The physiologic S3 is a benign finding commonly heard in children, adolescents, and young adults, but it is rarely present in adults after age 40 and, when present, is often associated with a thin, asthenic body habitus. This is a low-frequency sound that follows A2 by 120 to 200 ms and occurs during rapid filling of the ventricle.259,260 It is best heard at the apex in the left lateral position with the stethoscope bell pressed lightly against the skin and is differentiated from the pathologic S3 primarily by the "company it keeps."26!
Most agree that the pathologic S3 is an exaggeration of the physiologic S3, with a common mechanism of production.262 The exact genesis of the S3 remains controversial. Three major mechanisms of production have been proposed: the valvular theory, the ventricular theory, and the impact theory. The most popular theory has indicated that these sounds have their origins within the left or right ventricle or their walls.263 The dynamic interplay between the force of delivery of blood into the ventricle and the ability of the ventricle to accept this flow is an important factor in the genesis of this sound. When there is appropriate interaction between these factors, the S3 occurs when the ventricle suddenly reaches its elastic limits and abruptly decelerates the onrushing column of blood, thereby setting the entire cardiohemic system into vibration. Thus an S3 may be produced by excessive rapid filling into a ventricle with normal or increased compliance, as with high-output states and mitral regurgitation, or by a normal or less than normal rate of filling into a ventricle with decreased compliance, as in patients with hypertrophic cardiomyopathy. Likewise, decreased rates of filling into overfilled ventricles with large end-systolic volumes, as seen in patients with poor LV function and congestive heart failure, will produce this sound.264
Although this mechanism is likely responsible for the sound recorded within the ventricular cavity and on its epicardial surface, Reddy et al.217,265 have reported convincing data that the sound heard with the stethoscope can be due to the dynamic impact of the heart with the chest wall. The force of the impact and resulting intensity of S3 depend primarily on the size of the heart, the motion of the heart within the thorax, and the chest wall configuration. This theory explains the S3 present in hyperdynamic states as well as those with an increased end-systolic volume secondary to LV dysfunction. In the latter, the space between the enlarged heart and the lateral chest wall is diminished, thereby facilitating a more forceful impact in early diastole. This results in an exaggerated rapid filling wave on the apex cardiogram and the prominent S3 pathognomonic of congestive failure (Fig. 10-75, lower panel). Table 10-9 tabulates the major factors responsible for the production of the S3 as recorded within the left ventricle and on the chest wall.
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