1. What conditions tend to make the aortic component of the second sound louder than normal?
ANS: a. Conditions that raise aortic systolic pressure, e.g., systemic hyper tension, which occasionally produces a drumlike sound or "tambour" S2. A tambour is a small drum that is covered only on one side. The tambour effect may persist even after the blood pressure has been lowered to normal by medication.
b. Conditions that produce a hyperkinetic systemic circulation, e.g., youth, or thyrotoxicosis.
Note: The loudness of the aortic closure depends on the recoil of the aorta and on ventricular performance . It follows, then, that a hypertensive patient in heart failure may not have a loud A2.
2. What conditions, besides a thin chest wall and pulmonary hypertension, tend to make the P2 louder than normal?
ANS: Conditions that produce increased blood flow into the pulmonary artery, as in ASD or VSD.
3. Why does the A2 tend to be loud when the heart is hyperactive as in thyrotoxico-sis and aortic regurgitation (AR)?
ANS: The intensity of the A2 is increased if the aortic valve closes when the aorta is energetically recoiling from the violent stretch due to the increased volume flung into it during systole.
Note: With severe AR the A2 may be soft, presumably because of the absence of adequate valve substance to cause a sudden deceleration of forward flow.
4. How does inspiration affect the loudness of each component of the S2?
ANS: The P2 commonly becomes louder because extra blood in the pulmonary artery on inspiration causes more energetic elastic recoil. The A2, on the other hand, becomes softer because inspiration decreases the volume ejected into the aorta and also places the aorta farther from the stethoscope.
Note: All sounds tend to become softer on inspiration if you listen over the upper chest, where excess lung space is interposed between the stethoscope and the heart on inspiration.
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