INTRODUCTION
Transesophageal echocardiography (TEE) provides an astutely trained clinician with essential information which can significantly influence clinical management and improve patient outcome in both cardiac and noncardiac procedures (
1,
2). In 2011, the American Society of Anesthesiologists/Society of Cardiovascular Anesthesiologists (ASA/SCA) Task Force published updated practice guidelines and classified hemodynamic instability as a category I indication for the use of TEE and the use in coronary revascularization for patients with poor ventricular function as category IIa (
3). The use of TEE in routine coronary artery surgery is also now considered IIa (
3,
4). The European Association of Echocardiography (EAE) and the SCA recommend that TEE should be used for both elective and emergency open cardiac surgery unless contraindicated (
3,
4).
TEE provides an enormous amount of information during cardiac surgery that may directly change surgical case management in up to 13% of cases prebypass and in 6% postbypass (
5,
6,
7,
8), as well as anesthetic management in approximately 50% of coronary artery bypass graft (CABG) patients (
Table 15.1) (
5). The new information provided and subsequent interventions have been shown to be cost effective (
9). Skinner and Klein have also shown that preoperative studies may not accurately reflect patient pathology due to inadequacies of transthoracic echo, an inaccurate or incomplete report, and/or disease progression (
7,
10).
TEE provides a rational basis for decision making during weaning from bypass by being able to continuously assess cardiac function, cardiac output (CO), volume replacement, inotropic and vasoactive therapies, as well as, guide placement of intra-aortic balloon pumps (IABPs). TEE allows immediate assessment of the adequacy of revascularization by examination of regional wall motion abnormalities (RWMAs) both during on-pump and off-pump coronary artery procedures. Furthermore, TEE has proved reliable and comparable with the pulmonary artery catheter (PAC) thermodilution techniques for monitoring and quantifying CO.
The increasing age and comorbidity of patients undergoing coronary revascularization procedures make TEE an invaluable part of our monitoring armamentarium. For example, it allows us to optimally fluid resuscitate the patient and note the corresponding value of central venous pressure (CVP) or pulmonary artery pressure which can then be used in the intensive care unit. This is particularly important in hypertensive patients and those with ventricular systolic or diastolic dysfunction, in which venous pressure does not accurately reflect intracardiac volume (
11,
12).
NEW RWMA AFTER CARDIOPULMONARY BYPASS
What Does it Signify?
In two classic studies by Roizen and Smith, the occurrence of postoperative myocardial infarction was increased in patients who exhibited new RWMAs during CABG or aortic vascular surgery (
24,
25). The incidence of postoperative infarction was more strongly associated with new RWMAs than with new electrocardiographic changes. Swaminathan confirmed worsening RWMA immediately after CABG was associated with a twofold increase in long-term major adverse cardiac events (
26). Although TEE may be sensitive in diagnosing ischemia, a new RWMA does not always predict myocardial infarction. In the study of Leung et al. (
27), a myocardial infarction was subsequently diagnosed in only one of eight patients in whom a new, persistent RWMA had developed. This apparent discrepancy is consistent with the concept of “myocardial stunning,” in which an acute episode of myocardial ischemia can result in wall motion abnormalities that later resolve without any permanent injury.
What Should We Do?
The appearance of new RWMAs after bypass is common, but they may be caused by factors other than acute graft occlusion. These include transient ischemia resulting from the distal coronary embolization of air or debris, spasm of the left internal mammary artery, low coronary perfusion pressure, increased oxygen demand due to inotropic drugs, myocardial stunning, myocardial inflammation and surgical trauma, electrolyte disturbance, cardiac pacing, and conduction abnormalities. Any apparent dyskinesia due to conduction abnormalities can be differentiated from ischemia by looking for myocardial thickening. Although some investigators have suggested that the detection of new RWMAs warrants further surgical intervention, the sensitivity and specificity of new RWMA to predict graft failure confirmed by angiography in a large retrospective analysis do not support such an aggressive approach (
28); this has to be on an individual case basis. The additional morbidity/mortality associated with the resumption of bypass to
place another graft would likely outweigh the potential benefit in most cases. A more progressive approach is presented in
Table 15.4.
The surgeon can assess graft patency and flow by visual inspection to confirm the absence of graft kinking or torsion, by stripping the vein graft to confirm refill, by palpation, by transit time flow measurements (
29), and by the use of an epicardial surface Doppler flow probe. Decreased flow in an arterial conduit can result from poor distal runoff, a compromised anastomosis, or vasospasm that can be effectively treated with nitroglycerin, papaverine, or a calcium channel antagonist such as nicardipine or nifedipine.
Ventricular septal hypokinesis and dyskinesia are common immediately after separation from CPB and usually recover within 10 to 15 minutes
(Video 15.3). The abnormal conduction progression inherent with right ventricular (RV) pacing results in contractile dyssynchrony, which may be interpreted as a septal RWMA. Temporary atrioventricular or biventricular pacing may be considered to restore contractile synchrony (
30,
31). If septal dyskinesia persists or suddenly appears after a significant time postbypass, then the surgeon should be advised to check the LAD and RCA grafts if present. RWMAs in other areas of the LV need the patency of the graft to be checked sooner. If an RWMA persists or, more commonly, global dysfunction is seen with TEE, then circulatory support should be started either with inotropes or by inserting a circulatory assist device. The level of assist depends on the dysfunction seen. TEE aids placement of the devices and monitoring of recovery.
Differentiation between poor perfusion and stunned myocardium is more difficult. Possible strategies include epicardial scanning and the administration of a contrast agent to determine coronary flow patterns. If the area demonstrates flow of the contrast agent, the RWMA may resolve with time. The absence of contrast agent suggests a technical problem at the anastomosis or distal obstruction in the native coronary. Such information can help guide any possible surgical intervention. The technique of contrast perfusion can also be performed before bypass. If a specific area is likely to be infarcted, as demonstrated by the absence of contrast flow and significant wall thinning, surgical interventions are not likely to be of value. Both these techniques are uncommonly applied in routine operative practice, and their impact remains to be determined.
ACUTE CARDIAC DYSFUNCTION: ASSESSMENT AND MANAGEMENT
Cardiac dysfunction may develop at any time during the perioperative period. TEE examination of the heart and great vessels can provide a quick assessment of the primary factors related to hypotension: preload, afterload, myocardial contractility, valvular function, and integrity of the aorta. TEE can significantly affect the surgical and anesthetic management, especially in high-risk patients or in patients with acute hemodynamic collapse. The reader is reminded that post-CPB cardiac function must be interpreted in the context of the prebypass examination findings and the occurrence of any significant bypass events.
The TEE examination quickly provides data that guide pharmacologic therapy and volume resuscitation. In several studies, TEE significantly modified both surgical and hemodynamic decision making during the perioperative period (
32,
33). The echocardiographic findings associated with common causes of hypotension and cardiac dysfunction are presented in
Table 15.5 and discussed below.
Hypovolemia
Hypovolemia, a common cause of perioperative hypotension, is often related to the obstruction of venous inflow as a consequence of prebypass cannula placement, volume reequilibration after separation from
bypass, and bleeding. The assessment of LV chamber size by TEE has been shown to be a sensitive measure of LV preload. In the study of Cheung et al. (
34), the quantitative analysis of changes in the transgastric shortaxis (TG SAX) area could reliably detect even a 2.5% decrease in intravascular volume.
After separation from CPB, the LV is often noncompliant, especially when the LV is hypertrophied. This makes assessment of filling difficult when relying on a pressure reading from a CVP or PAC as higher pressures will be necessary to achieve optimal preload. Similarly, many dynamic indicators of fluid responsiveness rely on heart-lung interaction and are not valid in the “open chest”(
32,
35). TEE allows direct visualization of diastolic chamber size for assessment of fluid status. In addition, volume responsiveness can be assessed by tilting the patient head-down and confirming an increase in CO by aortic valve (AV) VTI in this situation. An interatrial septum that remains curved toward the right throughout the cardiac cycle is another indicator of raised left atrial (LA) pressure (
36).
Dynamic Mitral Regurgitation
The development of mitral regurgitation (MR) may be associated with hypotension, increased pulmonary pressures, RV failure, and decreased CO. Excessive volume resuscitation or increased afterload can result in LV distension with incomplete coaptation of the mitral leaflets and a central jet of regurgitation. Alternatively, ischemia or LV dysfunction can lead to papillary muscle dysfunction or LV distension. Significant MR may require mitral valve (MV) surgery or hemodynamic management, such as adjusting the systemic vascular resistance, administering inotropic agents, or decreasing the LV preload.
Right Ventricular Dysfunction
RV dysfunction is another common cause of perioperative hypotension. RV dysfunction is associated with RV dilation, tricuspid regurgitation, abnormal septal wall motion, and decreased LV chamber size. Management includes checking for ischemia (though more difficult to assess for the RV), optimizing the pulmonary vascular resistance (PVR), systemic arterial pressure, and contractility. The RV can be affected by pathology of the LV and vice versa. Following myocardial infarction, this ventricular interdependence can affect the shape (e.g., septal shift), size, and function (pressure-volume relationship) of the other ventricle, and is a predictor of outcome. The use of only retrograde cardioplegia can be associated with inadequate RV protection as the balloon on the cannula can obstruct the right cardiac vein preventing cardioplegia reaching the territory drained by it.
RV systolic dysfunction following CABG is commonly diagnosed by 2D echo images using ME fourchamber, ME RV inflow/outflow, the TG SAX views, and the newer TG RV view, TG RV inflow-outflow 130° (
37). Of note, tricuspid annular plane systolic excursion (TAPSE) is not a reliable indicator of RV dysfunction postbypass due to pericardiectomy. After open heart surgery, any residual intraventricular air is more likely to enter the right coronary because of its anterior position causing temporary RV ischemia and dysfunction. With the open chest, impairment of the free wall and RV distension can be visualized directly. Dysfunction and recovery can also be monitored by TEE while treatment is instituted using rest, administration of inotropic agents that also decrease PVR (e.g., milrinone, dobutamine), and titration of pulmonary vasodilators (nitric oxide, prostaglandin E
1, or nitroglycerin)
(Videos 15.4 and 15.5).
Low Ejection Fraction
Patients who have reduced left ventricular ejection fraction (LVEF) as evaluated prebypass (<40% EF) may need supplemental inotropic or chronotropic support as they are often on β-blockers and the ventricles can appear sluggish on TEE initially upon separation from bypass. This may be short lived and is monitored by TEE and therapy may be discontinued relatively quickly. A prebypass LVEF of <30% is likely to need inotropic support post bypass. TEE is used to monitor changes in contractility and filling in these patients. An increasingly sluggish LV post-CPB is an indication for insertion of an IABP. If this, in combination with inotropes, does not help then venoarterial (V-A) extracorporeal membrane oxygenation (ECMO) for temporary support or a left ventricular assist device (LVAD) is the next consideration.
Unexpected Diagnosis of Coexisting Problems
Unexpected findings are not uncommon in patients who have undergone a standard workup (
7,
10) and can be secondary to disease progression or previously undetected findings. Diagnosis of previously undetected pathologies can dramatically alter the surgical plan, for example, insertion of a mitral ring for severe MR, as well as impact on the postoperative management and outcome.
Intracardiac Shunts; Patent Foramen Ovale or Atrial Septal Defect
Up to 25% of adult cardiac surgical populations have an intracardiac shunt which can affect the surgical plan and long-term neurologic prognosis due to paradoxical air embolism. If a patent foramen ovale (PFO) is found incidentally during CABG surgery, the decision regarding closure depends on individual surgical preference (
38). When an open-chamber procedure is performed in conjunction with CABG surgery or in a patient with a stroke history, an incidental PFO could be closed. Practice may be swayed by the American Academy of Neurology cautioning against device closure of PFO in patients with cryptogenic ischemic stroke (
39).
A PFO can be most reliably detected when the interatrial septum is examined with both color flow Doppler (CFD) and after air contrast injection in the ME four-chamber and bicaval views. The passage of contrast bubbles in the LA within five cardiac cycles confirms the diagnosis of a PFO.
Intraoperative detection of a previously unsuspected PFO has relevance to ICU management and emphasizes the need for an echocardiographic report in the medical record and communication with the ICU staff. For example, if atelectasis develops post-CABG surgery resulting in an increase in RV afterload, the increase in right heart pressures can cause the shunt direction to change or exacerbate an existing right-to-left intracardiac shunt, with subsequent worsening hypoxia.
Pleural Effusions
Iatrogenic pleural effusions often develop when the pleura is opened during internal mammary artery harvesting and may be already present in patients with impaired ventricular function. This may have a marked effect on post-CPB ventilation and oxygenation as well as affecting the hemodynamic status of a patient with borderline cardiac function. Ultrasound can easily detect both left- and right-sided pleural effusions. Left pleural effusions can be seen in the ME descending aortic SAX view. Right-sided effusions are seen by turning the probe from the ME four-chamber view to the right
(Videos 15.6 and 15.7).
Previously Unknown Aortic Valve Pathology
Moderate aortic stenosis (AS) may be discovered during intraoperative TEE for CABG surgery. Quantification of AV disease and the decision when to perform a combined CABG and aortic valve replacement (AVR) procedure can be difficult, especially when LV function is compromised and the loading conditions may be altered. Evidence shows that a subsequent AVR after a previous CABG has a higher mortality than a single combined procedure (
40). The degree of calcification is important because even in the asymptomatic patient progression of the disease process may be rapid. Progression is quite variable, with a decrease in effective valve area ranging from approximately 0.1 to 0.3 cm
2/y. In a primary CABG procedure, it is therefore recommended that AVR should be considered in a patient with even moderate AS. Best practice dictates that patients are adequately investigated prior to surgery and decisions about concomitant AV surgery are discussed before patient is scheduled for surgery. The development of TAVR means that future progression of AS can be treated without the need for redo surgery, although it has its own risks associated with it.
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