Mitral regurgitation

Published on 07/02/2015 by admin

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Mitral regurgitation

Joshua D. Stearns, MD and Michael J. Murray, MD, PhD

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).

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