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332
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8—THE HEART
2. Wide Fixed Splitting
Wide xed splitting means that splitting occurs during inspiration and expiration, but the A2P2
interval remains constant.
3. Paradoxic Splitting (Reversed Splitting)
Paradoxic splitting means that audible expiratory splitting narrows or melds into a single sound
during inspiration. Paradoxic splitting occurs because the order of the S2 components has reversed:
A2 now follows P2, and as P2 is delayed during inspiration, the sounds move together.
B. SCREENING FOR ABNORMAL SPLITTING OF S
2
Fig. 40.1 reveals that all three abnormal second heart sounds—wide physiologic, xed, and paradoxic—
have audible splitting during expiration (dotted lines in Fig. 40.1). erefore, the best screening tool for
the abnormal S2 is audible expiratory splitting that persists when the patient sits up.
37–40
C. CLINICAL SIGNIFICANCE AND PATHOGENESIS
Table 40.1 lists the common causes of abnormal S2 splitting.
1. Wide Physiologic Splitting
Wide physiologic splitting may result from P2 appearing too late or A2 too early (Table 40.1).
18,38
e most common cause is RBBB.
In pulmonic stenosis, the A2P2 interval correlates well with severity of stenosis (gauged by the
RV systolic pressure, r = 0.87, p <0.001),41 although in many patients the clinician must listen
at the third interspace to hear splitting because the murmur is too loud at the second interspace.
TABLE 40.1 ■ Abnormal S2 Splitting
Splitting and Pathogenesis Etiology
WIDE PHYSIOLOGIC
P2 late
Electrical delay of RV systole RBBB
Prolongation of RV systole Pulmonic stenosis
Increased hangout interval Dilation of pulmonary artery
A2 Early
Shortening of LV systole Mitral regurgitation
WIDE AND FIXED
Increased hangout interval or prolongation of RV systole Atrial septal defect
Prolongation of RV systole Right ventricular failure
PARADOXIC
A2 late
Electrical delay of LV systole LBBB
Prolongation of LV systole Aortic stenosis
LV paced or ectopic beats
Acute cor pulmonale
RV paced or ectopic beats
Ischemic heart disease
LBBB, Left bundle branch block; LV, left ventricular; RBBB, right bundle branch block; R V, right ventricular; RV
systole and LV systole refer to the duration of right and left ventricular contraction.
40—THE FIRST AND SECOND HEART SOUNDS
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333
In most patients with pulmonary hypertension, the normal hangout interval disappears and S2
is single. S2 becomes wide in these patients only if there is associated severe RV dysfunction and
prolonged RV systole.
long-standing severe pulmonary hypertension
of pulmonary embolism is temporary, usually lasting hours to days).
31,32,42
Most patients with pulmonary hypertension and a wide S2 have either
31,32,42
or massive pulmonary embolism (the wide S2
43
2. Wide and Fixed Splitting
Patients with atrial septal defect have wide xed splitting of S2, although this is true only when their
pulse is regular (if the patient has atrial brillation or frequent extrasystoles, the degree of splitting
varies directly with the preceding cycle length).
30,44
e reason S2 is wide is not the same in every
patient: in some patients, hangout is increased; in others, RV mechanical systole is prolonged.44 S2 is
xed because hangout remains constant during respiration44 and because the presence of a common
left and right atrial chamber interrupts the normal respiratory variation of RV lling.
30
In patients with audible expiratory splitting (and regular rhythm), the absence of xed splitting
signicantly decreases the probability of atrial septal defect (LR = 0.1; see EBM Box 40.1), whereas
the presence of xed splitting increases the probability of atrial septal defect only modestly (LR =
2.6; see EBM Box 40.1). Patients with false-positive results (i.e., xed splitting without atrial septal
defect) commonly have the combination of RV failure and audible expiratory splitting from bundle
branch block or some other cause.
18
3. Paradoxic Splitting
In elderly adults with aortic ow murmurs, the nding of paradoxic splitting does not distinguish
signicant aortic stenosis from less severe disease (EBM Box 40.1).
D. S2 SPLITTING VS. OTHER DOUBLE SOUNDS
40
Other double sounds that mimic S2 splitting include the following (see also Chapter 42):
1. S2-Opening Snap
In contrast to the split S2, the S2-opening snap interval is slightly wider, the opening snap is loudest at the apex, and the opening snap ushers in the diastolic rumble of mitral stenosis at the apex.
Patients with S2-opening snap sometimes have a triple sound (split S2 + opening snap) during
inspiration at the upper sternal border.
2. S2-Pericardial Knock
In contrast to the split S2, the S2-knock interval is slightly wider, the pericardial knock is loudest
at or near apex, and the knock is always accompanied by elevated neck veins.
3. S2-Third Heart Sound
In contrast to the split S2, the S2-S3 interval is two to three times wider, and S3 is a low frequency
sound heard best with the bell.
4. Late Systolic Click-S
2
Clicks are loudest at or near apex and are often multiple. eir timing changes with maneuvers
(see Chapter 46).
IV. Intensity of S
2
Traditionally, a loud P2 has been regarded a reliable sign of pulmonary hypertension, but attempts
to conrm this teaching have been largely unsuccessful. For example, in mitral stenosis patients,
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8—THE HEART
the loud P2 dened either as an S2 that is louder at the left side of the upper sternum compared with the right side21 or as a split S2 with a louder second component (i.e., P2 > A2)20 did
not discriminate between patients with pulmonary hypertension and those without it (see EBM
Box 40.1). Furthermore, in patients with interstitial lung disease45 or those attending pulmonary
hypertension clinics,46 the nding of P2 > A2 was not an accurate sign of pulmonary hypertension.
Even when A2 and P2 were precisely identied by phonocardiography (e.g., A2 corresponds to aortic incisura on simultaneous aortic pressure tracing), the relative intensities of the two components
did not correlate well with pulmonary pressures.
45,47
Others have suggested that audible splitting
at the apex indicates pulmonary hypertension (because P2 should not be heard at the apex, and
any splitting at that location indicated that P2 was abnormally loud),33 but even this nding correlates better with the etiology of heart disease—it is common in atrial septal defect and primary
pulmonary hypertension—than it does with measurements of pulmonary pressure.
42,45,47
Nonetheless, one study of patients with cirrhosis did demonstrate that the loud P2 increased
probability of pulmonary hypertension (i.e., porto-pulmonary hypertension, LR = 17.6; EBM
Box 40.1, see Chapter 8). Also, the palpable S2 in patients with mitral stenosis accurately detects
pulmonary arterial pressures ≥50 mm Hg (positive LR = 3.6, negative LR = 0.05; see EBM Box
40.1). In this study, the palpable P2 was dened as an abrupt tapping sensation coincident with S2
at the second left intercostal space.
In patients with aortic ow murmurs, an absent or diminished S2 increases the probability of
signicant aortic stenosis (LR = 3.8, see Chapter 44).
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
References
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1.
Harvey W. De Motu Cordis HW (facsimile edition by Classics of Medicine library). Nonesuch; 1926.
2. McKusick VA. Rouanet of Paris and New Orleans. Bull Hist Med. 1958;32(2):137–151.
3. McCrady JD, Ho HE, Geddes LA. e contributions of the horse to knowledge of the heart and cir-
culation: IV. James Hope and the heart sounds. Conn Med. 1966;30(2):126–131.
4. Luisada AA, Portaluppi F. e main heart sounds as vibrations of the cardiohemic system: old contro-
versy and new facts. Am J Cardiol. 1983;52(8):1133–1136.
5. Ronan JA. Cardiac auscultation: the rst and second heart sounds. Heart Dis Stroke. 1992;1(3):113–116.
6. Sakamoto T, Kusukawa R, MacCanon DM, Luisada AA. Hemodynamic determinants of the amplitude
of the rst heart sound. Circ Res. 1965;16:45–57.
7. Hsieh BPC, Unver K, McNulty E, Schiller NB. e amplitude ratio of the rst to second heart sound is
reduced in left ventricular systolic dysfunction. Int J Cardiol. 2009;145(1):133–135.
8. Tassin A, Kobeissi A, Vitali L, et al. Relationship between amplitude and timing of heart sounds and
endocardial acceleration. Pacing Clin Electrophysiol. 2009;32(suppl 1):S101–S104.
9. Leech G, Brooks N, Green-Wilkinson A, Leatham A. Mechanism of inuence of PR interval on loud-
ness of rst heart sound. Br Heart J. 1980;43(2):138–142.
10. Burggraf GW, Craige E. e rst heart sound in complete heart block: phono-echocardiographic cor-
relations. Circulation. 1974;50(1):17–24.
11. Tei C, Shah PM, Cherian G, Wong M, Ormiston JA. e correlates of an abnormal rst heart sound in
mitral-valve-prolapse syndrome. N Engl J Med. 1982;307(6):334–339.
12. Perlo JK, Harvey WP. Auscultatory and phonocardiographic manifestations of pure mitral regurgita-
tion. Prog Cardiovasc Dis. 1962;5(2):172–194.
13. Wood P. An appreciation of mitral stenosis: Part 1. Clinical features. Part 2. Investigations and results. Br
Med J. 1954;1:1051–1063. 113–124.
14. Gershlick AH, Leech G, Mills PG, Leatham A. e loud rst heart sound in left atrial myxoma. Br Heart
J. 1984;52(4):403–407.
15. Stein PD, Sabbah HN, Barr I. Intensity of heart sounds in the evaluation of patients following myocar-
dial infarction. Chest. 1979;75(6):679–684.
16. Meadows WR, van Praagh S, Indreika M, Sharp JT. Premature mitral valve closure: A hemodynamic
explanation for absence of the rst sound in aortic insuciency. Circulation. 1963;28(2):251–258.
17. Garratt CJ, Grith MJ, Young G, etal. Value of physical signs in the diagnosis of ventricular tachycardia.
Circulation. 1994;90(6):3103–3107.
18. Perlo
19. Aronow WS, Kronzon I. Correlation of prevalence and severity of valvular aortic stenosis determined by
20. Whitaker W. Clinical diagnosis of pulmonary hypertension in patients with mitral stenosis. Q J Med.
21. Fowler NO, Noble WJ, Giarratano SJ, Mannix EP. e clinical estimation of pulmonary hypertension
22. Pilatis
23. Nakamura T, Hultgren HN, Shettigar UR, Fowles RE. Noninvasive evaluation of the severity of aortic
24. Aronow WS, Kronzon I. Prevalence and severity of valvular aortic stenosis determined by Doppler echo-
25. Hoagland PM, Cook EF, Wynne J, Goldman L. Value of noninvasive testing in adults with suspected
26. McGee SR. Etiology and diagnosis of systolic murmurs in adults. Am J Med. 2010;123(10):913–921.
27. Abe Y, Ito M, Tanaka C, etal. A novel and simple method using pocket-sized echocardiography to screen
28. Leatham A. Auscultation of the Heart and Phonocardiography. 2nd ed. Churchill Livingstone; 1975.
JK, Harvey WP. Mechanisms of xed splitting of the second heart sound.
18(5):998–1009.
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.
1954;23(89):105–112.
accompanying mitral stenosis. Am Heart J. 1955;49(2):237–249.
ND, Jacobs LE, Rerkpattanapipat P, et al. Clinical predictors of pulmonary hypertension in
patients undergoing liver transplant evaluation. Liver Transpl. 2000;6(1):85–91.
stenosis in adult patients. Am Heart J. 1984;107(5 Pt 1):959–966.
cardiography and its association with echocardiographic and electrocardiographic left ventricular hypertrophy and physical signs of aortic stenosis in elderly patients. Am J Cardiol. 1991;67(8):776–777.
aortic stenosis. Am J Med. 1986;80(6):1041–1050.
for aortic stenosis. J Am Soc Echocardiogr. 2013;26(6):589–596.
Circulation.
1958;
334.e1
29. Leatham A. e second heart sound: key to auscultation of the heart. Acta Cardiol. 1964;19:395–416.
https://t.me/medicina_free
30. Aygen MM, Braunwald E. e splitting of the second heart sound in normal subjects and in patients
with congenital heart disease. Circulation. 1962;25:328–345.
31. Shaver JA, Nadolny RA, O’Toole JD, etal. Sound pressure correlates of the second heart sound: an intra-
cardiac sound study. Circulation. 1974;49(2):316–325.
32. Curtiss EI, Matthews RG, Shaver JA. Mechanism of normal splitting of the second heart sound.
Circulation. 1975;51(1):157–164.
33. Harris A, Sutton G. Second heart sound in normal subjects. Br Heart J. 1968;30(6):739–742.
34. Nelson WP, North RL. Splitting of the second heart sound in adults forty years and older. Am J Med Sci.
1967;234(6):805–807.
35. Levine SA, Harvey WP. Clinical Auscultation of the Heart. WB Saunders; 1959.
36. Constant J. Bedside Cardiology. Little, Brown, & Company; 1985.
37. Breen WJ, Rekate AG. Eect of posture on splitting of the second heart sound. JAMA. 1960;
173(12):1326–1328.
38. Shaver JA, O’Toole JD. e second heart sound: newer concepts. Part 1: Normal and wide physiologic
splitting. Mod Concepts Cardiovasc Dis. 1977;46(2):7–12.
39. Shaver JA, O’Toole JD. e second heart sound: newer concepts. Part 2: Paradoxical splitting and narrow
physiological splitting. Mod Concepts Cardiovasc Dis. 1977;46(3):13–16.
40. Adolph RJ, Fowler NO. e second heart sound: a screening test for heart disease. Mod Concepts
Cardiovasc Dis. 1970;39(4):91–96.
41. Leatham A, Weitzman D. Auscultatory and phonocardiographic signs of pulmonary stenosis. Br Heart J.
1957;19(3):303–317.
42. Perlo JK. Auscultatory and phonocardiographic manifestations of pulmonary hypertension. Prog
Cardiovasc Dis. 1967;9(4):303–340.
43. Cobbs BW, Logue RB, Dorney ER. e second heart sound in pulmonary embolism and pulmonary
hypertension. Am Heart J. 1966;71(6):843–844.
44. O’Toole JD, Reddy PS, Curtiss EI, Shaver JA. e mechanism of splitting of the second heart sound in
atrial septal defect. Circulation. 1977;56(6):1047–1053.
45. Cobra SB, Cardoso RM, Rodrigues MP, Rodrigues MP. Usefulness of the second heart sound for predict-
ing pulmonary hypertension in patients with interstitial lung disease. S Paulo Med J. 2016;134(1):34–39.
46. Braganza M, Shaw J, Solverson K, etal. A prospective evaluation of the diagnostic accuracy of the physi-
cal examination for pulmonary hypertension. Chest. 2019;155(5):982–990.
47. Sutton G, Harris A, Leatham A. Second heart sound in pulmonary hypertension. Br Heart J. 1968;
30(6):743–756.
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CHAPTER
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41
The Third and Fourth Heart Sounds
KEY TEACHING POINTS
• The third and fourth heart sounds (S3 and S4) both originate from rapid diastolic filling of
ventricles. They are collectively called gallops. The S3 differs from the S4 in timing and
clinical significance.
• Right ventricular gallops appear at the left lower sternal border, intensify with inspiration,
and are associated with abnormalities of the jugular venous waveforms. Left ventricular
gallops appear at the apex and diminish in intensity during inspiration. All gallops are best
heard with the bell of the stethoscope.
• The S3 is an early diastolic sound. It is associated with a dilated ventricle, systolic
dysfunction, and elevated filling pressures. The S3 often disappears after the patient is
treated with diuretic medications.
• The S4 is a presystolic sound. It is associated with a stiff ventricle caused by ischemic,
hypertensive, or hypertrophic cardiomyopathy. Once heard, the S4 usually persists unless
the patient develops atrial fibrillation. Unlike the S3, the S4 does not predict the patient’s
hemodynamic findings.
I. Introduction
Although the third and fourth heart sounds (S3 and S4) are both sounds that originate in the
ventricle from rapid diastolic filling, they differ in timing and clinical significance. S3 appears in
early diastole and, if the patient is older than 40 years of age, the sound indicates severe systolic
dysfunction or valvular regurgitation. In persons younger than 40 years of age, S3 may be a normal
finding (i.e., the physiologic S3).1 S4 appears in late diastole, immediately before S1, indicating that
the patient’s ventricle is abnormally stiff from hypertrophy or fibrosis. If discovered in persons of
any age, the S4 is an abnormal finding.
In the late 19th century, the great French clinician Potain accurately described most features of
S3 and S4, their pathogenesis, and their distinction from other double sounds such as the split S1
or split S2.2 In his writings he called them gallops, a term he attributed to his teacher Bouillard.
II. Definitions
Several different terms have been used to describe these diastolic sounds.
2,3
335
336
lub dup lub dup lub dup
lub
du bub
lub
du bub
lub
du bub
be lub dup be lub
dup
be lub
dup
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8—THE HEART
A. GALLOP
A gallop is a triple rhythm with an extra sound in diastole (either S3, S4, or their summation). e
term refers only to pathologic sounds (i.e., it excludes physiologic S3) and, despite its connotation,
a patient may have a gallop whether the heart rate is fast or slow.
2,4
B. THIRD HEART SOUND (S3)
e third heart sound is sometimes called the ventricular gallop or protodiastolic gallop.2 It
appears in early diastole, 120 to 180 ms after S2.5 To mimic the sound, the clinician should first
establish the cadence of the normal S1 (lub) and S2 (dup):
And then add an early diastolic sound (bub)*:
e overall cadence of the S3 gallop (lub du bub) is similar to the cadence of the word
Kentucky.
C. FOURTH HEART SOUND (S4)
e fourth heart sound is sometimes called the atrial gallop or presystolic gallop.2 To mimic the
sound, the clinician establishes the cadence of S1 and S2 (lub dup) and then adds a presystolic
sound (be):
e cadence of S4 gallop (be lub dup) is similar to the cadence of the word Tennessee†.
D. SUMMATION GALLOP
e summation gallop is a loud gallop that occurs in patients with tachycardia. In fast heart
rhythms, diastole shortens, causing the events that produce S3 (rapid early diastolic filling) to
coincide with those producing S4 (atrial systole). e resulting sound sometimes is louder than
the patient’s S1 or S2.
Not all gallop rhythms in patients with tachycardia are summation gallops. e only way to
confirm the finding is to observe the patient after the heart rate slows. (In the past, slowing was
often induced by carotid artery massage, although in elderly patients this is no longer recommended. See Chapter 16). If slowing causes the gallop to disappear or evolve into two distinct but
fainter sounds (i.e., S3 and S4), it was a genuine summation gallop. If the sound evolves instead into
a single S3 or single S4, it was not a summation gallop.
*To pronounce the S3 gallop with correct timing, the “p” of dup (S2) must be dropped. In most patients the
accent is on S2 (lub du bub), although in others it falls on S1 or S3. e clinician can practice all three versions, always maintaining the same cadence, to become familiar with the varying sounds of S
†
Canadian teachers have suggested different mnemonics for the timing of S3 and S4: Montreal (pronounced
MON TRE al) for S3 and Toronto (tor ON to) for S4.
6
4,7
3.
41—THE THIRD AND FOURTH HEART SOUNDS
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337
E. QUADRUPLE RHYTHM
e quadruple rhythm consists of S1, S2, and both S3 and S4.4 It is an uncommon finding, usually
only evident in patients with slow heart rates. It is sometimes called the train wheel rhythm,
because the sound resembles that produced by the two pairs of wheels from adjacent train cars as
they cross the coupling of a railroad track.
be lub du bub be lub du bub be lub du bub
3,7
III. Technique
A. LOCATION OF SOUND AND USE OF STETHOSCOPE
S3 and S4 are both low frequency sounds (20 to 70 Hz), bordering on the threshold of human hearing.8
erefore, they are best heard with the bell of the stethoscope, applied lightly to the body wall with
only enough force to create an air seal.
the bell over the apical impulse or just medial to it. ey are sometimes only audible with the patient
lying in the left lateral decubitus position.9 Gallops from the right ventricle are best heard with the
bell over the left lower sternal border or, in patients with chronic lung disease, the subxiphoid area.
B. RIGHT VERSUS LEFT VENTRICULAR GALLOPS
Aside from their different locations, other distinguishing features of right and left ventricular
gallops are their response to respirations and association with other findings in the neck veins
and precordium. Right ventricular (RV) gallops become louder during inspiration; left ventricular
(LV ) gallops become softer during inspiration.10 e RV S4 may be associated with giant A waves
in the neck veins and sometimes a loud presystolic jugular sound (see Chapter 36).11 e LV S4
may be associated with a palpable presystolic movement of the apical impulse (see Chapter 38).
2,5
Gallops that originate in the left ventricle are best heard with
2,5
C. DISTINGUISHING THE S4-S1 SOUND FROM OTHER SOUNDS
ree combinations of heart sounds produce a double sound around S1: (1) the S4-S1 sound, (2)
the split S1, and (3) the S1-ejection sound. e following characteristics distinguish these sounds10:
1. Use of the Bell
e S4 is a low frequency sound, best heard with the bell. Firm pressure with the bell on the
skin—which tends to remove low frequency sounds—will cause the S4-S1 combination to evolve
into a single sound, in contrast to the split S1 and the S1-ejection sound, which remain double.
2. Location
e S4-S1 sound is heard best at the apex, left lower sternal border, or subxiphoid area (see the
section on location of sound and use of stethoscope). e split S1 is loudest from the apex to lower
sternal border, but sometimes is also heard well over the upper left sternal area. e aortic ejection
sound is heard from the apex to the upper right sternal border. e pulmonary ejection sound is
restricted to the upper left sternal area.
3. Effect of Respiration
Although the S4 may become louder (RV S4) or softer (LV S4) during inspiration, respiration does
not affect the interval between S4 and S1. In contrast, the split S1 interval varies with respiration
in up to one third of patients.
12
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8—THE HEART
Expiration makes the pulmonary ejection sound louder.12 e aortic ejection sound does not
vary with respiration.
13
4. Palpation
Only the S4-S1 sound is accompanied by a presystolic apical impulse (see Chapter 38). e intensity of the S4 (i.e., by auscultation) correlates moderately with the amplitude of the presystolic
impulse on apexcardiography (r = 0.46, p <0.01); similarly, the palpability of the presystolic
impulse correlates roughly with the amplitude of S4 on phonocardiography (r = 0.52, p <0.01).
14
IV. Pathogenesis
A. NORMAL VENTRICULAR FILLING CURVES
Filling of the right and left ventricles during diastole is divided into three distinct phases (Fig. 41.1).
e first phase, the rapid filling phase, begins immediately after opening of the atrioventricular
valves. During this phase, blood stored in the atria rapidly empties into the ventricles. e second
phase, the plateau phase (diastasis), begins at the moment the ventricles are unable to relax passively
any further. Very little filling occurs during this phase. e third phase, atrial systole, begins with the
atrial contraction, which expands the ventricle further just before the next S1.
B. VENTRICULAR FILLING AND SOUND
Both S3 and S4 occur at those times during diastole when blood flow entering the ventricles temporarily stops, that is, the S3 appears at the end of the rapid filling phase, and the S4 toward the
peak of atrial systole (Fig. 41.1). Sounds become audible if the blood decelerates abruptly enough,
which transmits sufficient energy to the ventricular walls and causes them to vibrate (an analogy
is the tensing of a handkerchief between two hands: abrupt tensing produces sound, whereas
slow tensing is silent).
fore whether gallops become audible: (1) the flow rate during entry and (2) the stiffness of the
ventricle. e greater the flow rate, the louder the sound. e stiffer the ventricle, the higher the
frequency of the sound.22 Since gallops consist of low frequencies that are difficult to hear (around
20 to 50 Hz), anything increasing their frequency content (i.e., stiff ventricles) makes the sound
more likely to be heard.
Even though S3 and S4 both result from rapid flow rates into stiff ventricles, the diseases caus-
ing them differ completely.
15–21
Two variables govern the suddenness of this deceleration, and there-
C. THE THIRD HEART SOUND (S3)
e S3 gallop appears when early diastolic filling is exaggerated, which occurs in two types of
cardiac disorders:
1. Congestive Heart Failure
e most common cause of the S3 gallop is congestive heart failure from systolic dysfunction. In
these patients, the S3 indicates that atrial pressure is abnormally elevated, an especially important
finding in patients with dyspnea, implying that heart disease is the principal cause of the shortness
of breath. In addition to elevated atrial pressure, these patients typically have a dilated cardiomyopathy and low cardiac output.
and cardiomyopathy (causing stiff ventricles) contribute to the sound, atrial pressure is the more
important clinical variable, because the sound disappears as soon as atrial pressure decreases with
diuresis.
23,24
Although both high atrial pressure (causing rapid flow rates)
41—THE THIRD AND FOURTH HEART SOUNDS
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339
Aorta
Aortic valve
Sudden deceleration
of rapid filling
Ventricular volume
Rapid filling
phase
S
3
Diastasis
Left atrium
Mitral valve
Left ventricle
S
4
Atrial systole
Mitral valve
opens
Fig. 41.1 Timing of third and fourth heart sounds. The figure depicts the three phases of diastolic filling of
the left ventricle (y-axis on graph, ventricular volume; x-axis, time). The S3 occurs at the end of the rapid filling
phase, when passive filling suddenly decelerates. The S4 occurs during atrial systole. Similar events on the
right side of the heart may produce a right ventricular S3 or S4. See text.
2. Regurgitation and Shunts
Patients with valvular regurgitation or left-to-right cardiac shunts also may develop an S3 gallop,
whether or not atrial pressure is high, because these disorders all cause excess flow over the atrioventricular valves. Patients with mitral regurgitation, ventricular septal defect, or patent ductus
arteriosus may develop a LV S3 from excess diastolic flow over the mitral valve into the left ventricle (in mitral regurgitation, the excess diastolic flow simply represents the diastolic return of the
regurgitant flow). Patients with atrial septal defect may develop a RV S3 from excess flow over the
tricuspid valve into the right ventricle.
3 phases of diastole
Mitral valve
closes
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