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The Dicrotic Arterial Pulse
By GORDON A. Ewy, M.D., JORGE C. Rios, M.D., AND FRANK I. MARCUS, M.D.
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SUMMARY
The study consisted of observations on nine male patients with palpable dicrotic
carotid pulses. Average patient age was 37 years. All had advanced myocardial failure
as evidenced by cardiomegaly and the presence of prominent atrial and ventricular
diastolic gallop sounds. Most of these patients were diagnosed as having primary
myocardial disease.
The indirect carotid pulse was characterized by a single systolic wave, a low dicrotic
notch, and a large dicrotic wave. The direct brachial arterial pressure pulse had a
similar configuration with a shortened ejection time index. The hemodynamic data on
these patients was characterized by low cardiac output, low stroke volume, elevated
pulmonary arterial wedge pressures, and high total systemic resistance. From these
observations we conclude that the presence of a marked dicrotic pulse in afebrile
patients at rest may indicate severe functional impairment of the myocardium.
Additional Indexing Words:
Dicrotic notch
Dicrotic wave
Primary myocardial disease
Hemodynannic data
THE dicrotic arterial pulse is characterized by two pulsations with each cardiac
cycle; the second is due to an accentuated
dicrotic wave (fig. 1). Paul Wood wrote,
". . . the dicrotic pulse is encountered chiefly
in patients sick with fever such as typhoid; the
peripheral resistance is low, the arteries are
lax, and the cardiac output probably normal."'
During the past 3 years we have observed a
number of patients with a palpable dicrotic
arterial pulse. None of them were febrile. It
was our clinical impression that these patients
had severe impairment of myocardial function.
Accordingly, nine of these patients were
assessed.
From
Methods
Each of the nine male patients studied had a
dicrotic carotid pulse that was readily palpable.
They ranged in age from 29 to 48 years with an
average age of 37 years. Seven had primary
myocardial disease, one (Z.C.) had advanced
hypertensive cardiovascular disease, and one
(C.R.) had coronary artery disease with a large
ventricular aneurysm. Two of the patients (Z.C.
and H.M.) had associated pulmonary emboli. All
patients had cardiomegaly by physical and
roentgenographic examination. All had both atrial
and ventricular, or summation diastolic gallop
sounds on auscultation and phonocardiograms;
none had cardiac murmurs. All were in normal
sinus rhythm.
Controls for the indirect carotid pulse recordings were obtained from nine normal male
subjects who ranged in age from 25 to 38 years
with an average age of 29 years. Controls for the
hemodynamic measurements and direct brachial
arterial tracings were obtained from 15 normal
subjects previously catheterized and reported on
by Perloff and associates.2 They ranged in age
from 16 to 36 years with an average age of 25
years. Differences were analyzed by the twotailed Student t-test.3
Indirect carotid arterial pulse recordings were
made in seven of these patients utilizing an airfilled funnel 2.5 cm in diameter that was
connected to a Statham physiologic transducer
(model PR 23-2G-300) by a 10-cm polyethylene
the Georgetown University School of
Medicine, Department of Medicine, Division of
Cardiology, District of Columbia General Hospital,
and the George Washington University School of
Medicine, George Washington University Medical
Division, District of Columbia General Hospital,
Washington, D. C.
This study was supported in part by grants from
the National Heart Institute, National Institutes of
Health, HE-5003 and HE-5433 and from the Special
Cardiac Research Fund, Georgetown University. Dr.
Marcus is the recipient of U. S. Public Health Career
Development Award HE-25,575.
Circulation, Volume XXXIX, May 1969
Peripheral vascular resistance
655
656
EWY ET AL.
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Figure
1
Indirectly recorded tracing of the carotid artery pulse
showing dicrotic arterial pulse. Note that one impulse is in systole and the second is in diastole. The
dicrotic pulse should be differentiated from the bisferiens arterial pulse in which both palpable impulses
are systolic. From top to bottom: low-frequency
apical phonocardiogram, indirect carotid arterial pulse
tracing, and electrocardiogram.
tubing. Recordings were made on an Electronics
for Medicine DR 8 recorder at paper speeds of 50
mm/sec or greater. Since the level of the dicrotic
notch is influenced by the time-constant of the
recording instrument, it is important to note that
the recording system used has a time-constant
approaching infinity.
Three measurements were made on both the
indirect carotid and direct brachial arterial
pressure pulse recordings in an effort to quantitate the differences in wave form that are obvious
when comparing the dicrotic and the normal
pulse (fig. 2). The first was to measure the peak
height of the dicrotic wave (d) above the level of
the dicrotic notch and to express this height as a
percentage of the total height of the systolic pulse
(t) measured from the onset or foot of the pulse
to the peak of the systolic wave (fig. 2). The
second was to measure the level of the dicrotic
notch (n) above the onset or foot of the systolic
wave and to express this distance as a percentage
of the total height of the systolic pulse (t). The
third was to express the area of the dicrotic wave
above the level of the dicrotic notch (fig. 2, black
area) as a percentage of the area of the systolic
Direct brachial arterial pressure pulse recordings. As
compared to the normal, the dicrotic pulse, as illustrated in panels 1 and 2, is characterized by a low
level of the dicrotic notch (n) and an increased height
of the dicrotic wave (d). The area under the dicrotic
wave (black) relative to the area under the systolic
wave (dashed lines) is larger in the dicrotic than in
the normal pressure pulse, iUustrated in panels 3 and 4.
(fig. 2, dashed area). Since the duration of
ejection appeared short, the ejection time index
was also measured. The ejection time index is the
systolic ejection time corrected for heart rate by
the method of Weissler and associates.4
Right heart catheterization was performed in
the standard manner, and pressures were obtained with the use of a Statham 23 Db
physiologic transducer and an Electronics for
Medicine DR 8 recorder. Left heart catheterization and left ventricular angiograms were obtained in the one patient (C. R.) who had a
ventricular aneurysm. Cardiac output was determined in duplicate by either the Fick principle
or by the dye-dilution technic, injecting indocyanine-green indicator into the pulmonary
artery and sampling from either the brachial or
femoral artery.
The effect of altering the arterial resistance on
the dicrotic pulse was studied in three patients by
distal occlusion of the artery. The brachial or
femoral artery was occluded distal to the recording
site by placing a blood pressure cuff around the
forearm or thigh and inflating it to a pressure
above systemic arterial pressure. In one of these
three patients, angiotensin was injected through
the same Cournand needle from which the pressure pulse was recorded. In another, a vasodilator,
tolazoline, was infused in a similar manner. In
addition, the effect of amyl nitrite inhalation was
recorded in three patients.
wave
Circulation, Volume XXXIX, May 1969
_
DICROTIC ARTERIAL PULSE
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Figure 3
The indirectly recorded carotid pulse. These recordings, two from patients (above) and two from normals
(below) were made utilizing an air-filled funnel
coupled to a Statham physiologic strain-gauge transducer. Note that the dicrotic pulses are characterized
by a single systolic wave, a low dicrotic notch, and
a large dicrotic wave. The configuration of the normal
indirectly recorded carotid pulse is illustrated below
for comparison.
Results
Indirect Carotid Pulse
Two indirect recordings of the carotid
arterial pulse from these patients are contrasted with two normal tracings in figure 3. The
contour of the systolic wave of the indirect
carotid pulse of these patients was characterized by a single peak. This configuration
contrasts with the two maxima found in the
indirect pulse recordings from normal subjects.5 The level of the dicrotic notch in the
patients was low, averaging 9% of the total
Circulation, Volume XXXIX, May 1969
pulse height (n/t) in contrast to the average
level of 46% in the normal. The dicrotic wave
was prominent. The height of the dicrotic
wave averaged 49% of the total pulse height
(d/t) in these patients compared to 6% in the
normal. The area of the dicrotic wave
averaged 44% of the area of the systolic wave in
the patients in contrast to 2% in normals.
Direct Brachial Arterial Pulse
The brachial arterial pressure pulse was
recorded directly in eight of the nine patients.
The level of the dicrotic notch was low,
averaging 10% of the total height of the
recorded pulse compared to the average level
of 40% in the normals (fig. 2). The height of the
dicrotic wave was increased, averaging 44% of
the total height of the pressure pulse in
contrast to an average height of 4% in the
normals. As in the indirect carotid pulse, the
area of the dicrotic wave was increased
compared to the area of the systolic wave in
the directly recorded brachial arterial pressure
pulse; 46% in these patients and 1.3% in the
normals. The average ejection time index was
0.04 sec shorter than the normal mean value of
0.42 sec of the controls (P = < 0.001).
Distal occlusion of the artery by a blood
pressure cuff or locally increasing the distal
constriction by intra-arterial infusion of angiotensin resulted in an accentuation of the
dicrotic wave (fig. 4). Inhalation of amyl
nitrite resulted in a decrease in the height of
the dicrotic wave and either no change or an
elevation of the level of the dicrotic notch (fig.
4).
Cardiac Catheterization
The hemodynamic findings are tabulated in
table 1. The cardiac output was low, with a
mean cardiac index of 1.74 L/min/m2. The
stroke volume was small, with a mean stroke
index of 17 cc/beat/im2. The pulmonary arterial wedge or the left ventricular end-diastolic
pressures or both, were elevated with a mean
pressure of 24.5 mm Hg. The mean total systemic resistance of 2,152 dyne-sec cm-'' was
twice as high as the mean value for the control patients.
EWY ET AL.
658
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ANGIOTENSIN
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( by brochial ortery infusion)
(inhalation)
FA
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Figure 4
From top to bottom: electrocardiogram, direct brachial arter pulse (BA) with pressure caibrations on the left, and direct femoral arterial pulse (FA) with pressure cdations on the
right. Note that the FA pressure pulse has a smauler dicrotic wave than the simultaneously
recorded BA. (Left panel) Control recordings of BA and FA pressure pulses. (Middle panel)
The effect of infusion of angiotensin into BA to increase arterial resistance. Note the increase
in the height of the dicrotic wave of the BA tracing and the lowered dicrotic notch. (Right
panel) BA and FA recordings following inhalation of amyl nitrite. The dicrotic wave is smaller.
Table 1
Hemodynamic Data from Nine Patients with Dicrotic Arterial Pulses
Age
Patient
Z.C.
R.L.
J.W.
R.B.
L.E.
C.R.
L.L.
E.H.
H.M.
Average:
Patients
(yr)
33
32
33
35
29
46
38
38
48
Diagnosis
HCVD
PMD
PMD
PMD
PMD
CAD-VA
PMD
PMD
PMD
BSA
(m 2)
Mean BP (mm Hg)
BA
Wedge
RA
2.20
1.38
1.64
1.85
2.15
1.68
1.97
2.02
2.15
120
73
75
84
80
68
83
87
89
7
11
15
8
20
12
11
11
28
18
25
32
27
27
24
15
1.89
12
i4.1
5
24.5
45.5
12
1.79
84
+ 15
88
SD
±0.32
±13
P
0.5
N.S.
37
±0.28
SD
Normals
25
CI
SI
(L/min/m2)
(cc/beat/m2)
TSR
dyne-sec cm -5
1.68
1.91
2.24
2.54
1.18
1.19
1.77
1.85
1.32
20
15
20
26
12
12
19
15
13
2,591
2,209
1,628
1,423
2,507
2,717
1,906
1,854
2,530
1.74
17
i 4.7
51
2,152
i466
1,099
±13
=±404
±0.46
3.79
±t0.85
0.001
0.001
0.001
Abbreviations: BSA = body surface area; m = meter; BP = blood pressure; BA = brachial artery; RA = right
atrium; wedge = pulmonary arterial wedge; CI = cardiac index; SI = stroke index; TSR = total systemic resistance;
HCVD = hypertensive cardiovascular disease; PMD = primary myocardial disease; CAD-VA = coronary artery
disease with ventricular aneurysm.
Normal values were calculated from the data obtained by Perloff and associates from 15 subjects.2 RA and wedge
pressure measurements were not obtained from the control subjects. The values listed represent the upper limits of
normal for our laboratory.
Cirecuaion, Volume XXX1X, Moy 1969
DICROTIC ARTERIAL PULSE
Discussion
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The English literature has few references to
the dicrotic arterial pulse. Textbooks of
cardiology" 6 refer to the work of Sir James
MacKenzie. In 1902, MacKenzie published his
classic book, The Study of the Pulse, Arterial,
Venous and Hepatic and of the Movement of
the Heart, in which he wrote: "When the
ventricular contraction is weak the systolic
wave is low, the dicrotic notch is deep,
reaching often to the base line, while the
dicrotic wave is much increased in size,
indicating a remarkable fall in arterial pressure." He illustrated the dicrotic pulse in a
patient with typhoid fever and attributed the
marked increase in the dicrotic wave to the
fact that".. the arterial relaxation was much
greater in the typhoid case."7 Paul Wood also
found this type of arterial pulsation in patients
with infectious or toxic reactions. He wrote,
".9. .a good sign of vascular relaxation is a
markedly dicrotic pulse and although not
necessarily serious should put the physician on
guard."'
Our studies indicate that the dicrotic pulse
in young patients who have elevated
peripheral vascular resistance and a low
stroke volume. Although these observations
appear to contrast with those in the literature,"1 6, 7 it is tempting to speculate that those
earlier observations were made on patients
occurs
E C G
B A
.
Figure 5
Electrocardiogram (E.C.G.) and direct recording of
the brachial arterial pulse (B.A.). Note that the postpremature beat has a more rapid upstroke velocity,
a larger systolic wave, a higher dicrotic notch, and
a smaller dicrotic wave than the control beat occurring
before the extrasystole.
Circulation, Volume XXXIX, May 1969
659
who had either typhoid myocarditis or a low
stroke volume secondary to severe dehydration from typhoid diarrhea.
The determinants of the dicrotic wave are
not completely understood. The dicrotic wave
of the normal arterial pressure pulse has been
ascribed to the rebound of arterial blood
against a closed aortic valve. However,
peripheral factors contribute materially to its
formation.8-12 There is a decrease or loss of the
dicrotic wave with age, hypertension, generalized atherosclerosis, and diabetes.5 10 13 Our
patients were relatively young, with a mean
age of 37 years. It may be that the arterial
resiliency of the young is necessary for the
generation of the dicrotic pulse.
What other factors contribute to the formation of the dicrotic pulse? Increasing local
arterial resistance in our patients heightened
the dicrotic wave. In the one patient studied,
local injection of an arterial dilator resulted in
a decrease of the dicrotic wave. These
observations confirm the importance of peripheral factors in the genesis of the dicrotic
wave. Three other observations bear on the
genesis of the dicrotic pulse: The first is that
the post-premature beats were less dicrotic
than the control beats (fig. 5). In the absence
of muscular subaortic stenosis, the more
forceful contraction of the post-premature
beat results in an increased stroke volume.
Second, in our patients with pulsus alternans,
the alternate beats with a higher pressure had
a smaller dicrotic wave and a higher dicrotic
notch than the beats with lower pressure. The
third observation was in a patient who had
pericardial tamponade and a dicrotic arterial
pulse only on inspiration (fig. 6A). In
tamponade it is known that the stroke volume
decreases with inspiration.14 In addition, the
ejection time index (an indirect measurement
of stroke volume) of the dicrotic beats was
0.04 sec shorter than that of the more normal
beats (fig. 6B). The dicrotic contour of the
brachial arterial pulse was not present following the removal of 500 ml of pericardial fluid.
These observations seem to indicate that a
small stroke volume or a weaker force of
660O
EWY ET AL.
f
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40
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B
Figure 6
Effect of respiration on brachial arterial pulse contour in a uremic patient with pericardial
tamponade.
(A) During tamponade. From top to bottom: electrocardiogram, direct brachial arterial
pressure pulse (BA), intrapericardial pressure recording (IP) and respiration: inspiration (in),
giving a downward deflection, and expiration (ex), giving an upward deflection. Note the
marked dicrotic pulse (arrows) on inspiration, when stroke volume would be small and the
almost normal contour of the pulse during expiration when the stroke volume would be larger.
The intrapericardial pressure is 20 mm Hg.
(B) Following removal of 500 ml of pericardial fluid by technic previously reported.15
From top to bottom: electrocardiogram, direct recording of brachial arterial pressure pulse
(BA), respiration, and intrapericardial pressure (IP). Following the relief of tamponade, note
the absence of the dicrotic pulse even during inspiration. The intrapericardial pressure decreased to a mean of 5 mm Hg with respiratory fluctuations between 11 and -1 mm Hg.
contraction, or both, may also be important in
the formation of the dicrotic pulse.
These observations concerning the role of
the arterial resiliency, peripheral resistance,
stroke volume, or force of myocardial contraction in the genesis of the dicrotic arterial pulse
are all in accord with the findings in our nine
patients. Those patients were relatively young,
with elevated peripheral resistance and low
stroke volumes. All had clinical and hemodynamic evidence of impairment of myocardial
function.
The dicrotic arterial pulse appears to be
determined by the presence of certain hemodynamic factors in relatively young patients.
Therefore, the dicrotic pulse is not necessarily
related to a specific disease entity as reported
by Meadows and co-workers.'6 We have
observed the dicrotic arterial pulse in a variety
of disease states, including primary myocardial disease, hypertensive cardiovascular disease, ischemic heart disease, acute myocardial
infarction, primary pulmonary hypertension,
and intermittently in a patient with pericardiCirculation, Volume XXXIX, May 1969
DICROTIC ARTERIAL PULSE
al tamponade. A dicrotic arterial pulse has
been reported in constrictive pericarditis.17
In view of these studies, whenever a
dicrotic pulse is palpated in an afebrile
patient, we are oriented to think of severe
functional impairment of the myocardium.
661I
7.
8.
Acknowledgment
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We are indebted to Dr. A. C. deLeon for making
the hemodynamic data on the normal patients
reported by Perloff and associates2 available for
analysis. Dr. Nayab Ali made the recording used in
figure 6. Drs. A. C. deLeon, J. K. Perloff, James
Ronan, and R. A. Massumi kindly reviewed the
manuscript. The authors appreciate the help of Dr.
George Just of Mainz, Germany, for referring us to
the work of Dr. Kurt Wezler and to Volker Sonntag
for the German translations. The secretarial assistance
of Mrs. Yvonne McIlwain is gratefully appreciated.
9.
10.
11.
12.
References
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2. PERLOFF, J. K., CALVIN, J., DE LEON, A. C., AND
BOWEN, P.: Systemic hemodynamic effects of
amyl nitrite in normal man. Amer Heart J 66:
460, 1963.
3. YOUDEN, W. J.: Statistical Methods for Chemists.
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4. WEISSLER, A. M., HARRIs, L. C., AND WHITE, G.
D.: Left ventricular ejection time index in
man. J Appl Physiol 18: 919, 1963.
5. FREIs, E. D., HEATH, W. C., LUCHSINGER, P. C.,
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6. HURST, J. W., AND LOGUE, R. B.: The Heart,
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HONIG, C. R., TENNEY, S. M., AND GABEL, P. V.:
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ALEXANDER, R. S.: Factors determining the
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BECK, W., SCHRIRE, V., VOGELPOEL, L., NELLEN,
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SHABETAI, R., FOWLER, N. O., AND GUERON, M.:
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MASsUMI, R. A., Rios, J. C., Ross, A. M., AND
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MEADOWS, W. R., OSADJAN, C. E., AND SHARP, J.
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662
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Circulataon, Volume XXXIX, May 1969
The Dicrotic Arterial Pulse
GORDON A. EWY, JORGE C. RIOS and FRANK I. MARCUS
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Circulation. 1969;39:655-662
doi: 10.1161/01.CIR.39.5.655
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
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