13 Decision Making and Perioperative Transesophageal Echocardiography

“In the affair of so much importance, wherein you ask my advice, I cannot make for want of sufficient premises advise you what to determine, but if it please I will tell you how.”

—Benjamin Franklin

All too often in medicine, critical decisions are made without the benefit of a thorough consideration of data, evidence, and framework. The paucity of clinical outcomes research in echocardiography, especially in the perioperative period, dampens the prospects for evidence-based decision making. In the absence of evidence-directed practice, decision making typically is based on anecdote, clinical impression, and tradition, with little effort devoted to the process of reaching an intelligent conclusion. The quantity of information is increasingly abundant in medicine, and the operating room is no exception. Its acquisition, interpretation, and application for decision making can be cumbersome, distracting, and misguided. In the era of increasing information, there is an imperative to develop a systematic process of handling data streams, organizing ideas and thoughts, defining and prioritizing problems, and effecting care through a well-thought-out decision. A formalized approach to the acquisition of data and decision making (Figure 13-1) enhances the quality of the intraoperative echocardiogram, its interpretation, and the confidence with which the findings are communicated to other members of the operative and nonoperative teams. Poor decisions are not made by the physician with bad intentions. Poor decisions are more commonly the result of individuals relying on limited medical knowledge (a database typically defined by the narrow bounds of their profession), narrow framing, and false or tenuous anchors. The echocardiographer who is overly confident in the abilities of his or her surgical counterpart may be falsely anchored to the prior performances of the surgeon, with little or no reliance on a formalized decision-making process. The lack of a structured paradigm for decision making is most worrisome when clinicians with lesser ability or experience are making the decisions. The least accomplished clinicians often have the most inflated estimate of their own abilities, thus lending themselves to the vulnerabilities of limited skills plus lack of a decision-making process.¹

Figure 13-1 An algorithm for the decision-making process.

CPB, cardiopulmonary bypass; TEE, transesophageal echocardiography.

The intraoperative consultant in echocardiography is confronted with multiple channels of information (Boxes 13-1, 13-2, and 13-3). The broad database that is required to formulate an intelligent decision includes provider- and patient-specific data. Patient-specific data include history and demographics, preoperative diagnostic examinations, admitting diagnosis and comorbidities, the patient’s wishes, recommendations of referring physicians, and intraoperative data. Intraoperative data include hemodynamic data, visual inspection, surgical input, and the transesophageal echocardiographic (TEE) examination. A systematic TEE examination of the heart and great vessels permits the acquisition and interpretation of qualitative and quantitative echocardiographic data applied to intraoperative decision making. The provider-specific data are composed of an accumulated database of knowledge acquired from training, experience, and continuous medical education. Expertise is gained from experience and enhances the repertoire of experiences from which a practitioner can draw but does not alter the cognitive engine and does not immunize the practitioner from errors in decision making. Intuition and experience are not reliable predictors of success. Learning through methods of trial and error and self-education by exploratory problem solving have little role in the arena of cardiac surgery. Heuristic methods of decision making often create a systematic and predictable bias. It is acceptable to be wrong. It is unacceptable to be consistently wrong in the same direction. A structured process of assessing all the data and weighing various alternatives (cognitive engine) will enable the physician to formulate a concise, organized approach to problem solving, communicating the findings and management alternatives.

Decision making can be encumbered by cognitive and emotional attachments that limit clinicians’ intellectual flexibility. Poor problem solving and poor outcome can follow a single poor decision of great magnitude. However, the “creep effect” of a series of small poor decisions can insidiously lead to a poor outcome. The adherence to a poor course of action because of an attachment to the original decision is common in medicine. “The escalating commitment to a losing course of action often begins with small steps” (Roch Parayre, MBA, personal communication). In the perioperative setting, this process is most vivid in the care of critically ill patients with little or no hope for survival. Continued commitment of resources and intervention often contribute to patient discomfort and cost without benefit in quality of life or longevity. The prior commitment of resources often encourages further commitment and investment in a losing cause. The echocardiographic decisions during surgery may become part of an intraoperative sequence of diagnostic and therapeutic interventions in which the best course of action is a complete reversal in direction. Repeated attempts at repairing a mitral valve (MV) may follow an initial unsuccessful repair. The decision to replace the valve instead of repairing it often is not considered until late in the course. Repeated intervals of cardiopulmonary bypass (CPB) and aortic cross-clamping are not without their complications and associated morbidities. It often is difficult to retain an open mind and to consider alternative diagnoses or therapeutic alternatives. Effective decision-makers are able, if necessary, to abandon the original decision to repair an MV and move toward valve replacement.

An intraoperative TEE examination can correct preoperative inaccuracies in diagnosis or detect occult disease. With increasing emphasis on decreasing preoperative testing, avoiding redundant testing, and decreasing costs, accurate diagnoses of disease may not occur until the time of surgery. The increased reliance on the intraoperative TEE is fiscally wise but places greater responsibility and impact on the intraoperative echocardiographer. The detection of occult disease not appreciated during the preoperative evaluation often impacts operative management. It is necessary to reframe a problem when the data acquired reveal new insights. For example, the detection of mobile atheroma in the ascending aorta may influence positioning of an aortic infusion cannula or cross-clamp, hence changing circulatory management and the operation.^2–4 A change in clinical management in respect to otherwise asymptomatic and silent findings is often controversial. The change in the operation has typically not been discussed with the patient, as the findings were unanticipated. The intraoperative diagnosis of moderate aortic valve regurgitation (AR) that was not detected before surgery will create a clinical challenge for the surgical team regarding administration of cardioplegia and the decision whether to replace the aortic valve (AV). Hence, the decision to proceed with an unplanned aortic valve replacement (AVR) relies on the ability of the echocardiographer to establish the diagnosis and mechanism of valvular pathology, define the pertinent factors that sway the decision (preoperative symptoms of congestive heart failure [CHF], ventricular size and function, pulmonary hypertension), and communicate with the surgeon and the other pertinent stakeholders. It is important to realize that the decision to recommend AVR to a patient is not often guided by the degree of AR but rather by the degree of corresponding ventricular dilatation and dysfunction. The finding of moderate AR with normal ventricular systolic function and chamber size, normal left atrial pressure, and no preoperative history of CHF may sway the operative team to proceed with the originally planned surgery and to treat the occult finding medically with postoperative afterload reduction and follow-up serial echocardiograms. In contrast, in a patient with otherwise unexplained shortness of breath, pulmonary hypertension, and a dilated left ventricle (LV), the presence of moderate AR typically leads to AVR. The introduction of new findings to the operative team warrants a “time-out” approach to determine the impact of the findings on the intraoperative care.

Decision-Making Process

The process of decision making is, in essence, “deciding how to decide.”⁵ What is the primary issue that needs to be addressed? What are the pitfalls in the decision? What are the consequences of the decision? What tools and resources does the decision maker require? What information is needed to make an informed decision? Is there evidence to support one decision over another? How much time does the decision-maker need to make the decision? Rarely is there a valid reason for not taking enough time to make a well-thought-out decision, even in the high-productivity, high-throughput environment of the operating room. Does the decision-maker need help? The authors have applied the methods of Russo and Schoemaker⁵ to decision making in medicine:

1. Framing: Framing defines the question and the factors that influence or sway the decision maker. Framing sets the vantage point of the decision maker and defines the boundaries, parameters, and priorities. By framing a question in the early stages of problem solving, it permits focus and bounded rationality. However, the price of focusing on a specific issue may be loss of peripheral vision. Adopting a narrowed vantage point can inadvertently impose significant bias and limitation. The decision should be addressed from a variety of vantage points so that all aspects of the decision can be considered.

Failure to work beyond a single conceptual frame can lead to difficulties in communication among the different participants of the care team. In the setting of a complex MV repair, the intraoperative echocardiographer often is focused on performance of the TEE, successful remedy of hemodynamic disturbances, surgical intervention, and documentation. If the echocardiographer is also the anesthesiologist, his or her frame is broadened to include patient safety and comfort, vigilance, and maintaining body homeostasis. The surgeon’s frame includes his or her ability and limitations in achieving a competent surgical repair, alternatives in surgical management, and the covenant with the patient and family regarding surgical management (e.g., repair vs. replacement, bioprosthesis vs. mechanical prosthesis), patient overall outcome, and his or her reputation as a surgeon. The patient’s vantage point may differ from those of the operative team. The patient wants the mitral regurgitation (MR) to be fixed, for the symptoms to be resolved, to return to a “normal routine,” for the remedy to be long-lasting, and to be able to ride a Harley Davidson, which he or she would otherwise have to forfeit if he or she was taking lifelong warfarin (Coumadin). Hence, as a decision maker, broadening the understanding of the issues and consideration of multiple frames will account for the interests of multiple parties.

2. Data collection: Data collection is aimed at reducing uncertainty. Uncertainty is never eliminated and, hence, needs to be managed. The perioperative echocardiographer manages uncertainty not through pinpoint predictions but by uncertainty estimates. It is imperative in the decision-making process to systematically identify the causes that could lead to decision failure and to quantify the likelihood of such causes occurring. A dilated mitral annulus with a flail middle scallop of the posterior leaflet and two ruptured chordae are associated with a high rate of successful surgical repair. However, factors that are likely to affect this outcome include the technical ability of the surgeon, a parameter that is difficult to estimate and creates uncertainty in the expected outcome.

The data should include echocardiographic and nonechocardiographic data (see Boxes 13-1 through 13-3). The importance and impact of TEE decisions have been generally recognized and accepted. The ability to make an appropriate decision is predicated on a comprehensive examination. Confirmatory information is useful, as is contradictory information. The process of decision making also includes defining what information “not to collect.” Collecting as much data as possible typically leads to confusion and loss of direction in the reasoning process. A common hazard for the echocardiographer is the performance of an abridged examination because of either increased clinical demands or reliance on a preoperative examination. The conclusions drawn from an intraoperative examination and associated decisions should not be hurried and should be based on all aspects of the examination. Although physical injury from the TEE examination is a serious matter, the greatest risk of TEE is that of errors of omission or misinterpretation, leading to mismanagement and poor outcome.^6–11

3. Decision and implementation: A clinical decision is made based on the integration of knowledge, framing, and information (Box 13-4). Primary knowledge is “knowing what you know” and “knowing what you do not know,” with the latter prompting a practitioner to seek assistance. Second-order knowledge is “not knowing what you do not know”; hence diagnoses are missed rather than misinterpreted. The broader the repertoire of primary knowledge, the more informed is the decision maker and the more reliable is the decision.

BOX 13-4. DECISION PROCESS

Projecting the impact of:

• Progression of disease

• Risk for redo surgery

• Short- and long-term outcomes

• Associated risks (e.g., anticoagulation)

• Size mismatch of prosthesis

• Effect of prolonged cardiopulmonary bypass on immediate postoperative outcome

Does the decision account for:

• Inconsistencies (among two-dimensional/Doppler/patient symptoms/preoperative evaluation)

• Plausibility of alternate explanation

• Alternate therapy

• Current literature

• Preoperative evaluations

• Patient factors (age, cardiac status, ability to tolerate anticoagulation, etc.)

The echocardiographer is an intraoperative consultant who generates vital information that has a direct impact on intraoperative care and decision making. As consultants, suggestions and recommendations are offered, but rarely does the echocardiographer dictate the management to the operative team. The decision/recommendation is shared with the stakeholders (surgeons, perfusionists, nurses, referring cardiologists, postoperative intensivists, family and patient) and is communicated verbally and by written report. Decisions often are accompanied by discussion and sometimes persuasion. Making a sound decision concerning the surgical approach to an anatomic problem can benefit the patient only if it is effectively communicated to the operating surgeon. However, clinical judgment must take into account the skill set of the operative team and the pitfalls associated with each intervention. Persuading a surgeon to proceed with a complex reconstruction may appear to be the appropriate course of action according to an echocardiographer, but it may be the wrong thing to do if the surgeon is unfamiliar with the recommended repair (i.e., poor framing).

4. Learning from knowledge to wisdom: A systematic process for learning from the results of past decisions is designed to increase the decision maker’s primary knowledge base and defines an effective clinical quality improvement program. The ability to achieve success or failure may depend on the ability of the decision maker to learn from past decisions and the decisions of others.⁵ A fund of knowledge gained through training, continuous medical education, readings, and the performance of echocardiograms on a regular basis maintain the skills of the echocardiographer. Although it is often difficult to obtain feedback regarding the impact of decisions on long-term outcome, the increment in effort to seek such insight always renders the echocardiographer more prepared for the next clinical scenario that shares common cardiovascular themes (wisdom). Feedback can be sought from a variety of sources: surgeon, cardiologist, outpatient echocardiography data files, among others. Participation in quality improvement forums with cardiovascular anesthesiologists, cardiologists, and cardiac surgeons who tend to follow the patients longitudinally is a useful learning tool.

Although all four processes above are important, the initial framing of the problem prompts the subsequent steps of data collection, conclusion, and learning. Framing begins by articulating a question. By addressing the problem in terms of a specific question, a clinical situation is framed in a more manageable context. A framing strategy can be an effective method to rationally limit decision options and form the basis of communication.

Performance of the decision maker is judged based on final outcome. However, decision making should be based on the information the decision maker had at the time of the decision. A significant limitation of measuring performance during uncertainty is that it is often judged, not by the decision-making process, but by single case results. If the decision is followed by a good outcome, the decision maker often is applauded with little regard to the ability to reach an intelligent conclusion. A poor outcome does not necessarily imply a poor process or poor decision. High-risk surgery leads to poor outcomes in many cases despite robust decisions. In medicine, this often leads to individuals being reluctant to make any decision at all, knowing that a poor outcome is likely and that it will be linked to their decision making. The reality of performance assessment is that even if the decision to proceed with therapy is substantiated, a poor outcome often will reflect negatively on the abilities of the echocardiographer, anesthesiologist, surgeon, and the operative team. Conversely, a good outcome does not imply a good process or a good decision.⁵ The surgeon’s decision to perform a posterior sliding mitral valvuloplasty and quadrilateral resection of the posterior leaflet based on a dilated mitral annulus with normal leaflet motion as defined by TEE may result in a technically competent MV repair and good long-term results. The decision to perform a posterior sliding valvuloplasty may or may not have been a wise decision. Equally good results may have occurred with the insertion of an annular ring without leaflet resection. The measure of an outcome by recording a metric is a valid assessment of quality only if the metric is a function of the actions of the provider.¹² The outcome cannot be random; otherwise, there is no basis for estimating quality.

Cardiac Function and Regional Wall Motion Abnormalities

Framing

Ventricular function is a predictor of outcome after cardiac surgery and a predictor of long-term outcome in patients with cardiovascular disease. Patients with compensated CHF may have severely decreased ejection fraction (EF) with minimal symptoms. Regional ventricular dysfunction most commonly is caused by myocardial ischemia or infarction. Hence there is an imperative to detect ventricular dysfunction and institute treatment in an attempt to prevent acute or long-term consequences.

Is ventricular function normal or abnormal? Is the abnormal function global or regional? What is the coronary distribution that relates to an SWMA? Is the ventricle big or small? Is the myocardium thinned or hypertrophied? Is the abnormal function new or old? Does the medical or surgical intervention improve or decrease ventricular function?

Data Collection

Left ventricular systolic function is assessed echocardiographically based on regional and global wall motion. Methods of assessment include changes in regional wall thickness, radial shortening with endocardial excursion, fractional area change (FAC), and systolic apical displacement of the mitral annulus. Off-line measurements of EF can be calculated using Simpson’s rule. However, the EF most commonly is estimated online from the four-chamber, two-chamber, and short-axis images of the LV. Other measures include end-diastolic area (EDA), end-systolic area (ESA), and, most recently, three-dimensional analysis.

Regional assessment provides an index of myocardial well-being that can be linked to coronary anatomy and blood flow. Although the measurement of coronary blood flow is not achieved by TEE, the perfusion beds and corresponding myocardium for the left anterior descending, left circumflex, and right coronary arteries are relatively distinct and can be scrutinized by TEE using multiplane imaging. The transgastric and long-axis imaging views of the LV are the most widely used for evaluating wall motion abnormalities. Digital archival systems have gained popularity for their ability to capture a single cardiac cycle that can then be examined more closely as a continuous cine loop. Cine loops also can permit side-by-side display of images obtained under varying conditions (e.g., prebypass and postbypass). Regional myocardial ischemia produces focal changes in the corresponding ventricular walls before changes occur on the ECG.¹⁶ Changes progress from normal wall motion to hypokinesis or akinesis. Dyskinesis, thinning, and calcification of the myocardium suggest a nonacute process, likely a prior infarction.

Assessment of right ventricular systolic function is more problematic because it is less quantifiable. The crescent-shaped right ventricle (RV) is not amenable to quantitative measures of differences in chamber size during the cardiac cycle. Characterization of the RV is accomplished by comparing the size of the right ventricular chamber with that of the LV and assessing the relative contractile function of the right ventricular free wall and that of the interventricular septum.

Ventricular failure can be caused by diastolic dysfunction: the compromised ability of the ventricle to accommodate diastolic filling. Diastolic dysfunction is assessed echocardiographically by examining volumetric filling of the ventricle at the mitral or tricuspid valves and annular excursion. Normal diastolic filling is biphasic with an early (passive) component that exceeds the late (active) inflow velocities. Abnormalities of ventricular filling (e.g., impaired ventricular relaxation, restriction, constriction) produce characteristic changes in the spectral recordings of Doppler inflow velocities. Abnormalities of diastolic function can lend insight into the mechanisms of circulatory instability (see Chapter 12).

Discussion

Preexisting ventricular dysfunction suggests increased risk for surgery and poorer long-term outcome. The presence of such ventricular dysfunction may deteriorate intraoperatively, requiring the need for marked pharmacologic or mechanical support. A patient with a preoperative EF of 10% scheduled for coronary artery bypass grafting (CABG) and MV repair is at increased risk for intraoperative ischemia, acute heart failure, and difficulty maintaining hemodynamic stability during the immediate postbypass period. Anticipating such problems, consider placement of an intra-aortic balloon pump or femoral arterial catheter during the prebypass period (Figure 13-2). The same patient is likely to benefit from the administration of inotropic agents (see Chapter 32).

Figure 13-2 The prebypass transesophageal echocardiography (TEE) examination may have predictive value for postbypass circulatory management.

A 63-year-old woman with a medical history of hypertension, congestive heart failure, pulmonary edema, dilated cardiomyopathy, diabetes, and obesity was scheduled for coronary artery bypass grafting (CABG) and mitral valve (MV) repair. The preoperative evaluation documented moderate-to-severe mitral regurgitation (MR) with reversal of systolic pulmonary vein blood flow velocity. The prebypass TEE midesophageal four-chamber view showed a markedly dilated left ventricle (LV) and mildly dilated right ventricle (RV) with mildly decreased global dysfunction (A). The transgastric view was characterized by severe global dysfunction and an LV end-diastolic diameter of 6.6 cm (A). The fractional area change (FAC) was 17% [FAC = (left ventricular end-diastolic area [LVEDA] – left ventricular end-systolic area [LVESA])/LVEDA × 100]. Revascularization alone was unlikely to significantly improve MV function. The midesophageal bicommissural view of the MV (B) demonstrated marked dilation of the MV annulus (major axis = 4.8 cm) and tethering of the leaflets below the valve plane that was caused by LV chamber dilation. A femoral arterial line was inserted for monitoring of central aortic pressure and/or possibly placing an intra-aortic balloon pump. The patient underwent a CABG × 3 and MV annuloplasty for moderate MR. The separation from bypass was difficult, requiring milrinone, epinephrine, vasopressin, and placement of an intra-aortic balloon pump. TEE, which was used to initially confirm the location of the femoral guidewire (C), was later used to position the balloon pump just downstream to the left subclavian artery. Worsening of RV function that was characterized by increased central venous pressure, new-onset tricuspid regurgitation, and a hypokinetic RV can be appreciated by ventricular septal flattening and dilation of the RV (D). The LV ejection fraction did not decrease as might be expected; after correcting MR, the FAC improved slightly from 17% to 22% after bypass. Cardiac function continued to improve, and the counterpulsation device was removed without complication on the first day after surgery. The infusions of milrinone and epinephrine were continued for several days.

A marked decrement or unexpected decrease in global cardiac function after release of the aortic cross-clamp can be caused by poor myocardial preservation during cross-clamping or distention of the heart during bypass. The risk for such incidents can be reduced by the monitoring of the electrical activity of the heart and pulmonary artery pressures, as well as for distention of the RV and LV. Effective venting of the heart is often difficult to discern by visual inspection alone, especially with the use of minimally invasive surgery through small incisions. TEE imaging can diagnose ventricular distention produced by AV insufficiency.

Not all preexisting SWMAs benefit from coronary revascularization. Regions of akinesia and dyskinesia usually are the result of a myocardial infarction and may reflect nonviable myocardium, although “hibernating” myocardium is possible. Hypokinetic segments generally are viable and may represent active ischemia.¹⁷ Preoperative positron emission tomographic scanning can detect hibernating myocardium and may be cost-effective to guide CABG.^18–20 The detection of hibernating myocardium in an area of chronic ischemia and regional hypokinesis will direct the surgeon to revascularize the corresponding stenosed coronary artery. In contrast, an occluded coronary artery with downstream infarction may not benefit from revascularization because contractile function may be irreversibly lost. However, in this latter scenario, revascularization postinfarction may provide some benefit in decreasing the risk for ventricular aneurysm formation.²¹

Diastolic dysfunction is associated with significant increases in mortality during long-term follow-up.²² Characterization of abnormalities of diastolic function lends insight into the mechanisms of circulatory instability and hypotension. Severe left ventricular hypertrophy with a noncompliant LV and hyperdynamic systolic function may produce severe heart failure if adequate loading is not achieved. Hemodynamic indices obtained from a pulmonary artery catheter (PAC) may be misleading. The findings of a small left ventricular chamber size, blunted transmitral filling velocities, and an increased FAC demonstrate the cause of the hypotension. The decision to administer volume may be appropriate despite the increased pulmonary artery pressures.

If the intraoperative examination reveals new ventricular dysfunction, the intraoperative team must determine the cause and severity and then plan a treatment. Other causes of SWMAs such as conduction abnormalities (left bundle branch block or ventricular pacing) can be difficult to distinguish. Is the decrement in function potentially reversible with conservative therapy, or should additional intervention be considered? Treatment of myocardial ischemia may include optimizing hemodynamics; administering anticoagulants, nitrates, calcium channel blockers, or β-blockers; inserting an intra-aortic balloon pump; or instituting CPB and coronary revascularization. The presence of new-onset SWMAs after separation from CPB is worrisome for myocardial ischemia. Even the patient without coronary artery disease (CAD) remains at risk because of hypotension, a shower of air or debris into the coronary circulation, or coronary spasm. The patient with CAD undergoing CABG may have all the above risks, technical difficulties at the anastomotic site, injury to the native coronary artery (e.g., stitch caught the back wall or occlusion of the circumflex artery during MV surgery), or occlusion of the coronary graft by thrombosis or aortic dissection. The coronary arteries, grafts, and anastomoses should be carefully inspected for patency and flow. Graft patency in the operating room is difficult to determine. Techniques include manual stripping and refill, measuring coronary flow by handheld Doppler, or administration of echo contrast agents (see Chapter 12). Hybrid operating rooms have been increasing in number with the intent of providing advanced imaging of the coronary circulation at the time of surgery.²³ A new SWMA in the distribution of a new coronary graft can prompt the decision-making strategies listed in Table 13-1 (see Chapters 18, 32, and 34).

TABLE 13-1 Management Strategies for New-Onset Myocardial Ischemia after Bypass

Diagnosis	Plausible Treatment
Coronary graft occlusion	Revise coronary graft
Coronary air emboli	Increase coronary perfusion pressure, administer coronary dilators
Coronary calcium/atheroma emboli	Support circulation
Dissection of the aortic root	Repair dissection
Coronary spasm	Administer coronary dilators

Transesophageal Echocardiography as a Rescue Device: Management of Marked Hemodynamic Instability

Framing

There are many instances during the perioperative period when the patient may exhibit progressive, unremitting hemodynamic deterioration or acute cardiovascular collapse. Echocardiography offers a versatile modality to quickly and accurately diagnose the cause of hypotension and develop management strategies.

The echocardiographer may be summoned to evaluate an unstable patient in the operating room, intensive care unit, or emergency department with little or no preceding knowledge of the patient. Typically, there will be no consent for the TEE procedure; occasionally, a family member may be available to provide consent on the patient’s behalf. TEE may need to be postponed in the trauma patient with suspected cervical spine injury or esophageal injury. The trauma patient with an unstable cervical spine is at increased risk for spinal cord injury with passive movement of the head and neck. Until the cervical spine has been documented to be stable, TEE should be avoided and TTE is the alternative. The risk for further esophageal injury in patients with a penetrating trauma poses an additional challenge. Esophagoscopy before TEE is performed in patients with suspected esophageal injury. However, delay in diagnosis is not without cost. Time must be used efficiently because permanent vital organ injury relates to the magnitude and duration of hypotension and malperfusion. A number of issues should be considered to guide the discussion and development of rational management strategies.

What is the cause of the hypotension? Does the cardiac or vascular pathology detected by TEE explain the decrease in blood pressure? Is the heart big or small? Is it full or empty? What is the global function of both ventricles? Are there SWMAs? Is there fluid in the pericardium? Is the observed decrease in cardiac function the primary cause, or is it a consequence of the decreased blood pressure? Is this event related to the patient’s medical history or current operative procedure? What specific parameters of the ventricle may help explain the current episode of hypotension? What interventions or therapy can be performed to improve hemodynamics? Once therapy is initiated, what index or parameter should be monitored to guide management?

Data Collection

Clinicians must not underestimate the importance of medical history, chief complaint, and operative course when attempting to discern the causes of hemodynamic instability in the acute setting. Important hemodynamic indices include heart rhythm, rate, blood pressure, concentration of exhaled carbon dioxide, and central venous or pulmonary artery pressure, if available. Echocardiography can be used to develop a rational approach based on the critical factors of cardiac performance. The determinants of cardiac performance include stroke volume (SV) and heart rate (HR), as elucidated by the following equation: CO = SV × HR, where CO represents cardiac output. The three components of SV that can be affected are preload, afterload, and myocardial contractility. Although quantitative analysis is possible, qualitative online analysis generally will yield sufficient information to form the basis of initial therapeutic intervention. Preload of the ventricle can be determined by assessing EDA, afterload can be estimated by assessing the ESA, and contractility can be estimated by the velocity of circumferential shortening, FAC, or EF. Mechanical causes of hypotension must be considered (e.g., pericardial effusion).

Discussion

Initial inspection determines heart size and overall contractile function of both ventricles. Estimates of EDA and EF of the LV provide an index of ventricular load and global function. Attention to both right and left ventricular size and function helps distinguish between different inciting events.

The common causes of intraoperative or perioperative hypotension include intravascular hypovolemia, myocardial ischemia, myocardial infarction, and systemic vasodilatation, either pathologic from infection or inflammation, or iatrogenic from drug administration (e.g., vancomycin). Mechanical causes of hypotension typically are related to compressive forces impairing the heart’s ability to fill or eject (e.g., pericardial fluid, tension pneumothorax). The MV is inspected for incompetence. Acute mitral regurgitation is rare in the absence of myocardial ischemia or infarction. A diagnosis of dynamic LVOT obstruction, an uncommon cause during the perioperative period, is difficult to establish in the absence of more invasive monitoring such as TEE (Figure 13-3). Systemic hypotension with a dilated RV and a small, underfilled LV implies either primary right ventricular failure (e.g., myocardial ischemia or infarction in the distribution of the right coronary artery) or secondary right ventricular failure from acute increases in pulmonary vascular resistance (e.g., pulmonary embolus [Figure 13-4], pneumothorax, or protamine reaction).

Figure 13-3 Acute intraoperative hemodynamic deterioration.

A 65-year-old man with a medical history of hypertension, sleep apnea, and smoking was scheduled for resection of colon cancer. During the bowel resection, the patient had a profound episode of hypotension and new-onset hypoxia. Although the patient’s hemodynamic condition initially improved after administration of phenylephrine and ephedrine, the patient became more hypotensive and hypoxic with evidence of pulmonary edema. Transesophageal echocardiography (TEE) was requested and was emergently placed to diagnose the cause of cardiovascular collapse and guide management. The midesophageal four-chamber view showed a moderately hypertrophied left ventricle (A). Left ventricular (LV) systole was associated with displacement of the mitral leaflet and chordae down into the outflow tract. The resulting defect in leaflet coaptation of the mitral valve (MV) and abnormal chordal position that was noted in A were associated with overwhelming mitral regurgitation (MR) and LV outflow tract obstruction. B, Administration of inotropes (epinephrine and ephedrine) was discontinued; the management strategy was changed to volume resuscitation and pressor administration. The hemodynamics normalized and the examination was repeated 10 minutes later (C, D). Displacement of the mitral leaflet and chordae had resolved together with the findings of MR and outflow tract obstruction. The patient was believed to have experienced a profound acute decline in the systemic vascular resistance in response to the release of vasoactive substances during bowel manipulation. The initial exacerbation of the hemodynamics was created by the relative hypovolemia and use of inotrope, leading to dynamic LV outflow tract obstruction. The concomitant episodes of hypoxia and pulmonary edema, which were attributed to the severe MR and increased left atrial pressures, resolved with the decrease in MR. The application of TEE was critical in making the correct diagnosis, altering management strategies, and initiating the appropriate therapy.

Figure 13-4 Progressive hypoxia and hypotension after cardiac surgery.

A 58-year-old morbidly obese patient with a medical history of hypertension, diabetes, and smoking had recently undergone coronary artery bypass grafting × 3. Five days after surgery, the patient experienced development of new-onset atrial fibrillation together with progressive hypoxia and hypotension requiring readmission to the intensive care unit. The patient’s condition continued to deteriorate and required tracheal intubation, ventilator support, and infusions of vasoactive agents. Transesophageal echocardiography (TEE) was performed to evaluate cardiac function and rule out a pericardial effusion. The midesophageal four-chamber view (A) showed a dilated right ventricle (RV) coincident with a relatively underfilled left ventricle (LV) and abnormal positioning of the ventricular septum. The displacement of the septum into the LV was consistent with RV dysfunction and RV volume overload. Inspection of the right heart revealed a dilated hypokinetic RV and a serpiginous density that extended from the right atrium into the RV (B). The thrombus appeared to be entangled in the chordal structure of the tricuspid valve. Although no thrombus was noted in the pulmonary arteries, the diagnosis of pulmonary embolism was made and the patient underwent an emergent embolectomy. A right atriotomy was performed and a 64-cm thrombus was extracted from the RV together with additional clots from both the right and left pulmonary arteries (C). The postbypass TEE documented improved right ventricular function and filling of the LV. TEE was critical in making the diagnosis and the decisions to institute and guide therapy.

Decreased systemic vascular resistance during sepsis or a systemic inflammatory reaction is associated with decreased ESA and increased ventricular contractility (increased velocity of circumferential shortening), with concomitant increases in the EF and FAC. The increase in cardiac performance can be quantified by measuring the cardiac output (CO). In cases of hypotension associated with a markedly increased CO, the treatment of choice would be the administration of a vasopressor, such as phenylephrine or vasopressin. If decreased systemic vascular resistance and CO are present, administration of a positive inotrope having vasopressor actions, such as epinephrine or norepinephrine, might be more appropriate.

The distribution of the right coronary arterial system of most patients (right dominant system) includes the RV and the posterior descending coronary artery, which provides blood supply to the inferior and inferoseptal walls of the LV. Acute right ventricular dysfunction is not uncommon after the release of the aortic cross-clamp. Preservation of the RV is less reliable compared with the LV because of its exposure to ambient room temperature and variability in its coronary circulation. Open-chamber procedures increase the risk for right ventricular dysfunction because of retained intracardiac air. In the supine patient, the right coronary ostium is located in the least-dependent portion of the aortic root, predisposing it for the embolization of air bubbles. Air embolization to the right coronary artery produces acute ST-segment changes, marked global right ventricular dysfunction, and SWMAs of the inferior wall of the LV (Figure 13-5). Conservative treatment includes increasing the blood pressure to promote coronary perfusion while continuing CPB.

Figure 13-5 Air embolism after open-chamber procedure.

A 57-year-old patient underwent surgical intervention to treat severe mitral regurgitation (MR) and two-vessel coronary artery disease. After performing the mitral valve (MV) repair, the right superior pulmonary vein vent catheter was advanced through the mitral valve to facilitate deairing. The patient was positioned in Trendelenburg and the aortic cross-clamp removed. After ventricular ejection, the left atrium and ventricle (LV) were relatively clear of air and the left atrial vent was removed. An aortic vent that had previously served as the cardioplegia cannula was used to vent the residual air from the ascending aorta. The patient was separated from bypass in normal sinus rhythm and maintained good hemodynamics. The initial postbypass transesophageal echocardiogram (TEE) showed normal ventricular function and filling (A). Shortly after starting administration of protamine, the blood pressure decreased and the electrocardiogram demonstrated ST-segment changes consistent with ischemia. The protamine administration was stopped, and vasopressors and inotropes were quickly administered. The TEE documented reduced cardiac function in the right ventricle and hypokinesis in the inferior and inferoseptal walls of the LV. The transgastric short- and long-axis views of the LV (B, C) showed that the myocardium in the distribution of the right coronary artery, as designated by the arrows, was characterized by increased echogenicity. Note the significantly elevated ST segments observed in B and C compared with the baseline (A). The absence of pulmonary hypertension and adequate diastolic filling of the LV supported a diagnosis other than acute anaphylactic protamine response or pulmonary embolism. The most likely culprit was air embolization causing transient myocardial ischemia. Air bubbles that migrated from the LV chamber embolized into the ostium of the right coronary artery, which lies at the most anterior aspect of the sinus of Valsalva. TEE served a crucial role in quickly evaluating and diagnosing the cause of hypotension. The hemodynamics, which were temporarily supported by boluses of vasopressors and inotropes, stabilized, and the protamine dose was completed. The patient was transferred to the intensive care unit without any further incident.

Pericardial Effusion and Tamponade

Framing

Small effusions are common after cardiac surgery, especially after removal of chest tubes. In isolation, pericardial effusion may not require surgical intervention. Cardiac tamponade occurs when the pressure exerted by the presence of a pericardial effusion (or any structure adjacent to the heart) compresses the heart, limits diastolic filling of any of the chambers of the heart, and impairs CO. Cardiac tamponade is an emergency, necessitating immediate diagnosis and intervention.

Is a pericardial effusion present? If so, does it contribute to cardiac dysfunction and the patient’s present hemodynamic distress? What is the cause of the effusion (acute or chronic)? Is the pericardial effusion the sequelae of another cardiovascular event or process (i.e., aortic dissection or cardiac catheterization)? Are there invaginations of the free walls of the right atrium (RA), RV, or LA? Is the effusion free flowing or loculated? Where is it located? Is echocardiographic assessment consistent with tamponade? What is the coagulation status?

Data Collection

Echocardiography is the standard modality for diagnosis of pericardial fluid. However, the diagnosis of cardiac tamponade is a clinical diagnosis based on hemodynamics and the patient’s condition. Low CO, hypotension, equalization of pressures, and high venous pressures are all signs of cardiac tamponade. Echo findings consistent with tamponade include presence of pericardial fluid, compression of the atria, compression of the RV, and loss of normal respiratory variability of ventricular inflow velocities.

The TEE examination quickly determines whether pericardial effusion is present, the location of the effusion (loculated, free-flowing), and impact on chamber filling. Location of the effusion is paramount should pericardiocentesis be deemed necessary for acute decompression. Right atrial and right ventricular collapse are the most sensitive signs of increased pericardial pressure. The effusion need not be a large circumferential effusion to significantly impact cardiac function. Postcardiotomy pericardial clot may be smaller and more compartmentalized than a chronic circumferential effusion that may be free flowing. Interpreting the clinical significance on cardiac hemodynamics may be complicated by factors such as lability of hemodynamics, decreased intravascular volume, depressed cardiac function, mechanical ventilation and pulmonary dysfunction, soft-tissue changes, and chest tubes that obstruct some of the echocardiographic windows. Doppler is used as a complementary method of demonstrating the hemodynamic derangements of tamponade and to determine the clinical significance of an effusion. The echocardiographer should interrogate the phasic respiratory variation of blood flow through the tricuspid valve and MV. Although not specific for tamponade, the changes in respiratory variation of inflow velocity are the hallmark of increased pericardial pressure. Significant respiratory variation of blood inflow velocities also may be seen in constrictive pericarditis or conditions associated with changes in intrathoracic pressure, such as increased work of breathing, asthma, or positive-pressure ventilation, and may be exacerbated in patients on positive end-expiratory pressure. Other important data pertaining to the cause and possible intervention include coagulation status.

Discussion

The American College of Cardiology/American Heart Association/American Society of Echocardiography (ACC/AHA/ASE) Task Force assigned a Class I recommendation to the use of echocardiography in patients with suspected bleeding in the pericardial space. Echocardiography is portable, quick, and noninvasive, yet it is a sensitive and specific modality for the detection and impact of a pericardial effusion. Pericardial effusions can be diagnosed and cardiovascular effects determined by TTE or TEE. However, during the postcardiac surgery period, the presence of positive-pressure ventilation, chest tubes, and bandages may severely limit the capability of TTE to assess fluid in the pericardium.

The effusion need not be a large circumferential effusion to significantly affect heart function. Loculated effusion may impinge only on the LA and may not be discernible by the traditional acoustic windows used by TTE. A hemodynamically significant localized hematoma compressing only the LA may not produce right atrial and right ventricular collapse, or the constellation of equalization of pressures. Small effusions are common after cardiac surgery, especially after removal of chest tubes, and in heart transplant recipients in whom there is a mismatch between heart size and pericardial cradle. The presence of a pericardial effusion in the nonpostcardiotomy patient must lead to a search for the cause of the effusion. Pericardial effusion mandates close scrutiny of the aortic root for possible aortic dissection. Pericardial effusion in a trauma patient is worrisome for cardiac rupture, ventricular contusion, or foreign body injury.

Acute cardiac tamponade in the nonpostcardiotomy patient can develop after introduction of as little as 60 to 100 mL blood. Causes might include type A aortic dissection, myocardial infarction with rupture, acute pericarditis, bleeding from malignancy, myocardial contusion, or myocardial perforation from penetrating trauma. These life-threatening conditions may present with hypotension, tachycardia, plethora, and jugular venous distention. Other classic findings include narrowed pulse pressure, pulsus paradoxus, widening of the mediastinum on chest radiography, and electrical alternans on the ECG. Treatment is immediate decrease in pericardial pressure that could be accomplished through the removal of a relatively small volume of fluid. This temporizing measure can be life-saving until more definitive therapy is instituted.

Not all pericardial effusions require immediate intervention. Development of cardiac tamponade is related to the rate of accumulation of pericardial fluid and the capacity for the pericardium to stretch and accommodate fluid. Chronic pericardial effusions, which occur in cases of malignancy, uremia, connective tissue disease, Dressler syndrome, and postinfection pericarditis, uncommonly require emergent intervention. Acute pericardial effusions that occur postcardiotomy are usually more ominous and often result in hemodynamic compromise, requiring treatment (see Chapters 22 and 34).

Hemodynamics may improve temporarily with the administration of volume, altering intrathoracic pressure (decreasing peak inflation pressure), but still may require drainage of the effusion. Chronic malignant effusions will improve after pericardiocentesis but often require a pericardial window for more definitive therapy. Effusions resulting from acute aortic syndromes or cardiac trauma require timely surgical intervention. Postcardiac surgery patients may require urgent re-exploration for evacuation of pericardial hematoma and to address the cause of continued bleeding. If hemodynamics improve after sternotomy but minimal clot is found, the physiologic tamponade may be related to generalized tissue edema and pulmonary dysfunction. In cases of poor cardiac function, the sternal incision may need to remain open and covered with a sterile dressing until edema recedes and cardiac function improves.

Management of Ischemic Mitral Regurgitation

Framing

Ischemic heart disease is the most common cause of mitral insufficiency in the United States. Mechanisms of valve incompetence are varied and include annular dilatation, papillary muscle dysfunction from active ischemia or infarction, papillary muscle rupture, or ventricular remodeling from scar, often leading to a tethering effect of the subvalvular apparatus. Mitral regurgitation leads to pulmonary hypertension, pulmonary vascular congestion, and pulmonary edema with functional disability. Ventricular function deteriorates as the LV becomes volume overloaded with corresponding chamber dilatation. Left untreated, severe mitral regurgitation from ischemic heart disease has a poor prognosis, hence the imperative for diagnosis and treatment.^24–26 Less certain is the impact of lesser degrees of mitral insufficiency on functional status and long-term morbidity and mortality. Patients presenting for CABG often have concomitant mitral regurgitation of a mild or moderate degree. The intraoperative team is confronted with the decision whether to surgically address the MV during the coronary operation.

Does mitral regurgitation warrant mitral surgery? What is the mechanism of the regurgitation? What are the grade and chronicity of the mitral regurgitation? Is the mitral regurgitation likely to improve by coronary revascularization alone?

Data Collection

Pertinent data, including preoperative functional status and evaluation, need to be considered to appropriately interpret and place the intraoperative data in context. The preoperative echocardiogram and ventriculogram need to be reviewed. The intraoperative hemodynamic data are coupled with TEE information to complete the dataset needed to move forward with the decision-making process. The severity of mitral regurgitation on TEE is measured by the vena contracta, maximum area of the regurgitant jet, regurgitant orifice area, and pulmonary vein blood-flow velocities. Valvular disease causes changes in other cardiac structures. Chronic mitral regurgitation may be associated with a dilated LA, pulmonary hypertension, and right ventricular dysfunction. Wall motion assessment and the ECG are used for detecting reversible myocardial dysfunction that may benefit from revascularization. The hemodynamic and TEE data are coupled with provocative testing of the MV in an attempt to emulate the working conditions of the MV in an awake, unanesthetized state. It is not uncommon that preoperative mild-to-moderate mitral regurgitation with a structurally normal valve totally resolves under the unloading conditions of general anesthesia.^27–29

Discussion

Most cases of ischemic mitral regurgitation are categorized as “functional” rather than structural. In a study of 482 patients with ischemic mitral regurgitation, 76% had functional ischemic mitral regurgitation, compared with 24% having significant papillary muscle dysfunction.³⁰ The mechanism of ischemic mitral regurgitation is attributed to annular dilatation, secondary to left ventricular enlargement and regional left ventricular remodeling with papillary muscle displacement, causing apical tethering and restricted systolic leaflet motion.³¹ The importance of local left ventricular remodeling with papillary muscle displacement as a mechanism for ischemic mitral regurgitation has been reproduced in an animal model.³²

The mitral regurgitation is prioritized in accordance with the principal diagnosis (e.g., CAD), comorbidities, functional disability, and short- and long-term outcome. Ischemic mitral regurgitation is quantified and the mechanism of valve dysfunction is defined. Intraoperative mitral regurgitation is compared with preoperative findings. Discrepancies between the preoperative and intraoperative assessment of the valve may reflect the pressure and volume unloading effects of general anesthesia. In patients with functional ischemic 1 to 2+ mitral regurgitation, the MV often is not repaired or replaced. However, the need for surgical intervention in patients with 2+ mitral regurgitation under anesthesia remains a point of debate and has not been definitively answered by prospective studies. MV surgery typically is recommended to improve functional status and long-term outcome for patients with 3+ ischemic mitral regurgitation or greater.³⁰ Ignoring significant ischemic mitral regurgitation at the time of CABG can limit the functional benefit derived from surgery.

The risks to the patient of not surgically altering the MV and anticipated residual regurgitation are weighted against the risk for atriotomy, mitral surgery, extending CPB and aortic cross-clamp times, and the likelihood that the CABG surgery will be successful at decreasing the severity of mitral regurgitation. Added risk includes commitment to a mechanical prosthesis should a reparative procedure prove unsuccessful. Mitral regurgitation caused by acute ischemia may resolve after restoration of coronary blood flow (Figure 13-6). The reversibility of the regurgitation is difficult to predict: Factors supporting reversibility (and, hence, no immediate need to surgically address the valve) include a structurally normal MV, normal left atrial and left ventricular dimensions, including the mitral annulus, and SWMAs associated with transient regurgitation and pulmonary edema. Revascularization of the culprit myocardium with improvement in regional function may be all that is necessary to restore normal mitral coaptation.^33,34 Myocardial infarction with a fixed wall-motion defect or aneurysm, chronically dilated left-sided heart chambers, dilated annulus, or other structural abnormalities that are not reversible (ruptured papillary muscle or chordae, leaflet prolapse, leaflet perforation) suggest myocardial revascularization is unlikely to correct the valvular incompetence.

Figure 13-6

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