We have used an orderly approach and we have defined a rather elegant diagnosis, not only the etiology of the problem in this case, but the severity as well. We started out by analyzing arterial pulse. You recall it was normal. But, in this case, it told us a little something more, because one might expect with mitral regurgitation of this type a flicking, rapid upstroke to that carotid arterial pulse, because the ventricle is pushing against and overall reduced resistance, as the blood is regurgitated into the left atrium. But that was offset in this case by the ventricular contractility that was reduced to a degree, and they added up together to basically a normal impulse carotid arterial. Then we looked at the venous impulse. What about the venous impulse? The fact that it was normal, did that tell us anything? Well, it did in this case. This is a patient with mitral regurgitation that is longstanding and, as such, that left atrium keeps getting larger and larger over time and it acts as a buffer to the pulmonary circulation and you don’t get a big rise in pulmonary pressures and, therefore, the venous pressure in the neck was normal, the wave form was normal.

We started to get greater clues as we moved on to chest wall evaluation. The sustained, inferolaterally displaced left ventricular impulse with the palpable s3, it told us dilatation of the ventricle, some element of hypertrophy, and that third heart sound. Well, that was really due to two things in this case, the great degree of mitral regurgitation generated that third heart sound in part and in addition, contractility of the ventricle was reduced in this longstanding, chronic case of mitral regurgitation. Then we palpated the lower left sternal edge and we found an almost pathognomonic finding, that rocking motion we appreciated. Why? The left ventricle contracted, the left atrium expanded late in systole and that thrust forward the heart and it moved the chest wall, so that there was a little pearl there – that movement wasn’t as if it were a right ventricular movement due to hypertrophy or dilatation, no, it was that rocking motion of the left atrium expanding and pushing the heart forward.

And finally, we listened to the patient, last but not least, oh yes, we learned a lot, but it was all put into context by the non-acoustic events. We listened at the upper left sternal edge, normal findings at the upper left sternal edge. What did that tell us? It confirmed the normality of the pulmonary pressures or, at least, the near normality. This is a case, again, where the left atrium acts as a buffer to this mitral regurgitation over many years. And finally, we listened to very sophisticated acoustic events at the apex. The [mimics sounds] systolic murmur, the obscuring of that first heart sound, going to the second sound… we correlated this with the pressure curves of the left ventricle versus the left atrium and we heard that booming, low-frequency third sound due to flow and, to some degree, to diminished left ventricular function, and finally, the flow rumble, where you hear that low-frequency sound after the third sound, and those acoustic events in diastole, the [mimics sounds] and the [mimics sounds], they tell us that mitral regurgitation is severe. There’s so much blood in that left atrium, that as it gushes across the mitral valve in the next diastole, you hear a [mimics sounds] and an [mimics sounds], so the cadence is [mimics sounds] and it wasn’t the systolic murmur that told us the severity – it told us the lesion – it was the diastolic events that told us the severity.

We’ve put it all together, we’ve evaluated everything at the bedside, we know the diagnosis – mitral regurgitation; we know its severity – severe.