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CHAPTER
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44
Aortic Stenosis
KEY TEACHING POINTS
• The characteristic murmur of calcific aortic stenosis radiates broadly from the cardiac
apex to the right clavicle. The absence of this murmur is a compelling argument against
the diagnosis of aortic stenosis.
• The classic physical findings of aortic stenosis—delayed carotid upstroke, diminished
intensity of the second heart sound, sustained apical impulse, and late peaking
murmur—all increase the probability that the murmur represents moderate-to-severe
stenosis (vs. a more benign aortic flow murmur).
• Clinicians will have difficulty using bedside findings alone to distinguish moderate aortic
stenosis from severe aortic stenosis.
Introduction
I.
Aortic stenosis is any disorder of the aortic valve that obstructs the ejection of blood from the left
ventricle into the aorta. Its characteristic findings are a systolic murmur, abnormal carotid pulse,
and sustained apical impulse.
e pathology of aortic stenosis was recognized in the 1600s, but it was James Hope who in
1832 first clearly described the characteristic murmur.
II.
The Findings
A.
THE MURMUR
e murmur of aortic stenosis is early systolic, midsystolic, or holosystolic. Although it may be
loudest at the right second intercostal space (i.e., the classic “aortic” area), most aortic stenosis
radiates
right
the patient’s right shoulder. Radiation of sound in the neck first appears on the right side (clavicle
and neck), but as the stenosis worsens the sound appears on both sides of the neck and over both
clavicles. In contrast, isolated radiation a murmur to just the left clavicle or left neck is not characteristic of aortic stenosis alone and suggests stenosis of a great artery (see Chapter 43).
borders contains both high- and low-frequency vibrations, giving it a harsh or rough sound, like
that of a person clearing the throat. At the apex the murmur of calcific aortic stenosis sometimes
loses low frequency components and instead consists of a narrow band of high frequency sound,
thus making it sound like mitral regurgitation. is harmonic distortion of sound—the loss of low
above and below the third left parasternal space, obliquely and upwards towards the
clavicle and downward toward the apex, a distribution mimicked by placing a sash over
In calcific aortic stenosis, the most common modern etiology, the murmur at the upper sternal
1,2
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9—SELECTED CARDIAC DISORDERS
frequency components of sound when the stethoscope is moved “upstream” toward the apex—is
called the Gallavardin phenomenon.
3
B. ASSOCIATED CARDIAC SIGNS
Other traditional findings of severe aortic stenosis are the following: (1) a carotid pulse that is
abnormally small in volume and delayed (pulsus parvus et tardus); (2) a palpable apical impulse
that is abnormally sustained (see Chapter 38 for definition of sustained impulse) and (3) reduced
intensity of the second heart sound, which occurs because the inflexible aortic leaflets close with
less force than normal. Another traditional finding is a prominent A wave in the neck veins (i.e.,
the Bernheim phenomenon), although this wave is more often seen on pressure tracings than at
the bedside. Its mechanism is disputed.
4
III. Clinical Significance
A. DETECTING AORTIC STENOSIS
e presence of the characteristic aortic systolic murmur increases the probability of aortic stenosis (likelihood ratio [LR] = 10.5 for mild or worse aortic stenosis, see EBM Box 44.1); most
false positives (i.e., patients with a characteristic aortic murmur but no aortic stenosis) have
increased aortic flow without obstruction (e.g., from fever, anemia, pregnancy, or turbulence due to
EBM BOX 44.1 Aortic Stenosis Murmur*
Likelihood Ratio‡ if Finding Is
Present Absent
Finding (Reference)
Aortic systolic murmur,
detecting mild or worse
aortic stenosis
Aortic systolic murmur,
detecting severe aortic
stenosis
5,6
5,7,8
†
Sensitivity
(%)
79–90 85–87 10.5 0.1
83–98 71–76 3.5 0.1
Specificity
(%)
*Diagnostic standard: for mild or worse aortic stenosis, peak aortic velocity ≥2.5 m/sec5 or unstated
echocardiographic parameter6; for severe aortic stenosis, maximal inter-aortic cusp distance 8 mm,7 peak
aortic velocity ≥4 m/sec,5 or peak aortic gradient > 64 mm Hg.
†
Definition of findings: for aortic systolic murmur, either the broad apical-base pattern or small apical base
pattern (see Chapter 43).
‡
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
LRs
0.1 0.2 0.5 12510
Absence of murmur, arguing
against aortic stenosis
8
AORTIC STENOSIS MURMUR
Probability
Decrease Increase
+45%+30%+15%–15%–30%–45%
LRs
Presence of murmur, detecting
aortic stenosis
44—AORTIC STENOSIS
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371
nonobstructing calcification). Most importantly, the absence of the aortic flow murmur decreases
considerably the probability of aortic stenosis (LR = 0.1 for stenosis of any severity). Chapter 43
discusses further the differential diagnosis of systolic murmurs, and how the clinician—by observing the location of sound, the second heart sound, the quality of the murmur, and how the murmur responds to irregular heart beats and different maneuvers—can be more confident a systolic
murmur indeed represents aortic stenosis and not another valvular lesion.
B. SEVERITY OF AORTIC STENOSIS
Once clinicians are confident a murmur represents an aortic flow murmur, they must decide
whether or not the patient has significant aortic stenosis. Significant aortic stenosis refers to those
lesions with such severe obstruction that valvular replacement is indicated if the patient has symptoms of angina, syncope, or dyspnea. (e footnotes of EBM Box 44.2 define severe stenosis.)
Many of the traditional teachings about aortic stenosis originated during a time when congenital and rheumatic disease were more common than they are today. Because the primary cause
of aortic stenosis today is calcific aortic stenosis, some of these teachings may not be as relevant as
they were in the past. In comparison to congenital and rheumatic disease, calcific aortic stenosis
affects older patients, who commonly have aortic flow murmurs without stenosis (i.e., aortic sclerosis) and who often have ischemic heart disease, a disorder complicating the bedside evaluation
because patients then have two possible explanations (i.e., severe aortic stenosis or ischemic heart
disease) for symptoms of angina or dyspnea.
e patients whose clinical signs are summarized in EBM Box 44.2 (over 700 patients in all)
were all elderly. Importantly, all had aortic flow murmurs, and the bedside question was whether
or not the murmur represented severe aortic stenosis. Although some had mild aortic regurgitation, other significant valvular disease was excluded from most of these studies. In these studies,
syncope was the only classic aortic stenosis symptom that increased the probability of severe
aortic stenosis (LR = 3.1; the LRs for the other two classic aortic stenosis symptoms, angina and
dyspnea, were not significant).
10,18,19
1. Individual Findings
e following findings, in descending order of diagnostic accuracy (EBM Box 44.2), increase the
probability of severe aortic stenosis in patients with aortic flow murmurs: sustained apical impulse
(LR = 4.1), absent or diminished S2 (LR = 3.8), late peaking murmur (LR = 3.7), delayed carotid
artery upstroke (i.e., pulsus tardus, LR = 3.5), prolonged murmur (LR = 3), apical-carotid delay
(i.e., a palpable delay between the apical impulse and carotid impulse, LR = 2.6), brachioradial
delay (i.e., a palpable delay between the brachial and radial artery pulses, LR = 2.5), reduced
carotid artery volume (i.e., pulsus parvus, LR = 2.3), and a murmur with an added humming
quality (LR = 2.1).
e findings that decrease the probability of severe aortic stenosis in patients with aortic flow
murmurs are absence of brachioradial delay (LR = 0.04; see EBM Box 44.2), absence of an apicalcarotid delay (LR = 0.05), early systolic timing (LR = 0.1), blowing quality throughout (LR =
0.1), lack of radiation to the neck (LR = 0.1), and short duration of the murmur (LR = 0.2).
Brachioradial delay and apical-carotid delay were each investigated in only single studies and thus
require confirmation by others.
Two additional bedside findings are chest radiography (CXR) and electrocardiography (ECG).
e finding of calcification of the aortic valve on CXR detects severe stenosis with a sensitivity
of 31% to 81%, specificity of 63% to 96%, positive LR = 3.9, and negative LR = 0.5.
ventricular hypertrophy on ECG detects severe stenosis with a sensitivity of 49% to 94%, specificity of 57% to 86%, positive LR = 2.1, and negative LR = 0.5.
9,11,15,16,18,19
11,16,18,19
Left
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9—SELECTED CARDIAC DISORDERS
EBM BOX 44.2 Characteristics of Severe Aortic Stenosis (All patients
have Aortic Murmur)*
Likelihood Ratio‡
if Finding Is
Present Absent
Finding (Reference)
†
Sensitivity
(%)
Specificity
(%)
Arterial pulse
Delayed carotid artery upstroke
Reduced carotid artery volume
Brachioradial delay
14
Apical impulse
Sustained apical impulse
Apical-carotid delay
15
Heart tones
Absent or diminished S
12,17
S4 gallop
Murmur
Grade ≥3/6
Early systolic timing
Prolonged duration
Late peaking
Loudest over aortic area
Radiation to neck
Radiation to both sides of neck
Blowing quality
Humming quality
*Diagnostic standard: for severe aortic stenosis, aortic valve area <0.6 cm2/m2, 13 <0.75 cm2,
cm2,
sec.
†
Definition of findings: for late peaking murmur, murmur peaks at midsystole or beyond; for aortic area,
second right intercostal space.
‡
Likelihood ratio (LR) if finding present = positive LR; LR if finding absent = negative LR.
5,18
5
5,9,12
9,10,12,13
5,11–13
5
5
11,15
<0.9 cm2, 10; peak gradient >50 mm Hg,
5
10
5,9,11–13,16
2
11,12
5,9–13
31–91 68–93 3.5 0.4
5,10,11
44–80 65–81 2.3 0.4
97 62 2.5 0.04
78 81 4.1 0.3
97 63 2.6 0.05
44–90 63–98 3.8 0.4
29–50 57–63 NS NS
31–89 23–77 NS NS
4 61 0.1 1.6
83–94 49–84 3.0 0.2
83–91 70–88 3.7 0.2
58–75 41–73 1.8 0.6
90–98 11–51 1.4 0.1
5
50 74 1.9 NS
4 67 0.1 1.4
62 71 2.1 0.5
11,12
or aortic flow peak velocity >3.6 m/sec9 or ≥4 m/
14,16
<0.8
NS, Not significant.
SEVERE AORTIC STENOSIS
Probability
Decrease Increase
+45%+30%+15%–15%–30%–45%
LRs
0.1 0.2 0.5 12510
LRs
Absence of brachioradial delay
Absence of apical-carotid delay
Absence of transmission to neck
Murmur early peaking
Murmur short duration
Sustained apical impulse
Absent or diminished S
2
Late-peaking murmur
Delayed carotid artery upstroke
44—AORTIC STENOSIS
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373
e following findings are not helpful in identifying patients with severe aortic stenosis: narrow pulse pressure,20 fourth heart sound, third heart sound,16 reversed splitting of the second heart
sound,12 aortic ejection click,12 and intensity of the murmur (see EBM Box 44.2).
2. Why Positive LRs Are So Low
e highest positive LR for the findings listed in EBM Box 44.2 is 4.1 (i.e., sustained apical
impulse). In general, positive LRs are low when patients without disease also demonstrate the
physical finding (i.e., specificity is low and there are many false-positive results). e cause of falsepositive results in the studies of aortic stenosis is principally moderate aortic stenosis (defined as
aortic valve area of 0.8 to 1.2 cm2 or peak gradient of 25 to 50 mm Hg)*.
erefore, if “disease” is instead defined as “combined moderate-to-severe aortic stenosis,” the
positive likelihood ratios improve dramatically, especially for delayed carotid upstroke (positive
LR = 7.6, negative LR = 0.5), absent or diminished S2 (positive LR = 7.4, negative LR = 0.5),
prolonged duration of murmur (positive LR = 11.4, negative LR = 0.3), and late peaking murmur
(positive LR = 13.7, negative LR = 0.3).
5,9,12,13,21
is implies that clinicians examining patients with aortic flow murmurs can easily distinguish
patients with moderate-to-severe aortic stenosis from those with milder stenosis or no obstruction, but they have greater difficulty distinguishing severe stenosis from those with moderate
stenosis.
3. Combined Findings
One study has validated the use of combined findings in the diagnosis of aortic stenosis.11
According to this diagnostic scheme, the clinician evaluates five bedside findings and assigns the
following points: delayed carotid upstroke (3 points), diminished carotid volume (2 points), murmur loudest at right upper sternal border (2 points), single/absent second heart sound (3 points),
and calcification of the aortic valve on chest radiography (4 points).
is diagnostic scheme distinguishes moderate-to-severe aortic stenosis from other causes
of aortic flow murmurs. e probability of moderate-to-severe aortic stenosis is low with 0 to
6 points (LR = 0.2) and high with 10 to 14 points (LR = 10.6). Scores from 7 to 9 points are
unhelpful (LR not significant).
References may be accessed online at Elsevier eBooks for Practicing Clinicians.
(LR = 3.5, EBM Box 44.1) is lower than that for mild or worse aortic stenosis (LR = 10.5, EBM Box 44.1).
*is also explains why the LR for the characteristic systolic murmur in detecting severe aortic stenosis
References
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1. Vaslef SN, Roberts WC. Early descriptions of aortic valve stenosis. Am Heart J. 1993;125(5 Pt 1):
1465–1474.
2. Willius FA, Dry TJ. A History of the Heart and the Circulation. WB Saunders Co.; 1948.
3. Roberts WC, Perloff JK, Costantino T. Severe valvular aortic stenosis in patients over 65 years of age.
A clinicopathologic study. Am J Cardiol. 1971;27(5):497–506.
4. Henein MY, Xiao HB, Brecker SJD, Gibson DG. Bernheim “a” wave: obstructed right ventricular inflow
or atrial cross talk? Br Heart J. 1993;69(5):409–413.
5. McGee SR. Etiology and diagnosis of systolic murmurs in adults. Am J Med. 2010;123(10):913–921.
6. Patel A, Tomar NS, Bharani A. Utility of physical examination and comparison to echocardiography for
cardiac diagnosis. Indian Heart J. 2017;69(2):141–145.
7. Aronow WS, Schwartz KS, Koenigsberg M. Correlation of aortic cuspal and aortic root disease with
aortic systolic ejection murmurs and with mitral anular calcium in persons older than 62 years in a longterm health care facility. Am J Cardiol. 1986;58(7):651–652.
8. Loxdale SJ, Sneyd JR, Donovan A, Werrett G, Viira DJ. e role of routine pre-operative bedside echo-
cardiography in detecting aortic stenosis in patients with hip fracture. Anaesthesia. 2011;67(1):51–54.
9. Aronow WS, Kronzon I. Prevalence and severity of valvular aortic stenosis determined by Doppler echo-
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.
10. Forssell G, Jonasson R, Orinius E. Identifying severe aortic valvular stenosis by bedside examination. Acta
Med Scand. 1985;218(4):397–400.
11. Hoagland PM, Cook EF, Wynne J, Goldman L. Value of noninvasive testing in adults with suspected
aortic stenosis. Am J Med. 1986;80(6):1041–1050.
12. 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.
13. Abe Y, Ito M, Tanaka C, etal. A novel and simple method using pocket-sized echocardiography to screen
for aortic stenosis. J Am Soc Echocardiogr. 2013;26(6):589–596.
14. Leach RM, McBrien DJ. Brachioradial delay: a new clinical indicator of the severity of aortic stenosis.
Lancet. 1990;335(8699):1199–1201.
15. Chun PKC, Dunn BE. Clinical clue of severe aortic stenosis: simultaneous palpation of the carotid and
apical impulses. Arch Intern Med. 1982;142(13):2284–2288.
16. Nakamura T, Hultgren HN, Shettigar UR, Fowles RE. Noninvasive evaluation of the severity of aortic
stenosis in adult patients. Am Heart J. 1984;107(5):959–966.
17. 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.
18. Danielsen R, Nordrehaug JE, Vik-Mo H. Clinical and haemodynamic features in relation to severity of
aortic stenosis in adults. Eur Heart J. 1991;12(7):791–795.
19. Nitta M, Nakamura T, Hulgren HN, Bilisoly J, Marquess B. Noninvasive evaluation of the severity of
aortic stenosis in adults. Chest. 1987;91(5):682–687.
20. Hancock EW, Abelmann WH. A clinical study of the brachial arterial pulse form: With special reference
to the diagnosis of aortic valvular disease. Circulation. 1957;16(4):572–581.
21. Etchells E, Glenns V, Shadowitz S, Bell C, Siu S. A bedside clinical prediction rule for detecting moder-
ate or severe aortic stenosis. J Gen Intern Med. 1998;13(10):699–704.
374.e1
CHAPTER
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45
Aortic Regurgitation
KEY TEACHING POINTS
• The characteristic murmur of chronic aortic regurgitation is blowing, early diastolic, and
decrescendo in shape. It is heard best with the diaphragm of stethoscope positioned
near the lower left sternal edge and with the patient sitting up, leaning forward, and
holding his or her breath in exhalation.
• The presence of this characteristic murmur greatly increases probability of aortic regurgitation;
its absence is a compelling argument against regurgitation of moderate-to-severe degree.
• In patients with the characteristic murmur of chronic aortic regurgitation, the following
findings increase probability of moderate-to-severe regurgitation: diastolic blood pressure
≤50 mm Hg, pulse pressure ≥80 mm Hg, and a murmur of grade 3 or louder.
• In patients with the characteristic murmur of chronic aortic regurgitation, the following
findings decrease probability of moderate-to-severe regurgitation: diastolic blood
pressure >70 mm Hg and pulse pressure <60 mg.
• In comparison to chronic aortic regurgitation, the murmur of acute aortic regurgitation
(e.g., from endocarditis or acute aortic dissection) is often shorter and more likely to be
associated with tachycardia, hypotension, and narrow pulse pressure.
Introduction
I.
e principal problem in aortic regurgitation is defective closure of the aortic valve, which allows
blood to return from the aorta to the left ventricle during diastole. In patients with significant
chronic
impulse, and abnormally forceful and collapsing arterial pulses (pulsus celer).
hearts “larger than that of an ordinary ox” (the origin of the phrase cor bovinum) and the finding
during life of “violently throbbing” carotid arteries. In 1832, Sir Dominic John Corrigan, a Dublin
surgeon, taught clinicians how to diagnose the disease during life, by emphasizing the importance
of these dramatic arterial pulsations and the associated diastolic murmur.
II. The Findings
A. THE MURMUR(S)
Severe aortic regurgitation may cause three distinct murmurs: (1) the early diastolic murmur of
aortic regurgitation, (2) a systolic aortic flow murmur, and (3) the apical diastolic rumble of the
Austin Flint murmur.
regurgitation, the traditional physical findings are a diastolic murmur, dilated apical
In the 1700s, clinicians associated the postmortem finding of damaged aortic valves with
1,2
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9—SELECTED CARDIAC DISORDERS
1. Early Diastolic Murmur of Regurgitation
e most important physical sign of aortic regurgitation is the early diastolic murmur, which is
blowing, high-f requency, and decrescendo in shape (see Chapter 43)
LubP
EW
WW
WW
WW
e murmur may occupy all of diastole or just its early part.3 Pressing firmly against the
chest wall with the diaphragm of the stethoscope brings out the murmur, which is usually
loudest in the left parasternal area at the third or fourth intercostal space. In some patients,
the murmur is only audible when the patient sits up, leans forward, and holds his or her
breath in exhalation.
2. Systolic Aortic Flow Murmur
Severe aortic regurgitation also produces a short systolic aortic flow murmur, which results from
ejection over the aortic valve of the large stroke volume characteristic of the disease. e combination of this murmur and the early diastolic one causes a characteristic “to-fro” sound near the
sternum (see Chapter 43)
WW
WW
WW
Lub SHSHSH P
EW
is murmur may superficially resemble that of aortic stenosis, although the flow murmur of
pure regurgitation is shorter and associated with the peripheral pulse findings of severe regurgitation (see later).
3. Apical Diastolic Rumble: Austin Flint Murmur
a. Definition
e Austin Flint murmur is a diastolic rumbling murmur heard at the apex in patients with severe
aortic regurgitation, which resembles mitral stenosis even though the mitral valve is completely
normal. It was first described by the American physician Austin Flint in 1862.
e Austin Flint murmur is found in up to 60% of patients with moderate or severe aortic
regurgitation but is rarely heard in mild aortic regurgitation.
5,6
Austin Flint called his murmur
4
presystolic, but by this he meant it was loudest before S1 and thus different from the murmur of
aortic regurgitation, which began immediately after S2 and tapered off during diastole. About half
of Austin Flint murmurs have two diastolic components (mid-diastolic and presystolic), whereas
the other half have just a presystolic component.
6,7
b. Pathogenesis
e cause of the Austin Flint murmur is still debated. Although all hypotheses assume the
murmur depends on a strong regurgitant stream of blood being directed back toward the left
ventricle during diastole, these hypotheses differ in how this regurgitant stream causes an
apical rumbling sound. Proposed mechanisms include fluttering of the anterior leaflet of the
mitral valve, premature closure of the mitral valve from elevated left ventricular end-diastolic
pressure, collision of the regurgitant stream with the anterior mitral leaflet, ventricular vibrations caused by the regurgitant stream itself, and harmonic distortion of the aortic regurgitant
murmur.
6,8–10
Many of these mechanisms may operate together to create the sound.11 An
instructive video showing the blood flow responsible for the Austin Flint murmur is available
in the reference by Weir.
12
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377
B. WATER HAMMER PULSE AND INCREASED PULSE PRESSURE
Because of the large stroke volume and diastolic emptying of aortic blood into the left ventricle
(i.e., aortic runoff ), the arterial pulse wave of aortic regurgitation rises suddenly and collapses
abruptly. is abnormality has many names, although the most common ones are collapsing
pulse, Corrigan pulse, or the water hammer pulse.* In most patients with aortic regurgitation,
the collapsing pulse becomes more prominent as the examiner elevates the patient’s wrist.
13,14
is occurs because elevation of the arm with respect to the heart reduces the diastolic pressure in that arm, causing the vessel to collapse more completely with each beat. (e pounding
sensation of the water-hammer pulse is identical to the sensation felt by the examiner when
palpating a person’s blood pressure, with the cuff pressure just above the person’s diastolic pressure; see Chapter 17.)
C. ABNORMAL PULSATIONS OF OTHER STRUCTURES: THE
AORTIC REGURGITATION EPONYMS
e large stroke volume and aortic runoff of aortic regurgitation may induce pulsations in other
parts of the body, which has generated many eponyms of what is fundamentally a single physical finding (the number of eponyms for aortic regurgitation rivals those of some neurologic
reflexes).
capillary pulsation, best elicited by blanching a portion of the nail and then observing the
pulsating border between the white and red color (Quincke capillary pulsations, described
in 1868, although Heinrich Quincke should be known instead for inventing the lumbar puncture); (2) an anterior-posterior bobbing of the head, synchronous with the arterial pulsations
(de Musset sign, named after the French poet Alfred de Musset, who was afflicted with aor-
tic regurgitation)19; (3) alternate blanching and flushing of the forehead and face (lighthouse
sign); (4) pulsations of organs or their parts, including the uvula (Müller sign, 1899), retinal
arteries (Becker sign), larynx (Oliver-Cardavelli sign), spleen (Sailer sign, 1928),20 and cervix
(Dennisons sign).
simply as an interesting observation, not one of particular diagnostic value. Excellent videos of
patients with bounding carotids,22 Quincke pulse,
1,15–18
ese various bobbings include the following: (1) an abnormally conspicuous
21,†
In many of the original descriptions of these eponymous findings, the sign was presented
23,24
and Müller sign25 are available.
D. HILL TEST
In 1909, Leonard Hill of Britain observed that patients with severe aortic regurgitation often have
a systolic pressure in the foot that is much greater than a simultaneously measured systolic pressure
in the arm.
26,27
e Hill test specifically refers to the systolic pressure of the foot minus that of the
arm (in the supine patient). e correct technique for measuring the pressure in the foot is to wrap
the arm cuff around the patient’s calf and to measure the systolic pressure in the dorsalis pedis and
posterior tibial arteries by palpation. e higher of these two pressures is the “foot pressure.”
*
Corrigan actually emphasized the exaggerated visible pulsations of aortic regurgitation, not the palpable
ones. e term water hammer pulse was coined in 1836 by Sir omas Watson, who likened the pulse to a
Victorian toy called a water-hammer, which imparted to a child’s hands the same sensation of a collapsing
pulse of aortic regurgitation.
†
e eponym does not necessarily indicate priority: Sailor gave credit for the pulsating spleen to Tulp of the
1600s,20 and Dennison gave credit for the pulsating cervix to Shelly, one of his house officers.
2
21
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9—SELECTED CARDIAC DISORDERS
E.
AUSCULTATION OVER ARTERIES
Two auscultatory findings may appear over the peripheral arteries of patients with aortic regurgitation: pistol shot sounds and Duroziez murmur (or Duroziez sign).
Pistol Shot Sound
1.
a. Definition
Pistol
shot sounds are short, loud, snapping sounds with each pulse, heard over the femoral,
brachial,
or radial arteries. ey are identical in quality to the Korotkoff sounds heard when
measuring blood pressure. Pistol shot sounds are heard with only light pressure of the stethoscope
and, like the water hammer pulse, may first appear only after elevation of the patient’s arm.
Pistol shot sounds were first described by Traube in 1872.
b. Pathogenesis
Pistol
shot sounds occur because of sudden expansion and tensing of the walls of the vessels
during
systole. Consequently, they are not only associated with the collapsing pulses of aortic
regurgitation but also are inducible in normal individuals by administering intravenous vasodilator
medications.
chute suddenly fills with wind.
30
e sounds are analogous to the loud, snapping notes heard when a sail or para-
31
e quicker the vessel dilates, the louder the note, and in patients
28,29
14
with aortic regurgitation, the intensity of the pistol-shot sound correlates with the height of the
pulse pressure
2.
Duroziez Murmur or Sign
a. Definition
e Duroziez sign is a double to-fro murmur heard over the brachial or femoral artery. It is heard only
with firm pressure from the stethoscope. For the Duroziez sign to be positive, both a systolic and diastolic
murmur must be present (many normal persons develop systolic murmurs with pressure on the stetho-
32
and the change in pressure over time (dP/dt) of the pulse.
15,28,33–36
30
scope). e diastolic component often becomes louder with pressure applied distal to the stethoscope.
Although some claim the Duroziez murmur also may occur in normal individuals who have
increased flow because of fever, anemia, or peripheral vasodilatation,
33
the vascular sound produced in these conditions does not have the characteristic to-fro sound of the Duroziez murmur,
but instead resemble the continuous murmur of an arteriovenous fistula.
35
PuSHSHSHSHPuSHSHSHSHSHSHSH
Duroziez described his “double intermittent murmur” in 1861.
b. Pathogenesis
e diastolic component of Duroziez sign results from the blood actually reversing directions in
the artery during diastole.
III. Clinical Significance
A. DETECTING AORTIC INSUFFICIENCY
34,35
e presence of the characteristic early diastolic murmur of aortic insufficiency greatly increases
the probability that an aortic leak is actually present (likelihood ratio [LR] = 10.1, EBM Box
45.1). Although some patients with mild regurgitation have no murmur, the absence of the char-
acteristic murmur greatly decreases the probability of moderate-to-severe aortic regurgitation
(LR = 0.1, EBM Box 45.1).
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