Inspection and Palpation of Venous and Arterial Pulses

American Heart
Fighting Heart Disease
and Stroke
Inspection and Palpation
of Venous and Arterial
Examination of the Heart
Part 2
Examination of the Heart
Inspection and Palpation of
Venous and Arterial Pulses
Prepared on behalf of the
Council on Clinical Cardiology
of the American Heart Association
Michael H. Crawford, MD
Robert S. Flinn Professor of Medicine
Chief, Division of Cardiology
University of New Mexico School of Medicine
Albuquerque, New Mexico
Based on a text prepared by
Noble O. Fowler, MD, in 1978
Part 2
Examination of the Heart
A Series of Booklets
Part 1
The Clinical History
Mark E. Silverman, MD
Part 2
Inspection and Palpation of
Venous and Arterial Pulses
Michael H. Crawford, MD
Part 3
Examination of the Precordium:
Inspection and Palpation
Robert C. Schlant, MD, and J. Willis Hurst, MD
Part 4
Auscultation of the Heart
James A. Shaver, MD, James J. Leonard, MD,
and Donald F. Leon, MD
Part 5
The Electrocardiogram
Masood Akhtar, MD
Available from your local American Heart Association
©1972, 1978, 1990 American Heart Association
1 Cervical Veins
Patient Position
Separating Venous and Arterial Pulsations
Pathologic Findings
Increased Pressure
Prominent a Waves
Prominent v Waves
Cannon a Waves
Constrictive Pericarditis
Hepatojugular Reflux Test
15 Arterial Pulses
Pathologic Findings
Differences in Peripheral Pulses
Hyperkinetic Pulse
Pulsus Bisferiens
Hypokinetic Pulse
Pulsus Parvus et Tardus
Dicrotic Pulse
Pulsus Alternans
Pulsus Paradoxus
Special Tests
Allen’s Test
Valsalva’s Maneuver
Cervical Veins
As seen in Figure 1, the internal jugular veins arise from the transverse
sinuses in the posterior compartment and descend from the jugular
foramina at the base of the skull. They course down the sides of the neck,
lateral to the internal carotid artery in the superior part of the neck, then
anterior to the common carotid artery at the base of the neck, where they
join the subclavian veins to form the innominate veins. The left internal
jugular vein is usually smaller than the right and contains a pair of valves
in the lower part near the junction with the left innominate vein. The right
and left innominate veins form the superior vena cava, which is connected
to the right atrium. The internal jugular veins lie behind the sternocleidomastoid muscles. A triangle is formed at the base of these muscles by
each muscle splitting just before attachment to the clavicle. These triangles
bounded by the two heads of the sternocleidomastoid muscles and the
clavicles are called the internal jugular triangles. In acute care medicine,
they are important as a site for internal jugular cannulation. The external
jugular veins are formed below the ears by the confluence of superficial
veins from the scalp and proceed superficially and laterally along the
neck, joining the subclavian veins at the internal jugular triangles. The
external jugular veins have two pairs of valves, one at the entrance to the
subclavian veins and one in the midportion, approximately 4 cm above
the clavicle.
The height of the column of blood in the right internal jugular vein
reflects right atrial pressure since there are no valves or other obstructions
from this vein down to the right atrium. The left internal jugular and two
external jugular veins are less reliable for estimating right atrial pressure
because of the presence of valves and the fact that the left innominate
vein must cross the mediastinum and may be relatively obstructed by the
great vessels and other mediastinal structures. Inspiration augments flow
through the right heart into the lungs, which normally results in a decrease
in mean pressure in the right atrium and the right internal jugular vein.
Pressure rises again during expiration.
Recordings of right atrial pressure reveal several waveforms (Figure 2).
First is the a wave, generated by atrial contraction during the latter part of
diastole, followed by the x descent, which represents atrial relaxation. The
x descent is interrupted by ascent of the v wave, generated by continued
filling of the right atrium during ventricular systole while the tricuspid valve
is closed. The v wave is terminated by onset of the tricuspid valve opening,
which permits blood to flow passively from the right atrium to the right
ventricle in early diastole. The v wave is followed by the y descent as right
atrial pressure decreases during mid-diastole. Occasionally, a c wave is
evident on the x descent, caused in the right atrium by upward
displacement of the tricuspid valve early in systole. In recordings over the
right internal jugular vein in the neck, the c wave may also be due to
transmission of the upstroke of the underlying carotid arterial pulse.
Subclavian Vein
Figure 1. Anatomy of cervical veins, From Ewy GA: Evaluation of the neck veins. Hosp
Pract 1987;22:72-75,79-80. Reproduced with permission.
Figure 2. Internal jugular venous waveforms in relation to first (S1) and second (S2) heart
sounds. From Ewy GA: Evaluation of the neck veins. Hosp Pract 1987;22:72-75,79-80.
Reproduced with permission.
Patient Position
Examination of the character of the waves in the neck veins is often
facilitated by proper lighting in the examining room (Figure 4). The best
technique is to direct tangential light across the neck to highlight lowamplitude venous pulsations. In normal individuals, the most prominent
characteristic of the internal jugular venous pulse may be the x descent,
which is accentuated during inspiration and becomes more shallow during
expiration. In older individuals and patients with heart disease, tl’ie a wave
may be the most prominent pulsation. The v wave is usually the most
difficult to observe unless pathologic conditions exist (see below).
Since right atrial pressure is often very low, optimal positioning of the
patient to visualize the column of venous blood above the level of the
clavicle is critical. The examiner must position the patient’s upper thorax
so that the column of blood in the internal jugular vein is visible in the
neck. In general, in positioning the patient, the lower the pressure in the
venous system, the more supine the patient’s position should be; the
higher the pressure, the more upright the patient’s position should be. This
is best accomplished by using an examining table that breaks in the
middle, allowing the entire thorax to be raised and lowered. Raising and
lowering the head alone is usually not sufficient. The overall height o~f the
pulsating column is an indicator of mean right atrial pressure, which can
be estimated based on a simple anatomic fact (Figure 3). In most
individuals, the center of the right atrium is approximately 5 cm from the
attachment of the second rib to the sternomanubrial junction (sternal angle
of Louis). This relation is maintained in every position between supine and
sitting upright. Thus, the vertical height of the column of blood in the neck
can be estimated from the sternal angle, to which 5 cm is added to obtain
an estimate of mean right atrial pressure in centimeters of blood. This
amount can then be converted to millimeters of mercury by multiplying by
0.736. Normal values are less than 8 cm of blood or less than 6 mm Hg.
Obviously, this estimation may be erroneous in patients with deformed
chest walls or malpositioning of the heart.
Figure 4. Proper positioning and lighting for examining cervical venous pulses. Note that
light soume is tangential to neck veins being examined and that examining table breaks at
patient’s hips so neck is not flexed. Photo courtesy of Noble O. Fowler, MD.
Figure 3. Estimating right atrial pressure with column of blood in right internal jugular vein
(see text for details). From O’Rourke RA: Physical examination of the arteries and veins
(including blood pressure determination), in Hurst JW (ed): The Heart, ed 6. New York,
McGraw-Hill Book Co, 1985, pp 138-151. Reproduced with permission.
Timing the various waves may be difficult, especially in patients with
rapid heart rates. The best way to determine correct timing of cervical
venous pulsations is to palpate the carotid pulse on the opposite side of
the neck. The a wave occurs just before the carotid pulse and the v wave
just after it. Alternatively, the physician can auscultate the heart and note
that the a wave occurs just before the first heart sound and the v wave just
after the second heart sound. Finally, the apical precordial impulse can be
observed and its timing substituted for that of the carotid artery.
Separating Venous and Arterial Pulsations
It is occasionally difficult to distinguish between venous pulsations and
those of the underlying internal or common carotid artery. This can be
accomplished in several ways. First, the carotid upstroke is usually one
dominant wave, whereas the venous pulse should have two waves. Venous
pulsations are also more lateral to carotid pulsations, especially in the
superior part of the neck. Perhaps the best way to distinguish pulsations is
to apply light pressure at the base of the neck, which results in cessation
of venous pulsations but does not influence the higher pressure of the
carotid artery pulsations (Figure 5).
Figure 5. Light pressure at base of neck, shown here with a tongue blade, is useful for
identifying external jugular veins and obliterating internal jugular vein pulsations to separate
them from carotid pulsations. Photo courtesy of Noble O. Fowler, MD.
Pathologic Findings
Increased Pressure
Several cardiac diseases cause increased right atrial pressure. If neck
pulsations are not seen in the patient in the supine position, the trunk must
be progressively elevated to the full upright position until venous pulsations
are observed. If the jugular venous pressure is very high (greater than 15 cm
of blood), rhythmic movement of the earlobes may be noted because of
transmission of pulsations to the confluence of venous drainage in this
area. Prominent carotid pulsations usually do not cause movement of the
earlobe because the carotid artery is more medial in the upper part of the
neck. The importance of locating the jugular venous pulse cannot be
overemphasized. In the patient with edema and ascites, the presence or
absence of elevated jugular venous pressure is critical in differential diagnosis of cardiac versus hepatic disease. Occasionally with very high jugular
Figure 6. Left panel shows distention of left external and left anterior jugular veins without
venous distention of right veins. At right, normal right external jugular vein is shown by
applying pressure near its termination, confirming that previous invisibility was related to
normal venous pressure on right. Patient’s head and trunk are elevated 45° from horizontal
position. Venous pressure was 14 mm Hg in left antecubital vein and 6 mm Hg in right
antecubital vein. Left innominate vein was compressed by dissecting aneurysm, which was
responsible for elevation in venous pressure limited to left upper extremity and left side of
head and neck. Photo courtesy of Noble O. Fowler, MD.
Figure 7. Collateral venous pattern in patient with superior vena cava obstruction as
demonstrated by venography. Photo courtesy of Noble O. Fowler, MD.
venous pressure, venous pulsations will not be noticed even in the full
upright position. In this case, the external jugular veins are usually distended,
suggesting very high venous pressure. The absence of venous pulsations
even in the supine position suggests low central venous pressure.
Unilateral cervical venous engorgement sometimes occurs because of
localized obstructions in the venous drainage system. An example of this
is seen in Figure 6, where compression in the mediastinum by an
enlarged aorta led to cervical venous engorgement. Obstruction of the
superior vena cava not only results in bilateral high venous pressure but
usually causes formation of collateral venous channels through which
venous blood flow from the upper body is diverted to the unobstructed
lower body venous channels and the right atrium via the inferior vena
cava. These channels often occur in subcutaneous areas over the upper
thorax as shown in Figure 7. They also may result in venous stars, or
small skin veins arranged in a radial pattern from a central source. Venous
stars can be distinguished from cutaneous arterial angiomata (spiders) by
compressing the central vessel and quickly releasing it. If blood flow
returns from the periphery inward toward the central vessel, it is a venous
star; the reverse is true of spider angiomata.
-0.2 see.
Figure 8. Jugular venous pulse recording in patient with tricuspid stenosis.
Prominent a Waves
Any condition that accentuates right atrial contraction or elevates right
atrial pressure can result in a large a wave. Pulmonary hypertension is a
common cause of large a waves because of high right-sided pressures
and vigorous atrial contraction observed in this condition. For example, in
mitral valve disease, pulmonary thromboembolism, and car pulmonale, the
a wave may become the predominant wave of the venous pulse. In
tricuspid valve stenosis, or atresia, the a wave may become very large
because of the accentuated atrial contraction in the presence of
obstruction to atrioventricular flow. In tricuspid stenosis, the y descent is
gradual and prolonged, reflecting the diminished rate of atrioventricular
flow through the narrowed tricuspid valve (Figure 8).
Prominent v Waves
s., s, s, s_,
r: ;"
Pu I se
Figure 9. Jugular venous pulse in severe tricuspid insufficiency. Pulse is almost entirely
composed of large regurgitant or c-v wave, thus superficially resembling carotid arterial
pulse. $1, first heart sound; S2, second heart sound.
Large v waves may be seen in concert with large a waves when right
atrial pressure is elevated by any cause. Large v waves exceeding the
height of the a waves are usually caused by tricuspid regurgitation. In this
condition, the tricuspid valve is incompetent and allows blood to
regurgitate retrogradely into the right atrium during ventricular systole. The
more severe the tricuspid regurgitation in general, the higher and the
earlier the v wave. In wide-open tricuspid valve incompetence, the right
atrial pressure wave may resemble the right ventricular pressure wave
leading to one large dominant wave in the neck coinciding with the carotid
pulse and the apical impulse (Figure 9).
Cannon a Waves
The presence of various rhythm disorders may lead to the regular or
irregular occurrence of abnormal cervical venous waveforms. An example
is the cannon a wave, which occurs when there is a right atrial contraction
during ventricular systole, while the tricuspid valve is closed. In this
situation, blood does not enter the right ventricle during atrial contraction
and regurgitates up the jugular veins, causing a large a wave. Irregular
cannon a waves are seen during complete heart block when there is
dissociation between atrial and ventricular contraction (Figure 10). Regular
cannon a waves can be observed in junctional tachycardia when there is
Electrocardio gram
Figure 10. Irregular cannon a waves in patient with complete heart block.
retrograde activation of the atria from the junctional focus, causing atrial
contraction to occur simultaneously with ventricular systole in every
cardiac cycle (Figure 11).
Constrictive Pericarditis
A thickened and rigid pericardium restricts cardiac filling so that right
atrial and internal jugular venous pressures are elevated. Elevated atrial
pressure results in more rapid filling, but the limitation of ventricular filling
caused by the noncompliant pericardium abruptly terminates filling. Thus,
the large pressure gradient to filling and abrupt termination of filling during
both the early and later phases of diastole result in prominent x and y
descents. The overall pattern is that of a jerky, saw-tooth waveform created
by the heightened a and v waves and more accentuated x and y descents
(Figure 12). In addition, venous pressure does not respond normally to
respiration since right heart blood flow to the lungs can no longer be
effectively augmented by inspiration due to the pericardial constriction.
The jugular venous pulse pressure does not decrease during inspiration
and may actually increase. Increased blood flow into the thorax caused by
negative intrathoracic pressure produced by inspiration may not be
accommodated by the constricted right ventricle; thus, right atrial pressure
rises inappropriately during inspiration. This inspiratory increase in venous
pressure is termed Kussmaul’s sign. It is not specific for constrictive
pericarditis and can occur in other conditions such as severe right
ventricular failure or right ventricular myocardial infarction.
I<--- I sec.-->l
Figure 12. Rapid y descent of jugular venous pulse in patient with constrictive pericarditis
who is in atrial fibrillation.
Figure 11. Regular cannon a waves during junctional tachycardia disappear after
restoration of sinus rhythm by carotid sinus massage.
Hepatojugular Reflux Test
Patients suspected of having cardiac decompensation, pulmonary
hypertension, or right heart failure may have a normal resting jugular
venous pressure. The hepatojugular reflux test is useful for ascertaining
right ventricular reserve in these conditions. This test consists of placing
the palm of the hand flat on the upper abdomen and pushing firmly for
10-15 seconds while observing the jugular venous pulse. This maneuver
increases intra-abdominal pressure and the pressure gradient for venous
flow from the abdomen to the thorax, resulting in augmented venous
return. With normal cardiac function, this increased venous return will be
readily accommodated by the heart without a change in right atrial pressure;
hence, there is no discernible change in jugular venous pulsation.
However, in patients with right ventricular dysfunction, pulmonary
hypertension, or constrictive pericarditis, increased venous blood flow
cannot be adequately accommodated, and pressure rises progressively in
"the right atrium and internal jugular vein (Figure 13).
The term hepatojugular reflux is in fact a misnomer since the jugular
venous blood does not come exclusively from the liver. Indeed, there is no
actual reflux of blood into the jugular venous system but rather a general
increase in pressure due to lack of accommodation of increased flow from
the abdomen to the thorax. Normal individuals may exhibit a brief rise in
jugular pressure immediately after abdominal pressure has begun, but
pressure will return to baseline during the remainder of the maneuver.
¯ .,IJJj jj j JJJ J j j.jj J JJ J J J J j JJ~lJ~lJ.j
Figure 13. Elevation in right atrial (RA) pressure observed during abdominal pressure in
patient with mild congestive heart failure.
Arterial Pulses
Perhaps because arterial pulsations can be readily appreciated, arterial
palpation is one of the earliest practices in physical diagnosis. Evidence
suggests that it was the major method of determining the presence or
absence of life in ancient societies and is still used today in deciding whether
to initiate cardiopulmonary resuscitation. Thus, a high level of expertise in
arterial pulse palpation is important for every practicing physician. Arterial
pulses are palpable because of their higher pressures and increased
thickness of the arterial wall as compared with veins. The routine physical
examination includes palpation of the carotid, subclavian, brachial, radial,
abdominal aortic, femoral, popliteal, posterior tibial, and dorsalis pedis
arterial pulses. It is beyond the scope of this publication to present the
anatomy and physical examination approaches to all arteries, but certain
major concepts and key diagnostic features are reviewed in detail.
Transmission of left ventricular blood pressure to the peripheral arterial
system after the aortic valve has opened during cardiac systole is the
origin of the arterial pulse. Its character is influenced by resistance to
blood flow in the arterial system, distensibility of the arteries, and inertia of
the blood mass. After the aortic valve opens, the velocity of blood flow in
the aorta initially rises rapidly, leading to the anacrotic (Greek derivation
meaning "upbeat") shoulder of the ascending aortic pressure tracing.
Peak pressure occurs somewhat later, then falls in the latter part of systole
until the aortic valve closes. Aortic valve closure abruptly ceases blood
flow to the aorta, resulting in the incisura on the aortic pressure recording,
followed by a small positive wave caused by elastic recoil of the aorta.
Pressure then falls throughout diastole as blood runs off into the
periphery. This character of the ascending aortic pulse wave recording
changes as the arterial waveform is sampled more peripherally in the
arterial system. The major changes are a progressive dampening of
pressure waveform components and a delay in the time at which the peak
pulse pressure arrives in relation to onset of systole, as indicated by the
QRS complex on the electrocardiogram (ECG). For example, the carotid
pulse occurs 30 msec after the QRS complex, the brachial pulse 60 msec
after the QRS complex, the radial pulse 80 msec after the QRS complex,
and the femoral pulse 75 msec after the QRS complex. Finally, as the
pulse wave moves peripherally, the various waves are distorted by
influences of reflected waves from more peripheral arteries (Figure 14). For
example, in the carotid pressure wave, the incisura is replaced by the
smoother and later dicrotic notch followed by the dicrotic wave.
Figure 14. Intra-arterial recordings from various locations (see text for details). From
O’Rourke RA: Physical examination of the arteries and veins (including blood pressure
determination), in Hurst JW (ed): The Heart, ed 6. New York, McGraw-Hill Book Co, 1985,
pp 138-151. Reproduced with permission.
The second major use of arterial pulse palpation is to assess the
magnitude of the left ventricular ejection impulse. The carotid pulse is
usually used for this assessment since it is most readily palpated and is in
proximity to the heart. Accentuated pulses represent an increase in pulse
pressure (the difference between peak systolic and end-diastolic arterial
pressure). Proximal aortic pulse pressure is proportional to left ventricular
stroke volume. However, arterial distensibility influences this relation. If
distensibility decreases because of age or disease, arterial pulse pressure
will be higher with a constant stroke volume.
The pads of the fingertips should be used to determine the character of
the carotid pulse. Some examiners suggest using the thumb, which has a
larger area for palpating. The timing of the pulse in relation to venous
waves and cardiac events such as heart sounds and the apical impulse
should be measured first, then the character of the pulse in terms of its
fullness, rate of rise, and abnormal pulsations. The normal carotid pulse
rises rapidly and tapers more slowly, is easily palpable, and occurs just
after the first heart sound between the a and v waves of the jugular
venous waveform and synchronous with the apical impulse in the
precordial area.
Pathologic Findings
There are two issues concerning examination of arterial pulses. First is
use of the palpable pulse to determine patency of the artery. For this
purpose, the pulses are usually graded on one of several numerical
scales. In one scale, 0 designates an absent pulse and 2+ a normal
pulse; 1 + therefore is a reduced pulse. Another system popular with
vascular surgeons uses a scale of 0-4+ for more gradations of reduced
pulses. These systems do not consider accentuated pulses since
increased pulses are more often a reflection of the magnitude of the
systolic ejection than of peripheral vascular patency. Many clinicians blend
the two systems and refer to a 2+ pulse as representing a normally patent
artery with normal cardiac function and 4+ as a normally patent artery
with an increased left ventricular systolic ejection impulse. In this system, a
1 ÷ pulse represents either reduced arterial patency or reduced cardiac
function. Therefore, it is recommended that physicians specify the aspect
of interpretation when grading a pulse.
Differences in Peripheral Pulses
The peripheral pulses should be evaluated bilaterally for patency. Impairment of one or both carotid pulses can be caused by atherosclerotic
narrowing and occlusion by thrombus or aortic arch disease resulting from
arteritis (e.g., Takayasu’s syndrome and syphilis). Unequal radial pulses
can result from aortic arch disease, dissecting aortic aneurysm, a cervical
rib, the scalenus anticus syndrome, arterial embolism, and thrombosis,
which may be due to previous cardiac catheterization or trauma. The right
subclavian artery occasionally arises from the aorta more distally than the
left (anomalous subclavian artery) and courses behind the esophagus,
resulting in reduced pulses in the right arm. Accentuated pulses in the
right arm can be caused by supravalvular aortic stenosis.
Femoral pulses may be impaired with atherosclerosis of the external or
common lilac arteries. On palpation, the normal femoral pulses should
slightly precede the radial pulses. The femoral pulses may be absent or
impaired bilaterally in Leriche’s syndrome (i.e., thrombotic occlusion of the
aortic bifurcation). They may be impaired either unilaterally or bilaterally in
dissecting aneurysm. Absent femoral pulses may result from thrombotic
occlusion of the aortic bifurcation or bilateral common lilac artery sclerosis
with thrombosis or saddle embolism to the aortic bifurcation. In a child or
young adult, if neither femoral pulse can be palpated or if both femoral
pulses are equally weakened and delayed, coarctation of the aorta is a
likely possibility. This is especially true if hypertension exists in the upper
extremities (Figure 15). Rarely, hypertension in the upper extremities and a
weak or absent femoral pulse result from coarctation of the abdominal
aorta, which often involves the renal arteries. With coarctation of the
thoracic aorta, the carotid pulses are often exaggerated. Weak or absent
femoral pulses are rarely found to be related to pseudoxanthoma
elasticum. The external lilac arteries may be hypoplastic, simulating
coarctation of the aorta.
Bilateral absence of either the dorsalis pedis or the posterior tibial
pulses occasionally occur in normal individuals. Bilateral absence of both
or unilateral absence of either usually indicates arterial obstructive
disease, more often resulting from arteriosclerosis than from embolism,
arteritis, or trauma. When the dorsalis pedis or the posterior tibial pulses
are abnormal, the more proximal pulsations of the popliteal and femoral
arteries and the abdominal aorta should be evaluated to determine the site
and cause of obstruction.
Hyperkinetic Pulse
A rapidly rising carotid pulse of increased amplitude suggests a
widened pulse pressure and increased left ventricular stroke volume.
Widened pulse pressure can be caused by high cardiac output states
such as anxiety, thyrotoxicosis, anemia, or systemic arteriovenous fistula.
In adults, the most common cause is aortic regurgitation, where blood is
regurgitated retrogradely from the aorta into the left ventricle during
diastole. The regurgitated volume is ejected with the forward stroke volume
during systole, increasing total left ventricular stroke output (Figure 16).
This increased stroke volume together with the fall in diastolic pressure
due to regurgitation may result in a marked increase in pulse pressure. It
should be mentioned that increased pulse pressure can also occur in the
elderly with a normal stroke volume, due to decreased distensibility of the
arterial tree that magnifies the arterial pulse waves. In children, patent
ductus arteriosus is a common cause.
mm Hg
Brochiol Artery
~, 150’
E I00
E 50
160-I Femoral Artery
Figure 16. Hyperkinetic pulse recorded from femoral artery of patient with aortic
K-I se c.-~
Figure 15, Brachial and femoral artery recordings from patient with coarctation of aorta.
Exaggeration of the right carotid pulse may be found with supravalvular
aortic stenosis. In hypertensive patients who are middle-aged or older, the
right common carotid artery just above the clavicle may show an
exaggerated pulse and a seemingly increased diameter. This finding is
often considered evidence of a carotid aneurysm. However, arteriograms
usually show that such findings result from kinking or buckling of an
elongated artery, not from a true aneurysm.
Palpation of a carotid artery may disclose a vibration (thrill) with an
associated audible bruit. Such a thrill may be caused by localized disease
of the carotid artery. A systolic murmur is found with mild obstruction
produced by thrombosis. A thrill in the carotid artery also may be referred
from elsewhere, most commonly from valvular aortic stenosis. Thrills may
be felt in high output states such as thyrotoxicosis, severe anemia, or
beriberi heart disease and are usually of brief duration.
Hypokinetic Pulse
The cause of a reduction in left ventricular stroke volume will lead to a
reduced pulse pressure or a hypokinetic pulse. A generalized decrease in
systemic arterial pressure can also lead to a diminution in pulse pressure
and a hypokinetic pulse. Thus, the major issue in evaluation of a
hypokinetic pulse is to differentiate between cardiac and peripheral causes
since both are associated with low systemic arterial pressure. For example,
marked hypovolemia will result in reduced blood pressure that cannot be
elevated by increased arterial tone or augmented cardiac activity.
Pulsus Parvus et Tardus
A carotid pulse that is slow-rising, late-peaking, and of low amplitude is
characteristic of severe valvular aortic stenosis (Figure 18). In this
condition, there also may be a palpable vibration (thrill) on the ascending
limb of the pulse. It is often difficult to palpate the carotid pulses of such
patients because of lowered pulse pressure and lack of a rapid rise on the
upstroke of the pulse. This pulse must be distinguished from the
hypokinetic pulse discussed above.
Pulsus Bisferiens
The pulsus bisferiens, or twice-beating pulse, has a double impulse
during systole and is best appreciated in the carotid pulse (Figure 17). It
has three major causes: The combination of aortic stenosis and
insufficiency, severe aortic regurgitation without stenosis, and hypertrophic
obstructive cardiomyopathy. The pathophysiology of the bisferious pulse in
each of these conditions is somewhat different, and the three disease
states are readily separated by other features of the physical examination.
$1 ESM PzAz
Figure 18. Phonocardiogram and carotid pulse tracing from patient with severe aortic
valve stenosis. S1, first heart sound; S2, second heart sound; ESM, ejection systolic
murmur; A2, aortic valve component; P2, putmonic valve component.
Figure 17. Brachial artery recordings from patient with severe aortic regurgitation.
Dicrotic Pulse
The dicrotic pulse also beats twice, but the second pulse wave is in
diastole and is an accentuation of the normal dicrotic wave of the carotid
pulse. A dicrotic pulse has two major causes. One is severe left ventricular
failure with a low stroke volume and high peripheral vascular resistance
(Figure 19). Paradoxically, the dicrotic pulse can also be produced by high
output states with extremely low systemic vascular resistance as occurs
with a high fever and dehydration (i.e., typhoid fever). Thus, the
pathophysiologic origins of an accentuated dicrotic wave are complex.
45° Heod-up tilt
Figure 20. Patient in Figure 19 also develops pulsus alternans after elevation to 45°
head-up tilt.
suspicion of pulsus alternans may be confirmed by use of a sphygmomanometer. In milder cases, if cuff pressure is lowered slowly, all sounds
can be heard over the brachial artery distal to the cuff at the systolic
pressure level, but these sounds alternate in intensity. In more advanced
cases, when cuff pressure is raised above the systolic pressure level and
then lowered very slowly, only the alternate strong beats are audible over
the brachial artery at first. Then, as cuff pressure is lowered further,
perhaps by 10 mm Hg, frequency of the Korotkoff sounds may suddenly
double as the weaker beats also become audible.
Figure 19. Brachial artery recording from patient with congestive heart failure due to
primary cardiomyopathy.
Puisus Aiternans
Pulsus alternans is an alternation in the pulse amplitude on every other
beat that is best appreciated in the radial artery. The examiner must be
certain that the rhythm is regular since irregular rhythm can cause variations
in pulse amplitude (see below). This is usually a sign of severe left ventricular dysfunction and heart failure (Figure 20). It is often associated with a
tachycardia and may be present continuously or occur transiently after a
premature ventricular contraction. In the latter situation, the difference in
pulse amplitude diminishes over several beats and finally disappears.
This is a subtle sign that can be discerned only by careful attention to
the pulse amplitude. In addition, it is best to have the patient hold his or
her breath to remove the effects of respiration on pulse amplitude. The
Pulsus Paradoxus
Pulsus paradoxus is a classic physical finding of cardiac tamponade
due to increased fluid in the pericardial space. In pericardial tamponade,
unlike constrictive pericarditis, augmented right heart flow to the lungs can
be accomplished during inspiration but only at the expense of left
ventricular filling. Thus, the slight decrease in systemic arterial pressure
during normal quiet respiration is markedly accentuated and becomes
palpable (Figure 21). Once an inspiratory decrease in pulse amplitude is
appreciated by palpation, the maximum difference in systolic blood
pressure between inspiration and expiration is usually 20 mm Hg or more.
Normally, this difference is less than 10 mm Hg and is due to a slight
decrease in left ventricular stroke volume during inspiration and
transmission of reduced intrathoracic pressure to the aorta. Occasionally
in severe tamponade, peripheral arterial pressure approaches zero during
inspiration, an observation that is the origin of the term pulsus paradoxus.
Kussmaul, who described it, noted that the peripheral pulse disappeared
during inspiration, yet the apical impulse of the heart was still visible, thus
the term paradoxic pulse. However, in extreme degrees of pericardial
tamponade, this sign may disappear if pericardial pressure approaches
the point of mimicking constrictive pericarditis and right heart flow can no
longer be augmented. In this situation, Kussmaul’s sign, an inspiratory
increase in jugular venous pressure, should be noted. Pulsus paradoxus is
not specific for pericardial tamponade and can occur in severe obstructive
lung disease (Figure 22) and in patients with constrictive pericarditis,
especially if the constriction is partial and not uniformly distributed
throughout the pericardium. Reversed pulsus paradoxus has also been
described in patients on positive pressure ventilators.
During examination for a paradoxical pulse, the patient should breathe
as normally as possible and should not be asked to breathe deeply. If the
pulse wanes with inspiration in all accessible arteries and cardiac rhythm
is regular, a paradoxical pulse is present. In instances when the examiner
is uncertain, it may be desirable to use a blood pressure cuff to measure
and confirm existence of a paradoxical pulse. The blood pressure cuff is
inflated until no sounds are heard with the stethoscope over the brachial
artery, and then gradually deflated until sounds are heard in expiration
only. The cuff pressure is then lowered further until sounds are heard
throughout the respiratory cycle. The difference between these two
pressure levels is a measure of the magnitude of the paradoxical pulse.
Any reading exceeding 10 mm Hg is probably significant.
mm Hg
Respiration ~
Brochiol 150
Artery Ioo-L ~ ~ A.= ~.=
Pressure 50-J
mm Hg O~
Figure 21. Exaggerated inspiratory decrease in brachial artery pressure in patient with
cardiac tamponade (pulsus paradoxus).
I sec
Figure 22. Pulsus paradoxus in patient with obstructive lung disease.
Special Tests
Cardiac arrhythmias often alter peripheral pulse characteristics. Irregular
rhythms such as atrial fibrillation cause a variation in stroke volume from
beat to beat and result in varying amplitude of the arterial pulse. Any
interruption in cardiac activity due to arrhythmias can also be appreciated
in the periphery by the absence of pulsations. For example, an interruption
of the pulse frequency of exactly double one cardiac cycle suggests the
presence of a premature ventricular contraction that usurped the next
sinus beat and resulted in a compensatory pause before the following
sinus beat.
Under certain circumstances in which atrial activation is not transmitted
to the ventricles, the peripheral pulses wax and wane in relation to the
varying time interval between atrial and ventricular systole. This variation of
pulse magnitude occurs most commonly in patients with ventricular
tachycardia and patients with atrioventricular block or dissociation. An
example is shown in Figure 23. It may be observed that the maximum
pulse occurs when atrial systole precedes ventricular systole by a short
interval. When there is a long interval or no preceding atrial beat, the
pulse is at a minimum. This finding may be a valuable clue to diagnosis of
ventricular tachycardia in patients who have a paroxysmal tachycardia of
unknown variety. A blood pressure cuff may help demonstrate or confirm
this mechanism. This finding is absent in ventricular tachycardia when
there is retrograde conduction from ventricles to atria.
a. 60-
Figure 23. Variation in pulse magnitude due to variable atrial contribution to ventricular
filling in patient with complete atrioventricular block and escape ventricular rhythm of
70 beats/min.
Allen’s Test
Small arteries in the hand cannot ordinarily be palpated, yet arterial
defects due to trauma or arterial disease may lead to dysfunction of the
hand. Adequacy of arterial circulation in the hand can be determined by
Allen’s test, in which firm compression of the arteries against the distal
ulnar and radial bones with the examiner’s fingers and thumbs occludes
both the radial and ulnar pulse at the wrist. The patient then flexes the
hand several times until all the blood has drained from the hand, as
evidenced by pallor. The examiner then releases either the ulnar or radial
artery and observes the flow of blood through the hand. Release of either
artery should result in rapid full perfusion of the hand since both arteries
are connected by collateral channels through the palmar arcade. With this
technique, specific arterial insufficiencies in various regions of the wrist
and hand can be determined. It is especially useful to ascertain the
adequacy of ulnar artery perfusion of the hand before cannulating the
radial artery in a critically ill patient.
Valsa~va’s Maneuver
When subtle degrees of cardiac dysfunction are suspected in a patient
without overt congestive heart failure, the Valsalva maneuver can be used
to detect this decrease in cardiac reserve. In Valsalva’s maneuver, the
patient bears down against the closed glottis, which increases intrathoracic
pressure and effectively ends venous flow into the thorax, markedly
reducing cardiac filling, resulting in a progressive fall in blood pressure.
The fall in blood pressure causes a reflex tachycardia, both of which can
be experienced by palpating a peripheral arterial pulse during the
maneuver. After 15 seconds of bearing down, the patient releases the
maneuver and breathes normally. There is an immediate increase in
venous return to the heart and, subsequently, left ventricular stroke
volume, which results in an increase in blood pressure that is higher than
before the maneuver because the reflex vasoconstriction that occurred
during the strain phase results in increased vascular resistance. The
increase in pulse amplitude is readily appreciated in a peripheral artery, as
is the ensuing reflex bradycardia. This is the normal response to the
Valsalva maneuver (Figure 24A).
In the presence of reduced left ventricular performance, there may
already be heightened sympathetic arterial tone. Thus, the fall in blood
pressure during the maneuver does not result in the usual tachycardia,
and there is no overshoot in blood pressure or reflex bradycardia (Figure
24B). If the patient has unrecognized overt heart failure, the so-called
square wave pattern is seen. In this situation, increasing intrathoracic
pressure increases pulmonary venous flow from the lungs into the left
ventricle since there is a great deal of excess blood in the lungs. This
results in an elevation of blood pressure during the Valsalva maneuver and
no appreciable reflex changes in heart rate. Once the strain phase is
released and pulmonary venous return falls, blood pressure returns to
baseline (Figure 24C). This abnormality in the Valsalva response is readily
determined by palpating an arterial pulse. The square wave response to
blood pressure in the Valsalva maneuver can also be observed in patients
with large atrial septal defects.
~ IO0
Suggested Reading
Dell’Italia L J, Starling MR, O’Rourke RA: Physical examination for exclusion of
hemodynamically important right ventricular infarction. Ann Intern Med 1983;99:608-611
Ducas J, Magder S, McGregor M: Validity of the hepatojugular reflux as a clinical test for
congestive heart failure. Am J Cardiol 1983;52:1299-1303
Ewy GA: Venous and arterial pulsations, in Horwitz LD, Groves BM (eds): Signs and
Symptoms in Cardiology. Philadelphia, JB Lippincott Co, 1984, pp 135-155
Ewy GA: Evaluation of the neck veins. Hosp Pract 1987;22:72-75,79-80
Ewy GA: The abdominojugular test: Technique and hemodynamic correlates [published
erratum appears in Ann Intern Med 1988;109:947]. Ann Intern Med 1988;109:456-460
O’Rourke RA: Physical examination of the arteries and veins (including blood pressure
determination), in Hurst JW (ed): The Heart, ed’6. New York, McGraw-Hill Book Co, 1985,
pp 138-151
O’Rourke RA, Crawford MH: Physical findings in heart failure and their physiologic basis, in
Mason DT (ed): Congestive Heart Failure. New York, Yorke Medical Books, 1976, pp
Figure 24. Direct systemic arterial pressure recordings during Valsalva maneuver in three
patients (see text for details). From O’Rourke RA, Crawford MH: Physical findings in heart
failure and their physiologic basis, in Mason DT (ed): Congestive Heart Failure. New York,
Yorke Medical Books, 1976, pp 183-190. Reproduced with permission.
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