Acute Mitral Regurgitation
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Patients with acute MR typically present with some degree of pulmonary edema.
Because the left atrium has not had time to adapt ( as in chronic MR ), it
remains relatively poorly compliant and thus is not able to handle the excess
volume as the regurgitant fraction is returned to it with each ventricular
contraction. This leads to increased left atrial pressures which are
transmitted backwards to the pulmonary circulation. Intubation with the
application of PEEP is often necessary, especially if the patient is in
cardiogenic shock.

The main goals of therapy are to minimize the mitral valve regurgitant
fraction and improve forward flow through the aortic valve.  If there is no
hypotension, afterload reduction is the mainstay of therapy with nitroprusside
and intra-aortic balloon pump being the most common agents used. I would
titrate the NTP until symptoms resolve or to a systolic BP of 90 to 100.
Although their use is becoming somewhat controversial, a Swan-Ganz catheter
will allow more precise titration of therapy in this situation. It will give
you a measure of forward flow ( Cardiac output), PA pressures, and PCWP. In
addition the height of the "v" wave on the PCWP tracing gives an estimate of
the degree of regurgitant flow - for example, initial  25 mmHg '"v" waves that
diminished to 15 mmHg after starting nitroprusside would be evidence for a
positive therapeutic effect.

Patients who are hypotensive with acute MR ( it sounds like this one was) are
much more difficult to treat and have extremely high mortality. In this
situation I think a Swan-Ganz is absolutely necessary as any proposed therapy
could just as easily have negative as well as positive effects. Inotropic
agents may be beneficial with Dobutamine being the preferred agent due to its
vasodilating properties (if the sytemic BP will tolerate it).  Otherwise
Dopamine can be tried in order to raise systemic BP to the minimal clinically
accepted level while recognizing that its alpha effects could increase
regurgitant flow and thus decrease forward flow.

As far as fluids are concerned, one of the goals in dealing with regurgitant
leisons is to decrease cardiac chamber sizes, thus shrinking the valve annulus
( in this case the mitral valve annulus ).  This decreases the size of the
valve orifice and thus can decrease the regurgitant fraction and increase
forward flow. Fluids ( colloids or crystalloids ) could paradoxically decrease
forward flow. Diuresis can be beneficial. Mitral regurg leads to left sided
volume overload, thus increasing preload is unlikely to result in improved
contractility, and careful diuresis is unlikely to decrease myocardial
contractility.

All of this is assuming that myocardial contractility is not significantly
impaired and that acute MR is the major hemodynamic problem. If a large amount
of LV is infarcted or there is RV infarction associated with an inferior MI,
then the situation becomes even more complex.

Hope this helps,

Pat Melanson
Dept of Emergency Medicine and
Division of Critical Care Medicine
Royal Victoria Hospital
Montreal, Quebec