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Balance Between Right and Left Ventricular Output

Dean L. Franklin, Robert L. Van Citters and Robert F. Rushmer


Circ Res. 1962;10:17-26
doi: 10.1161/01.RES.10.1.17
Circulation Research is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright 1962 American Heart Association, Inc. All rights reserved.
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Balance Between Right and Left


Ventricular Output
By Dean L. Franklin, Robert L. Van Citters, M.D.,
and Robert F. Rushmer, M.D.

The right and left ventricles differ greatly


in their size, shape, architecture, and function.1' 2' 3' 4 Even so, these chambers must
eject quantities of blood precisely equal, except for the flow from the bronchial arteries
into the pulmonary veins, which is probably
less than 1 per cent of the systemic flow.5
This balance in right and left ventricular outputs must be maintained under equilibrium
conditions and also must be rapidly restored
during or after transitions from one flow rate
to another, in spite of many apparently adverse factors. For example, the right ventricle generally begins to empty before the
left. Consequently, the time course of ejection must be different in the two chambers.6' T Von Capeller8 reported that left
ventricular output could increase 40 per cent
without a change in right ventricular output
when the two ventricles were pumping into
different systems. Conversely, congenital defects in the partitions of the heart commonly
lead to a sustained right ventricular output
which is three to five times greater than the
output of the left ventricle. On the other
hand, the outputs of the two ventricles appear
to be equalized even after destruction of much
of the right ventricular wall9 or after extensive damage to the left ventricular wall by
myocardial infarction. These observations
indicate the extent to which the individual
ventricles may adjust their outputs under
varying conditions.
One of the oldest controversies in the field
of pulmonary circulation concerns the effects
From the Department of Physiology and Biophysics, University of Washington School of Medicine,
Seattle, Washington.
Supported by Grants H716 and H4531 from the
National Heart Institute, National Institutes of
Health, Bethesda, Maryland.
Eeceived for publication July 14, 1961.

of respiration on the blood flow into the


pulmonary artery.10' n Some investigators
believe that the act of inspiration increases
pulmonary resistance and reduces pulmonary
flow, while others believe that inspiration increases "venous return" and augments right
ventricular output. In either case, the outputs of the two ventricles should be augmented at different phases of the respiratory
cycle so that the fluctuations should be out
of phase. Similarly, during sudden changes
in the circulatory flow (e.g., exercise) or redistribution of blood (e.g., during changes in
posture), accelerated right ventricular flow
has been postulated to precede the augmented
left ventricular output by an interval related
to the circulation time through the lungs.
Actually, entrance of blood into the pulmonary artery should cause an efflux of blood
from the pulmonary veins after an interval
equal to the pressure pulse propagation time.
The restoration of balance in the right and
left ventricular outputs is generally explained in terms of the length-tension relationship
emphasized by Starling.12 According to this
hypothesis, increased inflow into the right
ventricle would cause that chamber to distend progressively over a few beats as the
energy release and stroke volume attained a
new higher level. After traversing the pulmonary vascular bed, the additional flow
would progressively distend the left ventricle. Thus, during the transition from one
flow level to another, the filling pressures
and outputs of the two ventricles would be
demonstrably out of phase with adjustments
in the left ventricular output lagging several
cycles behind. Recently, Guz et al.13 reported
that the outputs of the two ventricles were
out of phase during respiratory variations
when the two flows were measured simultaneously.

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17

18

FRANKLIN, Van CITTEES, RUSHMER

HYPOTHESIS

This study was designed to test the hypothesis that balance in ventricular output is
maintained or restored in accordance with the
Starling mechanism and to determine the extent to which changes in the output of the
two ventricles are out of phase during spontaneous cardiovascular adjustments.
EXPERIMENTAL DESIGN

The balance of ventricular output has


usually been studied either by comparing
venous or arterial pressure in intact animals
or men, or by measuring flow in and out ot'
the ventricles in anesthetized thoracotomized
animals. Exposed to an abnormal environment, the hearts of thoracotomized animals
are greatly reduced in size14 and beat rapidly.
Furthermore, general anesthesia depresses or
distorts neural reflex adjustments and eliminates spontaneous activity.
In order to circumvent these difficulties and
limitations, the outputs of both ventricles
were recorded simultaneously by flowmeters
chronically implanted in intact conscious
dogs, and the spontaneous cardiovascular adjustments to respiratory activity, changes in
posture, and exercise were studied.
Methods
The patterns of right and left ventricular ejection in eight dogs were recorded simultaneously
from two pulsed ultrasonic flowmeters positioned
on the ascending aorta and on the main pulmonary
trunk (fig. 1). The pulsed ultrasonic flowmeter,
which has been described previously, is based on
the principle that sound waves passing through
moving fluid travel iit a greater net velocity downstream than upstream.1"'-18 Briefly, two barium
titanate crystals are mounted diagonally across a
bivalved plastic cylinder. Bursts of ultrasonic
waves (3 megacycles) travel along the diagonal
path between the crystals, alternating in direction
400 times per second. When the fluid between the
crystals is motionless, the transit time of sound is
precisely equal in the two directions. If the fluid
is moving along the channel, the difference between
the transit times upstream and downstream is
linearly related to the flow velocity as sampled
across the tube. The plastic cylinder prevented
expansion of the vessels. Records could be calibrated to indicate volume flow by computation and
by perfusion of known volumes through the gauges
in situ (seefig.1).

Additional variables were recorded in SOUK; of


the experiments. The diameter of the left ventricle
was measured continuously by sonocardiometry17
in two dogs (fig. 1, dogs V34 and V44). Left ventricular pressure was recorded routinely through
an indwelling polyethylene cannula extending from
the left atrial cavity through the back to the outside (seefig.1). At times, this pressure was determined by retrograde arterial catheterization.
Pressure in the right ventricle was recorded
through a catheter inserted into the jugular vein
in some instances and through an indwelling atrial
cannula in others. In three additional dogs, ultrasonicflowmeterswere installed on the inferior vena
cava and on the ascending aorta, to determine the
extent to which the flow into the right ventricle
altered before the flow into the left (fig. 5). In
all experiments, the heart rate was continuously
recorded by a ratemeter triggered by the steeply
rising phase of the pressure or flow pulses.
Stroke volume was recorded by means of an
electronic integrator which was reset after the completion of each cycle, so that the deflection was
proportional to the area under the flow curve of
each cardiac cycle. For each systole a step was
produced, the height of which was proportional to
the stroke volume. To facilitate inspection, the deflections indicating the stroke volumes of the two
ventricles were adjusted until the amplitudes were
approximately equal, even though the aortic flowmeter did not register the flow through the coronary arteries. In some records, the cardiac output
was indicated continuously by means of an integrator circuit with a long time constant (figs. 3
and 4). In the experiment illustrated in figure 5,
cardiac output was indicated by an integrator that
returned to the baseline every 2.5 seconds (stroke
flow integrated).
The flowmeters and cannulas were installed under
aseptic conditions and the experiments were conducted from 5 to 30 days after the surgery. Five
of the eight dogs were active and appeared healthy
within a. few days after surgery; the other three
remained lethargic and displayed rapid and forced
breathing. Previous experience had indicated that
these signs were characteristic of postoperative
atelectasis, usually with hydrothorax. This diagnosis was confirmed by thoracentesis and by postmortem examination in these animals. Experiments were conducted on these three dogs to
determine the effect of pulmonary collapse on the
functioning of the right and left ventricles. In
one, a pressure drop of some 40 mm. Hg within
the main pulmonary artery was demonstrated by
withdrawing a catheter and was ascribed to obstruction of the pulmonary artery by angulation
of the flow section. These studies of ventricular
function under abnormal thoracic conditions proCirculation Research, Volume X. January 1962

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19

RIGHT AND LEFT VENTRICULAR OUTPUT

duced most illuminating results. In the animals


which appeared healthy, the lungs were well inflated, the pleurnl spaces were free of fluid, and
the pulmonary artery nnd aorta were widely
pa tout.
Results

Typical wave forms of the instantaneous


flow velocity through the pulmonary artery
and aorta in a healthy dog are illustrated in
figure 1 (dog V22). The ejection patterns
from the two ventricles had distinctive differences in the healthy dogs. Ejection from
the right ventricle generally preceded the
onset of outflow from the left by intervals
ranging up to 0.02 seconds. In no case did
left ventricular ejection begin before right
ventricular ejection, although the patterns
sometimes appeared to begin simultaneously
(fig. 1, dogs V34 and V44).
The right ventricular ejection pattern displayed a gradually rising flow, reaching a
rounded peak in midsystole. Left ventricular
outflow rose abruptly to a sharp peak in early
systole and then declined toward zero flow,
slowly at first and then more rapidly. At
the end of systole, left ventricular ejection
was terminated abruptly by a retrograde
surge of blood, apparently associated with
a snapping closure of the aortic valve. Right,
ventricular ejection continued after left
ventricular outflow had ceased.
The temporal relations between the outflow
pattern and the change in the diameter of
the left ventricle are illustrated in figure ]
(dog V34). The ejection velocity reached a
peak early in systole when the diameter was
diminishing most rapidly. During late systole,
the left ventricular diameter decreased more
gradually as the ejection slowed. Thus, the
ejection patterns are consistent with the
changing ventricular diameter to the extent
that a single dimension can serve as an indicator of the change in the volume of the
ventricle.
The peak in the ventricular systolic pressure rose rapidly during the isovolumetric
contraction period and during early systole
when the ejection velocity increased most
rapidly (fig. 1, dog V44). The pressure
Circulation Research,

then leveled off and descended during the


later portions of systole as the ejection
slowed. The patterns of right and left ventricular pressure are very similar in wave
form but very different in amplitude. Systolic pressure was much lower in the right
ventricle than in the left, reflecting the lower
hydraulic impedance to flow through the pulmonary circulation as compared with the
systemic circulation. On this basis the peak
ejection velocity of the right ventricle might,
be expected to be higher and occur earlier.
The slower ejection of the normal right ventricle must, therefore, reflect differences in
either the architecture or the effective rate of
myocardial shortening of the two A'entricles.
The ventricular ejection patterns of the
healthy dogs differed from those of the dogs
with hydrothorax and atelectasis as illustrated in figure 2. In each animal with pulmonary atelectasis, the right ventricular ejection pattern displayed an abrupt rise in flow
velocity, reaching a peak in early systole.
The velocity then descended toward the zero
level, gradually at first and then more quickly. In addition, systole terminated with a
retrograde surge, which was more abrupt than
is observed under more nearly normal conditions. Thus, the right ventricular ejection
pattern altered to conform more closely to
the left ventricular ejection pattern under
conditions in which the outflow resistance was
increased (i.e., pulmonary atelectasis and pulmonary stenosis).
EFFECTS OF RESPIRATORY ACTIVITY

In the dogs that appeared healthy, the flow


velocity and stroke volume (integrated flow1)
from the pulmonary artery and aorta changed
very little during normal respiratory activity.
Pulmonary flow reached higher levels during
the inspiratory phase. Although these small
respiratory fluctuations in the output of the
two ventricles appeared to be almost exactly
in phase, careful examination indicated that
the right ventricular changes preceded the
left ventricular fluctuations by one cardiac
cycle in most instances. Tn contrast, flow
patterns recorded from the animals with hy-

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20

FRANKLIN, Van CITTERS, RUSHMER


DOG a

V22

DOG * * V 4 4

Pulmonary Flow
|,,T , li. 14 . L

Right Ventricular Pressure

Left Verrtriculor Pressure

Pulmonary Flow

MO-

Aortic Flow

Left Ventricular Diameter

FIGURE 1

The instantaneous flow velocity patterns from the pulmonary artery are generally rounded
with peak flows in midsystole in a healthy dog (V22). Aortic flow reaches a much higher
peak in early systole and has a much sharper retrograde surge at the end of systole. The
relations het-ween the flow patterns and left ventricular diameter (V34), and between
flow and right and left ventricular pressures (V44) are shown.

drothorax aud pulmonary atelectasis consistently revealed greatly accentuated fluctuations


in outflow from both the right and left ventricle. These greatly exaggerated fluctuations
were nearly 180 degrees out of phase with
the right ventricular stroke volume approaching minimal values at times when left ventricular stroke volume approached peak levels
(fig. 2B). As the hydrothorax was alleviated
by thoracentesis, the respiratory fluctuations
in the ventricular stroke volumes became attenuated and were almost in phase (fig. 20).
Tn three animals, injection of fluid into the
thorax produced greatly augmented respiratory fluctuations, which were again out of
phase.
CHANGES IN POSTURE

When a dog is induced to stand erect, the


long hydrostatic columns of blood should
cause distention of the dependent veins, so

that "venous return" and stroke volume


would be transiently reduced, first in the
right ventricle and then in the left. Records
obtained as a dog was elevated into an erect
position and lowered again to the normal
standing position are illustrated at slow paper
speed (0.25 mm./sec.) in the left hand column of figure 3. On an expanded time scale
(50 mm./sec), the changes in right and left
ventricular output could be followed stroke
by stroke. A progressive fall in stroke volume
in both ventricles accompanied the increase
in heart rate. There was, however, a slight
discrepancy in stroke volume between the two
ventricles, as designated by arrows 1 and 2
in figure 3. When the animal was permitted
to resume the standing position, the sequence
of ventricular adjustments was similar, but
there were more examples of reciprocal
changes in ventricular stroke volume. The
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21

EIGHT AND LEFT VENTRICULAR OUTPUT


B. HYDROTHORAX

A. CONTROL

C POSTTHORACENTESIS
(2 LITERS)

(ATELECTASIS)
PULMONARY ARTERY

AORTA

RIGHT VENTRICLE
y_ , r : : : : : ; .rf u , r t r : t ; . : . - : - ? i i

c:;

I Sc

10 Sec
RESPIRATION
Insp I

FIGURE 2

7n healthy dogs, the respiratory fluctuations in right and left ventricular outflow
are very slight and almost in phase. (B) In dogs with hydrothorax and pulmonary atelectasis, the respiratory fluctuations are exaggerated and almost ISO degrees out of phase.
The pulmonary flow pattern closely resembles the typical aortic flow pattern with the
peak velocities reached in early systole. (C) Relief of hydrothorax by thoracentesis reduces the magnitude of the respiratory fluctuations and brings them more nearly in phase.

onset of increased right ventricular output in


advance of the left ventricular adjustment
was only occasionally observed in this series
of experiments.
RESPONSES TO EXERCISE

An abrupt onset of exercise without previous warning might produce a transient imbalance between right and left ventricular
outputs. A highly trained dog, standing
quietly on a motor-driven treadmill, can be
induced to exercise almost instantaneously
and unexpectedly by the mere closing of a
switch.
The sequence of events at the onset of such

an exertion was analyzed, stroke by stroke,


in dogs with flowmeters on the pulmonary
artery and aorta. The instantaneous flow
patterns in the pulmonary artery and aorta,
as well as the integrated stroke volume records, are presented for comparison in figure
4. In general, the stroke volumes of the two
ventricles increased together at the onset of
exercise, but on any record occasional cycles
showed ventricular stroke volumes which
varied in opposite directions (see numbered
arrows) without any consistent pattern.
The changes in stroke volume of the two
ventricles were so evenly matched that it

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22

FRANKLIN, Van CITTERS, RUSHMER

PULMONARY
ARTERIAL
FLOW

. : ..

f&Sl,

Itt ;.....
RIGHT VENTRICULAR STROKE VOLUME
12

JJ.JJJJJJJJJJJIJIjJ

Jjfffffin J^
ASCENDING AORTIC FLOW

LEFT VENTRICULAR STROKE VOLUME

* 41
JJJJJJJJjJJiimrfMJjjJJJjJJJJJJJJJj.
CARDIAC OUTPUT

HEART RATE - PPM


240180t-.SMM/Ste-l

25 VV

;,.

FIGURE 3

2'fee pulmonary and aortic flow velocity and right and left ventricular stroke volumes are
all greatly reduced transiently when the dogs assume an erect position. These changes
all occur simultaneously and accompany ai transient tachycardia such that the cardiac output remains unchanged. A similar effect of smaller magnitude occurs during the return
to normal standing position.

would be difficult to state with confidence that


either ventricle responded before the other.
In many different exercise responses at treadmill speeds up to 4 m.p.h. on grades up to
12 per cent, there was no obvious tendency
for the output at the right ventricle to increase before that of the left.
During the exercise responses illustrated in
figure 4, the heart rate reached a high peak
abruptly after the treadmill started and then
diminished transiently before ascending to a
sustained plateau. During the wide excursions iu heart rate, the stroke volume varied
reciprocally so that the cardiac output rose
smoothly and progressively.
When an increased "venous return" was
experimentally induced by a rapid intravenous injection of saline, the right ventricular
stroke volume increased progressively for

a few beats and then diminished. The left


ventricular output increased similarly after a
lag of at least three cardiac cycles. This observation demonstrates that a phase lead of
the right ventricle can be readity detected by
the techniques employed here and, in fact,
was noted during abnormal respiratory activity (pulmonary atelectasis) and during experimentally accelerated "venous return." The
expected phase lead of right ventricular output did not occur during any of the responses
to exercise observed in this series.
If increased cardiac output is initiated by
increased "venous return," the inflow into
the right ventricle through the inferior vena
cava should be augmented before outflow from
the left ventricle increases. In the experiment illustrated in figure 5, three different
exercise responses were recorded at three
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23

EIOHT AND LEFT VENTRICULAR OUTPUT


PULMONARY ARTERIAL FLOW
Exercise

Treadmill exercise- 3 m.p.h. - 12% grade-

RIGHT VENTRICULAR STROKE VOLUME

JJJJJJ
ASCENDING AORTIC FLOW

0-

- I *'."*. N,

LEFT VENTRICULAR STROKE VOLUME


4
1

o-1
CARDIAC OUTPUT

0-

HEART RATE - PPM.

240180-^120- *"
60FIGURE 4

Slow paper records (0.25 mm./sec.) demonstrate that peak flow velocity in the aorta
and pulmonary artery and aorta are increased during exercise. Both right and left ventricular stroke volume diminish just before the treadmill is turned, on ("anticipation"?)
and increase transiently at the beginning of exercise. These changes in stroke volume
appear to occur essentially simultaneously except for random imbalance in specific cycles.

different paper speeds. In the record at slow


paper speed (0.1 rain./see.) showing the entire exercise response, the changes in all variables appear to be completed very promptly.
Tn the response recorded at faster paper speed
(10 mm./sec.) the heart rate and peak instantaneous flow velocity increased over several cardiac cycles. The increase in cardiac
Circulation

output is indicated by the steeper slope of


the integrated stroke flow record. Large
fluctuations in right a trial pressure and inferior vena caval flow appeared at the onset
of exercise and may have been associated with
the vigorous respiratory excursions, which
lasted an interval equivalent to two or three
cardiac cycles. At the end of that time the

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24

FRANKLIN, Van CITTERS, RUSHMER


EXERCISE
3mjin-5%gra
OJmm^ec

CONTROL
50mm*t
HEART RATE

EXERCISE
5 0 mm/sec

EXERCISE
10 mm /sc

AORTIC FLOW
(INSTANTANEOUS)

STROKE FUCW
(IMTEGRATEDI

RT ATRIAL PRES

1VC FLOW

EXERCISE

FIGURE 5

The time relations between increased inflow through the inferior vena cava and the outflow through the aorta at the onset of treadmill exercise are illustrated by records from
three responses from the same dog recorded at different paper speeds. Left ventricular
outflow as indicated by the slope of dotted lines in middle record, is increased by the time
that increased inferior vena ca'val floio is established.

inferior vena caval flow was sustained at a


higher mean level, and the slope of the integrated stroke volume record was steeper (see
dotted line in middle of record). Thus, right
ventricular inflow and left ventricular outflow appeared to increase almost simultaneously. Faster paper speeds did not permit
more accurate timing because of the fluctuations in the vena caval flow. However, the
increase in cardiac output at the onset of
exercise could not be clearly ascribed to accelerated inflow into the right ventricle, or
to increased "venous return." Furthermore,
a phase lead of right ventricular adaptation
in advance of left ventricular adjustments
could not be established by these observations.
Limitations of the Experiment

All but three of the dogs studied in this


series of experiments were active aud appeared healthy at the time of the experiments

(i.e., presented no obvious evidence of malfunction). However, all the dogs had recently undergone thoracic surgery and could
not reasonably be regarded as "normal," even
20 or 30 days after the operation. In the best
of these preparations, there was no abnormal
collection of fluid in the chest and adhesions
of pleura and pericardium were minimal.
However, all showed evidence of the previous
surgical manipulations within the thorax. In
three dogs, frank thoracic pathology was present in the form of rather' severe hydrothorax
and pulmonary atelectasis. Furthermore,
demonstrable obstruction in the pulmonary
artery had been produced in one dog by angulation of the plastic flow section. In the other
animals, the aortic and pulmonary arteries
were Avidely patent within thefloAvsections,
although the cross-sectional area had been
slightly reduced to prevent changes in circumference by the pressure pulses. Coronary
Circulation

Research,

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25

RIGHT AND LEFT VENTRICULAR OUTPUT

flow was not included in the output of the


aortic flowmeter.
The differences in wave form between right
and left ventricular ejection patterns cannot
be ascribed to deficiencies in the ultrasonic
flowmeters, which were identical at the two
sites and had frequency responses flat to 30
c.p.s. or above. Right ventricular ejection
patterns were distorted to resemble wave
forms typical of the left ventricular outflow
when the pulmonary resistance was increased
(i.e., by pulmonary atelectasis and pulmonary
stenosis).
The sudden and unexpected starting of a
treadmill is a desirable method of producing
an abrupt response to exercise but is likely
to cause a startle reaction which could complicate the picture to some extent. For example, the transient increase in the heart rate
at the onset of exercise was not characteristically observed in earlier experiments in which
the treadmill was accelerated rapidly rather
than started at full speed by the switch (see
fig. 4). Furthermore, in trained animals, the
ventricular performance often changes before
the exercise when the slightest clue is given
that the treadmill is about to be started.18
Extrapolations

The observation that the stroke volumes of


the right and left ventricles change almost,
if not precisely, in phase under different conditions was unexpected, since it was contrary
to popular opinion based on many studies on
anesthetized thoracotomized animals. Since
pulmonary atelectasis apparently caused the
ventricular responses to be greatly accentuated and almost 180 degrees out of phase, it
is tempting to assume that this abnormal situation is common to standard open-chest dog
preparations.
The precise balance between right and left
ventricular outputs suggests that the pulmonary circulation may normally offer so
little resistance to flow that even a slight increase in the output of the right ventricle is
promptly reflected in flow from the left. Interposing abnormally high resistance between
the two ventricles in the form of pulmonary

atelectasis or pulmonary obstruction accompanied by forced breathing consistently produced cyclic right and left ventricular responses that were grossly out of phase.
A number of factors could operate to cause
the ventricular stroke volumes to change together. Both ventricles beat the same number
of times per minute and have corresponding
changes in diastolic filling interval. Furthermore, during cardiovascular adjustments both
ventricles are likely to be bombarded by discharges along sympathetic nerves to produce
changes in the performance of the myocardium.
Summary

The right ventricular ejection pattern is


characterized by early onset, gradual rise to
peak flow velocities in midsystole and gradual
return to baseline. Left ventricular ejection
begins very shortly after right ventricular
systole, abruptly reaches peak flow, and diminishes during the remainder of the systolic
interval, terminating with a brief, sharp,
retrograde surge as the aortic valves close.
The duration of ejection is shorter in the left
ventricle than in the right. In healthy dogs,
respiratory activity produces very slight fluctuations in right and left ventricular output
that are almost in phase. In dogs with hydrothorax and pulmonary atelectasis, the right
and left ventricular outputs fluctuate in
greatly exaggerated fashion with each forced
respiratory effort. Under such conditions, the
changes in right and left ventricular stroke
volume are nearly 180 degrees out of phase.
Pulmonary outflow resistance is increased and
the right ventricular ejection pattern closely
resembles those generally characteristic of the
left ventricle. Assume that the erect posture
causes cardio-acceleration and large changes
in right and left ventricular stroke volume,
which are essentially synchronous. Treadmill
exercise with sudden and unexpected onset
produces changes in the outputs of the right
and left ventricles without obvious lead or lag
of one ventricle over the other. These experiments do not support the concept that changes
in "venous return" are dominant mechanisms
inducing alterations in cardiac output.

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26

FRANKLIN, Van CITTERS, RUSHMER

Acknowledgment
The contributions of Mr. Donald Baker, Mr.
William Schlegel, Mr. Nolan Watson, Mr. Donald
Harding, and Mr. Raymond Smith in the construction, maintenance, and operation of the electronic
recording and computing systems are gratefully
acknowledged.

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