Download Isolated Ventricular Systolic Interaction During

944
Isolated Ventricular Systolic Interaction
During Transient Reductions in
Left Ventricular Pressure
John C. Woodard, Edna Chow, and David J. Farrar
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The volume and pressure of one ventricle have been demonstrated to modulate the volume and pressure in the
contralateral chamber during systole and diastole. To quantitate the isolated systolic effects of left ventricular
(LV) pressure on right ventricular (RV) mechanics, we rapidly withdrew blood from the LV immediately after
diastole via an apex cannula during a single cardiac cycle in eight open-chest, open-pericardium anesthetized
pigs (45 kg) and studied the effects on the RV. Reductions in LV pressure of up to 75 mm Hg were achieved
in midsystole without changing LV or RV diastolic volume or pressure. Resultant changes in RV flow and
pressure development during these single unloaded beats may therefore be considered to result from pure
systolic interaction. The instantaneous left-to-right systolic pressure gain [G(t)] was determined as the ratio
of RV pressure change to LV pressure change as a function of time during systole, and the mean LV-to-RV
systolic pressure gain was determined as the ratio of changes in mean systolic RV pressure to changes in mean
systolic LV pressure. During LV unloading, there was an average reduction of 62.6+12.3% in the mean systolic
LV pressure, which resulted in decreases of 13.6±6.4% in mean RV systolic pressure, 17.9±10.4% in RV stroke
volume, and 27.0±113% in RV stroke work. G(t) was found to vary significantly within systole, reaching a
minimum of 0.042±0.014 mm Hg/mm Hg at normalized time 0.70 of the systolic duration and a maximum of
0.079+0.029 at the end of RV ejection. The midsystolic value for G(t) was 0.055±0.028, and the mean systolic
gain was 0.054±0.017 mm Hg/mm Hg. These results demonstrate that, independent of diastolic conditions,
there is a substantial transmission of systolic forces from the LV that contributes to RV ejection and that the
pressure interaction gain varies within the systolic portion of the cardiac cycle. (Circulidon Research
1992;70.944-951)
KEY WORDS * ventricular systolic interaction * ventricular interdependence * ventricular function
It is well established that the volume and pressure in
one ventricle may directly interact with the volume
and pressure in the contralateral chamber.1-19
Ventricular interaction may be divided into that occurring during passive ventricular filling (diastolic interaction) and that occurring during contraction (systolic
interaction). Diastolic interaction has been appropriately termed "ventricular interference"3 and manifests
itself as decreases in ventricular compliance with increases in contralateral chamber pressure and volume,
an effect that is potentiated at high end-diastolic volumes by the presence of the pericardium.'
The same shared ventricular anatomy that is responsible for diastolic interaction also permits transmission
of contractile forces between the ventricles. Since these
forces are much greater in the left ventricle (LV) than
in the right ventricle (RV), there could be a substantial
left-to-right systolic ventricular interaction that contributes to RV performance. However, only a few studies or
From the Medical Research Institute and the Department of
Cardiovascular Surgery, California Pacific Medical Center, San
Francisco.
Supported in part by grants 1-RO1-HL-32202 and 1-RO1-HL45608 from the National Heart, Lung, and Blood Institute.
Address for reprints: David J. Farrar, PhD, California Pacific
Medical Center, 2351 Clay Street, Room S637, San Francisco, CA
94115.
Received May 29, 1990; accepted December 27, 1991.
computer models have attempted to quantitate LVto-RV systolic interaction,6'18'19 and there have been no
studies determining the variation in systolic ventricular
interaction during the cardiac cycle.
Therefore, the purpose of the present study was to
measure isolated systolic LV-to-RV interaction in the
intact heart with a new technique using transient reductions in LV pressure during the systolic portion of a single
beat. By this means, the dependence of RV pressure on
LV systolic pressure could be quantitated as a function of
time during systole, independent of end-diastolic conditions. The results demonstrate a substantial contribution
of LV pressure to RV systolic performance.
Materials and Methods
Eight farm pigs (weight, 42-48 kg; average, 44.6 kg)
were premedicated with ketamine (20 mg/kg) and then
anesthetized with thiamylal sodium (initial bolus of 4.5
mg/kg and supplemental doses of 2.5 mg/kg every 15
minutes). A tracheostomy was performed, and the animal was ventilated using a mixture of oxygen and room
air. Blood gases were maintained in the physiological
range by adjustment of respiratory rate, fraction of
inspired oxygen, and tidal volume. Administration of 3
mg pancuronium bromide every 15 minutes was used
for muscle relaxation during data collection.
After the heart was exposed via a median sternotomy
and supported in a pericardial cradle, a cannula (16 mm
Woodard et al Ventricular Systolic Interaction
945
and pneumatic drive pressure were recorded for timing
purposes from an electromagnetic flow probe (Carolina
Medical Electronics) and a Statham transducer, respectively. Data were recorded on a direct-writing chart
recorder (model 2800, Gould, Cleveland, Ohio) and
digitized on a PDP 11/23 minicomputer (Digital Equipment Corp., Marlboro, Mass.) at a rate of 100 samples
per second.
Experimental Protocol
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FIGURE 1. Schematic diagram of experimental preparation
illustrating the method for pressure unloading the left ventricle
and the instrumentation used to measure the resulting ventricular interaction. AoP, aortic pressure; PA flow, pulmonary
artery flow; PAP, pulmonary artery pressure; RVP, right
ventricular pressure; LVP, left ventricular pressure; RVAP,
right ventricular anteroposterior dimension; RVSFW, right
ventricular septal-free wall dimension; LVSFW, left ventricular septal-free wall dimension; VAD, ventricular assist
device. Triggering the ventricular assist device from the R
wave allowed rapid withdrawal of blood from the left ventricle
via the apex cannula (arrow) during ventricular systole.
i.d.) was inserted into the apex of the LV and connected
to a ventricular assist device (VAD) (Thoratec, Berke-
ley, Calif.).20 The outlet port of the VAD was blocked,
and the one-way valves were removed so that blood was
both withdrawn and returned to the LV through the
apex cannula (Figure 1). Normal operation of a VAD
involves the cyclical application of vacuum and pressure
to the flexible blood sac in a rigid housing to fill and
empty the pump. However, in these experiments, the
VAD driver was modified to allow a single rapid filling
of the VAD triggered by the R wave of the electrocardiogram.
Cardiac dimensions were obtained using a sonomicrometer (Triton, San Diego, Calif.). The anteroposterior RV dimension was measured from a pair of hemispheric crystals sutured to the epicardium; septal-free
wall dimensions for both ventricles were obtained from
hemispheric crystals on the epicardium of the respective
ventricular free walls and a cylindrical crystal placed via
a 16-gauge needle track into the ventricular septum
(Figure 1).
Catheter-tipped manometers (SPC 350, Millar Instruments, Houston, Tex.) were inserted via stab
wounds in the ventricular free walls to measure RV, LV,
and pulmonary artery pressures. Aortic pressure was
recorded from a Statham transducer/fluid-filled catheter. An electromagnetic flow probe (Carolina Medical
Electronics, King, N.C.) was placed around the pulmonary artery to measure RV stroke volume. VAD inflow
Eight-second data sets were taken with respiration
suspended at end expiration. Control data, consisting of
the first five to eight cardiac cycles, were recorded with
the VAD driver supplying a pressure of 200 mm Hg,
which was well in excess of the LV systolic pressure and
thus ensured that the VAD blood sac was empty. After
the R wave of the unloaded beat, pneumatic drive
pressure was rapidly reduced to -100 mm Hg, allowing
the VAD to fill at a rate determined by the difference
between the pneumatic drive pressure and that in the
LV and the fluid impedance of the cannula. After each
data set, the VAD was emptied into the heart, and
sufficient time was allowed for stabilization before the
unloading sequence was repeated for a total of five sets
for each animal. Verification that end diastole was
unaffected by unloading was provided by the absence of
change in the end-diastolic pressure and cardiac dimensions from that of the preceding control beats.
Data Analysis
Data records were analyzed using software developed
in our laboratory. Any recording with unstable ventricular pressures or electrocardiographic evidence of arrhythmia during the control period was excluded. Pressure and flow waveforms from the five to eight cardiac
cycles before the unloaded cycle were averaged to
define the control beat, which was then subtracted from
the unloaded beat. The resulting differences in pressure
(as a function of time) were then used to calculate the
instantaneous gain. Because of heart rate differences
between animals, the period of systole was normalized
such that the time from end diastole to the end of RV
ejection ranged from 0.0 to 1.0. The intervening time
between these points was divided into 5% incremerts,
and the corresponding pressures and flows at each of
the 21 points were calculated by linear interpolation of
the sampled points.
The instantaneous left-to-right pressure gain is defined as the ratio (mm Hg/mm Hg) of RV pressure
change to LV pressure change (from the control to the
unloaded beat). Instantaneous gains were calculated for
the last 70% of systole, by which time the LV pressure
was consistently reduced in all animals. The "midsystolic" gain was defined as the average gain between
normalized systolic times of 0.4 and 0.6. Mean pressure
gain was defined as the ratio of changes in mean RV
systolic pressure divided by changes in mean LV systolic
pressure. The mean systolic pressures were in turn
calculated by integration of LV and RV pressures
during systole. RV stroke volume was computed by
integration of pulmonary artery flow, and RV stroke
work was computed from the product of mean RV
developed pressure and stroke volume. The instantaneous changes in pulmonary artery flow as a result of
Circulation Research Vol 70, No 5 May 1992
946
UNLOAD
200 .0
L OR:IIVE P
100 . O
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FIGURE 2. Typical data recordings.
The upper four tracings are ventricular
assist device pneumatic drive pressure (L
drive P), left and right ventricular pressures (LVP and RVP, respectively), and
pulmonary artery flow (Qpa) for a typical isolated systolic interaction experiment. The lower three tracings represent
the differences between each beat and
the preceding beat (del). Until the unloaded beat, the differences between consecutive beats are small, indicating the
stability of the preparation. During left
ventricular unloading, however, both
right ventricular flow and pressure are
markedly reduced as a result of systolic
ventricular interaction.
_:
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RVP
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sec
LV unloading were calculated as the ratio of RV flow
change to LV pressure change. RV ejection time was
defined as beginning at the rapid upswing of the pulmonary artery flow signal and terminating as the flow
signal crossed zero.
Mean data from each animal were calculated from
the five data records. These mean values were then
pooled and are presented as the mean±SD. Paired t
tests were performed on the data from control and
unloaded beats, with a value of p<0.05 considered
statistically significant. A one-way analysis of variance
with repeated measures followed by the Fisher post hoc
test was used to determine if the instantaneous pressure
gain varied with time during the systolic period.
Results
Hemodynamic measurements from a typical data set
are shown in the top four tracings of Figure 2. In the
seventh beat ("unload" in Figure 2), VAD drive pressure was reduced from 200 to -100 mm Hg (first
tracing), allowing ventricular emptying into the VAD
and causing a rapid fall in LV systolic pressure (second
tracing). Ensuing reductions in the RV pressure and
pulmonary artery flow are shown on the third and
fourth tracings. Beat-to-beat changes in each variable
were calculated by digitally shifting each recorded variable by one cardiac cycle and subtracting, thus producing the difference from one beat to the following beat.
These beat-to-beat changes in LV pressure, RV pressure, and pulmonary artery flow are shown on expanded
scales on the lower three tracings of Figure 2 and
demonstrate the stability of the preparation up to the
unloaded beat, in which there are reductions in all three
variables.
Pooled ventricular pressures and pulmonary artery
flow for all experiments are shown superimposed in the
left panels of Figure 3 as a function of normalized
systolic time, with the control beats indicated by open
symbols and unloaded beats represented by filled symbols. The right panels of Figure 3 present the changes in
4.6
these variables calculated by subtracting the data at
time points. It can be seen that control and
unloaded beats begin with unchanged end-diastolic
pressures in both ventricles (at normalized systolic time
0.0). For the unloaded beats, pneumatic and mechanical
delays were such that 60 msec elapsed between the R
wave of the electrocardiogram and the flow of blood
into the VAD; thus, the initial rise in LV pressure in the
unloaded beat was unchanged (Figure 3, top left panel).
Once VAD flow was established, LV pressure fell
progressively throughout systole, ending at a value
somewhat below that of the previous end diastole.
Concomitant reductions in systolic RV pressure and
flow are evident throughout the cycle.
The maximum reduction in LV pressure was 81±11
mm Hg or 88%, which occurred at a normalized systolic
time of 0.80. This resulted in instantaneous reductions
of 3.5±+1.5 mm Hg (14%) in RV pressure and 1.5+±0.9
1/min (21%) in pulmonary artery flow at the same
systolic time. Corresponding reductions were seen
throughout systole of the unloaded beat. Changes in RV
pressure and pulmonary artery flow between control
and unloaded beats increased rapidly in the initial phase
to a normalized systolic time of -0.3. From a time of
0.3-0.75, however, those differences were fairly constant, despite a continuing fall in LV pressure.
Pooled LV-to-RV systolic pressure gain as a function
of normalized systolic time, calculated from the differences between control and unloaded data, are shown in
the upper panel of Figure 4. Over the normalized
systolic time period from 0.3 to 0.7, there was a significant (p<0.001) decrease in gains from 0.072+0.022 to
0.042±0.014 mm Hg/mm Hg, reflecting the fact that
the change in LV pressure was increasing over this
time, whereas the change in RV pressure was relatively constant. From normalized systolic time of 0.75
to the end of systole, the pressure gain increased to the
highest value of 0.076±0.028 mm Hg/mm Hg at a time
of 1.0, which also was significantly greater than the
minimum gain at time 0.70. The corresponding
common
Woodard et al Ventricular Systolic Interaction
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FIGURE 3. Graphs showing
control and unloaded beats.
Left panels: Pooled left ventricular pressure (LVP), right ventricular pressure (RVP), and
pulmonary artery flow (Qpa)
(mean +SD) are shown for control (open circles) and unloaded
(filled circles) beats. Normalized
systolic time extends from 0
(representing end diastole) to 1
(indicating the end of right ventricular ejection). Right panels:
Pooled differences between normalized control and unloaded
beats are shown.
-80
12
-1
10
8
-2
6
-3
4
-4
2
-5
0
0.0
0.2
0.4
0.6
0.8
Normalized Systolic Time
1.0
0.2
0.0
changes in pulmonary artery flow divided by changes
in LV pressure also varied between a maximum of
0.043+0.021 1 minm mm Hg-1 at time 1.0 to a minimm Hg-1 at time 0.80
mum of 0.021±0.009 1. min
(Figure 4, bottom panel).
Overall hemodynamic data, pooled from all experiments for both control and unloaded cardiac cycles,
appear in Table 1. During the unloaded beat, LV peak
systolic pressure and mean systolic pressure were significantly reduced, but LV end-diastolic pressure was
unchanged. There were corresponding reductions in
RV peak and mean systolic pressure without changes in
RV end-diastolic pressure. No significant difference
between end-diastolic dimensions or pressures are evident between control and unloaded beats. However,
most systolic dimensions were significantly changed by
unloading: the LV end-systolic septal-free wall dimension was significantly reduced, as was the RV endsystolic anteroposterior dimension. The fractional
change from diastole to systole was significantly increased for the LV, whereas the diastolic-to-systolic
dimensional change in the RV was reduced in the
septal-free wall direction but increased in the anteroposterior direction. LV unloading also reduced RV
ejection time and resulted in significant reductions in
RV stroke volume and stroke work.
The midsystolic LV-to-RV systolic pressure gain was
0.055+±0.028, and the mean systolic pressure gain was
0.054±0.017 mm Hg/mm Hg (Table 2). For each millimeter of mercury drop in mean systolic LV pressure,
there was a 0.13±0.07-ml reduction in RV stroke volume
and a 0.66+0.28-mJ fall in RV stroke work (Table 3).
'
0.4
0.6
0.8
1.0
Normalized Systolic Time
Discussion
Classification of ventricular interaction into "diastolic" and "systolic" provides a useful framework for
conceptual understanding of two different mechanisms
mediated by a common anatomy. However, consensus
on the significance of systolic interaction has not been
achieved, partially because of the variety of conditions
under which it has been measured and the lack of clear
delineation between systolic and diastolic events. We
have chosen the label "isolated" systolic interaction to
indicate the following: alterations in systolic function
occurring purely as a result of changes in systolic
variables of the other ventricle. Previous studies of
"csystolic interaction"2711,16 fall outside this definition,
because end-diastolic conditions were uncontrolled and
these papers more properly document a melding of
actual isolated systolic interaction with the systolic
sequelae of changes in end-diastolic conditions.
In our study, at constant end-diastolic conditions in
both ventricles, during a single cardiac cycle, LV pressure was rapidly reduced after the isovolumic contraction phase. Utilization of this method ensures that
preload in the septum and free walls remains unchanged from the previous beat and therefore that the
potential work of the heart during the unloaded beat
was identical to the control beat. Measurement of
cardiac dimensions verified that end-diastolic conditions were constant, but during the unloaded beat, the
intraventricular septum shifted to the left, RV septalfree wall contraction was reduced, and the systolic
change in anteroposterior dimension was slightly enhanced. Mean LV pressure was reduced by 63±12%,
resulting in reduced RV pressure, stroke volume, and
948
Circulation Research Vol 70, No 5 May 1992
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0.6
0.8
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Normalized Systolic Time
FIGURE 4. Graphs showing instantaneous pressure gain and
change in pulmonary artery flow (Qp). LV, left ventricular;
RI, right ventricular; LVP, LV pressure. Top panel: The
ratio of change in RV pressure to change in LV pressure
(pressure gain) is shown as a function of time and pooled for
all pigs. The gain is presented as a function of normalized
time, defined as in Figure 3. Error bars indicate standard
deviation. Bottom panel: The instantaneous change in Qp,,
flow as a result of each millimeter of mercury reduction in
LVP is presented as a function of normalized systolic time.
stroke work. Also, the duration of RV ejection was
shortened. The gains, ranging from 0.042 to 0.076
mm Hg/mm Hg, suggest that systolic gain is time varying, with the highest gains at the earlier and later parts
of systole and the lower gains occurring around midsystole. The mean systolic LV-to-RV interaction gain was
0.054 mm Hg/mm Hg.
A quantitative relation between the developed pressure in one chamber and the volume of the other has
been obtained in isolated, isovolumically beating hearts
by Santamore et al,11 who found that reducing LV
volume from its "ideal" value caused a 5.7% decrease in
RV developed pressure. Weber et al,2 using an isolatedheart preparation, concluded that the degree of this
left-to-right systolic interaction was independent of RV
volume. However, in another isolated-heart preparation, Yamaguchi et a112 showed that, with increases in
LV volume, the slope of the RV end-systolic pressurevolume relation increases and the volume intercept
decreases. These changes support the concept that RV
stroke work is augmented at increasing LV pressures
and volumes. Their data also imply that any change in
contralateral ventricular geometry may alter regional
preload in the opposite ventricular free wall and that
this is, in part, responsible for the increased end-systolic
pressure-volume relation that is seen at increasing
volumes in the contralateral ventricle. A leftward shift
in the end-systolic pressure-volume relation intercept
without a change in slope had also been previously
reported by Maughan et al,6 who maintained constant
contralateral ventricular volume using a servo system.
Using aortic occlusion to produce an abrupt increase
in LV afterload, Langille and Jones19 demonstrated
coincident increases in LV and RV peak systolic pressure, from which a pressure gain of 0.086 mmHg/
mm Hg may be derived, which is substantially higher
than our midsystolic gains of 0.058. However, Maughan
et at6 measured pressure gain at end systole in isolated,
blood-perfused canine hearts and calculated a left-toright systolic pressure gain of 0.08, which is very close to
our value of 0.076 at end ejection. Maughan et al found
that this left-to-right gain was half that of right-to-left
gain over a wide range of ventricular volumes.
Elzinga et at7 have also measured the ejection performance of the RV during rapid changes in LV afterload in isolated feline hearts. Differences in RV stroke
volume of 30-50% were observed when the LV contracted isovolumically or against a low impedance load,
which implies a greater interaction than we found.
However, although RV end-diastolic pressure was controlled in their preparation, their results do not represent isolated systolic interaction, because of the inevitable variations in RV end-diastolic volume brought
about by changes in left-side volume and the ensuing
diastolic interaction.
In the computer model of ventricular interaction of
Santamore and Burkhoff,18 the LV-to-RV interaction
gain is predicted to be 0.095 mm Hg/mm Hg, with no
provision for any time-varying phenomena. This gain
was theoretically calculated from the ratio of Erf/
(Ervf+Es), where Er,f and Es are the elastances of the RV
free wall and interventricular septum from Maughan et
al.10 This theoretical gain is greater than our mean gain
of 0.054 but lies within the 95% confidence interval for
our peak gain, which extends from 0.055 to 0.097.
Because their gain was calculated for steady-state conditions, a direct comparison with our instantaneous
value is difficult to interpret.
Our measurements of time-varying gain show higher
values (0.072) in early ejection than after peak ejection
(0.042). The systolic interaction gains might have been
even higher if LV pressure could have been reduced
earlier in the cycle. Although the absolute magnitude of
the gains appears small because of the large difference
in the systolic pressures of the two ventricles, this belies
their true significance. Our results indicate that if the
changes in flows and pressures are expressed as a
percentage of the control values in each ventricle, a
100% reduction in LV pressure would result in a 23%
decrease in mean RV pressure generation. Similarly,
complete unloading of the LV would result in a 43%
decrease in RV stroke work and 29% reduction in RV
stroke volume. The 10-msec decrease in ejection time
observed in our study is most probably a result of
ejection occurring at a lower RV pressure, with the rate
of pressure decline being unchanged.
One possible shortcoming in the ventricular unloading method is that a cannula in the LV apex may
potentially disrupt normal ventricular contractile function to some degree. However, -5 g myocardium is
Woodard et al Ventricular Systolic Interaction
949
TABLE 1. Data for Control and Unloaded Cardiac Cycles
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Pressures
LV
PSP (mm Hg)
MSP (mm Hg)
EDP (mm Hg)
RV
PSP (mm Hg)
MSP (mm Hg)
EDP (mm Hg)
Aortic (mm Hg)
PAP (mm Hg)
Dimensions
LV
ED SFW (mm)
ES SFW (mm)
ASFW (%)
RV
ED SFW (mm)
ES SFW (mm)
ASFW (%)
ED AP (mm)
ES AP (mm)
n
Control beat
Unloaded beat
Change (%)
8
8
8
96.3+7.2
75.3±8.7
9.9±4.2
67.3±11.9*
28.2±9.1*
10.1±4.2t
-30.1
-62.6
2.0
8
8
8
8
7
29.8±6.0
22.1±5.2
3.6±1.0
83.5±9.8
23.2±5.8
26.7±5.3*
19.1±4.1*
3.5±1.1t
64.9±10.0*
21.5 5.3*
-10.4
-13.6
-2.8
-22.3
-7.3
7
7
7
55.5±6.0
51.9±5.7
6.5±2.2
55.5±6.Ot
44.5 ±4.6*
19.4±7.1*
0.0
-14.3
199.0
7
7
7
45.1±9.6
40.3±10.2
11.3±4.6
45.1±9.6t
43.8±8.9t
2.5±6.5*
0.0
8.7
-75.2
7
7
7
63.1±6.9
61.4±6.8
2.7±1.5
63.1±6.9t
60.4±6.4*
4.2±2.2*
0.0
-1.6
55.6
AAP (%)
SW, SV, and Tej
RV
-26.7
8
114.1±36.0
83.6±30.9*
SW (mJ)
-17.9
8
32.5±5.1
26.7±6.5*
SV (ml)
-3.9
7
245.0±23.0*
255.0±29.0
Tej (msec)
Values are mean±SD. n, Number of pigs; LV, left ventricular; PSP, peak systolic pressure; MSP, mean systolic
pressure; EDP, end-diastolic pressure; RV, right ventricular; PAP, pulmonary artery pressure; ED, end diastole; SFW,
septal-free wall dimension; ES, end systole; A, change between diastole and systole; AP, anteroposterior dimension;
SW, stroke work; SV, stroke volume; Tej, ejection time.
*p<0.05 and tp=NS compared with control beat by paired t test.
removed from the ventricular apex for cannula insertion, which comprises only 2-3% of the average porcine
heart and therefore may be considered negligible. An
additional small amount of tissue may be rendered
noncontractile by cannula fixation sutures. Shortening
of the heart in the base-apex direction may also be
slightly altered by some "tethering" action of the canTABLE 2. Systolic Left Ventricular-to-Right Ventricular Pressure
Gains at Normalized Systolic Times
LV-to-RV
systolic pressure gain
Normalized time
(mm Hg/mm Hg)
1.0
0.076±0.028
Maximum
0.7
0.042±0.014
Minimum
0.4-0.6
0.055±0.028
Midsystolic
0.0-1.0
0.054±0.017
Values are mean±SD. LV, left ventricular; RV, right ventricular. Normalized time was 0 at end diastole and 1.0 at end ejection.
Mean systolic gain was calculated from changes in mean LV and
RV systolic pressures.
Mean
nula and VAD, which are attached to the heart but
which still allow movement. But these effects are unlikely to significantly alter our results since any effect
would alter the control and unloaded beats in a similar
manner. Our preparation probably introduces less artifact than isolated-heart preparations, which use rigid
sewing rings in the mitral and tricuspid positions with
interruption of the mitral chordae. Interruption of the
chordae has been demonstrated to significantly change
TABLE 3. Changes in Right Ventricular Function During Reductions in Left Ventricular Pressure
Changes in Normalized
time
RV function
0.0-1.0
0.13+0.07
ARV SV/ALV MSP (ml * mm Hg-')
0.0-1.0
0.66+0.28
ARV SW/ALV MSP (mJ * mm Hg-1)
AQpa/ALV MSP (1 * min' *mm Hg-1) 0.037±0.016 0.4-0.6
Values are mean+SD. RV, right ventricular; A, change; SV,
stroke volume; LV, left ventricular; MSP, mean systolic pressure;
SW, stroke work; Qpa, pulmonary artery flow. Normalized time
was 0 at end diastole and 1.0 at end ejection.
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Circulation Research Vol 70, No 5 May 1992
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global systolic performance in the ejecting heart and
modify ventricular geometry.21
Ventricular systolic interactions are primarily mediated via the intraventricular septum. Although the
septum may be considered to be morphologically part of
the left ventricle,2 its motion (thickening) during systole
in the normal heart contributes equally to LV and RV
ejection.22 The LV free wall is also implicated in RV
function, as shown by reduction in RV developed
pressure during LV free wall ischemia"l and after LV
free wall transsection.17 Further evidence of both septal
and free wall-mediated interaction mechanisms is illustrated by unchanged systemic venous pressure,9 RV
pressure, and maximum RV dP/dt23 after prosthetic RV
free wall replacement. One study explained these findings with cineangiography, showing that contraction of
the LV influenced RV ejection by two means: bulging of
the interventricular septum into the RV cavity and
pulling the patch toward the septum.24
Farrar et a125 and Chow and Farrar26 have studied the
effects of steady-state reductions in LV pressure on RV
function. These studies found that reducing LV peak
systolic pressure by up to 90% produced parallel shifts
but no changes in slope in the RV septal-free wall
pressure-dimension relation and preload-recruitable
stroke work. Thus, reduced LV pressure produced a
septal shift without major changes in RV output, which
we also found under conditions of RV ischemia.27 These
studies of ventricular interaction have direct clinical
significance in patients with LV assist devices for endstage heart failure, because good RV function is required while the device is operating with reduced LV
pressure.28 However, the findings of these studies cannot be attributed to isolated systolic interaction because
of concomitant changes in diastolic function. To separate these two effects, we29 previously used a computer
simulation of LV pressure unloading with a LV assist
device, which was based on the Santamore-Burkhoff
model.18 These results showed that diastolic and systolic
interaction tend to counteract each other during steadystate LV pressure unloading in the normal heart. The
simulation predicted that although systolic function of
the RV may be diminished when LV pressure is reduced
(via systolic interactions), the concomitantly increased
RV diastolic compliance (via diastolic interaction) allows the RV to compensate by operation at higher
end-diastolic volumes. That is, the heart may provide
diastolic compensation for the reduction in systolic
function caused by depressurization of the contralateral
ventricle.
This study confirms that there are substantial contributions from LV pressure to RV systolic function. In
contrast to other methods, as a result of systolic ventricular interactions we were able to observe instantaneous
changes in RV pressure throughout systole in response
to reductions in LV pressure and in the absence of
preload changes in either ventricle. The results suggest
that systolic ventricular interaction is time varying
within the cycle.
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Isolated ventricular systolic interaction during transient reductions in left ventricular
pressure.
J C Woodard, E Chow and D J Farrar
Downloaded from http://circres.ahajournals.org/ by guest on April 13, 2017
Circ Res. 1992;70:944-951
doi: 10.1161/01.RES.70.5.944
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