Our patient has acute mitral regurgitation. Not only do we know that diagnosis, we know the severity, it is severe, and we know the likely etiology, likely due to chordal rupture. And, beyond that, in terms of etiology, very possibly due to infective endocarditis.

Now, when we did our bedside examination, a compelling finding at the apex was the systolic murmur. An unusual feature of that murmur was that it was decrescendo. And that is rather typical of acute mitral regurgitation. Because, as the ventricle contracts, regurgitating blood into the atrium, that atrium in acute mitral regurgitation, has not been stretched over time. It, therefore, is not a giving, very compliant atrium and, therefore, as the regurgitant jet goes into the atrium, the pressure rises quite high in the atrium and that high pressure in the atrium tends to reduce the regurgitation into the atrium and reduce turbulence and, hence, the murmur wanes in late systole. A typical finding.

The fourth sound, again, due to a strong left atrium, an atrium that can contract well into the ventricle, finding the ventricle less compliant that normal, and you hear the fourth sound.

A third sound, again, due to poor compliance of the ventricle due to the acute nature of the mitral regurgitation, and you hear a third sound in early diastole. Alternatively, because of the mitral regurgitation, that third sound could partially be due to flow.

And there were many supportive findings on physical examination. In the first place, the carotid vessel, rapid in upstroke. That's rather typical of an acute regurgitant lesion of the mitral valve. Because, as the ventricle contracts, it finds less resistance in the atrium and it contracts more vigorously and, when contractility is enhanced like that, the carotid vessel is rapid rising due to the reduced resistance to ventricular contraction.

The jugular venous pulse was our first clue to right sided involvement from the acute mitral regurgitation. The jugular venous pulse "a" wave was giant and that reflected the fact that the right ventricle was hypertrophied. And how do we know the right ventricle was hypertrophied? Because when we palpated the parasternal edge we could feel a sustained right ventricular impulse and that, in turn, we found that on auscultation, was there was pulmonary hypertension because we heard such a very prominent pulmonary second sound. And why the pulmonary hypertension? Because in acute mitral regurgitation, that non compliant left atrium reflects those very high pressures that come from the ventricle all the way back into the pulmonary circulation.

In summary, this is a rather classic case of acute mitral regurgitation, and the beauty of our bedside examination is that we not only defined the diagnosis itself, we defined its severity, severe, and we defined its likely etiology. In most of these cases, ruptured chordae are the ultimate anatomic defect. And now we must look further and evaluate our patient to define further our suspicions that this could be due to infective endocarditis.