Acute MR can result from papillary muscle dysfunction or rupture caused by
myocardial ischemia or infarction, infective endocarditis with flail or perforated
leaflets, severe myxomatous disease with rupture of a chorda that results in a flail
leaflet, or trauma.
The pathophysiologic features of acute MR differ from those of chronic MR in
that compensatory increases in left atrial and LV compliance do not occur.
This results in a sudden increase in pulmonary venous pressure that leads to
acute pulmonary edema, and frequently cardiogenic shock.
Afterload reduction should be initiated urgently with sodium nitroprusside and
should be guided by systemic BP and central hemodynamic monitoring.
Approximately 50% of patients with acute MR can be stabilized in this manner,
allowing MVR to proceed under more controlled conditions.
Diuretics, with or without nitrates, can be used (as systemic BP tolerates) to
relieve pulmonary congestion. However, the direct venodilatory effect of
nitroprusside may render other preload-reducing maneuvers unnecessary.
Intra-aortic balloon counterpulsation is indicated in cases of severe
hemodynamic instability to reduce SVR and improve forward cardiac output.
Surgery is indicated urgently in patients with acute MR and hemodynamic
compromise whose condition cannot be stabilized medically.
In those with infective endocarditis who are hemodynamically stable, MVR
should be delayed for several days while antibiotic therapy is initiated. If refractory
hemodynamic deterioration develops, surgery should not be delayed