Acute mitral regurgitation is suggested by the sudden onset of dyspnea, orthopnea and paroxysmal nocturnal dyspnea. the absence of longstanding cardiac symptoms and the presence of an apical holosystolic decrescendo murmur with loud third and fourth heart sounds.
Ruptured chordae tendineae
Ruptured chordae tendineae are the most common cause of acute mitral regurgitation. Etiologies of ruptured chordae tendineae most commonly include infective endocarditis and myxomatous degeneration of the mitral valve prolapse syndrome. Less often, rupture could be due to either other connective tissue diseases or trauma. Normal chordae tendineae have a tensil strength greater steel but, rarely, spontaneous rupture occurs without apparent cause. Rupture of the chordae tendineae does not result from myocardial ischemia or infarction.
Mitral valve apparatus
As shown in this illustration, the mitral valve apparatus is composed of five components: the mitral ring, or annulus; the anterior and posterior leaflets; the numerous primary, secondary and tertiary chordae tendineae; the anterolateral and posteromedial papillary muscles; and the left ventricular walls supporting the papillary muscles where they insert. Abnormalities of any of these components may result in mitral regurgitation, including left ventricular dysfunction or dilatation.
MR presenting features
This table compares the presenting features of patients with acute and chronic mitral regurgitation. In acute mitral regurgitation, the sudden onset of severe pulmonary congestion is typical. The murmur may be of recent onset or there may be a change in the character of a preexisting murmur. This contrast with chronic mitral regurgitation wherein the onset of pulmonary congestion is late and insidious and the murmur is usually present for many years.
Anatomic / physiologic features of acute MR
The anatomic and physiologic features of acute mitral regurgitation are illustrated here. With acute mitral regurgitation, the left atrium is relatively small and not very compliant. The large regurgitant volume that is ejected by the left ventricle into the small left atrium causes markedly elevated left atrial pressures, particularly in late systole, when the equilibration of the left ventricular and left atrial pressures causes diminishing mitral regurgitation and a decrescendo contour to the murmur. This results in early pulmonary vascular changes, pulmonary hypertension and right ventricular hypertrophy.
Acute vs. chronic MR
In contrast, with chronic mitral regurgitation, the dilated, thin walled, more compliant left atrium accomodates the large regurgitant volume from the left ventricle with little or no elevation of left atrial pressure. As a result, the mitral regurgitation murmur remains holosystolic and plateau shaped, the pulmonary vessels remain relatively normal and pulmonary hypertension and right ventricular hypertrophy are delayed in onset.
Key bedside findings - JVP / precordium
The key bedside findings to differentiate acute and chronic mitral regurgitation relate to the differences in left sided pathophysiology. This table compares these findings. Acute mitral regurgitation results in a giant "a" wave in the jugular venous pulse, reflecting pulmonary hypertension, whereas in chronic mitral regurgitation, the dilated left atrium buffers against the rise in right sided pressures and results in a normal jugular venous pulse. With acute mitral regurgitation, the apical impulse remains in the normal location. In chronic mitral regurgitation, the volume overload leads to dilatation and displacement of the apex. The apical and left sternal edge systolic impulses in our patient were sustained. With the acute onset of mitral regurgitation and the resulting acute pulmonary hypertension, these impulses are often brief and non sustained.
Key bedside findings - auscultation / rhythm
With acute MR, the enhanced left atrial contraction produces a fourth heart sound. With chronic MR, the left atrial contraction is weak or absent, thus, and S4 is uncommon when the MR is severe. In both lesions, an S3 is present, reflecting the severity of the lesion. An apical systolic murmur is present in both. In acute MR, the murmur is usually decrescendo, whereas in chronic MR, the murmur is plateau shaped. In acute MR, the rhythm is sinus, whereas in chronic MR, the rhythm is often atrial fibrillation due to enlargement and fibrosis of the left atrium.