including RV distension, acute severe tricuspid regurgitation, increase in pulmonary pressures, and LV failure secondary to a low preload.31 Another cause of RV dysfunction after LVAD placement is based on the concept of ventricular interdependence. Rapid reductions in LV end-diastolic pressure may result in movement of the ventricular septum toward the LV free wall. Functionally this causes abrupt alternations in RV size and geometry and can influence the severity of tricuspid regurgitation. If identified, the most effective short-term treatment is to reduce the LVAD flow, which subsequently increases the LV end-diastolic pressure and returns the septum to a more normal anatomic position.
Inflow Cannula. The inflow cannula is usually placed in the LV apex and is often directed anteroseptally and toward the mitral valve opening but away from the interventricular septum and lateral wall. It should not abut any of the LV walls in order to avoid obstruction of blood flow into the cannula.31 If the cannula is misdirected, withdrawal and inferior displacement by the surgeon generally rectifies the situation. Proper inflow cannula placement should be evaluated in at least two views: the midesophageal four-chamber view and the midesophageal long-axis view. A CFD sector should be placed across the opening of the inflow cannula and should demonstrate low-velocity, unidirectional, laminar (nonturbulent) flow (Figure 17–8). In addition, unobstructed flow should be demonstrated using continuous-wave Doppler from the inflow cannula with peak velocities less than 2.5 m/s (Figure 17–9).31 The cannula position should be assessed again after chest closure to ensure that it remains correctly positioned.
Midesophageal two-chamber view of the left ventricle (LV) demonstrating laminar flow with color-flow Doppler across the left ventricular assist device inflow cannula (arrow) positioned at the LV apex. (LA, left atrium)
Spectral pulsed-wave Doppler flow velocity across a left ventricular device inflow cannula in the midesophageal four-chamber view demonstrating low-velocity laminar flow.
Outflow Cannula. The outflow cannula of most devices is placed in the ascending aorta. This cannula may be seen in the midesophageal ascending aorta short-axis (Figure 17–10) or long-axis views. In order to assess the blood flow at the cannula anastomotic site, pulsed- or continuous-wave Doppler can be used. The peak velocity should be 1.0 to 2.0 m/s for an axial device and around 2 m/s for a pulsatile device.26
Midesophageal ascending aortic short-axis view demonstrating a left ventricular assist device outflow cannula (arrow) with color-flow Doppler showing flow across the cannula into the ascending aorta. (SVC, superior vena cava.)
Left Ventricle. After protamine administration, the LVAD speed can be safely increased and TEE should confirm LV unloading. A properly functioning LVAD should reduce the LV diameter, and the interventricular septum should remain in a neutral position. Persistent deviation of the septum to the right suggests inadequate reduction of left ventricular pressure, and an increased pump speed is warranted. Septal displacement towards the LV cavity is indicative of excessive LV unloading and may have adverse implications for RV function as discussed above. Detection of specific wall motion abnormalities and determination of ejection fraction are unreliable with a functional LVAD as preload reduction precludes normal contractility.26
TEE can be used to assess patients with reduced LVAD flows or function. The differential diagnosis includes right ventricular failure, pulmonary embolus, cardiac tamponade, hypovolemia, cannula obstruction or malposition, and device failure.31,38
Right Ventricular Failure or Pulmonary Embolus. RV failure and pulmonary embolus present with a similar echocardiographic picture. As mentioned previously, RV failure limits the preload for the LVAD, causing a low output state. The typical findings on TEE include a dilated and dysfunctional RV, severe tricuspid regurgitation, and an underfilled left ventricle. Patients with a pulmonary embolus tend to have elevated pulmonary artery pressures, whereas those with isolated RV failure may actually have low pulmonary artery pressures. If there is concern of a pulmonary embolus, the pulmonary arteries should also be examined.31
Cardiac Tamponade. Tamponade can be difficult to diagnose after LVAD placement, as fluid collections may be loculated, making them difficult to identify. For example, the typical findings of right heart compression may be absent if the fluid collection is located posteriorly and compresses the left atrium. Normal LVAD physiology, which reduces left heart filling pressures, also confounds this assessment.31
Hypovolemia. Clinically, hypovolemia will present with systemic hypotension, reduced jugular venous pressure or central venous pressure, and reduced LVAD output. Although this diagnosis does not typically require imaging, TEE may be a useful adjunct, demonstrating small RV and LV dimensions and ruling out other possible etiologies for the clinical picture, including RV failure and tamponade.
Inflow Cannula. Inflow cannula obstruction has a severely detrimental impact on VAD function and can be caused by a variety of pathological processes (Table 17–6).26,39 The cannula should again be examined in at least two views, typically the midesophageal four-chamber view and the midesophageal long-axis view.31 Color-flow Doppler across the cannula inlet demonstrating turbulent flow during LVAD diastole, and continuous-wave Doppler demonstrating a peak velocity greater than 2.5 m/s are suggestive of obstruction.26,39–41 Three-dimensional (3D) TEE images have also been used to visualize thrombus in the inflow cannula (Figure 17–11).
Table 17–6. Potential Causes of Inflow Cannula Obstruction. ||Download (.pdf)
Table 17–6. Potential Causes of Inflow Cannula Obstruction.
Compression of the ventricular septum
Compression of the papillary muscles
Compression of the left atrial wall (if the cannula is placed in the left atrium)
Migration of thrombus from an intracardiac site
A three-dimensional transesophageal echocardiographic view demonstrating a left ventricular assist device (LVAD) inflow cannula (arrow) in the apical region. A thrombus could be seen within the lumen of the cannula. (LV, left ventricle; LA, left atrium.)
The pulsatile LVADs contain valved conduits that direct flow through the device and prevent regurgitation in a manner similar to the native heart. Inflow valve regurgitation (IVR) is a common cause of LVAD mechanical dysfunction and is usually due to a torn cusp or commissural dehiscence of the prosthetic valve secondary to high pressures.37,41 The patient with significant IVR presents with clinical evidence of heart failure and elevated pump rates that result from increased device filling. Echocardiography will demonstrate ineffective LV unloading characterized by increased LV dimensions and aortic valve opening in addition to decreased outflow graft velocity and a decreased stroke volume.37,41
Outflow Cannula. Documented complications of the outflow cannulae include perforation and malposition. Air bubbles in the aorta near the outflow cannula anastamosis may suggest cannula perforation.26 An extreme case of cannula misplacement was reported in a hemodynamically unstable patient in whom the LV was dilated and the AV was opening with LVAD systole. The outflow cannula was not visualized on TEE and upon surgical exploration, was found in the right superior pulmonary vein.40