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8—THE HEART
D. THE FOURTH HEART SOUND (S4)
e S4 gallop occurs in patients with hypertension, ischemic cardiomyopathy, hypertrophic cardiomyopathy, or aortic stenosis—all disorders characterized by ventricles stiffened from hypertrophy or fibrosis.
2,23–25
Patients with the sound must be in sinus rhythm and have strong atrial
contractions, and most have normal atrial pressures, normal cardiac output, and normal ventricular
chamber size. Unlike the S3, the S4 is a durable finding that does not wax and wane unless the
patient develops atrial fibrillation (and thus loses the atrial contraction).
E. SUMMATION GALLOP AND QUADRUPLE RHYTHM
e summation gallop occurs because fast heart rates shorten diastole, primarily by eliminating the plateau phase (Fig. 41.1), which brings the events causing S3 close to those causing S4.
Diastolic filling is concentrated into a single moment, thus causing a very loud sound.
e quadruple rhythm typically occurs in patients who have had a long-standing S4 gallop
from ischemic or hypertensive heart disease but who then develop cardiac decompensation, high
filling pressures, and a S3.
Rarely, an intermittent summation gallop may appear in patients with slow heart rates due
to complete heart block (or VVI pacing).26 e gallop appears only during those moments of
atrioventricular dissociation when atrial systole and early diastole coincide (i.e., the P wave on
the electrocardiogram falls just after the QRS). Although the sound is technically a summation gallop, the clinician perceives what sounds like an intermittent S3. A similar mechanism
has been invoked to explain intermittent early diastolic sounds in patients with Wenckebach
heart block.
27
7
F. PHYSIOLOGIC S
3
Persons younger than 40 years of age with normal hearts may also have a S3 sound (i.e., physiologic S3), because normal early filling can sometimes be so rapid that it ends abruptly and causes
the ventricular walls to vibrate and produce sound. Compared with healthy persons lacking the
sound, those with the physiologic S3 are leaner and have more rapid early diastolic filling.1 e
physiologic S3 disappears by age 40, because normal aging slows ventricular relaxation and shifts
filling later in diastole, thus diminishing the rate of early diastolic filling and making the sound
disappear.
28
V. Clinical Significance
A. THE THIRD HEART SOUND
1. Congestive Heart Failure
EBM Box 41.1 shows that the presence of the S3 gallop is a significant finding indicating depressed
ejection fraction (likelihood ratio [LR] = 3.4 to 4.1; see EBM Box 41.1), elevated left atrial pressures (LR = 3.9), and elevated B-type natriuretic peptide (BNP) levels (LR = 10.1). Other studies
confirm its value as a predictor of poor systolic function.
the patient’s ejection fraction is greater than 30% (i.e., negative LR = 0.3 for detecting ejection
fraction <30%; see EBM Box 41.1).
In patients with a history of congestive heart failure, the S3 predicts responsiveness to digoxin46
and overall mortality.
47
36,45
e absence of the S3 gallop argues that
41—THE THIRD AND FOURTH HEART SOUNDS
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EBM BOX 41.1 The Third and Fourth Heart Sounds*
Likelihood Ratio†
if Finding Is
Present Absent
32,34,35,41
Finding (Reference)
The third heart sound
Detecting ejection fraction <0.5
Detecting ejection fraction <0.3
Detecting elevated left heart filling
pressures
32–35
Detecting elevated BNP level
Detecting myocardial infarction in
patients with acute chest pain
Predicting postoperative pulmonary
edema
39,40
Predicting postoperative myocardial
infarction or cardiac death
20,29–32
30,31
36,37
38
39,40
Sensitivity
(%)
11–51 85–98 3.4 0.7
68–78 80–88 4.1 0.3
12–37 85–96 3.9 0.8
41–65 93–97 10.1 0.5
16 95 3.2 NS
17 99 14.6 NS
11 99 8.0 NS
Specificity
(%)
The fourth heart sound
Detecting elevated left heart filling
pressures
Detecting severe aortic stenosis
Predicting 5-year mortality in patients
after myocardial infarction
*
Diagnostic standard: for ejection fraction, left ventricular ejection fraction <0.5 or <0.3 (as indicated above)
by scintigraphy or echocardiography (see Chapter 48); for elevated left heart filling pressures, pulmonary
capillary wedge pressure >12 mm Hg33 or left ventricular end diastolic pressure >15 mm Hg
elevated BNP level, ≥100 pg/mL36 or >1525 pg/mL37; for myocardial infarction, development of new
electrocardiographic Q waves, elevations of creatine kinase MB, or both; for severe aortic stenosis, peak
gradient >50 mm Hg42 or valve area <0.75 cm2.
†
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
BNP, B type natriuretic peptide; NS, not significant.
34,41
42,43
44
35–71 50–70 NS NS
29–50 57–63 NS NS
29 91 3.2 NS
43
341
; for
THIRD AND FOURTH HEART SOUNDS
LRs
0.1 0.2 0.5 12510
Absence of S3, arguing
against ejection fraction <30%
Probability
Decrease Increase
S
3
myocardial infarction
, detecting elevated left heart
S
3
filling pressures
S
, detecting ejection fraction <50%
3
S
, detecting myocardial infarction if chest pain
3
, predicting 5 year mortality if
S
4
myocardial infarction
+45%+30%+15%–15%–30%–45%
LRs
, predicting postoperative
S
3
pulmonary edema
S
, detecting elevated BNP level
3
, predicting postoperative
342
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8—THE HEART
2. Valvular Heart Disease
In patients with mitral regurgitation, the S3 is a poor predictor of elevated filling pressure (LR not
significant) and depressed ejection fraction (LR = 1.9).48 Some studies correlate the sound with
the severity of mitral regurgitation,20 whereas others do not.
48
In contrast, the S3 is a helpful finding in patients with aortic valve disease. In patients with aortic stenosis, the S3 detects both elevated filling pressures (LR = 2.3 for pulmonary capillary wedge
pressures ≥12 mm Hg) and a depressed ejection fraction (LR = 5.7 for EF <50%).48 In patients
with aortic regurgitation, the S3 detects both severity of regurgitation (LR = 5.9 for regurgitant
fraction ≥40%, see Chapter 45) and ejection fraction <50% (LR = 8.3).
20
3. Patients with Acute Chest Pain
In patients with acute chest pain presenting to emergency departments, the finding of an S3
increases the probability of myocardial infarction (LR = 3.2; EBM Box 41.1).
4. Preoperative Consultation
During preoperative consultation, the finding of S3 is ominous, indicating that the patient, without any other intervention, has an increased risk of perioperative pulmonary edema (LR = 14.6)
and myocardial infarction or cardiac death (LR = 8).
39
B. THE FOURTH HEART SOUND
e finding of the S4 gallop has less diagnostic value, simply because the disorders causing stiff
ventricles are so diverse and because the S4 does not predict the patient’s hemodynamic findings.
e finding does not predict ejection fraction, left heart filling pressures, or postoperative cardiac
complications.
aortic flow murmurs, presumably because many patients with mild stenosis have the finding for
other reasons, such as ischemic heart disease.
Nonetheless, when detected one month after myocardial infarction, the S4 is a modest predictor of 5 year cardiac mortality (LR = 3.2; see EBM Box 41.1). Experienced auscultators in the
val to widen, which could be recognized at the bedside, but proper interpretation of this finding
required knowledge of the patient’s PR interval, thus limiting its utility.49 In patients with chaotic
heart rhythms, the finding of a S4 excludes atrial fibrillation and suggests other diagnoses such as
multifocal atrial tachycardia.
S4 is rare in patients with chronic mitral regurgitation, because the dilated atrium of these
patients cannot contract strongly. erefore, finding a S4 gallop in a patient with mitral regurgitation is an important clue to the diagnosis of acute mitral regurgitation (e.g., ruptured chorda
tendineae; see Chapter 46).
23,24,34,39,40
It also does not predict significant aortic stenosis in elderly patients with
42,43
inter-
4-S1
50–52
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
References
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12. Perloff JK. Auscultatory and phonocardiographic manifestations of pulmonary hypertension. Prog
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presence of disease and examiner experience. Arch Intern Med. 1987;147(4):721–726.
15. Ozawa Y, Smith D, Craige E. Origin of the third heart sound. I. Studies in dogs. Circ. 1983;67(2):393–398.
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1983;67(2):399–404.
17. Kono T, Rosman H, Alam M, Stein PD, Sabbah HN. Hemodynamic correlates of the third heart sound
during the evolution of chronic heart failure. J Am Coll Cardiol. 1993;21(2):419–423.
18. Ishimitsu T, Smith D, Berko B, Craige E. Origin of the third heart sound: comparison of ventricular wall
dynamics in hyperdynamic and hypodynamic types. J Am Coll Cardiol. 1985;5(2 Pt 1):268–272.
19. Van de Werf F, Boel A, Geboers J, etal. Diastolic properties of the left ventricle in normal adults and in
patients with third heart sounds. Circulation. 1984;69(6):1070–1078.
20. Tribouilloy CM, Enriquez-Sarano M, Mohty D, et al. Pathophysiologic determinants of third heart
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21. Shah SJ, Marcus GM, Gerber IL, etal. Physiology of the third heart sound: novel insights from tissue
doppler imaging. J Am Soc Echocardiogr. 2008;21(4):394–400.
22. Glower DD, Murrah RL, Olsen CO, Davis JW, Rankin MS. Mechanical correlates of the third heart
sound. J Am Coll Cardiol. 1992;19(2):450–457.
23. Shah PM, Gramiak R, Kramer DH, Yu PN. Determinants of atrial (S4) and ventricular (S3) gallop
sounds in primary myocardial disease. N Engl J Med. 1968;278(14):753–758.
24. Shah PM, Yu PN. Gallop rhythm. Hemody namic and clinical correlation. Am Heart J. 1969;78(6):823–828.
25. Homma S, Bhattacharjee D, Gopal A, Correia J. Relationship of auscultatory fourth heart sound to the
quantitated left atrial filling fraction. Clin Cardiol. 1991;14(8):671–674.
26. Iga K, Konishi T. Intermittently audible the “third heart sound” as a sign of complete atrio-ventricular
block in patients with a VVI pacemaker. Int J Cardiol. 1999;71(2):135–139.
27. Konishi E, Kawasaki T, Shiraishi H, Yamano M, Kamitani T. Additional heart sounds during early
diastole in a patient with hypertrophic cardiomyopathy and atrioventricular block. J Cardiol Cases.
2015;11(6):171–174.
28. Van de Werf F, Geboers J, Kesteloot H, De Geest H, Barrios L. e mechanisms of disappearance of the
physiologic third heart sound with age. Circulation. 1986;73(5):877–884.
29. Gadsboll N, Hoilund-Carlsen PF, Nielsen GG, etal. Interobserver agreement and accuracy of bedside
estimation of right and left ventricular ejection fraction in acute myocardial infarction. Am J Cardiol.
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30. Mattleman SJ, Hakki AH, Iskandrian AS, Segal BL, Kane SA. Reliability of bedside evaluation in deter-
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31. Patel R, Bushnell DL, Sobotka PA. Implications of an audible third heart sound in evaluating cardiac
function. West J Med. 1993;158(6):606–609.
32. Marcus G, Vessey J, Jordan MV, et al. Relationship between accurate auscultation of a clinically useful
third heart sound and level of experience. Arch Intern Med. 2006;166(6):617–622.
33. Gadsbøll N, Høilund-Carlsen PF, Nielsen GG, et al. Symptoms and signs of heart failure in patients
with myocardial infarction: reproducibility and relationship to chest X-ray, radionuclide ventriculography
and right heart catheterization. Eur Heart J. 1989;10(11):1017–1028.
34. Zema MJ, Restivo B, Sos T, Sniderman KW, Kline S. Left ventricular dysfunction: bedside Valsalva
manoeuvre. Br Heart J. 1980;44(5):560–569.
35. Harlan WR, Oberman A, Grim R, Rosati RA. Chronic congestive heart failure in coronary artery dis-
ease: clinical criteria. Ann Intern Med. 1977;86(2):133–138.
36. Marcus GM, Michaels AD, de Marco T, McCulloch CE, Chatterjee K. Usefulness of the third heart
sound in predicting an elevated level of B-type natriuretic peptide. Am J Cardiol. 2004;93(10):1312–1313.
37. Narain VS, Puri A, Gilhotra HS, et al. ird heart sound revisited: a correlation with N-terminal pro
brain natriuretic peptide and echocardiography to detect left ventricular dysfunction. Indian Heart J.
2005;57(1):31–34.
38. Tierney WM, Fitzgerald J, McHenry R, etal. Physicians’ estimates of the probability of myocardial
infarction in emergency room patients with chest pain. Med Decis Making. 1986;6(1):12–17.
39. Goldman L, Caldera DL, Nussbaum SR, etal. Multifactorial index of cardiac risk in noncardiac surgical
procedures. N Engl J Med. 1977;297(16):845–850.
40. Goldman L, Caldera DL, Southwick FS, etal. Cardiac risk factors and complications in non-cardiac
surgery. Medicine (Baltimore). 1978;57(4):357–370.
41. Gupta S, Michaels AD. Relationship between accurate auscultation of the fourth heart sound and level
of physician experience. Clin Cardiol. 2009;32(2):69–75.
42. Aronow WS, Kronzon I. Correlation of prevalence and severity of valvular aortic stenosis determined by
continuous-wave Doppler echocardiography with physical signs of aortic stenosis in patients aged 62 to
100 years with aortic systolic ejection murmurs. Am J Cardiol. 1987;60(4):399–401.
43. Kavalier MA, Stewart J, Tavel ME. e apical A wave versus the fourth heart sound in assessing the
severity of aortic stenosis. Circulation. 1975;51(2):324–327.
44. Ishikawa M, Sakata K, Maki A, Mizuno H, Ishikawa K. Prognostic significance of a clearly audible fourth
heart sound detected a month after an acute myocardial infarction. Am J Cardiol. 1997;80(5):619–621.
45. Eagle KA, Quertermous T, Singer DE, etal. Left ventricular ejection fraction. Physician estimates com-
pared with gated blood pool scan measurements. Arch Intern Med. 1988;148(4):882–885.
46. Lee DCS, Johnson RA, Bingham JB, etal. Heart failure in outpatients: a randomized trial of digoxin
versus placebo. N Engl J Med. 1982;306(12):699–705.
47. Likoff MJ, Chandler SL, Kay HR. Clinical determinants of mortality in chronic congestive heart failure
secondary to idiopathic dilated or to ischemic cardiomyopathy. Am J Cardiol. 1987;59(6):634–638.
48. Folland ED, Kriegel BJ, Henderson WG, Hammermeister KE, Sethi GK. Implications of third heart
sounds in patients with valvular heart disease. N Engl J Med. 1992;327(7):458–462.
49. Barlow JB. Some observations on the atrial sound. S Afr Med J. 1960;34:887–892.
50. Cohen LS, Mason DT, Braunwald E. Significance of an atrial gallop sound in mitral regurgitation: A clue
to the diagnosis of rupture chordae tendineae. Circulation. 1967;35(1):112–118.
51. DePace NL, Nestico PF, Morganroth J. Acute severe mitral regurgitation. Pathophysiology, clinical rec-
ognition, and management. Am J Med. 1985;78(2):293–306.
52. Hultgren HN, Hancock EW, Cohn KE. Auscultation in mitral and tricuspid valvular disease. Prog
Cardiovasc Dis. 1968;10(4):298–322.
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CHAPTER
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42
Miscellaneous Heart Sounds
KEY TEACHING POINTS
• Miscellaneous heart sounds are classified by their timing: early systolic sounds (ejection
sounds), mid-to-late systolic sounds (click of mitral valve prolapse), and early diastolic
sounds (opening snap of mitral stenosis, pericardial knock of constrictive pericarditis, and
tumor plop of atrial myxoma).
• If a patient with a rigid prosthetic heart valve presents with chest pain, dyspnea, or
syncope, the clinician should carefully document the prosthetic heart sounds. In cagedball valves, the opening sounds should be loudest (early systolic for aortic position; early
diastolic for mitral position). In tilting-disc valves, the closing sounds should be loudest (S2
for aortic position; S1 for mitral position). Failure to elicit these findings may indicate valve
thrombosis.
In addition to the first, second, third, and fourth heart sounds, several other discrete, short
sounds may occur (Fig. 42.1). ese sounds include early systolic sounds (e.g., the aortic or pul-
monary ejection sound), midsystolic or late systolic sounds (e.g., systolic click of mitral valve prolapse), early diastolic sounds (e.g., opening snap of mitral stenosis, pericardial knock of constrictive
pericarditis, and tumor plop of atrial myxoma), and prosthetic valve sounds. All are high frequency
sounds best heard with the diaphragm of the stethoscope.
EJECTION SOUNDS
I.
The Finding and Pathogenesis
e ejection sound is the most common early systolic sound. It results from abnormal sudden halting of the semilunar cusps as they open during early systole.
typically have aortic stenosis, a bicuspid aortic valve, or a dilated aortic root.
ejection sounds have pulmonary stenosis, pulmonary hypertension, or a dilated pulmonary trunk.
Aortic and pulmonary ejection sounds are distinguished by their location, associated murmurs,
and how they vary during respiration. An aortic ejection sound is a loud high-frequency sounds
(often louder than S1) best heard at the apex, although commonly also audible at the upper right
sternal border.
sternal edge at the second or third intercostal space; they often diminish in intensity during inspiration. Ejection sounds associated with aortic or pulmonic stenosis occur immediately before the
onset of the systolic murmur.
Chapter 41 describes how to distinguish ejection sounds f rom other double sounds around S1,
including the combination of S4-S
4
It does not vary with respiration. Pulmonary ejection sounds are confined to the
4,5
1
and the split S1.
1,2
Patients with aortic ejection sounds
1,2
ose with pulmonary
2,3
343
344
4
Mid- and
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8—THE HEART
late systolic clicks
Ejection sound
S
S
Fig. 42.1 Miscellaneous heart sounds. The figure shows the timing of the miscellaneous systolic sounds
(ejection sounds and mid-to-late systolic clicks) and diastolic sounds (opening snap and pericardial knock),
in relation to the principal heart sounds (first, second, third, and fourth heart sounds). The tumor plop of atrial
myxoma, not depicted in the figure, has variable timing, ranging from 80 ms after A
snap) to 150 ms after A
II.
Clinical Significance
1
(i.e., timing of the third heart sound).
2
A2P2S
Opening snap
Pericardial knock
3
25
S
S
4
1
(i.e., timing of the opening
2
e primary importance of these sounds is their etiologic associations. In patients with aortic stenosis, the ejection sound implies that the stenosis is at the valvular level and that there is some mobility to the valve. Elderly patients with calcific aortic stenosis usually do not have ejection sounds,
because the calcific degeneration makes the valve leaflets inflexible. Children with noncalcific aortic
stenosis, in contrast, usually have the ejection sound. In one consecutive series of 118 patients with
aortic stenosis, the ejection sound was audible in 100% of patients with noncalcific valvular stenosis,
in 32% with calcific valvular stenosis, and in none with subvalvular or supravalvular stenosis.
4
MID-TO-LATE SYSTOLIC CLICKS
I.
The Finding and Pathogenesis
Mid-to-late systolic clicks occur in patients with mitral valve prolapse. ese sounds, which are
sometimes multiple, are caused by sudden deceleration of the billowing mitral leaflet as it prolapses backward into the left atrium during systole.
sternal border and is frequently associated with a late systolic murmur.
e hallmark of the click of mitral valve prolapse (and also of the associated murmur) is that
its timing shifts during maneuvers that change venous return. For example, the straining phase
of the Valsalva maneuver or the squat-to-stand maneuver, both of which decrease venous return,
causes the mitral leaflets to prolapse earlier in systole, thus shifting the click (and murmur) closer
to S
(see Fig. 46.1 in Chapter 46).
1
Clicks have been heard by clinicians for over a century, although they were ascribed to pleu-
ropericardial adhesions or other extracardiac causes
the sound coincided with systolic prolapse of the posterior mitral leaflet.
II. Clinical Significance
e presence of the characteristic click or murmur alone is sufficient grounds for the diagnosis of
11,12
mitral valve prolapse.
Chapter 46 discusses these findings further.
6
e click is loudest at the apex or left lower
7,8
9
until the 1960s, when Barlow demonstrated
7
10
42—MISCELLANEOUS HEART SOUNDS
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345
OPENING SNAP
I. The Finding and Pathogenesis
e opening snap is an early diastolic sound heard in patients with mitral stenosis.* e sound
occurs because the stenotic mitral leaflets (although fused, they are mobile) billow like a large
sail into the ventricle during early diastole but then abruptly decelerate as they meet the limits of
movement.
then followed by the mid-diastolic rumbling murmur of mitral stenosis. e opening snap is best
heard between the apex and left lower sternal border.
of S1, S2, and opening snap (RUP = S1; bu = S2; DUP = opening snap):
1,6
e abrupt deceleration causes a loud, medium-to-high frequency sound, which is
e clinician can mimic the sound of snap and murmur together by first setting up the cadence
U
bu DUP
P
R
R
UPbu DUP
R
U
bu DUP
P
and then adding the murmur:
bu DUP
R
U
P
RRR
RRRRR
U
bu DUP
P
RRR
RRRRR
U
bu DUP
P
In some patients the opening snap is so loud it is easily heard at the second left intercostal
space, where it then mimics a widely split S2. Careful attention to inspiration in these patients,
however, may reveal a triple sound (split S2 and opening snap) at this location, confirming the last
sound to be the opening snap.
e opening snap of mitral stenosis was first described by Bouillard in 1835.
1
II. Clinical Significance
According to traditional teachings, the opening snap is inaudible in patients with mitral stenosis
whose valve leaflets have become so thickened and inflexible they cannot create sound.
is an inverse correlation between the opening snap amplitude and degree of calcification of the
mitral valve (r = −0.675, p<0.01).
14
e interval between the A2 component of S2 and the opening snap (A2-OS interval) has been
used to gauge the severity of mitral stenosis. Patients with more severe obstruction tend to have a
narrower A2-OS interval than those with milder disease. is occurs because the mitral valve opens
when the pressure in the relaxing ventricle falls below the atrial pressure; the more severe the obstruction, the higher the atrial pressure and the sooner this crossover occurs. Nonetheless, determining the
A2-OS interval is primarily a phonocardiographic exercise, not an auscultatory one.15 Furthermore,
the A2-OS interval also depends on variables other than severity of stenosis, such as ventricular
relaxation time and heart rate, which further complicates interpreting it accurately at the bedside.
e opening snap does indicate that the accompanying diastolic murmur represents mitral
stenosis and not a flow rumble from increased flow over a nonstenotic valve (see Chapter 46 for
discussion of flow rumbles).
6,13
ere
15
PERICARDIAL KNOCK
e pericardial knock is a loud early diastolic sound heard in 20% to 94% of patients with constrictive pericarditis (see Chapter 47). It is heard over a wide area between the apex and left lower
*
Patients with tricuspid stenosis also may have an opening snap, but all of these patients also have mitral stenosis
and the mitral opening snap. Differentiating tricuspid and mitral opening snaps by auscultation is difficult.
346
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8—THE HEART
sternal border. Compared with the third heart sound, the pericardial knock is a higher frequency
sound (easily detected with the diaphragm of the stethoscope), appears over a wider area of the
precordium, and occurs slightly earlier (although still later than the opening snap or widely split
second heart sound).
16
e pericardial knock results from the sudden deceleration of the filling ventricle as it meets
the borders of the rigid pericardial sac.
16,17
In this way, it is similar to the third heart sound,
although the more abrupt deceleration of constriction is what probably makes the pericardial
knock higher-pitched and louder than the third heart sound (see Chapter 41).
TUMOR PLOP
e tumor plop is an early diastolic sound representing prolapse of the pedunculated tumor from
the atrium over the mitral (or tricuspid) valve into the ventricle18 In two large series of patients
with myxoma (283 patients), it was detected in 15% to 50% of patients.
19,20
Characteristically, the
intensity and timing of the tumor plop vary between examinations: the plop may occur as early
as the timing of an opening snap, or as late as that of the third heart sound. It is often associated
with a diastolic murmur that mimics the rumbling sound of mitral stenosis.
19
An audio recording of a pansystolic murmur and tumor plop sound from a patient with a
mitral valve myxoma can be found in reference by Doshi.
21
PROSTHETIC HEART SOUNDS
I. Introduction
Abnormal prosthetic heart sounds may be the only clue explaining the patient’s dyspnea, syncope,
or chest pain. To recognize these abnormal sounds simply and quickly, the clinician must first
understand the normal prosthetic heart sounds. is section focuses on rigid mechanical valves,
such as caged-ball valves (Starr-Edwards)† single tilting-disc valves (Bjork-Shiley, MedtronicHall), and bileaflet tilting-disc valves (St. Jude Medical).
22–24
II. Principles
e important observations are (1) timing and intensity of opening and closing sounds, which
typically have a clicking or metallic quality and are often audible without a stethoscope, and (2)
associated murmurs. Any new or changing sound or murmur requires investigation.
A. OPENING AND CLOSING SOUNDS
In patients with caged-ball valves, the opening sound is louder than the closing sound. In patients
with tilting-disc valves (both single disc and bileaflet), the closing sounds are loud and the opening sounds are only faint or inaudible (Fig. 42.2).
1. Caged-Ball Valves
In the aortic position, the caged-ball valve produces a loud opening sound, which is an extra systolic sound occurring just after S1 with timing identical to the aortic ejection sound (i.e., instead
of just S1 and S2, lub dup…lub dup, the clinician hears ledup dup…ledup dup). Caged-ball valves
†
e Starr-Edwards valve is no longer manufactured, although it is still in use.
42—MISCELLANEOUS HEART SOUNDS
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Prosthesis
type
Caged-ball
valves
Tilting-disc
valves
Fig. 42.2 Prosthetic valve sounds. The normal findings of prosthetic valves are based on references 22–24.
AC, Closure sound of aortic prosthesis; AO, opening sound of aortic prosthesis; MC, closure sound of mitral
prosthesis; MO, opening sound of mitral prosthesis; P2, pulmonary component of second heart sound; S1,
first heart sound; S2, second heart sound. See the text.
Aortic position Mitral position
P
2
S
1
AO
S
1
AO
AC
P
2
AC MC
CM
S
2
MO
S
MO
2
in the mitral position produce an extra diastolic sound when they open, with timing identical to
that of the opening snap (i.e., instead of S1 and S2, lub bup…lub bup, it is lub budup…lub budup).
ese opening sounds should always be louder than the corresponding closing sound (i.e., closing
sounds are coincident with S2 in aortic prostheses and with S1 in mitral prostheses). e finding of
an inaudible or abnormally soft opening sound indicates something is interfering with excursion
of the ball, such as thrombus.
2. Tilting-Disc Valves
ese valves produce distinct, metallic closing sounds coincident with S1 (mitral position) or S2
(aortic position). Patients whose closing sounds are abnormally quiet may have significant valve
dysfunction.
B. MURMURS
In the aortic position, all rigid valves (caged-ball and tilting-disc) typically produce short midsystolic murmurs that are best heard at the base and sometimes radiate to the neck. Diastolic
murmurs in these patients suggest perivalvular regurgitation and require investigation.
In patients with rigid valves in the mitral position, any holosystolic murmur suggests perivalvular regurgitation and requires investigation. A normal finding in patients with the caged-ball
valve in the mitral position (but not tilting-disc valves) is an early-to-midsystolic murmur at the
left sternal border. is murmur does not indicate regurgitation but instead represents turbulence
caused by the cage of the valve projecting into the left ventricular outflow tract.
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
22–24
22,24
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