What did we hear when we listened at the apex in our patient? Let’s listen again together. We’ll use the cotton swab placing it on the carotid vessel, we’ll use the bell of the stethoscope again to accentuate low-frequency sounds. If we watch the cotton swab, we’ll be able to identify systole. Let’s listen together. [Cut-away] Well, we clearly heard a fourth sound at the apex. We did not just hear the expected [sounds], but in this case, we heard [sounds]. And you know what? In a patient with an inferior wall infarction, that is expected. The incidence of fourth heart sounds is extremely high in this setting. That is because the compliance of the left ventricle is reduced due to the infarct and, for that reason, when the atrium kicks blood into the ventricle, the blood rapidly decelerates from the stiffness of that ventricle, and you hear the fourth sound. [Sounds]

We also heard an additional, rather subtle finding and that is that the first heart sound was a bit reduced. It’s tough to appreciate, but it was a bit reduced. Now, that can be from more that one reason: reduced left ventricular contractility in the setting of inferior wall infarction, where A-V nodal problems are significant, and conduction can be delayed, a long PR interval can also cause that. So, in summary, we heard a fourth sound, a somewhat reduced first sound and a second sound.

You know, it may he just as important, what we did not hear, and we should think about the things we didn’t hear. I can give you a few examples. For example, what we didn’t hear was a low-frequency third sound. We didn’t hear [sounds], or if you have a fourth sound with it [sounds]. A third sound is more significant than a fourth in terms of reduced ventricular function. Listen carefully for it. Another thing we didn’t hear was the murmur at the apex of mitral regurgitation. In this clinical setting, it could mean papillary muscle dysfunction from the infarction causing the leak of that mitral valve back into the left atrium, appreciated as [sounds]. We didn’t hear that. And, finally, we didn’t hear the pericardial friction rub. We didn’t hear it anywhere in the precordium, but be aware of that, because pericarditis can be a complication of acute myocardial infarction, and when you hear it, it has a rather distinctive quality, in fact, so much so, that I’d like to share it with you. I am going to have us listen to another patient, and share with you what it sounds like when you hear a pericardial friction rub. That pericardial friction rub has a cadence to it when all components are there, it sound [sounds]. Let me, let me plug in this tape and share that with you. Everybody listen together. In this case I am going to listen with the diaphragm of the stethoscope with firm pressure. Everybody listen. [Cut-away] that was a classic pericardial friction rub. [Sounds] Some or all of the components can vary with respiration.

In summary, our patient had an expected fourth sound at the apex, a slight diminution of S1. Do the thorough examination. What you don’t hear may be as important as what you do hear.