Physiological consequences of mitral regurgitation
The immediate results of sudden-onset mitral regurgitation are a decreased cardiac output and an increased pulmonary vascular pressure. The ventricle ejects some of its stroke volume into the left atrium, and thus the forward cardiac output is reduced; the left atrium experiences high pressures and these are passed on to the pulmonary circulation.
Mild mitral regurgitation is usually well tolerated. To compensate for the reduced forward flow, the left ventricle becomes dilated and hypertrophied. The increase in total (forward as well as regurgitating) stroke volume tends to compensate for the low cardiac output.
The left atrium enlarges, but at the early stages the LA pressures remain more or less the same.
Moderate mitral regurgitation (a regurgitant fraction of over 60% of stroke volume) is usually associated with some degree of congestive heart failure. The left atrium is grossly dilated, and this tends to stretch the mitral annulus even further, worsening the degree of regurgitation. The LV ejection fraction is preserved until a very late stage; however one must recall that most of this ejection is propelled backwards into the pulmonary circulation.
However, the LV can only compensate to a certain degree, and at the late stages of mitral regurgitation it begins to decompensate, giving rise to worsening congestive heart failure.
Severe mitral regurgitation is biventricular failure. The LV is failing because it cannot produce a sufficient amount of forward flow (as it is much easier for blood to flow backwards into the low-pressure pulmonary circulation). The RV is struggling against increased pulmonary arterial pressures; it also dilates and hypetrophies.
Strategies to compensate for the physiological consequences of mitral regurgitation
Nothing concrete can be said about preload management in mitral regurgitation. Some preload is essential, but increasing it beyond a certain individual point will result in greater stretch on the mitral annulus, leading to greater regurgitation. Thus, the only way to know who needs fluids and who doesn't is with the careful observation of what happens after a small fluid bolus.
These people need a rapid heart rate. With bradycardia, LV volume is allowed to bloat unreasonably during diastole, and this leads to a decompensation (an overdistended ventricle pumps inefficiently). Forward cardiac output is thus reduced not only because of a decrease in rate, but also a decrease in stroke volume.
With an increased heart rate, the cardiac output is maintained, and diastolic overdistension is avoided.
The atrial kick is not as important in this setting. The distended atrium would not be able to contract well even if it wanted to; with onset of AF its already low function is not so greatly diminished as to impact on the cardiac output.
Contractility is all-important. Not only will you increase cardiac output by increasing total stroke volume (and thus the forward fraction), you will also increase the contractility of the muscle immediately surrounding the mitral annulus, thus constricting the annulus (and reversing the valve lesion, to some extent). Thus, it is important to avoid cardiodepressant drugs like beta-blockers, and it is rewarding to used catecholamine inotropes such as dobutamine. Because right heart failure and pulmonary hypertension tend to be present, one can occasionally get away with mixing dobutamine and milrinone together.
Because forward flow is what you are interested in increasing, any resistance to forward flow is undesirable. Thus, afterload reduction tends to decrease the regurgitant fraction and increase the forward ejection fraction. The use of vasopressors is therefore unhelpful, and arterial vasodilators are probably very useful.
Again, nitroprusside is widely quoted as a good choice of vasodilator, probably owing to its selective effects on arterial smooth muscle.