734
Independence of Myocardial Oxygen Consumption
from Pressure-Volume Trajectory during Diastole in
Canine Left Ventricle
Hiroyuki Suga, Yoichi Goto, Osamu Yamada, and Yuichiro Igarashi
From the Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Fujishirodai, Suita, Osaka, japan
Downloaded from http://circres.ahajournals.org/ by guest on July 31, 2017
SUMMARY. We have found that myocardial oxygen consumption is linearly correlated with the
systolic pressure-volume area in the canine left ventricle. This pressure-volume area is a specific
area in the pressure-volume diagram that is circumscribed by the end-systolic pressure-volume
relation line, the end-diastolic pressure-volume relation curve, and the systolic segment of the
pressure-volume trajectory. This area is equivalent to the total mechanical energy generated by
ventricular contraction, consisting of the external mechanical work and the mechanical potential
energy. In the present study, we specifically changed the course of the diastolic segment of the
pressure-volume trajectory without changing the systolic segment of the pressure-volume trajectory and the systolic pressure-volume area. Although the fractions of external mechanical work
and mechanical potential energy in the pressure-volume area were markedly changed, the
simultaneously measured left ventricular oxygen consumption remained unchanged. This result
indicates that the myocardial oxygen consumption is predominantly determined by the total
mechanical energy generated during systole, or the systolic pressure-volume area, independent
of how the total mechanical energy is converted effectively to external mechanical work during
the cardiac cycle (Circ Res 55: 734-739, 1984)
WE have recently found that left ventricular oxygen
consumption is closely correlated with the left ventricular systolic pressure-volume area (PVA) (Suga
et al., 1981a). We defined PVA as a specific area in
the pressure-volume (P-V) diagram that is circumscribed by the end-systolic P-V relation line, the
end-diastolic P-V relation curve, and the systolic
segment of the P-V trajectory (Suga, 1979b).
As shown in Figure 1, PVA in a normal ejecting
contraction consists of two areas: one is the rectangular area within the P-V trajectory, and the other
is the triangular area between the end-systolic P-V
line and the end-diastolic P-V curve on the left side
of the P-V trajectory. The former area represents the
external mechanical work, and the latter the mechanical potential energy. Thus, PVA represents the
total mechanical energy generated by each ventricular contraction, of which external mechanical work
is the effective stroke work output of the ventricular
pump, and the potential energy is the remaining
part unused for the pumping. The P-V trajectory
during diastole divides PVA into these two parts.
The potential energy will be eventually converted to
heat unless it is further converted to an additional
external mechanical work by afterload reduction
during diastole (Suga, 1979a).
The purpose of the present study was to investigate whether left ventricular oxygen consumption
was affected by a shift of the course of the P-V
trajectory during diastole when there was no change
of the course of the systolic segment of the P-V
trajectory. This procedure was performed as a new
method which variably reconverts the external mechanical work once performed during systole back
into the mechanical potential energy during diastole.
PVA was supposed to be unaffected by this procedure in a stable heart because the systolic segment
of the P-V trajectory was kept unchanged with our
servo control pump system.
We found that left ventricular oxygen consumption remained the same even when the external
mechanical work performed during systole was variably reconverted to the mechanical potential energy
during diastole. This finding indicates that ventricular oxygen consumption is determined exclusively
by the cardiodynamic events during systole, independent of the events during diastole, and the external mechanical w,ork and the mechanical potential energy are interchangeable during the cardiac
cycle without any extra energy cost.
Methods
The left ventricular preparation and the experimental
setup we used were the same as described previously
(Suga et al., 1981a, 1982, 1983a). Briefly, two dogs were
anesthetized with sodium pentobarbital (30 mg/kg, iv).
The heart lung section was isolated in one dog, and its left
subclavian artery and the right ventricle via the right atrial
appendage were connected via the cross-circulation tubings with the other dog's common carotid arteries and
external jugular vein. The lung lobes were removed and
the cross-circulated beating heart was excised from the
chest.
A thin latex balloon was fitted via the mitral ring in the
Suga et al. /Diastole and Cardiac Oxygen Consumption
P-V
Loop
Ex i e r n a 1
Me c h an i c a ]
Work
Pressureflren
Vo 1 ume
(PVfl)
0
Ventricular
Volume
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FIGURE 1. Schematic illustration of systolic pressure-volume area
(PVA) and its two components, external mechanical work and potential energy, in a normal ejecting contraction. End systole is the time
at which the P-V loop touches the end-systolic P-V relation line. The
systolic segment of the P-V loop consists of the segments for the
isovolumic contraction phase and the ejection phase. The diastolic
segment of the P-V loop consists of the segments for the isovolumic
relaxation phase and the filling phase. In the main protocol of the
present study, the P-V trajectory for the isovolumic relaxation phase
was curtailed by advancing the onset of diastolic filling to change the
course of the diastolic segment of the P-V loop.
left ventricle, and connected to the servo pump (Suga et
al., 1979). The balloon and the water housing of the pump
were primed with water. Ventricular volume was measured by the displacement of the piston of the pump, and
ventricular pressure, by a miniature gauge placed inside
the apical end of the intraventricular balloon. The servo
pump system enabled us to change the courses of the
P-V trajectory during systole and diastole and to have
end-diastolic volume, ejection pressure, and stroke volume
at our disposal.
Left ventricular pressure and volume signals were displayed on a storage oscilloscope and photographed. The
same signals were fed to an analog-to-digital converter,
and PVA and its two components, i.e., external mechanical
work and mechanical potential energy, were determined
with a digital computer (Suga et al., 1983b). PVA and its
two components were expressed in mm Hg ml/beat per
100 g of left ventricle. 1 mm Hg ml = 1.33 X 10"" J.
The determination of PVA required the identification
of the end of systole as in our previous studies (Suga et
al., 1983b). Our definition of end systole was the same as
proposed previously (Suga et al, 1973, 1979). Briefly, we
first determined ventricular volume Vd where the peak
isovolumic pressure was zero. Then, the P-V ratio, namely,
the slope of the line connecting Vd and the instantaneous
P-V data point on the P-V trajectory, was calculated in
the computer. End-systole was identified as the time when
the P-V ratio became maximal, i.e., E™*.
Left ventricular oxygen consumption was determined
in the same way as described previously (Suga et al.,
1981a, 1982, 1983a). Coronary venous flow returning to
the right heart was continuously drained out hydrostatically through an electromagnetic flowmeter. Oxyhemoglobin percent saturations of both coronary arterial and venous bloods were determined with an oximeter (Erma
Optical Works, PWA-200). Coronary arterial blood of a
known saturation was sampled, and its oxygen content
735
was determined with a Lex O2 Con oxygen content analyzer to obtain an oxygen saturation-to-content conversion
factor. Coronary arteriovenous oxygen content difference
was then determined from the coronary oxyhemoglobin
saturation difference and the saturation to content conversion factor.
Because the right ventricle was maintained collapsed
by the continuous hydrostatic drainage of the coronary
venous return, the measured oxygen consumption of the
heart was assumed to be exclusively of the left ventricle.
Left ventricular oxygen consumption (Vo2) was expressed
in ml O2/beat per 100 g of left ventricle; 1 ml O2 is
equivalent approximately to 20 J under normal aerobic
conditions.
We used the following experimental protocols. In a
given contractile state of the left ventricle without any
inotropic interventions to the cross-circulated heart preparation, we produced steady state normal ejecting contractions that had a rectangular P-V trajectory loop, as
shown in the leftmost column of Figure 2. Both Vo2 and
PVA were determined when ventricular pressure, coronary flow, and coronary venous oxyhemoglobin saturation
reached steady state at 2-3 minutes after each specified
loading condition was imposed.
Then, the course of the diastolic segment of the P-V
trajectory was due to two to four different pathways by
appropriately advancing the onset of filling, as shown in
the middle and rightmost columns of Figure 2. This procedure did not affect the systolic segment of the P-V
trajectory, due to both the servo control pump system and
the stability of the ventricle preparation. Vo2 and PVA
were determined for these contractions with different
courses of the diastolic segment of the P-V trajectory.
Beside this main protocol, we produced isovolumic
contractions at different end-diastolic volumes, as shown
in Figure 3A, and produced ejecting contractions with a
constant stroke volume whose systolic segment of the
0.2 sec
200
p
mmHg 100
0
45
V
-dV/dt
200r
ml/sec_2Oo[
f
-vv
PVR
FIGURE 2. Time tracings of left ventricular pressure (P), volume (V),
and time-derivative of V (—dV/dt). The bottom row shows the contours of left ventricular systolic pressure-volume area (PVA), external
mechanical work (EW), and mechanical potential energy (PE) in the
three differently loaded contractions shown above each. Note that the
course of the diastolic segment of the P-V loop was markedly shifted
and the fractions of EW and PE in PVA were changed.
Circulation Research/Vo/. 55, No. 6, December 1984
736
P-V trajectory was markedly shifted, by changing the
onset of ejection (Figure 3B). In these ejecting contractions,
the diastolic segment of the P-V trajectory was kept unchanged with the servo control pump system.
At the end of each experiment, the atria and the right
ventricular free wall were trimmed off the heart, and the
left ventricle was weighed. The mean left ventricular
weight of eight hearts was 76 ± 9 (SD) g.
Results
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Figure 3 shows representative scatter diagrams of
Vo2-PVA data points obtained in one left ventricle.
Panel A of Figure 3 shows a set of data of isovolumic
contractions in a stable contractile state. There was
a high and linear correlation between Vo2 and PVA
over the physiological range. All other left ventricles
showed similar findings (Suga et al., 1981a).
Panel B of Figure 3 shows the data of the contractions whose PVA was changed by shifting the systolic segment of the P-V trajectory, as seen in the
inset P-V diagram. The linear regression line fitted
to the V02-PVA data points of these contractions
plus one unloaded contraction was close to that
fitted to the isovolumic contractions of the same left
ventricle in panel A.
Panel C of Figure 3 shows the results obtained in
the main protocol. This panel shows one set of Vo2PVA data of contractions, whose diastolic segment
of the P-V trajectory was widely shifted without
any changes in its systolic segment, as seen in the
inset P-V diagram. In spite of these changes and the
resulting significant decreases in the external me-
-
chanical work and increases in the mechanical potential energy, Vo2, as well as PVA, remained unchanged. The linear regression line of these data,
together with one unloaded contraction, was close
to those of the same left ventricle in panels A and
B.
Panel D of Figure 3 pooled all those data points
in panels A through C. The correlation coefficient
was close to 1, and the scatter of the data points
around the linear regression line was small. The
three solid circles are identical with those data points
in panel C in the main protocol. These three data
points are within the 95% confidence range of the
sampled data, indicating that the Vo2-PVA point
was not affected by the marked shift of the diastolic
segment of the P-V trajectory. We observed similar
results in all eight left ventricles.
Figure 4 shows more explicitly the independence
of Vo2 from the relative magnitude of external mechanical work (EW) in PVA. This figure plots Vo2
against EW:PVA ratio in the main protocol in all
eight left ventricles. PVA in each left ventricle was
set to a constant in the range between 1000 and
2500 mm Hg ml/beat per 100 g. The coefficient of
variation (Snedecor and Cochran, 1971) of PVA
around each mean PVA in each left ventricle was
computed. The mean coefficient of variation across
all eight hearts was only 4.0 ± 1.6%, indicating the
constancy of a given PVA. The EW:PVA ratio therefore indicates the fraction of external mechanical
work in a constant PVA. This ratio is dimensionless,
and can vary between 0 and 1. The greatest EW:PVA
ft
•<3
1
_
E
0
V ml
30
0
PVfl
1000
2000
3000
mmHg ml/beat/1OOg
1000
2000
3000
PVR mmHg m1/best/1OOg
1000
2000
3000
mmHg m1/beoi/1OOg
0
PVR
1000
2000
3000
PVfl mmHg ml/beat/lOOg
FIGURE 3. Correlograms of the left ventricular oxygen
consumption per beat (V02) on the ordinates and systolic
pressure-volume area (PVA) on the abscissas. The diagonal solid lines are the linear regression lines. The inner
pairs of dashed curves are the 95% confidence zones of
the regression lines. The outer pairs of dashed curves are
the 95% confidence zones of the sampled data. The insets
depict the P-V trajectories from which the V02-PVA data
were obtained. Panel A shows isovolumic data. The
regression equation of V01 on PVA is Voi = 0.000031
PVA + 0.034. The correlation coefficient is 0.97. Standard deviation of the sampled data from the regression
is 0.005 ml O2/beat per 100 g. Panel B shows data of
ejecting contractions whose PVAs were changed by shifting the systolic P-V trajectory. The regression line is V02
= 0.000032 PVA + 0.033. The correlation coefficient is
0.95. Standard deviation from regression is 0.004. Panel
C shows data of ejecting contractions with external
mechanical work returned to the ventricle during diastole
in the main protocol. The regression line is V05 =
0.000029 PVA + 0.026. The correlation coefficient is
0.93. Standard deviation from regression is 0.003. Panel
D pools all data shown in panels A, B, and C in the same
left ventricle preparation. The regression line is V02 =
0.000030 PVA + 0.034. The correlation coefficient is
0.98. Standard deviation from regression is 0.005.
Suga et al. /Diastole and Cardiac Oxygen Consumption
O
O)
O
O
c5
a>
_D
\
CM
ED
CN
o
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0
0.25
0.5
0.75
EW/PVfl rat io
1
FIGURE 4. Constancy of left ventricular oxygen consumption (VoJ in
spite of the marked changes in the ratio of external mechanical work
(EW) to a constant PVA in each of eight hearts. Each set of connected
symbols corresponds to an individual heart.
ratio in each run was obtained in the contraction
whose diastolic segment of the P-V trajectory was
vertical in the P-V diagram, as in normal contractions in situ. EW-.PVA decreased as the course of the
diastolic segment of the P-V trajectory was shifted
to the right by advancing the onset of ventricular
filling, as seen in the bottom PVA patterns (from
left to right) in Figure 2.
As seen in Figure 4, Vo2 did not change, or
changed only little, with the wide changes in
EW:PVA ratio between 0 and 0.8. The mean coefficient of variation of Vo2 around each mean Vo2
was only 3.9 ± 1.8%, indicating the constancy of
Vo2 despite the marked changes in EW:PVA ratio.
These results indicate that, when PVA remained
unchanged, Vo2 also remained constant, in spite of
the marked changes in the fraction of external mechanical work in PVA by the shift of the diastolic
segment of the P-V trajectory.
Discussion
The present results have indicated that myocardial
oxygen consumption is virtually independent of the
cardiodynamic events during diastole. The diastolic
cardiodynamic events are represented by the course
of the diastolic segment of the P-V trajectory. This
independence of myocardial oxygen consumption
from diastolic cardiodynamic events is consistent
with the concept of PVA.
The physical and physiological significance of
PVA was first derived from the time-varying elastance model of the canine left ventricle (Suga et al.,
737
1973; Suga, 1979b). PVA was equivalent to the total
mechanical energy generated in the model during
the gradual increment in the time-varying elastance
from the end-diastolic compliant level to the endsystolic stiff level (Suga, 1979b; Piene and Sund,
1982).
In a given contractile state, PVA is explicitly determined by the systolic segment of the P-V trajectory because both the end-systolic P-V relation line
and the end-diastolic P-V relation curve are considered to be constant for any given left ventricle (Suga
et al., 1973, 1979). Thus, the course of the diastolic
segment of the P-V trajectory is not related to the
determination of PVA when the contractile state
remains unchanged.
PVA consists of the external mechanical work and
the mechanical potential energy (Suga, 1979b). The
diastolic segment of the P-V trajectory is directly
related to the division of PVA into these two energy
components. In normnal ejecting contractions, the
diastolic segment of the P-V trajectory during the
isovolumic relaxation phase is vertical. In the present
study, the diastolic segment of the P-V trajectory
was variably shifted so that the isovolumic relaxation phase was curtailed and the fraction of PVA
contributed to the external mechanical work in one
cardiac cycle was reduced.
We interpreted the shift of the diastolic segment
of the P-V trajectory as follows. The external mechanical work performed during systole is equal to
the area under the systolic segment of the P-V
trajectory. This is the work that was performed by
the left ventricle on the outside environment. The
area under the diastolic segment of the P-V trajectory is equivalent to the mechanical work performed
by the environment on the ventricle during diastole.
The net external mechanical work output is therefore equal to the external mechanical work performed during systole, minus the mechanical work
paid back from outside to the ventricle during diastole. This net work is represented by the area within
the P-V trajectory during one cardiac cycle. The area
for the mechanical potential energy is therefore increased by the amount of the mechanical work
returned to the ventricle from outside. Thus, in the
present main protocol, the fraction of external work
in PVA once determined by the end of systole was
decreased during diastole. Therefore, the present
results indicate the total myocardial oxygen consumption is determined by the total mechanical
energy generated during systole, independent of
how much of this total mechanical energy is converted to effective pump work output during the
entire cardiac cycle.
Although our present finding may appear to be
consistent with Monroe's (1964) finding that as
much as 90% of myocardial oxygen consumption
was determined during systole, we consider that
there is a substantial difference between Monroe's
experiments and ours. Monroe's experiment was
738
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limited to quasi-isovolumic contractions whose volume was rapidly reduced to zero at different times
during cardiac cycle. These were quick volumereleased contractions. Thus, there was no return of
mechanical work to the left ventricle from outside
during diastole. Instead, the mechanical potential
energy generated during systole was partially converted to external mechanical work during the quick
volume release in early diastole. In this sense, Monroe's type of contraction is opposite to ours in the
direction of external mechanical work performed
during diastole.
Our present results, together with Monroe's
(1964), therefore would indicate that, whether the
relaxing ventricle performs mechanical work on the
environment or has work performed on it from
outside, the oxygen consumption of the ventricle is
determined predominantly by the cardiodynamic
events during systole, and is affected little by the
cardiodynamic events during diastole.
In the isolated cat papillary muscle, Cooper (1979)
found that a significant proportion (36%) of myocardial oxygen consumption was saved by a quick
release of force and length of isometrically contracting muscle at the peak of force. This curtailment of
Vo2 is greater than Monroe's (1964) 9% in the canine
left ventricle. Besides the difference in species, Monroe's (1964) preparation was blood perfused at 37°C,
whereas Cooper's preparation was superfused by a
non-blood perfusate at 29°C. These differences in
experimental conditions might be related to the
marked disparity between the two results.
Cooper's (1979) speculative mechanism for the
difference between his own observation and Monroe's deserves mention. Cooper's papillary muscle
preparation remained isometric until the length release, whereas Monroe's ventricle had compressed
intraventricular air before the volume release, and
the ventricular contraction was not purely isovolumic. This quasi-isovolumic contraction had experienced the shortening deactivation (Brutsaert and
Paulus, 1977) by the time of the release, and the
oxygen consumption was largely terminated by the
end of systole. This situation did not occur in Cooper's purely isometric muscle. If this speculation is
reasonable, our present finding of the independence
of oxygen consumption from diastolic cardiodynamic events may also be related to the shortening
deactivation during the systolic ejection phase.
However, we consider that shortening deactivation was small in our present ejecting contractions,
according to our previous observations (Suga et al.,
1979). We had observed that the amount of endsystolic pressure deficit from the peak isovolumic
pressure at the same volume due to shortening
deactivation was only a few percent in ejecting
contractions with ejection fractions between 0 and
50%, although it amounted to 10-15% at an ejection
fraction of 75%. Therefore, we consider that shortening deactivation may not be the sole mechanism
Circulation Research/Vol. 55, No. 6, December 1984
underlying the present independence of myocardial
oxygen consumption from the diastolic cardiodynamic events.
As seen in the top tracings in Figure 2, neither
peak pressure nor its time integral, i.e., tension time
index (Sarnoff et al., 1958), changed much despite
large changes in diastolic conditions. The constancy
of these two measures cannot, however, be the cause
of the constancy of oxygen consumption in our main
protocol (see Fig. 4). The reason is that neither peak
pressure nor tension time index proved to be a good
correlate of ventricular oxygen consumption in our
previous study (Suga et al., 1981b).
Although we conclude that myocardial oxygen
consumption is independent of the diastolic cardiodynamic events, we are not concluding that the
relaxation is a passive process during which the
myocardium is not utilizing energy. Relaxation of
muscle is known to be the process of detachment of
crossbridges by ATP following the sequestration of
calcium by sarcoplasmic reticulum using ATP (Katz,
1977). Thus, the relaxation phase is an energetically
active period during which myocardium utilizes
ATP. Moreover, unlike the relaxation phase of the
ventricle, the crossbridge breaking and the calcium
reuptake are known to start in the contraction phase
before the start of the relaxation phase (Brutsaert et
al., 1978; Allen and Kurihara, 1982). Therefore, we
conclude, simply, that the total energy utilization
during one cardiac cycle is not influenced by the
mechanical events that occur during ventricular relaxation.
The following speculation would be possible for
the mechanism underlying the observed independence of the left ventricular oxygen consumption
from the P-V trajectory during diastole. Myocardial
oxygen consumption is primarily utilized for the
basal metabolism, the excitation-contraction coupling, and the mechanical contraction (Gibbs, 1978;
Suga et al., 1983b). The basal metabolic oxygen
consumption is assumed to be constant despite the
changes in the diastolic segment of the P-V trajectory (Monroe and French, 1960). Because PVA remains unchanged despite the changes of the diastolic P-V trajectory, the total mechanical energy
generated by the contractile machinery remains the
same by the definition of PVA (Suga, 1979b). In
addition, excitation-contraction coupling is assumed
to be unaffected by the change in diastolic P-V
trajectory because the total amount of calcium ions
released from the sarcoplasmic reticulum is determined by the end of systole (Allen and Kurihara,
1981), and, therefore, the energy needed to uptake
the same amount of calcium ions will be the same.
It seems unlikely that the diastolic events affect the
calcium level in the next systole, because we did not
observe any change in the ventricular contractile
state in terms of the end-systolic pressure at a given
end-systolic volume when the diastolic P-V trajectory was markedly shifted. Thus, the change of the
Suga et al. /Diastole and Cardiac Oxygen Consumption
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diastolic P-V trajectory does not seem to have affected the primary deteminants of Vo2 in the present
study.
Our present finding indicates that external mechanical work and mechanical potential energy are
interchangeable during diastole without any change
in myocardial oxygen consumption. This finding is
consistent with our previous finding that the oxygen
cost of external mechanical work and that of potential energy are the same (Suga et al., 1980). If the
oxygen cost of the work and that of the potential
energy were different, the present interchangeability
without any change in myocardial oxygen consumption would not have been observed.
To summarize, we specifically shifted the diastolic
segment of the P-V trajectory in the P-V diagram
without changing the systolic segment of the P-V
trajectory and PVA. Although the fraction of external mechanical work in the total mechanical energy
generated during systole was markedly changed by
the shift of the diastolic segment of the P-V trajectory, oxygen consumption of the left ventricle remained unchanged. The result suggests for the first
time that the external mechanical work and the
mechanical potential energy of the left ventricle are
interchangeable in one cardiac cycle without any
change in myocardial oxygen consumption. The result also corroborates the concept that the myocardial oxygen consumption of the left ventricle is
primarily determined by the systolic cardiodynamic
events independent of the diastolic cardiodynamic
events.
Received April 16, 7984; accepted for publication August 14, 1984.
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INDEX TERMS: Heart • Cardiac mechanics • Cardiac energetics
• Systole • Relaxation
Independence of myocardial oxygen consumption from pressure-volume trajectory during
diastole in canine left ventricle.
H Suga, Y Goto, O Yamada and Y Igarashi
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Circ Res. 1984;55:734-739
doi: 10.1161/01.RES.55.6.734
Circulation Research is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1984 American Heart Association, Inc. All rights reserved.
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http://circres.ahajournals.org//subscriptions/