Mitral regurgitation can develop acutely or insidiously as a result of a large number of disorders. Chronic mitral regurgitation is usually the result of rheumatic fever (often with concomitant mitral stenosis); con-genital or developmental abnormalities of the valve apparatus; or dilatation, destruction, or calcification of the mitral annulus. Acute mitral regurgitation is usually due to myocardial ischemia or infarction (papillary muscle dysfunction or rupture of a chorda tendinea), infective endocarditis, or chest trauma.
The principal derangement is a reduction in forward stroke volume due to backward flow of blood into the left atrium during systole. The left ventricle compen-sates by dilating and increasing end-diastolic volume (Figure 21–8). Regurgitation thorugh the mitral valve initially maintains a normal end systolic volume in spite of an increased end diastolic volume. However, as the disease progresses the end systolic volume increases. By increasing end-diastolic volume, the volume-overloaded left ventricle can maintain a normal cardiac output despite blood being ejected retrograde into the atrium. With time, patients with chronic mitral regurgitation eventually develop eccentric left ventricular hypertrophy and progres-sive impairment in contractility. In patients with severe mitral regurgitation, the regurgitant volume may exceed the forward stroke volume. In time, wall stress increases, resulting in an increased demand for myocardial oxygen supply.
The regurgitant volume passing through the mitral valve is dependent on the size of the mitral valve orifice (which can vary with ventricular cav-ity size), the heart rate (systolic time), and the left ventricular–left atrial pressure gradient during systole. The last factor is af fected by the relative resistances of the two outflow paths from the left ventricle, namely, SVR and left atrial compliance. Thus, a decrease in SVR or an increase in mean left atrial pressure will reduce the regurgitant volume. Atrial compliance also determines the predomi-nant clinical manifestations. Patients with normal or reduced atrial compliance (acute mitral regurgita-tion) have primarily pulmonary vascular congestion and edema. Patients with increased atrial compli-ance (long-standing mitral regurgitation resulting in a large dilated left atrium) primarily show signs of a reduced cardiac output. Most patients are between the two extremes and exhibit symptoms of both pul-monary congestion and low cardiac output. Patients with a regurgitant fraction of less than 30% of the total stroke volume generally have mild symptoms. Regurgitant fractions of 30% to 60% generally cause
moderate symptoms, whereas fractions greater than 60% are associated with severe disease.Echocardiography, particularly TEE, is useful in delineating the underlying pathophysiology of mitral regurgitation and guiding treatment. Mitral valve leaflet motion is often described as normal, prolaps-ing, or restrictive (Figure 21–9). Excessive motion or prolapse is defined by systolic movement of a leaflet beyond the plane of the mitral valve and into the left atrium.
To calculate regurgitant fraction (RF), forward stroke volume (SV) and the regurgitant stroke vol-ume (RSV) must be measured. Although they can both be estimated by catheterization data, pulsed Doppler echocardiography provides reasonably acute calculations. Stroke volume is measured at the left ventricular outflow tract (LVOT) and at the mitral valve (MV), where
Stroke volume = cross-sectional area (A) × (TVI) and cross-sectional area (A) can be approximated as,
A = 0.785 × (diameter)2
The time–velocity integral (TVI) is the integral of the velocity versus the time signal obtained with pulsed Doppler. The TVI reflects the distance the blood has traveled during a heart beat. By knowing the area through which the blood travels and the distance traveled, it is possible to estimate the stroke volume. This is the case because the area is expressed in centimeters squared, and the distance is expressed in centimeters. The product of these measures is cubic centimeters or milliliters—hence, the stroke volume for each heartbeat.
Thus, the volume of blood that enters through the mitral valve must be the same as that passing through the left ventricular outflow track. Any dif-ference between the two represents the amount of the volume that initially entered the left ventricle, but that did not pass the LVOT. This is the volume that regurgitated into the left atrium.
RSVmitral regurgitation =(AMV ×VTIMV)− (ALVOT × TVILVOT),
RF = RSV/SV
An RSV greater than 65 mL usually correlates with severe mitral regurgitation.
Afterload reduction is beneficial in most patients and may even be lifesaving in patients with acute mitral regurgitation. Reduction of SVR increases forward SV and decreases the regurgitant volume. Surgical treatment is usually reserved for patients with moderate to severe symptoms. Valvuloplasty or valve repair are performed whenever possible to avoid the problems associated with valve replace-ment (eg, thromboembolism, hemorrhage, and prosthetic failure). Catheter-mediated valve repairs are continually being refined, potentially reduc-ing the need for “open” surgery. Anesthesiologists skilled in advanced perioperative echocardiogra-phy assist in correctly identifying the leaflet(s) to be repaired and determining the repair’s success. Three-dimensional echocardiography is increas-ingly employed to assist in the assessment of the mitral valve (see Figure 5-29).
Anesthetic management should be tailored to the severity of mitral regurgitation as well asthe underlying left ventricular function. Factors that exacerbate the regurgitation, such as slow heart rates and acute increases in afterload, should be avoided. Bradycardia can increase the regurgitant volume by increasing left ventricular end-diastolic volume and acutely dilating the mitral annulus. The heart rate should ideally be kept between 80 and 100 beats/min. Acute increases in left ventricular afterload, such as with endotracheal intubation and surgical stimula-tion under “light” anesthesia, should be treated rap-idly but without excessive myocardial depression. Excessive volume expansion can also worsen the regurgitation by dilating the left ventricle.
Monitors are based on the severity of ventricular dysfunction, as well as the procedure. Mitral regur-gitation may be recognized on the pulmonary artery wedge waveform as a large v wave and a rapid y descent (Figure 21–10). The height of the v wave is inversely related to atrial and pulmonary vascular compliance, but is directly proportional to pulmo-nary blood flow and the regurgitant volume; thus, the v wave may not be prominent in patients with chronic mitral regurgitation, except during acute deterioration. Very large v waves are often apparent on the pulmonary artery pressure waveform, even without wedging the catheter. Color-flow Doppler TEE can be invaluable in quantitating the severity of
the regurgitation and guiding therapeutic interven-tions in patients with severe mitral regurgitation. By definition, blood flow reverses in the pulmonary veins during systole with severe mitral regurgitation.
Patients with relatively well-preserved ventricular function tend to do well with most anesthetic tech-niques. Spinal and epidural anesthesia are well toler-ated, provided bradycardia is avoided. Patients with moderate to severe ventricular impairment may be sensitive to depression from high concentrations of volatile agents. An opioid-based anesthetic may be more suitable for those patients—again, provided bradycardia is avoided.
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