Chapter 10: THE HISTORY, PHYSICAL EXAMINATION, AND CARDIAC AUSCULTATION HEART SOUNDS
Heart sounds are of two types: high-frequency transients associated with the abrupt terminal checking of valves that are closing or opening and low-frequency sounds related to early and late diastolic filling events of the ventricles. Sounds related to closing and opening of the AV valves include mitral and tricuspid closing sounds (M1, T1), nonejection sounds, and the opening snaps; sounds related to closing and opening of the semilunar valves include aortic and pulmonic closure sounds (A2, P2) and early valvular ejection sounds or clicks. Low-frequency sounds include the physiologic heart sound (S3) and the pathologic S3 gallop associated with early ventricular filling events and the presystolic atrial S4 gallop associated with late diastolic events resulting from the atrial contribution to ventricular filling. With tachycardia, these sounds may fuse, producing a summation gallop.216,217
The First Heart Sound
The first heart sound (Sj) as recorded by high-resolution phonocardiography consists of four sequential components: (1) small, low-frequency vibrations, usually inaudible, that coincide with the beginning of LV contraction and felt to be muscular in origin, (2) a large, high-frequency vibration, easily audible, related to mitral valve closure (Mj), (3) a second high-frequency component, following closely, related to tricuspid valve closure (Tj), and (4) small, low-frequency vibrations that coincide with accelerated flow of blood into the great vessel. The two major components normally audible at the left lower sternal border are the louder Mj followed by Tj. They are separated by only 20 to 30 ms, and at the apex in the normal subject, and only a single sound (Mj) is usually appreciated. Splitting of the first heart sound is less evident with the tachycardia following coughing or with sustained handgrip exercises
The first high-frequency component of S1 coincides with the complete coaptation of the anterior and posterior leaflets of the mitral valve. This sound is due to the sudden deceleration of blood setting the entire cardiohemic system into vibration when the elastic limits of the closed, tensed valves are met. It is unlikely that complete coaptation of the complex valve leaflets and final tensing are simultaneous; presumably it is the latter event that is associated with vibrations perceived as M1. When T1 is more widely separated from M1, however, identical echocardiographic correlates have been demonstrated in patients with wide splitting of S1 due to Ebstein's anomaly of the tricuspid valve.216 This exaggerated T1, or "sail sound," and its wide separation from M1 have been a helpful sign in the diagnosis of this entity.217 Wide splitting of S1 with normal sequencing (M1, T1) is also present in right bundle branch block of the proximal type as well as in LV pacing, ectopic beats, and idioventricular rhythms originating from the left ventricle due to a delayed contraction of the right ventricle. In a similar manner, pacing from the right ventricle and ectopic beats and idioventricular rhythms originating from the right ventricle will produce reversed splitting of S1 (T1, M1) due to delay in LV contraction. Reversed splitting of S1 also may be present in patients with hemodynamically significant obstruction of the mitral valve, since mitral valve closure is delayed due to the increased left atrial pressure, which must be overcome by the rising LV pressure before closure can occur. Similar delay in M1 also may be found in mitral obstruction secondary to left atrial myxoma.
Figure 10-62 illustrates the sound and pressure correlates of M1. The first high-frequency component of M1 coincides with the downstroke of the left atrial c wave and is delayed from the left ventricular-left atrial pressure crossover by 30 ms. In the past, these findings have caused considerable confusion regarding the origin of both Mj and Tj, since it was assumed that these sounds occurred at AV pressure crossover.
However, the elegant studies of Laniado et al.2^ established that forward flow continued for a short period following left ventricular-left atrial pressure crossover due to the inertia of mitral flow, with Mj occurring 20 to 40 ms later, coincidentally with cessation of mitral flow and closure of the valve. An even greater delay between the occurrence of Tj and right ventricular-right atrial pressure crossover has been shown,219 and O'Toole et al.220 have shown that Tj also coincides with the downstroke of the right atrial c wave. These hemodynamic data, together with the echocardiographic correlates of Mj and Tj, confirm the prime role played by the AV valves in the genesis of Sj.
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