Anatomy of the mitral valve

The approach to repair of mitral valve incompetency continues to evolve, but regardless of the changes in technology, the successful anesthetic management of a patient with mitral regurgitation (MR) undergoing any surgical procedure is dependent on the anesthesia care provider understanding the anatomy and physiology of the mitral valve.

The mitral valve, so named because it resembles a bishop’s miter, is composed of a fibrous annulus and anterior and posterior leaflets. The combined area of the two leaflets being more than twice the area of the annulus itself. The two leaflets are connected to the anterolateral and posteromedial papillary muscles by first-order (primary), second-order (secondary), and third-order (tertiary) chordae tendineae. The anterior leaflet attaches to approximately one third of the annulus, and the ratio of its height to its base is greater than that of the posterior leaflet, which attaches to the other two thirds of the annulus. The two leaflets are connected at the sides of the annulus to comprise the anterolateral and posteromedial commissures. The posterior mitral valve has three components, the P1, P2, and P3 “scallops,” with corresponding segments on the anterior valve denoted as A1, A2, and A3. The P1 and A1 segments are attached at the anterolateral commissure, whereas the A3 and P3 segments adjoin at the posteromedial commissure.

Pathophysiology of mitral regurgitation

Incompetence of the mitral valve with regurgitation of blood from the left ventricle (LV) into the left atrium (LA) during systole is common (Figure 150-1). Although MR has a number of different causes, in most cases, MR occurs as a result of senescence of the mitral leaflets, and its prevalence increases with age. Degenerative MR is second only to calcific aortic stenosis as the most common valvular cardiac disorder in high-income countries. Mitral valve incompetence usually develops over many years, but incompetence of the valve can develop acutely for reasons other than degenerative disease (e.g., rupture of chordae tendineae from ischemic heart disease). Furthermore, acute MR can superimpose on chronic mitral insufficiency. Barlow disease of the mitral valve is another common condition resulting in MR, characterized by myxoid degeneration of the leaflets leading to thickened and redundant leaflets, mitral annular dilation, and chordal elongation.

Acute MR is usually quite symptomatic (Figure 150-2) and requires surgical intervention. However, the management of chronic regurgitation of the mitral valve is controversial; patients who are symptomatic or who have a decreased ejection fraction are at increased risk of developing complications and are usually considered candidates for surgery. Surgical repair or replacement of the valve not only relieves symptoms, but has increasingly been shown to improve long-term outcome, with reductions in morbidity and mortality rates. Patients who have MR and who have a decreased ejection fraction, an increased LV end-diastolic volume (LVEDV; i.e., dilated LV), chronic atrial fibrillation, or pulmonary hypertension have better long-term outcomes when the valve incompetence is surgically corrected earlier in the course of the disease. Increasing evidence indicates that life expectancy is improved in patients with MR who have surgery before the previously mentioned morbidities develop. Fortunately, the success of valve repair (compared with replacement) and the low morbidity and mortality rates associated with surgical intervention favor early elective surgery. In an effort to prevent progression to worsening disease and subsequent increase in morbidity and mortality rates, current efforts focus on identifying patients with asymptomatic mitral valve disease whose long-term outcome may be favorably impacted if their MR is corrected at an early stage.

Natural history of mitral regurgitation

Three-dimensional echocardiography has significantly changed the approach to evaluating MR. In the past, the mitral annulus was believed to be a fixed cartilaginous structure to which the anterior and posterior leaflets were attached. We now recognize that the annulus undergoes significant conformational changes throughout the cardiac cycle. During systole, the annulus “contracts,” or narrows, allowing the edges of the anterior and posterior leaflets to coapt, thereby preventing regurgitation of blood into the atrium during ventricular systole. The opposite occurs during diastole: the annulus “widens,” increasing the cross-sectional area of the mitral valve orifice, thereby facilitating inflow into the LV during diastole.

MR can be classified as acute, chronic compensated, or chronic decompensated. Acute MR (as might be caused by rupture of a chorda tendinea) leads to a large volume of blood being ejected retrograde into the LA during LV systole because LA pressure is considerably lower than aortic root pressure. In turn, increased LA blood volume leads to increased LA pressure, which is ultimately transmitted retrograde into the pulmonary vasculature. As a result, pulmonary artery pressure, pulmonary artery occlusion pressure (PAOP), and pulmonary capillary wedge pressure increase acutely. As described by Starling, the increase in end capillary hydrostatic pressure leads to transudation of fluid into the alveoli, which is manifested clinically by dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and rales (as can be heard on auscultation of the lungs) as well as pulmonary edema (as can be seen on chest radiograph).

In patients in whom incompetence of the valve develops over time (i.e., changes due to senescence), the volume of blood that regurgitates into the LA is initially small; therefore, cardiac output can be maintained by an equivalent increase in LVEDV, and stroke volume ejected into the aorta remains unaffected. The regurgitant volume in the left atrium is not large enough to increase PAOP and end capillary hydrostatic pressure. Consequently, there is no transudation of fluid into the alveoli. However, as the regurgitant volume increases, the LV hypertrophies to reduce the wall stress that accompanies the rise in total stroke volume (total stroke volume equals LA regurgitant volume plus stroke volume into the aorta). Over time, as the valve becomes more incompetent, the increasing volume of regurgitant into the LA dilates the LA while maintaining a relatively “normal” LA pressure. These compensatory changes allow cardiac output to be maintained and minimize the effects of increasing regurgitant volume on the pulmonary vasculature. The compensatory phase of MR may last for many years but, eventually, will manifest by LV dysfunction, the sine qua non of decompensated MR. It is not completely clear why or when a patient transitions from the compensated to the decompensated phase of MR, but, as mentioned previously, it is important to intervene surgically before the patient’s condition decompensates. Once LV dysfunction develops, it is difficult if not impossible to reverse, and life expectancy is considerably reduced.

Chronic compensated MR transitions to decompensated chronic MR when the LV begins to dilate to accommodate the LVEDV necessary to accommodate both the LA regurgitant fraction and the stroke volume ejected to the aorta (i.e., the total volume ejected from the LV). As the LV dilates, the myocardiocytes are no longer able to contract adequately to compensate for the volume overload, and stroke volume begins to decrease. The reduced stroke volume decreases cardiac output, and LV end-systolic volume subsequently increases. A vicious cycle ensues: an increase in end-systolic volume in the LV increases LVEDV, LA pressure, and PAOP. As the PAOP increases, alveoli begin to fill with fluid, leading to the symptoms and signs of pulmonary edema and congestive heart failure. Mild MR is associated with few, if any, complications. However, severe MR may lead to the development of a variety of sequelae (Box 150-1).

Concomitant disease

As was discussed earlier, the clinical manifestations of MR are due to dilation of the LA. This dilatation can lead to atrial fibrillation (with increased risk for thromboembolic events), an increased LA pressure manifested by pulmonary hypertension, and heart failure. Although these sequelae of MR can initially be managed medically, as soon as there is any evidence of end-diastolic enlargement of the LV, the mitral valve incompetence must be surgically corrected.

MR, per se, does not lead to coronary artery disease (CAD); however, CAD can lead to MR in two ways: myocardial ischemia and infarction can lead to necrosis and rupture of a papillary muscle, resulting in the acute onset of severe MR. Likewise, CAD resulting in regional wall motion abnormalities can lead to papillary dysfunction, as well as annular architectural changes, which both contribute to MR. Nevertheless, the principal etiology of MR in high-income countries is senescence of the mitral valve apparatus and valve leaflets. Because the incidence of CAD likewise increases with age, older patients often present for treatment of CAD and are found to have some degree of MR. If the MR is due to ischemia (e.g., as a result of regional wall motion abnormalities such as hypokinesis or akinesis in the subvalvular LV) the management can be challenging because none of the options for correcting these abnormalities is ideal. In such patients, depending on a variety of factors, the surgeon may chose to replace the valve rather than attempt to repair it because the success rate of repair in patients with MR due to ischemia is much lower than the rate in patients with MR because of degenerative changes.

Surgical correction of mitral regurgitation

Carpentier revolutionized the treatment of MR when, more than 30 years ago, he published his experience with repairing the mitral valve as opposed to replacing it. His findings, as well as those of others, have led to mitral valve repair being the preferred technique for correcting MR. Approximately 50,000 patients have mitral valve repair annually in the United States. The most common technique to repair the valve is annuloplasty, with or without surgical correction of any defects in the leaflets themselves, or repair of dysfunctional chordae tendineae or reattachment of a ruptured chorda tendinea (Figures 150-3 and 150-4).

The goal of annuloplasty is to implant an annuloplasty “device”—commonly referred to as a “ring”—onto the annulus to restore its structural integrity and function. The cardiac surgeon has multiple options from which to choose when selecting a ring to perform the annuloplasty: the plastic rings can be complete 360-degree rings or incomplete rings; rigid, semirigid or flexible; adjustable or nonadjustable; or either flat or saddle-shaped. The goal is to restore the annulus in such a way that the anterior and posterior leaflets coapt during ventricular systole. If there is redundancy or prolapse of one of the components of the valve leaflets, then the redundant tissue can be resected, or, alternately, if there is incompetence between subcomponents of the leaflets (e.g., between P2 and P3), such an area of the valve can be plicated. If there is incompetence of the valve leaflets because of abnormalities of the chordae, the surgeon can shorten them or reattach them if they are ruptured. Increasingly, in as many as 20% of institutions, mitral valve repair is being performed with minimally invasive techniques that involve mini right-sided thoracotomies with or without robotic assistance.

As the field has advanced, cardiologists are using a variety of new devices and advances in technology to repair incompetent valves in the cardiac catheterization suite using percutaneous techniques. The efficacy of percutaneous repair has been demonstrated in patients with MR who underwent repair using the MitraClip (Abbott Laboratories, Santa Clara, CA). At 12 months following MitraClip repair, mitral valve function and LV ejection fraction had improved. In addition, when compared with a control group, the MitraClip cohort demonstrated greater reduction in diastolic and systolic LV dimensions and volumes, LV mass, and peak wall stress.

Anesthetic considerations in the patient with mitral regurgitation

Understanding the nature and etiology of the patient’s MR is critical to formulating an anesthetic plan for patients undergoing mitral valve procedures. During the preoperative visit, in addition to the customary history and examination conducted on all patients about to undergo an anesthetic, the anesthesia provider must determine the etiology of the MR. Although senescence of the mitral valve is the most common cause of MR, patients may also have MR as a consequence of rheumatic fever, ischemic cardiomyopathy, or other less common causes. The anesthesia provider must also determine whether the patient has mild symptomatic chronic MR or acute regurgitation imposed on chronic MR. Any concomitant disease processes must be elucidated and medical therapies (e.g., the use of anticoagulants or β-adrenergic receptor blocking agents) must be considered.

In the operating room, the monitoring requirements and management of patients undergoing a midline sternotomy and atriotomy are the same as for other patients having cardiopulmonary bypass. Minimally invasive techniques may require special considerations and should be discussed with the surgeon, the cardiologist, or both in advance. Often, minimally invasive approaches to mitral valve repair require lung isolation, groin cannulation, and the placement of a cannula in the superior vena cava. In addition, surgeons may request that a coronary sinus catheter be placed via the jugular vein cannula site for retrograde perfusion.

The maxim for managing patients with MR is to maintain or decrease systemic vascular resistance during induction and maintenance of anesthesia because any increase in systemic vascular resistance will decrease LV output into the aorta, along with a corresponding increase in the severity of MR. Equal emphasis should be placed on avoiding tachycardia because of the adverse effects of decreased diastolic time on LVEDV, which, in turn, will limit cardiac output.

Intraoperative transesophageal echocardiography (TEE) is an integral part of the mitral valve repair process. Following induction of anesthesia and tracheal intubation, an orogastric tube should be inserted, the stomach suctioned (in this case, primarily to remove air), the gastric tube removed, and, unless the patient has a condition in which the use of TEE is absolutely contraindicated, an echocardiographic probe should be inserted into the esophagus. A preprocedural intraoperative examination using TEE should be performed, noting the patient’s systemic blood pressure and central venous pressure (or pulmonary artery pressure, if available) and to describe the anatomy of the mitral valve and the relative size of the cardiac chambers, with particular attention paid to the size of the LA. This baseline information is important because it provides the surgeon with valuable information about the nature and etiology of the MR and can help direct the repair. Hemodynamic conditions should be noted during the echocardiographic examination, with the goal of reproducing similar hemodynamics (i.e., systemic blood pressure) that a patient has while not under general anesthesia. The reduction of systemic vascular resistance that often accompanies the maintenance of a general anesthetic can significantly alter the severity of MR and may not highlight all areas of regurgitation. Volume loading, the use of vasopressors, or a combination thereof may be necessary to reproduce preoperative hemodynamic values.

Before the patient is separated from cardiopulmonary bypass, a second, postprocedural echocardiographic examination should be performed to assess the adequacy of the repair and to identify any concerns about the repair. One common concern (incidence 2%-16%) following a mitral valve repair with annuloplasty is that of systolic anterior motion (SAM) of the mitral valve and the LV outflow tract obstruction that it may, in turn, create. Likewise, the preprocedural intraoperative TEE may also help identify patients at high risk of developing SAM after repair and help surgeons modify their repair to reduce the likelihood of SAM. Often, with mild SAM, medical management, including volume loading, heart rate control, and increasing system vascular resistance may resolve the obstruction of the LV outflow tract. However, if obstruction of the LV outflow tract persists despite these maneuvers, the mitral valve repair may need to be revised, often by using a larger size annuloplasty and, at times, employing an Alfieri repair to reduce leaflet excursion during diastole.

Once the repair is determined to be successful, separation from cardiopulmonary bypass may ensue, anticoagulation (heparinization) can be reversed, the heart and vessels can be decannulated, and the patient managed as any other patient would be who has undergone cardiopulmonary bypass.

The care of patients having a minimally invasive technique is less complicated, but, in these patients, because of the concern about the adequacy of the repair of the mitral valve using minimally invasive techniques, the echocardiographic examination must be conducted more thoroughly. The degree of residual MR must be documented, and, because the use of these techniques has not been fully established, care must be taken to examine for and document any unanticipated sequelae.