Flail Mitral Leaflet

Hypertension Exercise Program

Cure High Blood Pressure Permanently

Get Instant Access

Figure 10-62: The apex phonocardiogram is displayed simultaneously with the cardiac cycle, as recorded by high-fidelity catheter-tipped micromanometers in the central aorta, left ventricle (LV), and left atrium (LA). The first high-frequency component of Mj is coincident with the downstroke of the left atrial cwave and is separated from left ventricular-left atrial pressure crossover by an interval of 30 ms. (From Shaver JA, Saderni R, Reddy PS, et al. Normal and abnormal heart sounds in cardiac diagnosis: I. Systolic sounds. Curr Probl Cardiol i985; i0:i0-53. Reproduced with permission from the publisher and authors.)

INTENSITY OF Sj

The primary factors determining intensity of Sj are (i) integrity of valve closure, (2) mobility of the valve, (3) velocity of valve closure, (4) status of ventricular contraction, (5) transmission characteristics of the thoracic cavity and thorax, and (6) physical characteristics of the vibrating structures.

Integrity of Valve Closure

In rare situations, usually in the setting of severe mitral regurgitation, there is inadequate coaptation of the mitral leaflets to a degree that valve closure is not effective. As a result, abrupt halting of the retrograde blood column during early ventricular contraction does not occur, and Sj may be markedly attenuated or absent. Such may be the case in severe mitral regurgitation due to a flail mitral leaflet, as shown in Fig. !0-63.

Flail Mitral Valve Leaflet

Figure 10-63: Base and apex phonocardiograms are recorded simultaneously with the mitral valve echocardiogram in a 62-year-old man who developed acute mitral regurgitation secondary to rupture of the chordae tendinae of a myxomatous valve. During diastole, multiple echoes arise from the flail posterior mitral leaflet (PML), and during early ventricular systole, effective mitral valve closure does not occur, resulting in an inaudible low-frequency vibration on the apex phonocardiogram. During systole, there is separation of the anterior (AML) and posterior mitral leaflets, resulting in severe mitral regurgitation. The murmur has a crescendo-decrescendo contour simulating the murmur of aortic stenosis ending prior to A1. Wide physiologic splitting of S1 is present. The prominent S4 present on the apex phonocardiogram was associated with an apical presystolic impulse. (From Shaver JA. The physical examination in cardiac diagnosis. Cardiol Consult 1985; 6:3. Reproduced with permission from the publisher and author.)

Figure 10-63: Base and apex phonocardiograms are recorded simultaneously with the mitral valve echocardiogram in a 62-year-old man who developed acute mitral regurgitation secondary to rupture of the chordae tendinae of a myxomatous valve. During diastole, multiple echoes arise from the flail posterior mitral leaflet (PML), and during early ventricular systole, effective mitral valve closure does not occur, resulting in an inaudible low-frequency vibration on the apex phonocardiogram. During systole, there is separation of the anterior (AML) and posterior mitral leaflets, resulting in severe mitral regurgitation. The murmur has a crescendo-decrescendo contour simulating the murmur of aortic stenosis ending prior to A1. Wide physiologic splitting of S1 is present. The prominent S4 present on the apex phonocardiogram was associated with an apical presystolic impulse. (From Shaver JA. The physical examination in cardiac diagnosis. Cardiol Consult 1985; 6:3. Reproduced with permission from the publisher and author.)

Mobility of the Valve

Severe calcific fixation of the mitral valve with complete immobilization will cause a markedly attenuated M1. This is seen most commonly in the setting of long-standing mitral stenosis.

Velocity of Valve Closure

The velocity of valve closure is the most important factor affecting the intensity of S1 and is determined by the timing of mitral valve closure in relation to the LV pressure rise in early systole.221 The relative timing of left atrial and LV systole may vary this relationship. As the PR interval progressively decreases from 130 to 30 ms, there is a progressive increase in the intensity of M1 and progressive delay in M1 relative to the onset of LV contraction. When left atrial and LV systole occur almost simultaneously at a PR interval of 10 ms, however, S1 again becomes soft. At short PR intervals (30-70 ms), the mitral valve leaflets are maximally separated by atrial contraction at the onset of LV systole. With LV contraction, the mitral valve closes at a high velocity with a large excursion. This results in a loud, late M1 occurring on a steeper part of the LV pressure curve when the retrograde blood column is suddenly decelerated at the moment the elastic limits of the mitral valve are met. At longer PR intervals, there is less separation of the mitral valve leaflets, which have already begun to close with atrial relaxation. When LV systole begins, there is less excursion of the mitral valve until tensing occurs, and S1 occurs earlier relative to the onset of LV contraction at a lower LV pressure. Thus less force is applied to the mitral valve, its closing velocity is decreased, and less energy is generated when a column of retrograde blood is abruptly halted, resulting in a softer M1.

The clinical finding of marked variation in the intensity of S1 in a patient with a slow heart rate often will http://cardiology.accessmedicine.com/server-java/Arknoid/amed/hurst/co_chapters/ch010/ch010_p10.html (3 / 22) [2003-1-4 12:20:13]

alert the clinician at the bedside to the diagnosis of complete heart block with AV dissociation. Other conditions in which there are beat-to-beat variations in the intensity of S1 include Mobitz type I heart block and ventricular tachycardia with AV dissociation. Variations in the intensity of S1 also occur with atrial fibrillation with both normal and stenotic AV valves. The loud S1 occurs at short RR intervals, whereas a softer S1 occurs at longer RR intervals when the valve leaflets have closed partially.222

The position of the mitral valve at the onset of ventricular systole may be altered not only by the relative timing of atrial and ventricular systole but also by altering the rate of LV filling during atrial systole. Leonard et al.221 have shown that the timing and intensity of both S1 and S4 in hypertensive patients can be influenced by variations in venous return. It is suggested that the mitral leaflets have a greater separation when venous return is decreased to the noncompliant hypertensive left ventricle because there is more effective atrial volume transport into a relatively underfilled ventricle. This results in a softer S4 that migrates toward an increased S1. When venous return is increased, the atrial contribution of ventricular filling is now operating on the steeper portion of the LV pressure volume curve. The S4 becomes louder and earlier, and S1 is decreased in amplitude due to partial atriogenic closure of the mitral valve. This is the most likely explanation of a soft S1 frequently noted in hypertensive patients with normal PR intervals.

Status of Ventricular Contraction

The status of ventricular contractility is also an independent factor determining the amplitude of S^.221-222 In normal subjects, both exercise and catecholamine infusion have been shown to increase the amplitude of Sj, whereas administration of blocking agents decreases it.224 In both situations, the prime factor in altering the intensity of S1 is the rate of pressure development in the ventricle. This increased rate of pressure development partially explains why S1 is increased in patients with anemia, arteriovenous fistulas, pregnancy, anxiety, and fever. It is also likely that these high-output states, often associated with tachycardia, result in wider separation of the AV valves at the onset of ventricular systole due to high flow through a shortened diastolic period. Similarly, the loud T1 in an ASD is due to high flow through the tricuspid valve, secondary to the left-to-right shunt at the atrial level. A decrease in the intensity of S1 associated with a decrease in the rate of LV pressure development may be found in myxedema, cardiomyopathy, and acute MI.223,224 Beat-to-beat variation in the intensity of S1 (auscultatory alternans) also has been found in patients with pulsus alternans, in whom beat-to-beat alteration in the rate of LV pressure development occurs.

Transmission Characteristics of the Thoracic Cavity and Chest Wall

The degree of attenuation of heart sounds generated by the vibrating cardiohemic system is a function of both sound frequency and the distance of the heart from the chest wall. The higher-frequency heart sounds are attenuated to a greater extent than are lower-frequency sounds. Conditions such as obesity, emphysema, and large pleural or pericardial effusions will decrease the intensity of all auscultatory events, whereas a thin body habitus would tend to increase the intensity.

Physical Characteristics of the Vibrating Structures

Alterations in the physical characteristics of the vibrating structures also may vary the intensity of S1. Both MI and ischemia induced by pacing have been shown to decrease the intensity of S1 secondary to these alterations.224

S1 IN PATHOLOGIC CONDITIONS

Careful attention to the intensity of S1 is an extremely important aspect of cardiac auscultation, often giving clues to the proper diagnosis and degree of abnormality of the involved structures. The following conditions are examples where alterations in the intensity of S1 play a key role in the correct diagnosis.

Sj in Mitral Stenosis

A loud, late Mj is the hallmark of hemodynamically significant mitral stenosis.225 When Mj is loud, it is associated with a loud opening snap, and the intensity of both Mj and the opening snap correlates with valve motility Fig. 10-64, left). When calcific fixation of the stenotic mitral valve occurs, Mj is soft, and the opening snap is absent. The relationship between sound and pressure and echocardiographic mitral valve motion is shown in Fig. 10-65. Significant scarring of the mitral valve is evident as a result of the rheumatic process. The increased left atrial pressure delays the time of pressure crossover between the left atrium and the left ventricle. As a result, Mj occurs later and at a much higher than normal LV pressure, at a time when there is a more rapid rate of development of LV pressure. The presystolic gradient between the left atrium and the left ventricle prevents preclosure of the mitral valve leaflets. As a result, the closure of the leaflet begins from a domed position within the LV cavity and takes place over a much greater distance than normal following the onset of LV contraction. Both these factors increase the velocity of mitral valve closure and the momentum of blood directed toward the mitral valve leaflets, resulting in a loud Mj when the elastic limits of the stenotic mitral valve are met. A similar mechanism is responsible for the booming Sj with after vibrations in left atrial myxoma (see Fig. !0-65, center).

Atrial Myxoma Picture

Figure 10-65: External sound, equisensitive LV and left atrial pressures (catheter-tipped micromanometer), LV dP/dt, and left atrial sound are recorded simultaneously with the mitral valve echocardiogram in a patient with hemodynamically significant mitral stenosis. A significant presystolic gradient is present due to atrial contraction, and the onset of the rapid closure of the mitral valve (B) is delayed until the LV pressure exceeds left atrial pressure. This occurs 40 ms after the beginning of the LV pressure rise at a time when LV dP/dt is much higher than normal. Following left atrial-left ventricular pressure crossover, there is rapid ventriculogenic closure of the mitral valve (BC), resulting in a very loud Mj coincident with the C point of the mitral valve echocardiogram. Its separation from A2 is determined by both the level of the left atrial pressure and the rate of LV pressure decline. (From Shaver JA, et al. Normal and abnormal heart sounds in cardiac diagnosis: I. Systolic sounds. Curr Probl Cardiol j985; !0:!0-53. Reproduced with permission from the publisher and the authors.)

Figure 10-65: External sound, equisensitive LV and left atrial pressures (catheter-tipped micromanometer), LV dP/dt, and left atrial sound are recorded simultaneously with the mitral valve echocardiogram in a patient with hemodynamically significant mitral stenosis. A significant presystolic gradient is present due to atrial contraction, and the onset of the rapid closure of the mitral valve (B) is delayed until the LV pressure exceeds left atrial pressure. This occurs 40 ms after the beginning of the LV pressure rise at a time when LV dP/dt is much higher than normal. Following left atrial-left ventricular pressure crossover, there is rapid ventriculogenic closure of the mitral valve (BC), resulting in a very loud Mj coincident with the C point of the mitral valve echocardiogram. Its separation from A2 is determined by both the level of the left atrial pressure and the rate of LV pressure decline. (From Shaver JA, et al. Normal and abnormal heart sounds in cardiac diagnosis: I. Systolic sounds. Curr Probl Cardiol j985; !0:!0-53. Reproduced with permission from the publisher and the authors.)

S1 in Mitral Valve Prolapse

Tei et al.226 have reported a loud M1 heard over the apex in patients with nonrheumatic mitral regurgitation; this is indicative of holosystolic mitral valve prolapse (see Fig. 10-64, right). Patients with the more common middle to late systolic prolapse have a normal S1, whereas a soft or absent S1 may indicate a flail mitral leaflet (see Fig. 10-65). The increased amplitude of leaflet excursion with prolapse beyond the line of closure explains the loud M1 associated with holosystolic prolapse. An alternate explanation may be a summation of a normal M1 and an early nonejection click of valvular prolapse.

S1 and LBBB

In LBBB, M1 is decreased in intensity and is frequently delayed, at times resulting in reversal of sequence of S1.227 The reason for the delay and the decreased intensity of M1 in this condition is multifactional, with different mechanisms operative in different patients, depending on the degree of completeness of the LBBB, the site of block (proximal versus peripheral), and especially the status of LV function.228 The primary factors involved are (1) delay in onset of LV contraction, (2) degree of LV dysfunction, (3) presence of concomitant first-degree heart block, and (4) presence of a noncompliant left ventricle facilitating atriogenic preclosure of the mitral valve. It is likely that more than one factor is operative in most patients with LBBB, with one or two factors predominating.

S1 in Acute Aortic Regurgitation

One of the important auscultatory findings in acute aortic regurgitation is attenuation or absence of M1.222 Severe regurgitation into a left ventricle that has not had time to adapt to the acute volume overload causes a marked increase in the LV end-diastolic pressure, resulting in premature closure of the normal mitral valve in middiastole. With the onset of LV systole, minimal mitral valve excursion occurs, causing a marked reduction in the intensity of M1.

Systolic Ejection Sounds

Ejection sounds are early systolic ejection events that can originate from either the left or the right side of the heart. These sounds may be classified as valvular, arising from deformed aortic or pulmonic valves, or as vascular, or root events caused by the rapid, forceful ejection of blood into the great vessels. The presence or absence of valvular ejection sounds is of great benefit in defining the level of RV or LV outflow tract obstruction, whereas root ejection sounds give insight into abnormalities of the great vessels with or without systemic or pulmonary hypertension.

Was this article helpful?

0 0
Reducing Blood Pressure Naturally

Reducing Blood Pressure Naturally

Do You Suffer From High Blood Pressure? Do You Feel Like This Silent Killer Might Be Stalking You? Have you been diagnosed or pre-hypertension and hypertension? Then JOIN THE CROWD Nearly 1 in 3 adults in the United States suffer from High Blood Pressure and only 1 in 3 adults are actually aware that they have it.

Get My Free Ebook


Post a comment