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479
Pulse Wave Reflection: Can It Explain the Differences
Between Systemic and Pulmonary Pressure and Flow
Waves?
A Study in Dogs
G.C. van den Bos, N. Westerhof, and O.S. Randall
With technical assistance by F.O.M. Pot
From the Laboratory for Physiology, Free University, Amsterdam, The Netherlands
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SUMMARY. We have studied the effect of changes in pulse wave reflection on the configurations
of pressure and flow in systemic and pulmonary circulation. Electromagnetic flow transducers, atrial
catheters, and pacing leads were implanted in 10 dogs. In four animals, the flow transducer was
placed on the pulmonary artery, in another four on the ascending aorta, and in two additional dogs
on both vessels. One week later, ascending aortic and/or pulmonary artery flow and pressure
(catheter tip manometer) were measured under general anesthesia (Nembutal, 30 mg/kg, iv). When
the pulmonary circulation was studied (six dogs), measurements were made before and during
serotonin infusion (0.5-0.75 mg/min). When the systemic circulation was studied (six dogs),
measurements were made before and during nitroprusside infusion (50-200 jug/min). To quantify
the arterial load, we calculated pulmonary and systemic input impedances. To estimate the amount
of reflection, we used a reflection index which we defined as the amplitude ratio of reflected and
forward wave. Nitroprusside decreased total peripheral resistance, increased total arterial compliance,
and decreased the reflection index; similarity between aortic pressure and flow wave shapes
increased, and they looked more like their pulmonary counterparts. Serotonin increased pulmonary
vascular resistance, decreased pulmonary arterial compliance, and increased the reflection index.
Resemblance of pressure and flow waves decreased. The differences in wave shapes can thus be
explained by the amount of reflection: the less reflection the more pressure and flow resemble each
other. (Circ Res 51: 479-485, 1982)
THE configurations of pressure and flow in pulmonary artery and ascending aorta are determined by
the interaction of ventricles and pulmonary or systemic input impedance, respectively. The characteristics of the ventricles differ (Rushmer, 1964; Elzinga
et al., 1980). Although a comparative study has not
been done, the literature indicates that pulmonary
and systemic input impedances are also different
(Milnor et al., 1966; Noble et al., 1967; Reuben et al.,
1971; Westerhof et al., 1973; Pouleur et al., 1978;
Hopkins et al., 1979, 1980). Consequently, resemblance of pulmonary and aortic flow waves is small;
the same is true for pulmonary and aortic pressure
waves (Fig. 1). Figure 1 also shows that in the pulmonary circulation, pressure, and. flow waves look
alike, but that this is not so in the systemic bed.
Rushmer (1964) has pointed out that the differences
between aortic and pulmonary flow waves tend to
disappear when left ventricular function deteriorates
or when the right ventricle faces an abnormally high
load for a long time.
Measured pressure and flow waves consist of forward and reflected waves (Westerhof et al., 1972; van
den Bos et al., 1976). The forward wave (equal in
shape for pressure and flow, since characteristic
impedance is real and frequency independent; see
McDonald, 1974) runs into the system and is reflected
from distributed sites. Under all physiological and a
large variety of pathological conditions, the reflected
pressure wave is in phase with the forward wave:
addition of forward and reflected wave results in a
measured wave which is larger than the forward wave.
The reflected flow wave is out of phase with the
forward wave so that summation of forward and
reflected wave now renders a measured wave smaller
than the forward wave. Consequently, the more the
forward wave is reflected, the less measured flow
resembles measured pressure. The differences in
wave shapes in the two systems and the observation
that pulmonary pressure and flow waves look more
alike than their systemic counterparts could be partly
explained if reflection in the pulmonary bed were
less. In the circulation under control conditions, the
major source of reflection is the periphery, which was
described by von Kries as early as 1890. Changes in
peripheral resistance could thus alter the amount of
reflection.
We have studied systemic and pulmonary flow and
Circulation Research/Vo/. 51, No. 4, October 1982
480
O.5 sec.
Pulmonary A
flow
Pulmonary A
Pressure
kPa/mmHg
FIGURE 1. Pressure and flow pulses in pulmonary artery (top) and aorta (bottom).
Aortic
Pressure
kPa/mmHg
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pressure waves in anesthetized dogs. We decreased
systemic and increased pulmonary resistance, since
we would expect that the wave shapes in both beds
might then become more alike. Similarly, vasodilation
in the systemic circulation might increase resemblance of pressure and flow waves, and vasoconstriction in the pulmonary bed might decrease the normally existing resemblance.
Methods
rates higher than the atrial rate, we either used two pacemakers triggered from the same source or we paced the
ventricles only.
We have recorded on paper (Elema EMT 81) and analog
tape (SE 7000): ECG II, left atrial pressure (Statham 23 dB)
in all dogs; ascending aortic pressure and flow (Transflow
systems 601) in group A and C; pulmonary artery pressure
and flow in group B and C.
We have used 10 male, mongrel dogs (20.5-43.0 kg). One
week before the experiments transducers, catheters (left
atrium) and pacemaker wires (right atrium and ventricle)
were implanted under general anesthesia and sterile conditions, through a left thoracotomy in the 4th intercostal
space. In four dogs, the electromagnetic flow transducer
(constructed in our workshop) was put on the ascending
aorta (group A)—in another four, on the pulmonary artery
(group B)—while, in two additional animals, we have put
flow transducers on both vessels (group C).
In the actual experiments, the dogs were anesthetized
with Nembutal (30 mg/kg, iv), intubated, and connected to
a respirator (Pulmomat Drager; mixture of 20% O2 and 80%
N2O). Nembutal was added in the course of the experiment
if necessary. We produced total atrioventricular block (Randall et al., 1981).
Catheter tip manometers (Millar Mikro-TIP PL 350, 6F
or 7F) were introduced into the aorta (group A) from a
femoral artery or into the pulmonary artery (group B) from
a femoral or jugular vein. In the two dogs in group C, tip
manometers were put into aorta as well as pulmonary
artery. The tips of the catheters were positioned at the
upper rim of the flow transducer. Because of catheter
"whip," this was not always possible in the pulmonary
artery. When flow and pressure had to be analyzed for
input impedance, the two waves were synchronized by the
computer program (superposition of back flow and pressure
incisura).
Pacing catheters were put into the right atrium and
ventricle if necessary. The heart was paced at a series of
rates by a pacemaker triggered from the right atrial ECG.
This signal, converted to a TTL pulse, was first passed
through a digitimer (Devices D 4030). This arrangement
provided synchronization of atrial and ventricular contractions. The digitimer could be programmed to trigger the
pacemaker at every first, second, third, or fourth atrial ECG,
etc., until the ventricles beat at their own rate. For heart
Croup A
Protocol
After control recordings had been made, systemic resistance was decreased with nitroprusside (50-200 fig/min).
Croup B
After control recordings had been made pulmonary resistance was increased with serotonin (0.5-0.75 mg/min).
Group C
In these dogs, the procedure was performed in sequence,
i.e., serotonin was given followed by nitroprusside or vice
versa.
When a steady state had been reached during the infusions, recordings were again made. Recordings during control and intervention were made at a series of heart rates
ranging from the intrinsic ventricular rate to the maximum
rate at which the heart could be paced (about 3 Hz) without
causing mechanical alternans. At each heart rate in groups
B and C, the respirator was disconnected for about 20
seconds.
Calculations and Analyses
Pressure and flow signals of series of heart beats (from
5 to 15) in the steady state at each pacing rate were passed
through a filter (3 dB point at 80 Hz; -12 dB/octave). Beats
were either sampled from periods when the respirator had
been disconnected or from a complete respiratory cycle.
The data was then converted from analog to digital at a rate
of 200/sec. We performed Fourier analyses on individual
beats. When the amplitude of pressure harmonics was less
than 1% and of flow harmonics less than 2% of the first
harmonic, these harmonics were considered to be contaminated by noise and discarded. Impedance was calculated
by dividing pressure and flow moduli and subtracting their
phase angles. The impedance for each heart rate was calculated by averaging the results of individual beats. We
481
van den Bos et al./Systemic and Pulmonary Reflection
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performed this procedure for several heart rates to improve
resolution of the impedance plot. A computer program
subsequently placed the moduli and phase data in classes
of frequencies (the class interval was equal to the lowest
determined frequency) and determined the mean of each
class. A line drawn through these means gives the average
impedance.
Systemic peripheral resistance was calculated as the ratio
of mean aortic pressure and cardiac output. Characteristic
impedance was defined as the average of the impedance
moduli above 4 Hz. For pulmonary peripheral resistance,
mean left atrial pressure was subtracted from mean pulmonary artery pressure, and this difference was divided by
cardiac output.
Total arterial compliance was calculated by fitting the
three-element windkessel (Westerhof et al., 1971) to the
impedance by means of a least squares method.
Forward and backward (= reflected) waves were calculated from measured flow and pressure in the pulmonary
artery and ascending aorta using the characteristic impedance of these two arteries (Westerhof et al., 1978).
To quantitate reflections, we used a reflection index
which we calculated as the ratio between maximum ampli-
SYSTEMIC
CONTROL
1O
<D
c
SO
1O
2O
3O
O
PULMONARY
CONTROL
F27
SO
3O
frequency
SEROTONIN
F
2O
3O
frequency
Pd
A. Systemic circulation before (C) and during nitroprusside (N)
S17
C
80
19.2 22.3 16.6 15.4 1.25
N
92
10.0 14.0
7.7 35.9 0.28
O12
2D
4
TABLE 1
HR
S17
3 OO-3
T3
0
Hemodynamic Variables before and after Drug Infusion
Experiment
NITROPFIUSSIDE
N
89
90
19.2
9.4
23.3
12.6
15.9
7.3
22.3
15.4
0.86
0.61
M09
C
N
95
93
13.6
10.9
17.6
13.8
10.8
9.0
29.2
25.6
0.47
0.43
M19
C
N
94
94
16.8
10.0
19.2
13.4
14.5
8.3
26.8
23.7
0.63
0.42
A06
C
N
78
78
14.9
10.9
18.3
14.1
12.1
8.8
13.4
15.6
1.11
0.70
A24
C
N
129
128
16.2
7.3
18.1
10.6
14.3
5.5
66.3
47.3
0.24
0.15
B. Pulmonary circulation before (C) and during serotonin (S)
S17
C
S
92
90
2.0
3.4
4.9
6.5
.9
1.6
31.8
21.0
0.053
0.15
O12
C
S
119
121
2.3
4.5
4.6
5.7
1.4
1.3
16.7
14.8
0.076
0.27
F12
c
s
70
60
3.9
4.2
6.8
7.9
4.7
3.6
18.6
27.7
0.094
0.095
F26
c
s
90
90
3.4
3.7
5.2
6.3
3.4
3.0
19.6
17.1
0.074
0.152
F27
c
s
90
88
2.1
3.8
4.1
7.5
1.8
2.3
23.9
29.8
0.018
0.060
F28
c
s
71
71
2.4
2.7
3.1
4.1
1.8
1.3
24.0
39.7
0.034
0.047
P = mean blood pressure in kPa (10 kPa = 75 mm Hg), P. =
systolic pressure in kPa, Pd = diastolic pressure in kPa, F = cardiac
output in ml/min, HR = heart rate in beats/min, Rp = peripheral
resistance in 109 Pa-sec-m" 3 (104 dyne-sec-cm" 5 ).
-1OO
FIGURE 2. Input impedance in systemic (top) and pulmonary (bottom) bed in one dog, before and during nitroprusside or serotonin
infusion, respectively. Each symbol represents one heart rate. Moduli are in 10'' Pa • sec-m~' (or 104 dyne sec.cm~"); phases in degrees;
frequency in Hz.
tudes of reflected and forward waves (since the ratio is the
same for pressure and flow, one can use either of the two).
Results
Table 1 presents pressures, flow, and peripheral
resistance of all experiments at comparable heart rates
for control and nitroprusside in the systemic (A), and
for control and serotonin in the pulmonary arterial
bed (B).
Nitroprusside lowered systolic, diastolic, and mean
blood pressure and decreased peripheral resistance.
The effect on cardiac output was inconsistent.
Serotonin raised mean and systolic pulmonary
pressure, but the changes in diastolic pressure and
cardiac output were variable. Pulmonary vascular resistance increased.
To be informed about the arterial loads, we have
calculated systemic and pulmonary input impedance
before and during nitroprusside and serotonin. Figure
2 gives an example for one dog (all data points from
all used heart rates are shown), and illustrates that
variability in a dog is considerable. In Figure 3 we
have presented average impedance plots in each dog
before and during nitroprusside (3a) or serotonin (3b)
infusion. The figure illustrates that there is also con-
482
Circulation Research/Voi. 51, No. 4, October 1982
characteristic impedance and total arterial compliance
(Table 2). Nitroprusside had a tendency to increase
slightly the systemic characteristic impedance. Systemic compliance increased considerably (213%, range
69-420) with nitroprusside. During serotonin infusion, pulmonary compliance fell by 66% (range 42-
SYSTEMIC
86).
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We have also calculated the forward and reflected
wave for one heart beat before and during nitroprusside and serotonin infusion (Fig. 5). After nitroprusside, the reflected wave decreases; the incisura in the
pressure pulse moves to a lower level and pressure
begins to resemble flow. In the pulmonary circulation
before serotonin, the reflected wave is small and the
measured pressure and flow wave look alike. After
serotonin, the amplitude of the reflected wave has
increased considerably and the similarity between
flow and pressure becomes less. The increased reflection causes the incisura in the pressure pulse to move
to a higher level. Figure 6 gives the reflection index in
the systemic and pulmonary bed before and during
the interventions. Nitroprusside significantly decreases the index in the systemic bed, while serotonin
significantly increases it in the pulmonary circulation.
PULMONARY
F12 j
F=2B
1
1
1
ID
2O
3O
frequency '
Discussion
1
1O
SO
3Q
frequency
ID
2O
3O
frequency
The arterial bed can be described by resistance,
compliance and inertance (Westerhof et al., 1977).
Changes in any of these parameters alter the characteristics of the system so that pressure and flow will
also change. Generation of pressure and flow waves
in a set of tubes causes reflection of these waves
(Westerhof et al., 1978). The amount of reflection is
expressed in the reflection coefficient, also a property
of the system. Consequently, changes in the parameters that describe the system influence the reflection
coefficient. Since the configurations of pressure and
flow are to a major extent determined by the amount
of reflection any change in the parameters will alter
the wave shapes.
SYSTEMIC
-1OO1
PULMONARY
B
FIGURE 3. Average input impedances in aorta (A) and pulmonary
bed (B) for the six dogs before (drawn line) and during nitroprusside or serotonin, respectively (dashed line). Units as in Figure 2.
siderable variability between dogs. Figure 4 shows the
average systemic and pulmonary impedance and their
standard errors for all animals.
The changes in the impedance during nitroprusside
and serotonin mainly concern the mean term (Rp in
Table 1) and very low frequencies. Nitroprusside
decreased the moduli and phase angles of low frequency harmonics so that flow and pressure were less
out of phase. During serotonin infusion, the moduli
and phase angles of low frequency harmonics increased: flow and pressure were less in phase.
From the input impedance, we have also calculated
•O
0
I
OO4
\\
1O
S
a
SO
3O
frequency
ID
2O
3O
frequency
o
FIGURE 4. Average input impedance in aorta (left) and pulmonary
bed (right) for all dogs before (drawn line) and during nitroprusside
or serotonin, respectively (dashed line). Units as in Figure 2.
Standard errors are shown at 5 Hz intervals.
van den Bos et al. /Systemic and Pulmonary Reflection
483
TABLE 2
Characteristic Impedance (Zc)* and Arterial Compliance (C)t
Pulmonary circulation
Systemic circulation
Experiment
Control
Nitroprusside
Zc
C
0.0266
2.42
0.0295
1.82
0.0176
3.27
0.0198
3.42
0.0258
1.71
0.0159
7.62
0.0265
12.58
0.0424
9.42
0.0183
5.52
0.0382
8.38
0.0287
3.65
0.0258
15.95
S17
Ol2 Zc
C
M09 Zc
C
M19 Zc
C
A06 Zc
C
A24 Zc
C
Experiment
S17
Zc
C
O12
Zc
C
F12
Zc
C
F26
F27
F28
Zc
c
Zc
c
Zc
c
Control
Serotonin
0.0119
12.15
0.0256
6.36
0.0078
16.37
0.0155
33.33
0.0170
15.59
0.0054
22.71
0.0202
4.42
0.0165
3.05
0.0165
4.83
0.0221
4.55
0.0194
3.33
0.0097
13.22
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* 109 Pa-sec-m"51 = 104 dyne-sec-cm- 5
tlO- 9 m 3 -Pa"' = 10" 4 cm 5 -dyne"'.
Reflections occur at distributed sites, but the periphery supposedly plays a major role. Welkowitz
(1977) argues, on the basis of his analog model of the
arterial tree, that normally little reflection occurs in
SYSTEMIC
O.5 sec
CONTROL
the peripheral bed. Westerhof et al. (1972) clearly
show that changes in peripheral resistance alter the
reflection coefficient. We have therefore used such
changes to alter pulsewave reflection: serotonin in the
pulmonary and nitroprusside in the systemic circulation. Our general hemodynamic results with these
drugs are comparable to those in the literature (Reuben et al., 1971; Gundel et al., 1981). Our study shows
that differences in the amount of reflection can explain the dissimilarity in the pattern of flow and
pressure in systemic and pulmonary circulation: the
less reflection the greater the resemblance of flow and
pressure waves.
When we infused serotonin, the amount of reflection in the pulmonary bed increased significantly. A
larger reflected wave must now be added to the
forward pressure wave and subtracted from the forward flow wave. Thus, flow and pressure wave lose
similarity. On the other hand, when we infused nitro-
IMITROPRUSSIDE
SYSTEMIC
PULMONARY
PULMONARY
O.5
BBC
X
UJ
O.5--
a
Q
UJ O.25
11
UJ
tr
CONTROL
SEROTONIN
FIGURE 5. Measured (heavy line), forward (thin line) and reflected
(dashed line) wave in ascending aorta (top) and pulmonary artery
(bottom) before and during infusion of nitroprusside and serotonin,
respectively.
o-1- FICURE 6. Reflection index in systemic and pulmonary bed before
and during nitroprusside or serotonin.
Circulation Research/Vo/. 51, No. 4, October 1982
484
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prusside, the amount of reflection in the systemic
circulation decreased significantly. A smaller reflected
wave has to be added to the forward pressure and
subtracted from the forward flow wave. Pressure and
flow wave become more alike.
We have expressed the amount of reflection as the
reflection index (Fig. 6): the ratio between the maximum amplitude of reflected and forward wave. Usually, reflection is quantitatively expressed by means
of the reflection coefficient (Westerhof et al., 1972).
This is a complex parameter in the mathematical
sense with a modulus and phase which are both
functions of frequency and therefore not easy to
interpret. Our reflection index, on the other hand,
gives one number for each heart beat. Even though
this number is not easily obtained (one has to calculate
forward and reflected waves), it is easy to understand.
Calculation of this index clearly illustrates the changes
in the amount of reflection occurring with serotonin
and nitroprusside.
Under control conditions, the amount of reflection
is less in the pulmonary than in the systemic circulation. Serotonin increases pulmonary reflection (as was
predicted by Pollack et al., 1968), while nitroprusside
decreases systemic reflection. The amount of reflection in the systemic bed is now comparable to that in
the pulmonary circulation during control. The same
holds for the constricted pulmonary bed and the
systemic circulation under control conditions. In both
situations, the pulmonary pressure begins to resemble
aortic pressure and the pulmonary flow begins to
resemble aortic flow. We should realize, however,
that the resemblance is restricted to wave shapes.
That the wave shapes are not exactly alike is in part
due to the differences in pump function of right and
left heart: configurations of flow and pressure are
determined by the characteristics of the ventricle as
well as the arterial impedance.
Peripheral resistance is only part of the load faced
by the heart. Milnor (1975) has indicated that this
load can best be described by the input impedance.
Calculation of input impedance is only permitted for
linear systems. Although the linear behavior of the
entire arterial tree has been challenged (Milnor and
Nichols, 1975; Milnor and Bertram, 1978), several
reports show that linearity is a reasonable assumption
(Dick et al., 1966; Noble et al., 1967; Li et al., 1981).
We have measured the input impedances before and
during the interventions (Fig. 4). These impedances
mainly differ in their mean term (= peripheral resistance) and the characteristic impedance. The mean
term is considerably higher and the characteristic
impedance slightly higher in the systemic bed. The
changes in the impedance caused by the drugs mainly
concerned the mean term and the low frequency
range. This can best be seen in Figure 7 which shows
the data of Figure 4 plotted on an expanded frequency
axis. These changes in the low frequency ranges
indicate a change of compliance. When we calculated
arterial compliance, nitroprusside increased this parameter while serotonin decreased it (Table 2). This
SYSTEMIC
V
0
PULMONARY
O.O4-
V
1
S
3
4
5
6.,
frequency
5
6
frequency
FIGURE 7. Average input impedance in systemic (left) and pulmonary (right) circulation before (drawn line) and during nitroprusside or serotonin (dashed line). Data of Figure 4 replotted on
expanded frequency axis. Units as in Figure 2.
need not be a direct effect of the drugs since compliance is also dependent on pressure (Bergel, 1961). The
large changes in compliance (Table 2) causes small
changes in the impedance plot (Figs. 4 and 7). Moreover, major changes in general hemodynamics caused
by serotonin and nitroprusside were only reflected in
the impedance plot by changes in the mean term and
the lowest frequencies.
Gundel et al. (1981) have expressed doubts about
the use of the impedance concept for clinical work.
They suggest that the concept is appropriate principally for physiological studies—Impedance on the
one hand and the combination of peripheral resistance
and compliance on the other are both ways to describe
the arterial system. However, in our opinion the
combination of peripheral resistance and compliance
is easier to understand and therefore more practical
as a description of the load to the heart.
We wish to acknowledge Dr. JC.J. van Ryssen for his help
during the experiments, C. Pieksma for typing the manuscript, A.
van der Vos for his help with the computer programming and J.
Meijer and H. Verbeek for the illustrations.
Dr. O.S. Randall was on sabbatical leave from the University of
Michigan, Department of Cardiology, Ann Arbor, Michigan.
Address for reprints: Dr. C.C. van den Bos, Physiological Laboratory, Free University, Van der Boechorststraat 7, 1081 BT Amsterdam.
Received November 23, 1981; accepted for publication July 22,
1982.
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of the systemic arterial tree. Med Biol Eng 11: 710-723
Westerhof N, Elzinga G, Sipkema P, Bos GC van den (1977)
Quantitative analysis of the arterial system and heart by means
of pressure-flow relations, edited by HC Hwang, NA Norman.
In Cardiovascular Flow Dynamics and Measurements, Baltimore,
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Westerhof N, Bos GC van den, Laxminarayan S (1978) Arterial
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INDEX TERMS: Pulmonary artery • Aorta • Reflections • Imped-
Pulse wave reflection: can it explain the differences between systemic and pulmonary
pressure and flow waves? A study in dogs.
G C van den Bos, N Westerhof and O S Randall
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Circ Res. 1982;51:479-485
doi: 10.1161/01.RES.51.4.479
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