By using our bedside skills we have defined our patient's pathology, and that pathology is severe disease of the left and the right heart - left ventricular and right ventricular dysfunction. And how did we define that? Starting out originally with a very simple observation such as the blood pressure. Narrow pulse pressure, slightly elevated diastolic. That may be seen in patients with severe left ventricular failure. We then supported this by feeling the arterial pulses, first the carotid and then the peripheral pulses. They were small, or hypokinetic, a finding seen in severe left ventricular failure.

Then we went to the venous pulse, a reflector of disease of the right heart. And what did we see? An elevated central venous pressure to be sure and, in addition, a giant "a" wave in the neck, and it is called giant, because the right atrium is making a giant effort to put blood into the right ventricle, but that right ventricle is not distensible, it is not compliant, so when the right atrium contracts, that big wave is reflected up into the venous impulse contour.

Then we examined the chest wall and what do we find? Again, left and right sided findings. The apical area, where the left ventricle, not only was inferolaterally displaced, reflecting its dilatation and enlargement, but where we palpated presystolic and early diastolic components to the impulse. These are the palpable equivalent of what we hear as the S4 and the S3. Those low frequency vibrations are such that you can actually feel them on the chest wall when they are intense enough. And on the right side, the right ventricle reflected in the parasternal edge, almost identical findings telling us wait, it isn't just left ventricular disease we have here, it's also right ventricular disease.

And then we listened, we listened at the upper left sternal edge. The splitting of the second heart sound was normal, but the intensity of P2 told us this patient has an element of pulmonary hypertension, probably from their left ventricular failure.

And then we moved down to the lower left sternal edge. We got a big help by watching respiration and listening at the same time. Because, when this patient breathed in we just didn't hear [sounds], but what we heard when they breathed in was [sounds], third and fourth sounds on inspiration telling us that the right side is struggling, as reflected in the S3 and the S4. As blood is rushing into the ventricle in early diastole and as the atrium contracts in late diastole, or presystole, that blood decelerates because of the stiff, non compliant, right ventricle and, again, you hear those filling sounds enhanced in inspiration, which tells us it is right sided.

An then the apex, well, of course, we heard the S3 and S4 at the apex. They were so prominent we heard them even with the diaphragm. Most of the times, you want to listen with the bell, but that's how prominent they were. But in our case, we heard something else too, we heard the murmur of mitral regurgitation, and the real question is: oh gee, is mitral regurgitation then the reason for all this? And the answer is probably not. Probably not because mitral regurgitation can be the result of pump failure in addition to in some cases being its cause. When that ventricle is dilated and the papillary muscles get pulled upon because of the dilatation, you unseat the mitral valve and you get mitral regurgitation due to the dysfunction of that apparatus that makes up the entire mitral valve.

Well, we should probably conclude then that our patient likely has a cardiomyopathy, a disease of both the left and right heart, of the muscle, but we are obligated to rule out anything we can remedy. So, we must be sure to be vigilant, look for other causes and amongst them are atypical presentations of coronary artery disease.