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326 CHAPTER 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts
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FIG. 8-41 Anatomic Basis for Cardiac Murmurs II. Same symbols as in Fig. 8-40.
A2 is soft or absent at the apex. If the valve is stenotic but not calcied (as
in congenital aortic stenosis), S2 may split during expiration (paradoxically)
reecting delayed aortic valve closure (Fig. 8-38). Normal inspiratory splitting of S2 suggests mild stenosis. When a stenotic valve remains exible, an
ejection or early systolic click, caused by doming of the valve, precedes the
murmur in early systole, but disappears when the valve calcies. An apical S4
is common. Precordial Thrust: Left ventricular hypertrophy accentuates the
precordial apical thrust. In the left lateral decubitus position, a double apical
Cardiovascular Signs 327
A.
B.
C.
D.
E.
F.
G.
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Normal arterial
waves
Dicrotic pulse
Bounding pulse
Tardus pulse
(Plateau pulse)
Pulsus alternans
Bigeminy
Inspiration
Pulsus paradoxus
FIG. 8-42 Arterial Pulse Contour. A. Normal pulse contour. B. Dicrotic pulse. C. Bounding or collaps-
ing pulse. D. Tardus or Plateau pulse. E. Pulsus alternans. F. Bigeminal pulse. G. Pulsus paradoxus.
thrust is sometimes felt, the rst impact reects atrial contraction, the second
reects LV systole. Arterial Pulse: Severe aortic stenosis produces a slowly rising carotid pulse contour (tardus or anacrotic pulse, Fig. 8-42D) felt as a sustained
push rather than the normal brief tap. Decreased pulse amplitude is often palpable, but it is best assessed by calculating pulse pressure. Physical ndings
do not reliably assess the severity of aortic stenosis.
can be asymptomatic until severe, when exercise induces dyspnea, angina, or
syncope. The most common etiologies are rheumatic valvulitis, valve sclerosis,
and congenital bicuspid valve. X-ray Findings: Aortic valve calcication may
be seen on plain chest radiographs.
rosis without stenosis is shorter and accompanied by normal heart sounds at
the base. The apical systolic murmur of MR has a blowing quality and is often
holosystolic. A systolic diamond-shaped murmur occurs with both valvular
and subvalvular stenosis.
Hypertrophic obstructive cardiomyopathy (IHSS). Asymmetric LV hyper-
trophy with prominent hypertrophy of the basal interventricular septum is
associated with dynamic outow obstruction starting shortly after the onset
of systole. Obstruction is caused by apposition of the anterior mitral leaet to
the hypertrophied septum. Mitral insufciency may occur as well. A family
Symptoms: Aortic stenosis
DDX: The systolic murmur of aortic scle-
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history of autosomal dominant inheritance is often present. Unexplained
sudden deaths in the family suggests hypertrophic cardiomyopathy with
or without obstruction. Palpation: The apical impulse is often double. The
Murmur:
at the apex and left sternal border. It is less intense in the right second interspace and usually does not radiate to the carotids. At the apex, the murmur
may have a blowing holosystolic quality, like MR. The murmur varies with
LV end-diastolic volume, peripheral resistance, and contractility. The outow obstruction and murmur are intensied by reducing LV end-diastolic
volume by standing and/or the Valsalva maneuver, conversely the valvular
aortic stenosis murmur becomes softer. Raising diastolic blood pressure by
handgrip reduces the dynamic obstruction and murmur. Squatting or lifting
the legs increases venous return and LV end-diastolic volume, reducing the
obstruction and murmur.
upstroke in contrast to the diminished and delayed pulse of valvular stenosis.
A double peaking or bisferiens pulse may be present. Heart Sounds: As in
valvular stenosis, an S4 is frequent. There is no systolic ejection click with
subaortic stenosis. Symptoms: The symptoms are identical to those of severe
valvular stenosis. The diagnosis is conrmed by echocardiography.
Supravalvular aortic stenosis. This rare congenital anomaly results from narrowing of the ascending aorta or a small-holed diaphragm distal to the valve.
It produces most of the signs of valvular stenosis, but A2 is accentuated and
the carotid murmurs are unusually loud. The nding of a systolic blood pressure that is >10 mm Hg greater in the right arm than the left is typical of
supravalvular aortic stenosis.
A systolic ejection murmur beginning well after S1 is best heard
Arterial Pulse: The arterial pulse wave has a sharp
Aortic valve sclerosis. Aortic sclerosis is caused by leaet thickening and
calcication (sclerosis) without signicant obstruction (stenosis). A mediumpitched murmur of moderate intensity is heard in the aortic region and may
be heard at the apex. It is often brief, conned to early systole, and is usually softer than an aortic stenosis murmur. The murmur may be faintly heard
in the carotids. A2 is usually present at the apex. DDX: Because the murmur is seldom loud or long or accompanied by an abnormal carotid pulse,
it shouldn’t be confused with aortic stenosis. Preservation of A2 at the apex
speaks against severe calcic aortic valvular stenosis.
Valvular pulmonic stenosis. Pulmonary stenosis is usually congenital,
alone or with the tetralogy of Fallot. It can be acquired with carcinoid tumors.
A diamond shaped ejection murmur is loudest in the second left interspace
(Figs. 8-39C and 8-40E). Its intensity, conguration, and pitch resemble an
aortic stenosis murmur, but its intensity increases with inspiration. Carotid
transmission may occur (left > right). Slow RV ejection delays P2 widely
splitting S2. Lower pulmonary artery pressure reduces the intensity of P2
(Figs. 8-20 and 8-39C). An early ejection click indicates valvular rather than
infundibular stenosis. An accentuated precordial thrust or sternal lift indicates RVH. DDX: The murmur resembles the pulmonary ow murmur of an
ASD, but P2 is not diminished with ASD.
Infundibular pulmonic stenosis. The infundibulum is the funnel-shaped
portion of the right ventricular chamber leading to the pulmonary artery.
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Congenital narrowing produces a form of pulmonic stenosis. In contrast to
valvular stenosis, the ejection murmur and the systolic thrill are usually in the
third left interspace and there is no ejection click. Although this lesion may
be isolated, it is usually accompanied by a VSD, as in the tetralogy of Fallot.
Ostium secundum ASD.
genital left-to-right interatrial shunt, causes the high-volume, high-velocity
ow across the pulmonic valve (Fig. 8-41A). A medium-pitched murmur is
heard in the second or third left interspace with maximum intensity a little
before mid-systole (Fig. 8-39E). This murmur is sometimes accompanied by
a low-pitched diastolic ow murmur along the lower left sternal border from
increased ow through the tricuspid valve. S2 is widely split, and usually the
split is xed. P2 is not diminished.
able from pulmonic stenosis. Compared to pulmonic stenosis, it is usually
lower pitched, peaks earlier in systole, and rarely becomes as loud.
Ostium primum ASD. The congenital opening in the interatrial septum is
near the AV valves and often associated with a cleft mitral valve leaet. There
is a harsh systolic murmur at left sternal border and, if MR is present, an
apical systolic murmur transmitted to the axilla. Sometimes a mid-diastolic
murmur is heard at the lower left sternal border. S2 is accentuated with xed
splitting during inspiration and expiration. The right ventricular impulse is
prominent. If MR is present, the LV apical impulse may be accentuated and
laterally displaced.
Coarctation of the aorta. See also Coarctation of the aorta, page 368. The
coarctation is in the descending aorta, so the murmur is heard best in the
posterior interscapular area, and faintly heard, if at all, on the anterior chest.
A continuous bruit can sometimes be heard over the sternum from the dilated
internal mammary arteries.
Ventricular septal defect. Congenital VSDs occur alone and in Eisenmenger
and Fallot syndromes. Blood ows from the high pressure left ventricle into
the much lower pressure right ventricle through an opening in the interventricular septum (Fig. 8-41B). VSD is more common in the membranous than
muscular septum. The high-pitched murmur is typically pansystolic with
peak intensity in the fourth and fth left interspace. It may be transmitted
over the entire precordium and to the interscapular region. With muscular
septal defects, the murmur may not persist throughout systole. The intensity
and harshness diminish and the midsystolic accentuation is lost when pulmonary hypertension supervenes. Loud murmurs may be accompanied by a
thrill. When the defect is large S2 may be accentuated. DDX: With pulmonary
hypertension, imaging may be needed to distinguish VSD from persistent
ductus arteriosus. Faint murmurs must be distinguished from benign systolic murmurs. VSD may complicate MI, typically at the cardiac apex; large
acquired defects are rapidly fatal.
Overlling of the right ventricle, due to a con-
DDX: The murmur may be indistinguish-
Tricuspid regurgitation (TR). Right ventricular contraction produces back-
ow of blood into the right atrium and major veins, with a pulsatile increase
in CVP (Fig. 8-41H). Faint murmurs are in early systolic, loud murmurs are
heard throughout systole, both augmenting with inspiration. They are high
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pitched and blowing, best heard with the diaphragm. Maximum intensity is
along the lower left sternal border and may be sharply localized or transmitted to the apex. Right ventricular hypertrophy may be present with a palpable right ventricular precordial thrust. When severe, tricuspid insufciency
produces engorged neck veins with prominent v-waves and hepatic pulsation. There are no characteristic heart sound changes.
maximum intensity, large jugular v-waves, and augmentation with inspiration is diagnostic. Congenital TR occurs with Ebstein anomaly. It is acquired
in rheumatic heart disease, right ventricular failure, endocarditis, carcinoid
tumor, and pulmonary embolism.
Mitral regurgitation. MR results from myxomatous degeneration of the
valve, endocarditis, rheumatic valvulitis, ruptured chordae, papillary muscle
ischemia or rupture, MI, and a dilated mitral valve ring due to LV dilatation. Blood ows back through the mitral orice at almost constant velocity
throughout systole (Fig. 8-41F). With severe MR, the left ventricle empties
prematurely, so A2 is early, widely splitting S2.
this loud high-pitched murmur with maximum intensity at the apex begins
with S1, continues throughout systole, and ends at or near S2 (Fig. 8-39H).
However, many variations occur. The murmur may mask S1, begin with S1
and decrescendo to end in early-to-mid systole, or begin in mid-to-late systole
and crescendo to end with, or even after, S2. Faint murmurs are well localized; loud murmurs are transmitted to the axilla. Eccentric jets may produce
murmurs with radiation to the base and carotids, or to the lung bases and
spine. There is insignicant variation with phases of respiration or rhythm
irregularities. A rumbling diastolic murmur from the increased ow volume
across the mitral valve may be heard.
difcult to appreciate being embedded in the murmur. S2 is widely split with
severe regurgitation. A2 may be difcult to appreciate at the apex being lost in
the terminal portion of the murmur. An S3 is sometimes heard with moderate
or severe MR.
thrust suggest LV hypertrophy and dilatation, respectively. An increased left
parasternal thrust or lift may reect the enlarged left atrial systolic rather than
right ventricular disease. DDX: The murmur must be distinguished from aortic stenosis which is often loud at the apex as well as at the base. Comparison
of the duration and quality at the apex and base differentiates the two.
Palpation: Accentuation and lateral displacement of the apical
Heart Sounds: S1 is often diminished or
DDX: The location of
The Murmur: Classically,
Mitral valve prolapse—midsystolic click and apical late systolic murmur.
The valve undergoes myxomatous degeneration, producing redundant leaflet tissue (especially the posterior leaet), an enlarged valve annulus, and
elongated chordae tendineae. As the ventricular volume decreases during
systole, one or more valve leaet scallops billow, prolapsing backward into
the atrium and losing coaptation with resultant MR.
of the population, more frequently in women. It can be inherited, probably
as an autosomal dominant with reduced expression in males.
The systolic crescendo murmur is heard best at the apex in mid to late systole.
It is usually short, relatively high pitched, and blowing, persisting into S2. It
may transmit to the back left of the spine. In unusual cases, it is described as
cooing, honking, or whooping. It may be inaudible or so loud as to be heard
without a stethoscope. It typically moves closer to S1 on standing (decreased
venous return, smaller LV volume) and becomes shorter and later in systole
This occurs in 2% to 5%
The Murmur:
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when squatting or recumbent (increased venous return, larger LV volume).
Auscultation during a Valsalva maneuver while erect may reveal a murmur
inaudible at rest with the patient supine. Heart Sounds: A clicking sound is
sometimes heard during mid-systole, coincident with the onset of the murmur; the click may occur without a murmur. Associated Dysrhythmias:
Ventricular premature beats, paroxysmal atrial tachycardia, atrial brillation,
sinus bradycardia, periods of sinus arrest, and positional atrial utter may all
occur in association.
Noncardiac Signs: The incidence of chest wall abnor-
malities is increased, particularly pectus excavatum. Mitral valve prolapse is
common in Marfan syndrome. Symptoms: Most persons are asymptomatic.
A minority develop easy fatigue, shortness of breath, nonanginal chest pain,
palpitation, or syncope. Complications: There is an increased relative risk
for cerebral transient ischemic attacks, chordae tendineae rupture, congestive
cardiac failure, endocarditis, and sudden death, though these are rare.
Ruptured interventricular septum, papillary muscle, or chordae tendineae. Sudden appearance of a loud pansystolic murmur and hemody-
namic shock suggests rupture of the interventricular septum, a chorda
or papillary muscle, or severe papillary muscle dysfunction. There may
be a precordial thrill; severe pulmonary edema occurs with chordae or
papillary muscle injury. The murmur is usually grade II-IV/VI; however, severe mitral insufciency can be associated with a surprisingly
soft murmur. When the septum ruptures, there are signs of right-sided
failure, low cardiac output, and poor peripheral perfusion. Prompt recognition and treatment can be lifesaving.
Diastolic Murmurs: Early, mid, and late diastolic murmurs are almost always
pathologic and reect valve leaet dysfunction. Flow from the aorta or pulmonary artery back into a ventricle results in a diastolic regurgitant murmur
beginning with S2 that may persist throughout diastole. The diastolic murmur of mitral stenosis does not start with S2 because ventricular pressure
continues to fall after S2 until it becomes less than atrial pressure (the period
of isovolumic relaxation).
Aortic regurgitation (aortic insufciency). Flow driven by the decreas-
ing transvalvular pressure gradient from early to late diastole produces the
decrescendo murmur. The high pitch is caused by blood being forced through
a relatively small orice at high pressure (Fig. 8-40D). The Murmur: The
high-pitched blowing decrescendo murmur immediately follows S2; it may
not last throughout diastole (Fig. 8-39B). The murmur is best heard with the
diaphragm held rmly against the chest while the patient is leaning forward
in full expiration. The point of maximum intensity is in the right second or
left third interspace. There is often an accompanying aortic systolic murmur.
Transmission down the right rather than the left sternal border suggests aortic
root aneurysm. Heart Sounds: S1 is usually normal; A2 may be accentuated.
Palpation: Accentuation and lateral displacement of the apical thrust sug-
gest LV hypertrophy and dilatation.
ing quality. Vasodilatation, high pulse pressure, and pistol-shot sounds may
be found. Nailbed pulsation is easily seen. DDX: The quality and location
do not distinguish aortic from pulmonic regurgitation, but maximal intensity in the aortic area, an accentuated and displaced apical thrust, increased
Arterial Pulse: The pulse has a collaps-
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pulse pressure, brisk carotid upstrokes, pulsus bisferiens, and Duroziez sign
all favor AI. Common causes are rheumatic valvulitis, congenitally bicuspid
aortic valve, and endocarditis. Marfan syndrome, aortic dissection, sinus
of Valsalva aneurysm, and aortic valve annular ectasia are less common.
Syphilitic aortitis is increasingly uncommon.
Pulmonic regurgitation. Most commonly the result of pulmonic valve ring
dilation in pulmonary hypertension which leads to backow of blood from
the pulmonary artery into the right ventricle resulting in RV volume and pressure overload (Fig. 8-40F).
in quality and timing from aortic regurgitation, it is usually softer and transmits less widely (Fig. 8-39D). The point of maximum intensity is in the second or third left interspace. In the absence of pulmonary hypertension, the
murmur is medium to low pitched. Heart Sounds: P2 may be accentuated.
Palpation: A right ventricular precordial thrust may be palpable. Pulmonary
valve regurgitation occurs with pulmonary hypertension of any cause (mitral
stenosis, left-sided heart failure, pulmonary emphysema, idiopathic pulmonary hypertension, congenital heart lesions, obstructive sleep apnea, chronic
pulmonary emboli) and after pulmonary valvotomy.
Tricuspid stenosis. Tricuspid stenosis results from rheumatic valvulitis, con-
genital heart disease, and carcinoid tumors. Right atrial contraction against
the stenotic valve orice causes presystolic accentuation of the murmur and
giant a-waves in neck veins. Impedance to right ventricular lling leads
to elevated CVP (Fig. 8-41G). The Murmur: The diastolic murmur is low
pitched and rumbling and has a presystolic crescendo when atrial brillation is absent. It is best heard with the bell lightly placed. When stenosis is
mild, the murmur is late diastolic. With increasing severity, it is heard in mid
and even early diastole. Increased venous return during inspiration accentuates the murmur.
gressively increases as stenosis worsens. Heart Sounds: S1 is accentuated.
Sometimes a tricuspid opening snap is identied. Palpation: The point of
maximum intensity is sharply localized at the lower-left sternal border in the
fourth or fth interspace. In severe stenosis, signs of central venous congestion (elevated CVP, hepatomegaly, ascites, edema) are found, mimicking right
ventricular failure.
of mitral stenosis by its location and inspiratory accentuation. The diastolic
rumble accompanying severe TR or a large ASD identical to the mid-diastolic
rumble of tricuspid stenosis.
Venous Pulse: Giant a-waves are present. The CVP pro-
The Murmur (Graham Steell): Indistinguishable
DDX: The murmur can usually be distinguished from that
Mitral stenosis. In mild mitral stenosis ventricular lling is minimally
delayed and the period of rapid lling shortens, resulting in a mid-diastolic
murmur. With moderate or severe stenosis, ventricular lling is prolonged,
so atrial systole increases the pressure gradient across the valve, producing a
presystolic crescendo murmur. The accentuated S1 results from thickened but
exible leaets. Pulmonary hypertension produces the accentuated P2. The
opening snap is attributed to thickened but exible leaets, tethered at their
commissures, bulging into the left ventricle when atrial pressure exceeds LV
pressure; the snap is absent with immobile leaets (Fig. 8-41E). The Murmur:
This low-pitched rumbling murmur is heard best in the left lateral position
near the apex. It is usually sharply localized, so the bell must be placed lightly
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directly on the apex. Sometimes, a loud murmur is discovered only by carefully inching the bell over the entire apex. In mild stenosis the murmur is middiastolic. As the orice narrows, the murmur starts earlier and ends later, until
it is almost pandiastolic. There is always a pause after S2 before the murmur
begins. A long murmur often has a presystolic crescendo (Fig. 8-39G). Heart
Sounds:
If there is pulmonary hypertension, P2 is accentuated and occurs early but
is still delayed by inspiration. When the murmur is loud, there is usually
a mitral opening snap shortly after A2, heard best at the left sternal border
between the second and fourth interspaces. This is commonly mistaken for a
split S2. The opening snap disappears when the mitral cusps become calcied
and rigid.
in the left decubitus position. There is often a palpable right ventricular thrust
indicating right ventricular hypertrophy.
similar murmur that is localized nearer the sternum. A similar diastolic apical rumble may be heard with increased mitral diastolic ow due to severe
MR. The apical diastolic murmurs of aortic and pulmonic regurgitation have
a blowing, not rumbling quality. Congenital stenosis is rare. Mitral stenosis
nearly always results from rheumatic heart disease.
Aortic insufciency. The Austin Flint or aortic insufciency murmur is often
associated with uttering of the anterior mitral valve leaet. However, neither this phenomenon nor others accompanying chronic aortic regurgitation
seem consistently to correlate with this apical diastolic murmur. Authors vary
on the criteria for diagnosis; the methods of Levine and Harvey are cited here.
Some patients with severe AI and normal mitral valves have a murmur at the
cardiac apex similar in pitch and timing to mitral stenosis. The examiner confronted with a combination of aortic and mitral murmurs must decide if the
mitral valve is normal. AI is caused by rheumatic valvulitis, syphilis, or acute
endocarditis.
The mitral valve opening snap is absent in the Flint murmur.
S1 at the apex is accentuated if the thickened leaets are mobile.
Palpation: The murmur is often accompanied by a thrill at the apex
DDX: Tricuspid stenosis produces a
DDX: Accentuation of S1 or P2 favors organic mitral stenosis.
Continuous Murmurs: Murmurs heard throughout the cardiac cycle indicate
turbulent ow occurs without interruption. Therefore, ow must be from a
continuous high-pressure source to a low-pressure sump, e.g., from the aorta
to the pulmonary artery or a vein, or across a xed obstruction in the aorta.
Ductus arteriosus. A persistent ductus arteriosus is an arteriovenous stula
between the aorta and pulmonary artery (Fig. 8-41C) producing a continuous murmur throughout the heart cycle. The higher aortic pressure during
ventricular systole increases the murmur's pitch. Uncorrected, the increased
PA pressure leads to RVH and eventually right-to-left shunting with peripheral cyanosis conned to the lower extremities (Eisenmenger physiology).
Murmur: A murmur heard in the rst and second left interspace through-
out systole and diastole is usually caused by a persistent ductus. The murmur is medium pitched and rough, heard with the bell and diaphragm.
Louder murmurs are harsh. There is typically a late systolic crescendo and a
decrescendo after S2 producing a machinery murmur (Fig. 8-39F). Most frequently, transmission is to the interscapular region; occasionally it transmits
down the left sternal border, sometimes to the apex. As pulmonary artery
pressures approach aortic pressures, the murmur’s diastolic portion may
The
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disappear. Pulmonary hypertension may lead to TR. Increased mitral ow
can produce a diastolic rumble simulating mitral stenosis.
may be buried in the crescendo portion of the murmur. There is frequently
a short pause between S1 and the murmur. Palpation: The precordial thrust
of both ventricles can be accentuated.
the peripheral pulse can have a collapsing quality like AI.
in the toes but sparing the ngers is seen with persistent right to left shunt
in Eisenmenger physiology. The continuous murmur must be distinguished
from a venous hum.
Coarctation of aorta. See Coarctation of the aorta, pages 329 and 368.
Coronary arteriovenous stula and ruptured sinus of Valsalva aneurysm.
These conditions present similarly with a continuous mid-precordial murmur; imaging is needed for differentiation. The Murmur: A continuous murmur with late systolic accentuation (machinery or to-and-fro) is audible on
either or both sides of the lower sternum, often accompanied by a systolic or
continuous thrill. DDX: Although the to-and-fro murmur has the same quality as that in ductus arteriosus, the location is sufciently different to be distinctive. A mid-precordial to-and-fro murmur can occur with the combination
of VSD and aortic regurgitation, but the quality of the systolic and diastolic
components is distinct and there is no late systolic accentuation. Although a
venous hum may be audible behind the upper sternum, its accentuation is
diastolic, and it is abolished by pressure on the internal jugular vein.
Vascular Signs of Cardiac Activity: LV contraction maintains arterial blood
pressure and produces palpable pulsations in all accessible arteries. Right
atrial and ventricular contractions generate venous pulsations in the upper
body. Because arterial pressure is normally ~16 times higher than CVP, arterial pulsations are palpable whereas venous pulsations are not. This is useful
in determining the origin of visible pulsations.
Arterial Pulses: With large shunts
Heart Sounds: S2
DDX: Clubbing
Pulse contour and volume. The systolic arterial pressure contour is a function
of aortic compliance, LV stroke volume, and the rate of ow from LV to aorta.
These, in turn, are inuenced by LV contractility and the size of the aortic
valve orice and LV outow tract. The diastolic pressure contour reects the
run off during each cardiac cycle. The carotid pulse most accurately reects
the contour of the normal pulse contour and volume alterations are diagnostically signicant.
Normal arterial pulse. The palpable primary wave is a swift upstroke to the
peak systolic pressure, followed by a more gradual decline. A smaller upstroke caused by blood rebounding off the closed aortic valve, the dicrotic
wave, occurs near the end of ventricular systole but is not usually palpable
(Fig. 8-42A).
Twice peaking (dicrotic) pulses. There are two types of twice peaking arterial pulses (Fig. 8-42B). Most common is pulsus bisferiens with two palpable
waves during systole. Less common is the dicrotic pulse, which has one wave
palpable in systole and a second in diastole.
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CLINICAL OCCURRENCE: Pulsus Bisferiens: Severe aortic regurgitation
especially when associated with moderate aortic stenosis, hypertrophic subaortic stenosis, and hyperkinetic circulatory states, e.g., hyperthyroidism;
Dicrotic Pulse: Very low cardiac output as with dilated cardiomyopathy or
cardiac tamponade, especially in patients with normal aortic compliance.
Bounding or collapsing pulse (Corrigan pulse, water-hammer pulse). A large
stroke volume and/or vigorous LV contraction generates a steep pulse upstroke followed by rapid decline as blood runs off from the aorta. With high
pulse pressure the upstroke may be very sharp, whereas the down slope is
precipitous (Fig. 8-42C). It may be accompanied by the pistol-shot sound.
This is encountered in hyperthyroidism, anxiety, aortic regurgitation, persistent ductus arteriosus, and arteriovenous stula.
Plateau pulse (pulsus tardus). Characteristic of severe aortic stenosis, the
upstroke is gradual, and the peak delayed toward late systole (Fig. 8-42D).
Carotid palpation reveals gentle, sustained lifting movements in contrast to
the normal brief pulsatile tapping.
Absent pulses, pulseless disease. See Takayasu Aortitis, page 362.
Bigeminy (coupled rhythm). A normal beat is followed by a premature beat
and a pause (Fig. 8-42F). If the premature beat occurs with a very short coupling interval so that ventricular lling is incomplete, it has a smaller stroke
volume than the preceding normal beat and may not produce a palpable arterial pulsation and the radial pulse rate appears to be half the ventricular rate.
This is detected by auscultating the rhythm over the precordium.
Pulsus alternans. Greater and lesser volume pulse waves alternate despite a
normal rhythm and constant rate (Fig. 8-42E) signaling LV dysfunction. This
may not be palpable but is detected while auscultating the blood pressure: as
the cuff is slowly deated every other beat becomes audible rst, then, with
further deation, the rate appears to double as all beats are heard.
must be distinguished from bigeminal rhythm, in which a normal beat is followed by a premature beat.
Pulsus paradoxus. Normally, inspiration decreases intrathoracic pressure in-
creasing venous blood ow into the chest and right ventricle, decreasing LV
lling. The result is a small decrease in LV stroke volume and systolic blood
pressure. In pericardial tamponade total heart volume (pericardial sac and
chambers) is xed. With inspiration the right heart volumes expand, bulging
the septum leftward, resulting in further compromise of left heart volumes, exaggerating the fall in LV stroke volume and systolic arterial pressure. Labored
breathing associated with exacerbations of obstructive airway disease also
produces a paradoxical pulse. Under normal resting conditions the inspiratory
fall in arterial systolic pressure is <10 mm Hg. A paradoxical pulse exists when
inspiration creates a >10-mm-Hg drop in systolic arterial pressure. This is detected while auscultating blood pressure. Sometimes the exaggerated pulse
volume swings can be palpated (Fig. 8-42G). Pericardial tamponade, pulmonary emphysema, and severe asthma are causes. DDX: In AV asynchrony
pulse volume is variable so pulsus paradoxus cannot be accurately assessed.
DDX: This
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