Download the Right Atrium, Right Ventricle, and Left

Cardiac Hemodynamics During Stimulation of
the Right Atrium, Right Ventricle, and Left
Ventricle in Normal and Abnormal Hearts
By ALBERTo BENCHIMOL, M.D.,
IN
PREVIOUS
REPORTS
wel-3
AND
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genital complete heart block, and one had atrial
fibrillation. Included in the group were 11 normal
subjects, seven patients with documented coronary artery disease (postmyocardial infarction
with or without angina pectoris), two with idiopathic myocardial hypertrophy, and one each
with essential hypertension, mild mitral stenosis,
mild mitral insufficiency, congenital complete
heart block, idiopathic bradycardia, and postoperative constrictive pericarditis. Ages ranged
from 15 to 74 years with a mean of 47 years.
There were 14 males and 12 females.
The studies were performed under local anesthesia with mepivacaine hydrochloride (Carbocaine 1%i) and with meperidine (Demerol), 50
mg., as premedication. A no. 8 Zucker bipolar
electrode catheter* was introduced into the right
cubital vein and advanced to the right ventricle.
The right brachial artery was exposed and a
second no. 8 Zucker bipolar electrode catheter
was introduced into the artery and advanced to
the left ventricle. A no. 18 Cournand needle
was introduced into the right femoral artery for
measurement of arterial pressure and for sampling
of the indicator. The wires of the electrode
catheter were connected with an external transistorized pacemaker (Electrodyne, model TR
3) for control of the heart rate. This unit has
been modified to provide faster rates of pacing.
The range of rate could thus be varied from 60
to 180 per minute. This pacemaker delivers a
nonphasic round-topped DC pulse of between
2 and 3 msec in duration and its voltage can be
varied from 0 to 15 volts. Right ventricular pressure or right atrial pressure, left ventricular pressure, and femoral artery pressure were measured
simultaneously with a P23Db Statham pressure
transducer. The first derivative of the femoral
artery pressure was measured using an R/C differentiating circuit. Mean arterial pressure was
obtained by electronic filtering. Heart rate was
measured from lead II of the electrocardiogram
simultaneously recorded with the dye curve.
Ejection time was measured from the indirect
carotid artery tracing by using a Sanborn pulse
and
others4-9 have described the hemodynamic consequences of varying the rate of artificial pacing of the right ventricle in patients
with complete heart block. Since the wires of a
permanent pacemaker for treatment of complete heart block are implanted in the left
ventricle and previous data were obtained
from right ventricular pacing, it becomes important to determine whether the site of implantation of pacemakers is a critical determinant of cardiac output in man.
Experimental studies in dogs by Fletcher
and associates10 with electrodes implanted in
the apex, the high lateral wall, and the posterior septal region of the left ventricle have
shown no significant differences in cardiac
output and mean arterial pressure. Lister
and co-workers," however, have demonstrated in dogs that the pacemaking site significantly influences cardiac output. Since this
information has been available only in dogs,
we have undertaken to study in man (1) the
influence of pacemaking sites on the hemodynamics of normal subjects, in patients with
compensated heart disease, and in patients
with heart failure, and (2) the contribution of
atrial systole to the cardiovascular dynamics
of the normal and the abnormal heart.
Methods
A group of 26 persons was studied. Twentyfour had normal sinus rhythm, one had conFrom the Institute for Cardiopulmonary Diseases,
Scripps Clinic and Research Foundation, La Jolla,
California.
Supported in part by National Institutes of Health
Research Grant HE-07983-03 and Graduate Training
Grant HE-5513-03, and by the Timken-Sturgis Foun-
*U. S. Catheter and Instrument Co., Glens
New York.
dation.
Circulation, Volume XXXIII, June 1966
MARVIN S. LIGGETr, M.D.
933
Falls,
BENCHIMOL, LIGGETT
934
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wave crystal microphone (model no. 374).12
Peripheral resistance, ventricular power, mean
systolic ejection rate, stroke power, and stroke
work were calculated from standard formulas.
Peak systolic pressure was used in the formula
of Sarnoff and associates13 for calculation of the
tension-time index. All pressures, dp/dt, carotid
tracings, and electrocardiograms were simultaneously recorded in the eight-channel Dr-8 oscilloscopic photographic recorder* at a paper speed
of 200 mm/sec with 20-msec time lines. A minimum of six consecutive beats was recorded, and
measurements were made for each heart beat
and averaged.
The cardiac output was determined with the
indicator-dilution technique using indocyanine
green as an indicator. A precalibrated dye-dilution
tube (BD-X 412 LST) with a one-way stopcock
was filled with 6.25 mg of dye. The indicator
was rapidly injected into the right ventricle or
right atrium, and the tube was flushed with 10
ml of 5% dextrose in water. A 50 ml lubricated
heparinized syringe was placed on a withdrawal
infusion pump (Harvard Instruments, model 600900), and blood was withdrawn from the femoral artery at a constant rate of 38.2 ml/min. A
Gilford cuvette densitometer (model 130 IR) was
used to detect the injected dye. After the dye
curves had been inscribed, the blood was reinfused into the patient's arterial system. Cardiac
outputs were obtained in duplicate and averaged.
The output of the densitometer was connected
to a dye-dilution computer (Sanborn model 130),
and cardiac output was calculated by this
means.14 At the end of the procedure the response
of the densitometer to two concentration standards
was obtained by using the same flow rate and
densitometer attenuation. Zero and two calibration values of 2 and 4 mg of dye per liter of
blood were obtained.
Types of Studies Performed
1. Right Ventricular and Right Atrial
Stimulation at Identical Rates
Nineteen cases were studied. In 14 cases the
right ventricle was stimulated first. After a series
of two to three control measurements the right
tained at the end of this period. In 12 cases the
right atrium could not be stimulated at rates
above 120 to 140 per minute because of nonconduction at the A-V junction.
The patients were divided into three groups:
group 1, eight normal subjects; group 2, seven
patients with compensated heart disease, and
group 3, four patients in heart failure.
2. Right Ventricular Stimulation at Various Sites
Six patients were studied. Initially, two or
three control measurements were obtained. The
tip of the electrode catheter was then positioned
in the outflow tract of the right ventricle. Several
minutes elapsed before measurements were obtained to determine with certainty by using
a fluoroscope whether the tip of the catheter
had moved to another position in the ventricle.
The pacemaker
was
then turned
on
to a rate
of
minute. Measurements were made at
this stimulation site. Subsequently, the tip of the
catheter was located in the midportion of the
right ventricle, and another set of measurements
was obtained. Finally, the tip of the catheter was
positioned in the inflow tract of the right ven100
per
tricle, and the same procedure repeated. The
changes in the configuration of the QRS complex
of the electrocardiogram demonstrated that in
fact the site of stimulation had changed when
the catheter was repositioned in the ventricle.
3. Right Ventricular and Left Ventricular
Stimulation at Identical Rates
The tip of the electrode catheter
was
placed
in the midportion of each chamber. Six cases were
studied. In three cases the left ventricle was
stimulated first, and in the remaining three cases
the right ventricle was the first chamber to be
paced. After a series of two to three control
measurements the right or the left ventricle was
stimulated at a progressive increase in rate (80,
100, 120, 140, 160, and 180 per minute) up to a
maximum of 180 per minute. For each set of rates
the stimulation lasted from 3 to 5 minutes and
measurements wvere obtained at the end of the
period.
Results*
atrium or the right ventricle was stimulated at a
progressive increase in rate up to a maximum of
180 per minute. Nine pairs of determinations
were made for each chamber in the following
order: the patient's own rate, 80, 100, 120, 140,
160, and 180 beats per minute. The artificial
stimulation for any given rate lasted approximately 5 minutes, and measurements were ob-
Eight persons were studied. The mean control heart rate was 81 for right atrial pacing
and 80 for right ventricular pacing. When the
pacemaker was turned on with the rate of 80
*Electronics for Medicine, North White Plains,
New York.
*Complete data in rough form
from Dr. Benchimol.
Right Atrial and Right Ventricular Pacing at
Various Rates
Group 1. Normal Subjects
may
be requested
CircTlation, Volume XXXIII, June 1966
CARDIAC HEMODYNAMICS
935
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per minute, there was an initial fall in cardiac
index, stroke index, mean arterial pressure,
ventricular power, tension-time index, ejection
time, stroke power, and stroke work for both
atrial and ventricular stimulation. With an
increase in rate of pacing there was a mild
stepwise increase in cardiac index, tension-time
index, dp/dt of arterial pressure with a stepwise fall in stroke index, peripheral resistance,
ejection time, stroke power, stroke work, and
systolic ejection rate (figs. 1 and 2). At a
pacemaker rate of 120 per minute the mean
difference between right atrial and right ventricular pacing for the cardiac index, stroke
index, mean arterial pressure, ventricular
power, and ejection time was 0.14 +
0.53 L/min/m,2 3±+ 5 ml/beat/m,2 2 + 12 mm
'Iz
46
z.,500
-I
_ v
20
1
i
130
O
.
C
t0
C')
O
HEART
0
100
120
t PAC ON
beat/min.
RATE
140
160
ISO
Figure 2
Mean tension-time index (T.T.I.), dpldt of femoral
artery pressure, ejection time (E.T.), stroke power
(S.P.), stroke work (S.W.) and systolic ejection rate
(S.E.R.) in a group of normal subjects (group 1)
during artificial stimulation of the right atrium (RA)
and right ventricle (RV) at various heart rates. Pac =
pacemaker. C = control.
v
c
C
; tr
5.
3.
a.
lI
Ij
I
'
C
80
100
120
140
ISO
ISO
t PA C. ON
HEART RATE -beat/min.
Figure
1
Mean cardiac index (CI.), stroke index (S.l), mean
femoral artery pressure (F.A. mean), peripheral resistance (P. Res.) and ventricular power (V.P.) in a group
of normal subjects-(group 1) during artificial stimulation of the right atrium (RA) and right ventricle (RV)
at various heart rates. Pac = pacemaker. C = control.
Circulation, Volume XXXIII, June 1966
Hg, 0.6 ± 1 kg-m/min/m,2 and 36± 32* msec,
respectively. These figures were not statistically significant as P values were not less than
0.05. Further increase in rate of atrial and
ventricular pacing to a maximum rate of 180
per minute resulted in a fall in cardiac index
and ventricular power -and a rise in peripheral
resistance while -stroke index,' ejection time,
stroke power, stroke work, and systolic ejection
*The number to the right of
standard deviation.
+
sign represents 1
BENCHIMOL. LIGGETT
936
I
uGroup z- Compens. Heart Dis.
.
0- RA pc.
-
14.
RV poc.
~~~~~~~~~~~~*;
2.
CSIL
105
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I,
Dr
--
-0
initial fall in cardiac index, stroke index, ventricular power, and dp/dt of arterial pressure
for both right atrial and right ventricular
stimulation. As the rate of stimulation increased, cardiac index, tension-time index,
and peripheral resistance rose up to rates of
120 to 140 per minute for both right atrial
and right ventricular pacing. Further increase
in rate of stimulation resulted in a progressive
fall in cardiac index, stroke index, ejection
time, stroke power, stroke work, and systolic
ejection rate for both right atrial and right
ventricular pacing (figs. 3 and 4). Mean
arterial pressure, ventricular power, and
*t
4000
Ck
o- RA pac.
0a RV pac.
IT
IW Group 2 - Compens. Heart Dic.
.';
t1.4
<lt
k , 3000-
d
A:t1*t
t200
2000
-
-
I
CY
C
60
100
t PAC. ON
20
140
160
ISO
HEART RATE -beats/min.
Figure 3
Mean cardiac index (C.I.), stroke index (S.I.), mean
femoral artery pressure (F.A. mean), peripheral resistance (P. Res.), and ventricular power (V.P.) in
group 2 patients with compensated heart disease,
during stimulation of the right atrium (RA) and
right ventricle (RV) at various rates. Pac = pacemaker.
C = control.
continued to fall. At the point of maximal
stimulation cardiac index, stroke index, peripheral resistance, ventricular power, tensiontime index, dp/dt of arterial pressure, stroke
power, stroke work, and systolic ejection rate
were slightly higher for right atrial pacing as
compared with right ventricular pacing. However, there was considerable variation within
the group, and the difference was not statistically significant.
350
250
.4
rate
Xj
1301o
_
O-
C
80
100
120
140
160
ISO
t PAC. ON
HEART RATE -beats/min.
Figure 4
Group 2. Compensated Heart Disease
studied. The
70-
mean
Mean tension-time index (T.T.I.), dp/dt of femoral
control cardiac index was 2.94 L/min/m2
prior to right atrial and right ventricular
artery pressure, ejection time (E.T.), stroke power
(S.P.), stroke work (S.W.), and systolic ejection rate
Seven patients
were
pacing. When the pacemaker was turned
at a rate of 80 per minute, there was
on
an
(S.E.R.) in group 2 patients during artificial stimulation of the right atrium (RA) and right ventricle (RV)
at various rates. Pac = pacemaker. C = control.
Circulation, Volume XXXIII,
June
1966
937
CARDIAC HEMODYNAMICS
dp/ dt did not change significantly. For any
given rate of stimulation, cardiac index, stroke
index, mean arterial pressure, ventricular power, tension-time index, dp/dt, ejection time,
stroke power, stroke work, and systolic ejection rate were generally slightly higher for
right atrial pacing as compared with right
ventricular pacing, and this was more evident
at higher rates of pacing. At a pacemaker
rate of 100 per minute the mean difference
between right atrial and right ventricular
pacing for cardiac index, stroke index, mean
arterial pressure, ventricular power, and ejec-
tion time was 0.47 ± 0.62 L/ min/m,2 4 ± 6
ml/beat/rM,2 9 + 9 mm Hg, 1.6 + 1.2 kg-m/
min/m,2 and 25±27 msec, respectively. The
figures were not statistically significant. The
changes in ventricular power were significant
to the 0.001 level and the ejection time
to 0.01 with higher figures for right atrial
pacing.
Group 3. Heart Failure
Four cases were studied. The mean control cardiac index was below the limits of
normal being 2.33 L/min/m2 for right atrial
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Figure 5
Electrocardiogram (ECG), phonocardiogram (PCG) at the mitral area (MA), right ventricular
(RV) and femoral artery (FA) pressures in one subject of group 3 before and during pacing
of the right atrium and right ventricle. Note an increase in right ventricular systolic and
end-diastolic pressures during ventricular pacing. The femoral artery pressure is higher
during atrial pacing.
Circulation, Volume XXXIII, June 1966
BENCHIMOL, LIGGETT
938
pacemaker rate of 100 per minute the mean
difference between right atrial and right ventricular pacing for cardiac index, stroke index,
mean arterial pressure, ventricular power, and
ejection time was 0.49 ± 1.5 L/min/m,2 4 ± 12
ml/beat/m,2 12 ± 20 mm Hg, 1.2 + 2.6 kgm/min/m,2 and 18 ± 46 msec, respectively.
These figures were not statistically significant
as P values were not less than 0.05.
1.11L
t, 55
5
A-V Junction Conduction
90
LuC2
t0
7
2200
]
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1600-
Twelve patients developed varying degrees
of nonconduction at the A-V junction at rates
of atrial pacing above 120 to 140 per minute.
In these patients an increase in rate of pacing
resulted in a progressive increase in the P-R
interval up to a point at which the refractory
period of the A-V junction was reached ret 5000
-Group 3-H*art Failure
usRApac.
0*- RV puc.
1
Ku
C
80
100
120
140
160
p 2000
180
t PAC. ON
HEART RATE - beats/min.
Figure 6
300 F
200-r
K
Mean cardiac index (C.I.), stroke index (S.I.), mean
femoral artery pressure (F.A. mean), peripheral resistance (P. Res.) and ventricular power (V.P.) in a
group of patients with heart failure (group 3) during
artificial stimulation of the right atrium (RA) and
right ventricle (RV) at various rates. Pac = pacemaker. C - control.
pacing and 2.43 L/min/m2 for right ventricular
pacing. At lower rates of right atrial and right
ventricular stimulation (80 per minute) there
was a fall in cardiac index for right ventricular
pacing while cardiac index rose for right atrial
paciing. A stepwise increase in rate of stimulation up to a rate of 120 to about 140 per minute resulted in a mild increase in cardiac index
and mean arterial pressure while stroke index,
ejection time, stroke power, stroke work, and
systolic ejection rate fell. Further increase in
rate of pacing up to a maximum of 180 per
minute resulted in a fall in cardiac index and
ventricular power, a rise in peripheral resistance, and a further decline in stroke index,
ejection time, stroke power, stroke work, and
systolic ejection rate (figs. 5 to 7). At a
250L
'15I
p.>
PI
t
PAC. ON
HEART RATE -beats min.
Figure 7
Mean tension-time index (T.T.I.). ejection time (E.T.),
stroke power (S.P.), stroke work (S.W.) and systolic
ejection rate (S.E.R.) in patients in heart failure
(group 3) during artificial stimulation of the right
atrium (RA) and right ventricle (RV) at various rates.
Pac = pacemaker. C = control.
Circulation, Volume XXXIII, June 1966
CARDIAC HEMODYNAMICS
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sulting in nonconduction with consequent reduction in ventricular response. Further increase in rate of pacing beyond the refractory
period of the A-V junction resulted in a
greater degree of nonconduction with further
reduction in the ventricular response. An increase in the current of the pacemaker signal
had no effect on the characteristics of this
response. In three patients intravenous administration of 1 mg of atropine sulfate given
at the rates which produced nonconduction
at the A-V junction resulted in abolition of
the block with return of 1:1 conduction. Under
the influence of this drug the rate of atrial
pacing could then be increased up to a range
of 160 to 180 per minute with 1:1 conduction.
The effect of this drug on A-V junction conduction was apparent within 1 minute after
its administration. A systematic study of this
problem and the effect of various drugs on
this type of block is presently being made
in our laboratory.
939
tract and the midportion of the right ventricle
for cardiac index, stroke index, mean arterial
pressure, ventricular power, and ejection time
was 0.06 ± 0.3 L/min/m,2 2 ± 2.5 ml/beat/m,2
2±4 mm Hg, 0.29 + 0.5 kg-m/min/m,2 and
3 + 3 msec, respectively. The figures were not
statistically significant as P values were not
less than 0.05.
The mean difference between pacing the
midportion and the inflow tract of the right
ventricle for cardiac index, stroke index, mean
arterial pressure, ventricular power, and ejection time was 0.19 ± 0.13 L/min/m,2 2 ± 1
ml/beat/m,2 1 + 5 mm Hg, 0.36 + 0.5 kg-m/
min/m,2 and 1 ± 3 msec, respectively. The
figures were not statistically significant as P
values were not less than 0.05.
Right Ventricular Versus Left Ventricular Pacing
Six persons were studied. Three were nor4.
Right Ventricular Pacing Sites
Six persons were studied. Three were normal, two had compensated coronary artery
disease, and one had congenital complete
heart block. Since no differences were found
between patients with heart disease and normal subjects, the results will not be described
separately.
During this study the outflow tract of the
right ventricle was paced initially, and this
was followed by stimulation of the midportion
of the right ventricle and lastly by stimulation
of the inflow tract of the right ventricle. The
rate of stimulation was fixed at 100 per minute.
No significant differences were found for
the three pacing sites for cardiac index, stroke
index, systolic, diastolic, and mean arterial
pressures, dp/ dt of arterial pressure, right
ventricular pressure, ejection time, tensiontime index, stroke power, mean systolic ejection rate, and stroke work (fig. 8). Cardiac
index, ventricular power, stroke power, and
systolic ejection rate were slightly lower for
the group during mid-right ventricular pacing,
but this was not statistically significant. The
mean difference between pacing the outflow
Circulatson, Volume XXXIII, June 1966
1400
2
35
.
25
OUT
INF.
MID
OUT
I NF.
MID
6.-
1L1
100
240-
4200
90jJj-I--
3100IVA
700
2 00 i
600
OUT
INF.
MID
OUT
I NF.
MID
Figure 8
cardiac
index
Mean
(C.I.), stroke index (S.I.), mean
femoral artery pressure (F.A. mean), dp/dt of femoral
artery pressure, peripheral resistance (P. Res.), ventricular power (V.P.), ejection time (E.T.) and tension-time index (T.T.I.) in six patients during stimulation of the outflow tract (out), midportion (mid) and
inflow tract (inf.) of the right ventricle at a fixed
heart rate of 100 per minute.
BENCHIMOL, LIGGETT
940
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mal, two had compensated coronary artery
disease, and one had compensated isolated
mitral stenosis. The left ventricle was stimulated first in three cases, and the right ventricle
was stimulated first in the remaining three.
The rate of stimulation ranged from 80 to 180
per minute. The changes observed for cardiac
index, stroke index, and other parameters of
cardiac function as a function of heart rate
were essentially the same as those described
for right atrial and right ventricular pacing
in patients with compensated heart disease
(group 2 of study 1). For any given rate of
right ventricular and left ventricular stimulation, there were no significant differences for
cardiac index, stroke index, arterial pressures,
right and left ventricular pressures, dp/dt,
eV
3.5 - -o0
('I
N:
c,j
RVpoc.
0
]
S.
LVpac.
3.5$
(I)
C
100
80
1
120
140
160
ISO
PAC. ON
HEART RATE
-
beats/min.
Figure 10
Mean tension-time index (T.T.I.), dp/dt of femoral
pressure, ejection time (E.T.), stroke power
(S.P.), stroke work (S.W.), and systolic ejection rate
(S.E.R.) during artificial stimulation of the right
(RV) and left (LV) ventricles at various rates. Pac
pacemaker. C control.
artery
1700r
I
NL
1500-
C
so
t
100
PAC. ON
120
140
160
180
HEART RATE -beats/min.
Figure 9
Mean cardiac index (C.I.), stroke index (S.I.), femoral
artery pressure (F.A. mean), peripheral resistance
(P. Res.), and ventricular power (V.P.) in six subjects
during artificial stimulation of the right (RV) and
left (LV) ventricles at various rates. Pac = pacemaker.
C - control.
peripheral resistance, ventricular power, ejection time, tension-time index, stroke power,
systolic ejection rate, and stroke work (figs.
9 and 10).
At a rate of 140 per minute the mean difference between right ventricular and left ventricular pacing for cardiac index, stroke index,
mean arterial pressure, ventricular power, and
ejection time was 0.10 + 0.3 L/min/m,2 0.7
+ 2 ml/beat/m,2 3 + 3 mm Hg, 0.1 0.7 kgm/min/m,2 and 15 +27 msec, respectively.
These figures were not statistically significant
as P values were not less than 0.05.
Circulation, Volume XXXIII, June 1966
CARDIAC HEMODYNAMICS
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Discussion
Experimental studies in dogs by Wiggersl5
demonstrated that pacemaking sites significantly influence cardiac performance. He
showed that ectopic beats produced by ventricular stimulation resulted in less effective
contraction by the ventricle from which the
ectopic beats had originated as compared
with those from the opposite ventricle. Subsequent studies by Corday a nd Irving'6 in
dogs showed that the site of an ectopic ventricular focus is an important determinant of
cardiac output, coronary bloodi flow, and arterial pressure at rates below 1l60 per minute.
More recently, Lister and associates"' provided further data substantiating the fact that the
site of artificial ventricular stimulation from
the epicardium significantly alters cardiac performance in dogs.
Our observations on patients with normal
and abnormal hearts with endocardial right
ventricular and left ventricular pacing and at
various sites in the right ventricle do not
support the previous observations on dogs.
No significant differences were found at various pacing sites in the right ventricle or between the left ventricle and the right ventricle.
Therefore, we are in agreement with the work
of Fletcher,10 Levy,17 Starzl18 and their associates and, by Williams-Olsson cand Anderson,'9
who demonstrated that sites of artificial
pacing do not significantly alter cardiac performance. At any given rate of stimulation
up to a maximum of 180 per minute, right
ventricular and left ventricular stimulation
results in similar changes in cardiac output,
stroke volume, mean arterial pr-essure, ventricular power, and other parameters of ventricular performance in both normal and abnormal
hearts. Furthermore, our data, at a fixed rate
of 100 per minute at various pacing sites
in the right ventricle provide further documentation that the site of an ectopic focus
does not significantly affect ventricular performance in man, either in norrmal or abnormal
hearts. These data have practical application
because of an increase in the number of
permanent pacemakers which are being used
for treatment of complete heart block. The
Circulation, Volume XXXIII, June 1966
941
wires of these pacemakers are most commonly
implanted in the left ventricular wall. Our
data suggest that these wires may be implanted in the right ventricle if necessary since
the hemodynamics of these two pacing sites
are nearly identical.
Cardiac output in the group of normal
subjects increased only slightly with an increase in rate. For a wide range of rate cardiac
output remained relatively stable but fell at
rates above 150 per minute. However, in the
group of patients with heart disease with
or without failure in whom cardiac output
was lower in the control figures, it rose with
increase in rate up to a range between 120
and 150 per minute. A further increase in
rate resulted in a marked fall in cardiac
output. These data confirm Braunwald and
associates' observations20 who also did not
detect significant changes in cardiac output
during a wide range of atrial pacing. The
mechanisms involved in these two types of
responses of the normal and abnormal heart
are not known. It is conceivable that a normal
heart may accommodate large variations in
stroke volume at the expense of changes in
stroke work and ventricular power whereas
in the diseased heart cardiac output rises
with an increase in rate because, to a great
extent, there are considerable limitations on
the variation of the stroke volume. Therefore,
in these patients, the increase in heart rate is
the predominant mechanism for the increase
in cardiac output. The mechanisms of the fall
in cardiac output at faster rates have been
described by Wiggers and Katz,2' Wiggers,22
Nakano,23 and Wegria,24 and Miller25 and
their colleagues, and are most likely related
to a decrease in diastolic filling time which
results in a decrease in coronary blood flow
and myocardial hypoxia.
It has long been suggested that the atria significantly contribute to ventricular filling.26-30
Most of the earlier studies2628 31' indicated
that the contribution of the atria to cardiac
output ranged from zero to as much as 30%.
The importance of atrial systole to cardiac
function in man has only recently been the
object of systematic study.32 3 In previous
942
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observations33 on patients with complete
heart block we have shown that a properly
timed atrial contraction (P-R interval of 1 to
300 msec) results in an increase in ejection
time (13%), isometric contraction time (6%),
systemic arterial systolic pressure (15%), dp/dt
of arterial pressure (14%), and tension-time
index (33%) as compared with figures obtained during a time when atrial systole occurs
during ventricular systole. Furthermore, our
studies indicated that the contribution of
atrial contraction to the increase in these
parameters occurs at a wide range of ventricular rate (20 to 125 per minute). However,
no measurement of cardiac output was obtained during that study and the question
was not answered as to whether or not atrial
contraction significantly improves cardiac output in man. Gilmore and associates36 have
shown in dogs that the left ventricle produces
less stroke work than atrial pacing does for
any given left ventricular end-diastolic pressure for ventricular pacing.
The present study indicates that in normal
human hearts cardiac output, stroke volume,
ventricular power, and ejection time are only
slightly higher during atrial pacing than during ventricular pacing for any given rate up
to a maximum of 180 per minute. However,
in the group with compensated heart disease
and in the group with heart failure, the
contribution of atrial systole appears to be of
greater significance. This difference appears to
be slightly higher at faster rates of pacing.
More recently, Samet and associates35
indicated that synchronous atrial and ventricular pacing results in slightly higher cardiac
output than asynchronous pacing does. However, this difference is relatively small and
variable. Data obtained from patients with
atrial fibrillation and after conversion to regular sinus rhythm have shown variable improvement in cardiac function.37-39 Our own data39
did not demonstrate any significant increase
in cardiac output at rest or during exercise
after conversion to sinus rhythm.
Recently, Braunwald and associates40 emphasized that atrial contraction does not significantly elevate left ventricular end-diastolic
BENCHIMOL, LIGGETT
pressure in the presence of ventricular dilatation. Burchell41 also stated that atrial contraction does not appear to be an important
regulatory mechanism of cardiac output. It
does become apparent that under certain
circumstances atrial systole may become an
important factor to the cardiac function. However, this contribution is highly variable and
to a great extent unpredictable. Nevertheless,
this contribution to cardiac output is relatively small and in the majority of cases the human heart may function at a wide range of
work loads without the contribution of a coordinated atrial contraction.
Summary and Conclusions
Artificial stimulation of the right atrium and
the right ventricle at rates between 80 and 180
per minute was performed in eight normal
subjects, in seven patients with compensated
heart disease, and in four patients with heart
failure. For any given rate of atrial or ventricular stimulation there were no significant
differences for cardiac index, stroke index,
mean arterial pressure, ventricular power, and
ejection time in normal subjects. In patients
with compensated heart disease there was a
slight tendency for higher figures for these
parameters during atrial pacing, but these
differences were not statistically significant.
Stimulation of the right and left ventricles
at equivalent rates in the range of 80 to 180
per minute did not show any statistically
significant changes for cardiac index, stroke
index, mean arterial pressure, stroke work
and power, ventricular power, ejection time,
tension-time index, and peripheral resistance.
Stimulation of the outflow tract, the midportion and the inflow tract of the right ventricle at a fixed rate of 100 per minute did
not show any significant changes in cardiac
index, stroke index, mean arterial pressure,
and other related parameters.
It is concluded that pacing sites do not
significantly influence cardiac dynamics in
unanesthetized man. Furthermore, the contribution of atrial systole to the cardiac function
is minimal in normal subjects but slightly
greater in patients with heart disease.
Circulation, Volume XXXIII, June 1966
CARDIAC HEMODYNAMICS
943
Acknowledgement
direct arterial tracings with special reference
to pre- and post-operative findings. Amer J
Cardiol 5: 728, 1960.
SARNOFF, S. J., BRAUNWALD, E., WELCH, G.,
CASE, R. B., STAINSBY, W. N., AND MACRUZ,
R.: Hemodynamic determinants of oxygen
consumption of the heart with special reference
to the tension-time index. Amer J Physiol 192:
148, 1958.
BENCHIMOL, A., AKRE, P. R., AND DIMOND,
E. G.: Clinical experience with the use of
computers for calculation of the cardiac output. Amer J Cardiol 15: 213, 1965.
WIGGERS, C. J.: Muscular reactions of the mammalian ventricles to artificial surface stimuli.
Amer J Physiol 73: 346, 1925.
CORDAY, E., AND IRVING, D. W.: Disturbances of
Heart Rate, Rhythm and Conduction, ed. 1.
Philadelphia, W. B. Saunders Co., 1961, p.
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LEVY, J. M., MESEL, E., AND RUDOLPH, A. M.:
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with ectopic beats. Amer J Physiol 203: 1141,
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STARZL, T. E., GAERTNER, R. A., AND WEBB,
R. C.: Effects of repetitive electric cardiac
stimulation in dogs with normal hearts, com-
We thank Miss Marilyn Hanna, Mrs. Mary Vensel,
Miss Shirley Cardwell, and Miss Ann Wall for their
technical assistance.
13.
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Circulation, Volume XXXIII, June 1966
Cardiac Hemodynamics During Stimulation of the Right Atrium, Right Ventricle,
and Left Ventricle in Normal and Abnormal Hearts
ALBERTO BENCHIMOL and MARVIN S. LIGGETT
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Circulation. 1966;33:933-944
doi: 10.1161/01.CIR.33.6.933
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