|a u s c u l t a t i o n t u t o r
The classic murmur of mitral regurgitation is a high-pitched
holosystolic murmur beginning with the first heart sound and
extending to the second heart sound. The intensity usually is
constant throughout systolic ejection, often radiating to the axilla.
The harshness of the murmur does not correlate with the magnitude
of the valvular defect. Patients with severe disease often have a
third heart sound, a consequence of the increased ventricular filling
volume that is ejected into the left ventricle under higher than
normal pressure. Patients with mitral valve prolapse often have a
mid-to-late systolic click and a late systolic murmur. These patients
are usually female and often have orthostatic hypotension.
In the acute stage, which usually occurs with a spontaneous
chordae tendineae or papillary muscle rupture secondary to
myocardial infarction, a sudden volume overload occurs on an
unprepared left ventricle and left atrium. The volume overload on
the left ventricle increases left ventricular stroke work. Increased left
ventricular filling pressures, combined with the transfer of blood from
the left ventricle to the left atrium during systole, results in elevated
left atrial pressures. This increased pressure is transmitted to the
lungs resulting in acute pulmonary edema and dyspnea.
If the patient tolerates the acute phase, the chronic compensated
phase begins. The chronic compensated phase results in eccentric
left ventricular hypertrophy. The combination of increased preload
and hypertrophy produces increased end-diastolic volumes, which,
over time, result in left ventricular muscle dysfunction. This muscle
dysfunction impairs the emptying of the ventricle during systole.
Therefore, regurgitant volume and left atrial pressures increase,
leading to pulmonary congestion.
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