Examination of the arterial pulse
Assessment of the arterial pulse characteristics is an integral part of the
cardiovascular examination. Carotid, radial, brachial, femoral, posterior
tibial, and dorsalis pedis pulses should be routinely examined bilaterally to
ascertain any differences in the pulse amplitude, contour, or upstroke.
Popliteal pulses should also be examined when lower extremity arterial disease
The carotid pulse contour is very similar to that of the central aortic pulse;
a delay in the onset of the ascending limb of the carotid pulse, compared with
the central aortic pulse, is only about 20 msec. Thus, examination of the
carotid pulse provides the most accurate representation of changes in the
central aortic pulse. The brachial arterial pulse is examined to assess the
volume and consistency of the peripheral vessels.
UNEQUAL OR DELAYED PULSES
！ Inequality in
the amplitude of the peripheral pulses may result from:
• Obstructive arterial diseases, most commonly
• Aortic dissection
• Aortic aneurysm
• Takayasu's disease
• Supravalvular aortic stenosis in which the
right carotid, brachial, and radial pulses are larger in amplitude and volume
than those on the left side because of the preferential streaming of the jet
toward the innominate artery
Simultaneous palpation of the radial and femoral pulses is important to
determine if there is a delay in pulse transmission. In normal adults, the
upstrokes of the radial and femoral pulses normally appear simultaneously. A
delay in the onset of the femoral pulse, generally associated with a
diminished amplitude, suggests coarctation of the aorta.
！ Pulsus alternans is a
variation in pulse amplitude occurring with alternate beats due to changing
systolic pressure. It is best appreciated by applying light pressure on the
peripheral arterial pulse, and can be confirmed by measuring the blood
pressure. When the cuff pressure is slowly released, phase I Korotkoff sounds
are initially heard only during the alternate strong beats; with further
release of cuff pressure, the softer sounds of the weak beat also appear. The
degree of pulsus alternans can be quantitated by measuring the difference in
systolic pressure between the strong and the weak beat.
！ The most important cause of
pulsus alternans is left ventricular failure. In clinical practice, true
pulsus alternans is rarely seen in the absence of significant left ventricular
myocardial failure, and should prompt further investigation to determine the
severity and cause of left ventricular myocardial dysfunction.
Pulsus alternans also may be evident in the following situations:
• Left ventricular pulsus alternans without
systemic arterial pulsus alternans has been observed in patients with
hypertrophic cardiomyopathy and a significant rest or provocable outflow
The mechanism remains unclear; abolition of left ventricular alternans occurs
after successful myomectomy. (See
"Clinical manifestations of hypertrophic cardiomyopathy"
"Evaluation of obstructive hypertrophic cardiomyopathy"
• Pulsus alternans is rarely encountered in
patients with cardiac tamponade.
• It can occur in the presence of marked
tachypnea when the respiratory rate is one-half the heart rate due to an
inspiratory decrease in the pulse amplitude. The pulse abnormality disappears
when respiration is held transiently.
• It may be seen in patients with severe aortic
• Pulsus alternans is frequently precipitated by
ectopic beats; apparent pulsus alternans may be observed in patients with a
bigeminal rhythm. In the latter situation, the premature beats are usually out
of phase with the normal beats and postectopic pauses are appreciated.
Simultaneous auscultation of the sequence of the heart sounds and palpation of
the arterial pulse can differentiate between true pulsus alternans and
apparent pulsus alternans due to bigeminy.
Pulsus alternans should not be diagnosed when the cardiac rhythm is irregular.
！ The precise mechanism for
pulsus alternans remains unclear; alternating preload (Frank-Starling
mechanism) and incomplete relaxation have been proposed [2
Changes in afterload, which is lower after preceding the strong beat, may also
It also has been suggested that a change in ventricular contractility is the
primary mechanism, causing changes in end-diastolic volume and pressure. In
experimental animals, acute myocardial ischemia is associated with regional
pulsus alternans, leading to the hypothesis that alternating potentiation and
attenuation or deletion of contraction accounts for the pulse abnormality [3
Thus pulsus alternans may result primarily from an alternating contractile
state of the ventricle. The magnitude of the alteration of pressure and stroke
volume during pulsus alternans, indices of pump function, reflects the
interaction of an alternating contractile state with changes in preload and
！ Some respiratory
variation of pulse amplitude should be observed during examination of the
arterial pulse. Systolic arterial pressure normally falls during inspiration,
although the magnitude of decrease usually does not exceed 8 to 12 mmHg. These
changes in pulse amplitude are not usually appreciated by palpation but can be
established with the sphygmomanometer.
A more marked inspiratory decrease in arterial pressure exceeding 20 mmHg is
termed pulsus paradoxus. In contrast to the normal situation, this is easily
detectable by palpation, although it should be evaluated with a
sphygmomanometer. When the cuff pressure is slowly released, the systolic
pressure at expiration is first noted. With further slow deflation of the
cuff, the systolic pressure during inspiration can also be detected. The
difference between the pressures during expiration and inspiration is the
magnitude of pulsus paradoxus. The inspiratory decrease in systolic pressure
is accentuated during very deep inspiration or Valsalva; thus, assessment of
pulsus paradoxus should be made only during normal respiration.
！ Pulsus paradoxus is an important
physical finding in cardiac tamponade. (See
"Pulsus paradoxus in pericardial disease"
). In patients with
suspected cardiac tamponade, echocardiography should be performed to detect
pericardial effusion and ventricular diastolic collapse; the latter is more
specific and sensitive than pulsus paradoxus for the diagnosis of tamponade [4
Pulsus paradoxus may not occur despite cardiac tamponade in patients with
hemodynamically significant aortic regurgitation and atrial septal defect. (See
"Pericardial compressive syndromes"
In addition to tamponade, pulsus paradoxus can occur in chronic obstructive
pulmonary disease, hypovolemic shock, and infrequently in constrictive
pericarditis and restrictive cardiomyopathy. It is rarely observed in
pulmonary embolism, pregnancy, marked obesity, and partial obstruction of the
superior vena cava.
In hypertrophic obstructive cardiomyopathy, arterial pressure occasionally
rises during inspiration (reversed pulsus paradoxus); the precise mechanism
for this phenomenon is unclear [5
In addition to changes in the amplitude, configurational changes of the
carotid pulse may occur.
！ The mechanism for the marked
inspiratory decrease in arterial pressure with pulsus paradoxus appears to be
related to the inspiratory decline of left ventricular stroke volume due to an
increase in right ventricular end-diastolic volume and decreased left
ventricular end-diastolic volume. In cardiac tamponade, the interventricular
septum shifts toward the left ventricular cavity during inspiration (reverse
Bernheim's effect), a result of the normal increase in venous return to the
right side, thereby decreasing left ventricular preload [6
An inspiratory decrease in pulmonary venous return to the left side of the
heart also has been thought to contribute to decreased left ventricular
！ The normal carotid
arterial pulse tracing and the central aortic pulse waveform consist of an
early, the percussion wave, that results from rapid left ventricular ejection,
and a second smaller peak, the tidal wave, presumed to represent a reflected
wave from the periphery. The tidal wave may increase in amplitude in
hypertensive patients or in those with elevated systemic vascular resistance.
Radial and femoral pulse tracings demonstrate a single sharp peak in normal
Pulsus bisferiens is characterized by two systolic peaks of the aortic pulse
during left ventricular ejection separated by a midsystolic dip. Both
percussion and tidal waves are accentuated. It is difficult to establish with
certainty that the two peaks are occurring in systole with simple palpation (pulsus
bisferiens) versus one peak in systole and the other in diastole (dicrotic
！ Pulsus bisferiens is frequently
observed in patients with hemodynamically significant (but not mild) aortic
regurgitation. In patients with mixed aortic stenosis and aortic
regurgitation, bisferiens pulse occurs when regurgitation is the predominant
lesion. The absence of pulsus bisferiens does not exclude significant aortic
In most patients with hypertrophic cardiomyopathy the carotid pulse upstroke
is sharp and the amplitude is normal; pulsus bisferiens is rarely palpable but
often recorded. The rapid upstroke and prominent percussion wave result from
rapid left ventricular ejection into the aorta during early systole. This is
followed by a rapid decline as left ventricular outflow tract obstruction
ensues, a result of midsystolic obstruction and partial closure of the aortic
valve. The second peak is related to the tidal wave. Occasionally, a
bisferiens pulse is not present in the basal state but can be precipitated by
Valsalva maneuver or by inhalation of amyl
Pulsus bisferiens is occasionally felt in patients with a large patent ductus
arteriosus or arteriovenous fistula. A bisferiens quality of the arterial
pulse also is rarely noted in patients with significant mitral valve prolapse
and, very rarely in normal individuals, particularly when there is a
hyperdynamic circulatory state.
！ The mechanism of pulsus
bisferiens is not clear. It appears to be related to a large, rapidly ejected
left ventricular stroke volume associated with increased left ventricular and
！ A dicrotic pulse results
from the accentuated diastolic dicrotic wave that follows the dicrotic notch.
It tends to occur when the dicrotic notch is low, as in patients with
decreased systemic arterial pressure and vascular resistance (eg, fever). A
dicrotic pulse also may be present in patients with severe heart failure,
hypovolemic shock, cardiac tamponade, conditions associated with a decreased
stroke volume and elevated systemic vascular resistance, and during the
immediate postoperative period following aortic valve replacement [7
The precise mechanism for a dicrotic pulse in the last group is not clear; it
is more frequently observed in patients with pump failure postoperatively.
Dicrotic pulse is occasionally noted in normal individuals, particularly after
A dicrotic pulse is frequently confused with pulsus bisferiens at the bedside;
it is almost impossible to distinguish between these two types of pulse
configurations without a pulse recording. Thus, the potential exists for
mistaken diagnosis of aortic regurgitation due to malfunction of a prosthetic
！ The Corrigan or
water-hammer pulse is characterized by an abrupt, very rapid upstroke of the
peripheral pulse (percussion wave), followed by rapid collapse. It is best
appreciated by raising the arm abruptly and feeling for the characteristics in
the radial pulse.
The Corrigan pulse probably results from very rapid ejection of a large left
ventricular stroke volume into a low resistance arterial system. Thus, it
occurs most commonly in chronic, hemodynamically significant aortic
regurgitation. A bounding arterial pulse is not diagnostic of aortic
regurgitation; it can occur in many conditions associated with increased
stroke volume such as patent ductus arteriosus, large arteriovenous fistulas,
hyperkinetic states, thyrotoxicosis anemia, and extreme bradycardia. The
typical pulse characteristics of chronic aortic regurgitation may not occur in
acute aortic regurgitation, even when it is severe, since left ventricular
stroke volume may not increase appreciably, the systemic vascular resistance
may not be low, and the left ventricle is not dilated.
PULSES IN AORTIC STENOSIS
changes in the morphology of the arterial pulse may occur in the presence of
fixed left ventricular outflow tract obstruction, particularly valvular aortic
stenosis. Careful examination of the arterial pulse provides useful
information for the diagnosis and assessment of the severity of aortic
Increased resistance to left ventricular ejection due to fixed obstruction
reduces the stroke volume, prolongs left ventricular total ejection time, and
retards the rate of initial stroke output into the aorta and distal arterial
system. This results in a number of changes that can be appreciated with
palpation of the carotid pulse:
• Anacrotic character (anacrotic pulse) ！ An
anacrotic pulse gives the impression of interruption of the upstroke of the
carotid pulse. Aortic stenosis is likely to be hemodynamically significant
when the anacrotic notch is felt immediately after the onset of the upstroke.
When an anacrotic notch occurs very early on the ascending limb of the
arterial pulse, it can be appreciated in the radial pulse and suggests
moderate to severe aortic stenosis.
• Delayed upstroke of the ascending limb (pulsus
tardus) ！ A delayed peak and slower upstroke of the carotid pulse suggest a
prolonged left ventricular ejection time. The delay can be appreciated by
simultaneous palpation of the carotid pulse and auscultation of the interval
between S1 and S2 (duration of systole). Normally the peak of the carotid
pulse occurs closer to S1; in the presence of severe aortic stenosis, it is
usually closer to S2. In the presence of fixed outflow obstruction, the
central aortic pulse demonstrates a progressively slower rise of the ascending
limb, a lower anacrotic shoulder, and a peak closer to the incisura as the
severity of obstruction increases.
• Delayed peak
• Small amplitude (pulsus parvus) ！ The
amplitude of the pulse decreases with a diminished stroke volume.
• Shudder (thrill) on the ascending limb ！ A
thrill (carotid shudder) also is frequently palpable on the ascending limb of
The diagnosis and severity of aortic stenosis should not be determined by
changes in the carotid pulse configuration alone. The auscultatory findings of
aortic stenosis and evidence for left ventricular hypertrophy should be
The carotid arteries may become rigid and less compliant in elderly patients
due to arteriosclerosis. The usual changes in the carotid pulse due to aortic
stenosis are modified in this situation, particularly the amplitude, which may
not decrease even in the presence of severe aortic stenosis.