Pathophysiology Of Mitral Regurgitation

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Chronic Mitral Regurgitation

Mitral regurgitation is a volume overload state for the left ventricle because during diastole the ventricle receives not only the normal pulmonary venous return, but also the extra volume of blood, which goes into the left atrium during systole. The left ventricle thus has two outlets for systolic emptying in mitral regurgitation, namely, the aorta and the left atrium. The volume overload would result in left ventricular dilatation and enlargement. The left ventricular dilatation is accompanied initially by better compliance of the left ventricle, which helps to maintain relatively normal left ventricular diastolic pressure despite the large volume of blood entering the left ventricle during diastole. The left atrium also becomes enlarged when the regurgitation is significant. The left atrial enlargement is accompanied by increased compliance ofthe left atrium, which helps to maintain a normal left atrial pressure.

The two-outlet system allows supernormal emptying and therefore supernormal ejection fraction when the ventricular function is normal and preserved. The ejection fraction can still be maintained at near-normal levels, even when some left ventricular dysfunction develops because of the systolic advantage that the left ventricle has. The systolic tension is therefore maintained at normal levels (1-4).

The increased diastolic tension caused by increased dimension (radius) will act as a stimulus to hypertrophy. The hypertrophy is often eccentric rather than concentric (5). This will decrease the diastolic compliance of the left ventricle, leading to a rise in the diastolic left ventricular filling pressure. The raised diastolic pressure in the left ventricle may impede good subendocardial perfusion because the majority of coronary flow occurs in diastole. The decreased subendocardial perfusion may eventually lead to subendocardial fibrosis in late stages, which may further depress the compliance and begin to raise thepre-a wave pressure. Because the latter forms the baseline filling pressure over which the a and v wave buildup occurs in the atrium, the raised pre-a wave pressure will further raise the v wave pressure height in the left atrium. The upper normal left ventricular diastolic pressure for the end of diastole (post- a wave) is usually 12-15 mmHg, whereas the upper normal left ventricular pre-a wave pressure is 5-8 mmHg. The normal v wave in the left atrium may be between 12 and 18 mmHg. In chronic mitral regurgitation, even when the regurgitation is severe, the left atrial v wave height may only be mild to moderately elevated (20-35 mmHg). This would mean a persistent pressure difference between the left ventricle and the left atrium throughout systole, causing the regurgitant flow to last until the very end of systole and well into the isovolumic relaxation phase. The murmur, therefore, usually lasts for the whole of systole (thus termed pansystolic) and all the way to the S2 and slightly even beyond the S2. In addition, the gradient remains relatively large and constant from the beginning of systole to its end, giving rise to a plateau high-frequency systolic murmur.

Elevated left atrial pressure will cause some secondary pulmonary hypertension. This, together with the decreased left ventricular compliance and diastolic dysfunction, will eventually lead to systolic dysfunction, causing reduced stroke volume and ejection fraction (Fig. 1) (1-4).

Acute Mitral Regurgitation

If the mitral regurgitation is severe and acute in onset as with ruptured chordae, then there may not be enough time to develop compensatory dilatation of either the left atrium or the left ventricle. The large volume of regurgitant blood entering a relatively stiff and nondilated left atrium will result in a steep rise in the v wave pressure in the left atrium (sometimes as high as 50-70 mmHg). The entry of a large volume of blood during diastole into a nondilated left ventricle will tend to raise the diastolic filling pressure in the left ventricle. The raised pre-a wave pressure may further add to the v wave height. The high v wave buildup in the left atrium during systole would mean a decreased and rapidly falling pressure difference between the left ventricle and the left atrium toward the later part of systole. This will in turn limit the regurgitant flow during the later part of systole, making the regurgitant flow and the murmur decrescendo. In addition, the excess flow would cause more low and medium frequencies, making the murmur sound harsher (Fig. 2) (6-8).

Hyperdynamic Ejection Fraction Causes
Fig. 1.

Pulmonary Edema Fig. 2.

Table 1

Chronic Mitral Regurgitation

Pathophysiological changes

Clinical symptoms/signs

Two outlets

Systolic advantage

Increased LV and LA compliance

Increased LA size

Increased LA pressure

Reduced ejection fraction (late sign) Pulmonary hypertension

LV volume overload Increased radius

Retrograde flow from high-pressure LV into low-pressure LA

Increased flow across mitral valve in diastole due to (normal return + regurgitant flow)

ß Long asymptomatic period

& Atrial fibrillation & Palpitation

& Dyspnea

& Pulmonary congestion & Low-output symptoms

& Hyperdynamic apex & Displaced/large area apex

& Systolic murmur predominantly high frequency

& Mid-diastolic rumble

Signs of Severity

Low normal pulse volume

LV enlargement

Wide split S2 due to an early A2

Harsh low/medium frequencies in the regurgitation murmur iindicating a lot of flow S3 rumble (inflow rumble) Signs of pulmonary hypertension

LV, left ventricular; LA, left atrial.

Clinical Symptoms and Signs in Mitral Regurgitation

The pathophysiological changes as related to the clinical symptoms and signs in mitral regurgitation, together with clinical indicators of the severity of mitral regurgitation, are given in Table 1.

Even significant degrees of mitral regurgitation, when chronic, can be tolerated for many years because the left atrial pressure is kept at near- normal levels and the stroke volume and cardiac output maintained. Thus, there is often a long latent period when the patient remains asymptomatic. The left atrial enlargement may eventually lead to the development of atrial arrhythmias, especially atrial fibrillation. This may cause symptoms of palpitation. When the left atrial pressure begins to rise, patients may develop symptoms of dyspnea on exertion. When the left atrial pressure is significantly elevated, symptoms of pulmonary congestion, such as orthopnea and/or nocturnal dyspnea, may develop. When the mitral regurgitation is severe and acute or abrupt in onset, significant elevations in the left atrial pressure could occur, leading to dramatic symptoms of pulmonary congestion including pulmonary edema.

The enlarged left ventricle with supernormal ejection fraction in the early stages will lead to a hyperdynamic displaced large-area left ventricular apical impulse. The systolic advantage that the left ventricle has on account of the two outlets for systole often helps to maintain near-normal ejection fraction for a long time, and thus the apex beat is unlikely to be sustained. The increased flow across the mitral valve in diastole secondary to the normal pulmonary venous return, together with the regurgitant flow, would give rise to an S3 or a mid-diastolic rumble at the apex, especially when the mitral regurgitation is severe.

Reduced ejection fraction and significant pulmonary hypertension are often late signs if present, and then may be associated with low-output symptoms of fatigue and lassitude.

If mitral regurgitation is detected, the presence of some or all of the following signs (Table 1) would indicate that the mitral regurgitation is in fact severe: low normal pulse volume, large-area displaced hyperdynamic left ventricular apex beat, wide split S2 due to the early occurrence of the aortic component of S2, harshness of regurgitant murmur because of excessive flow adding some low and medium frequencies to the usual high frequencies ofthe regurgitant murmur, S3 and/or inflow mid-diastolic rumble at the apex, signs of pulmonary hypertension such as elevated jugular venous pressure with or without abnormal contour, sustained right ventricular impulse palpable in the subxiphoid area, and loud or palpable pulmonary component of the S2.

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    How in mitral regurgitation hyperdynamic apex can be palpated?
    2 years ago

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