You are on page 1of 10

Elastic energy as an index of right ventricular

filling
P Squara, D Journois, P Estagnasie, M Wysocki, A Brusset, D Dreyfuss
and JL Teboul
Chest 1997;111;351-358

The online version of this article, along with updated information and
services can be found online on the World Wide Web at:
http://chestjournals.org/cgi/content/abstract/111/2/351

CHEST is the official journal of the American College of Chest


Physicians. It has been published monthly since 1935. Copyright 2007
by the American College of Chest Physicians, 3300 Dundee Road,
Northbrook IL 60062. All rights reserved. No part of this article or PDF
may be reproduced or distributed without the prior written permission of
the copyright holder
(http://www.chestjournal.org/misc/reprints.shtml). ISSN: 0012-3692.

Downloaded from chestjournals.org on April 30, 2007


Copyright 1997 by American College of Chest Physicians

Elastic Energy as an Index of Right


Ventricular Filling*
Pierre Squara, MD; Didier Journois, MD; Philippe Estagnasie, MD;
Marc Wysocki, MD; Alain Brusset, MD; Didier Dreyfuss, MD; and
Jean Louis Teboul, MD

Background: Right ventricle (RV) preload assessment remains controversial because the complexity of RV geometry is an obstacle to wall stress modeling. We developed a method to evaluate
end-diastolic RV elastic energy (EL), a variable that integrates all the stretching effects of venous
return and that can be easily estimated at the bedside from the area under the diastolic RV
pressure-volume curve. The purpose of this study was to compare the clinical utility of EL and of
the two conventional variables used to assess RV filling, ie, right atrial pressure (Pra) and RV
end-diastolic volume (EDV).
Method: We studied 26 postoperative patients who required a rapid fluid challenge. Energetics
were evaluated by constructing the RV pressure-volume loop at the bedside using right heart
catheterization with RV ejection fraction (EF) derivation. Correlations between RV filling and RV
performance (ejection and mechanical efficiency) were studied. RV filling indexes were Pra,
EDV, and EL. Indexes of RV ejection were stroke volume (SV), RV stroke work (RVSW),
mechanical energy expenditure during ejection (EM), and total energy expenditure of contraction (ET). Indexes of RV mechanical efficiency were EF and the EM/ET ratio.
Results: Three important results were obtained. First, among RV ejection indexes, those that
correlated best with RV filling indexes were EM and ET. Second, we found significant linear
relationships between improved RV filling, as assessed by changes in EDV and EL, and improved
RV ejection, as assessed by changes in SV, RVSW, EM, or ET. Third, changes in EDV and EL also
predicted improved mechanical efficiency, as assessed by changes in EF and EM/ET. In all
situations, changes in EL yielded the strongest correlations.
Conclusions: Derivation of EL is simple and appears to be the best clinical means of assessing
Starlings law of the heart for the RV.
(CHEST 1997; 111:351-58)
Key words: energetics; hemodynamics; preload; right ventricle
Abbreviations: CO5cardiac output; Cv5ventricular compliance; EDP5end-diastolic pressure; EDV5end-diastolic
volume; EF5ejection fraction; EL5elastic energy; EM5mechanical energy expenditure during ejection;
ENM5nonmechanical energy expenditure during contraction; ESV5end-systolic volume; ET5total energy expenditure of contraction; PAPe5mean ejection pulmonary artery pressure; Pem5extramural right ventricle pressure;
Pra5right atrial pressure; RV5right ventricle; RVSW5right ventricle stroke work; SV5stroke volume

and optimization of right ventricle


A ssessment
(RV) preload is a major concern in the critically
ill. Although in vitro muscle fiber experiments define
preload as the weight that stretches the muscle
*From the Medical ICU, Victor Dupouy Hospital, Argenteuil
(Dr. Squara); the Department of Anesthesiology, Laennec,
Necker-Enfants Malades University Hospital, Paris (Dr. Journois); the Medical ICU, Louis Mourier, Bichat-Claude Bernard
University Hospital, Paris (Drs. Estagnasie and Dreyfuss); the
Medical ICU, Cite Universitaire Hospital, Paris (Dr. Wysocki);
the Cardiothoracic Surgery ICU; Ambroise Pare Hospital,
Neuilly (Dr. Brusset); and the Medical ICU, Kremlin Bicetre
University Hospital (Dr. Teboul), Kremlin Bicetre, France.
Manuscript received April 4, 1996; revision accepted September 13
Reprint requests: Dr. Squara, Reanimation polyvalente, Hopital
Victor Dupouy, 69 rue du Lieutenant-Colonel Prudhon, 95100
Argenteuil, France

before contraction, it is generally accepted that


end-diastolic sarcomere length is the most appropriate measure of preload.1-3 However, accurate determination of preload in the intact RV is difficult.
Accordingly, until the 1980s, RV preload was evaluated based on its relation to wall stress using the
Laplace law for a sphere or for an ellipsoidal shell,
which states that stress is a function of the product of
the wall distending pressure by the radius of wall
curvature.4,5 RV filling pressure was usually derived
from right atrial pressure (Pra). More recently, the
development of both ultrasonography and fast-response thermistor catheters has made it possible to
assess end-diastolic volume (EDV) at the bedside.6,7
In many situations, however, no correlation was
found between Pra (or transmural RV filling presCHEST / 111 / 2 / FEBRUARY, 1997

Downloaded from chestjournals.org on April 30, 2007


Copyright 1997 by American College of Chest Physicians

351

sure) and EDV,6 invalidating the current rationale


for RV preload assessment. Many studies have
shown the limitations of this rationale. First, the
physiologic unstressed volume of the RV may vary
with structural and functional changes induced by
pressure and/or volume overload.8-10 Below a threshold value, a change in volume does not result in a
measurable change in pressure, but only modifies
ventricular geometry. Therefore, muscle stress and
sarcomere length do not change significantly. Second, since the RV is crescent shaped,11 the local
distending pressure-stress relationship is heterogeneous along the RV walls and can change as a result
of septal shift,12 modifications in the radius of curvature of the RV free wall,9 or diastolic stiffness due
to impaired relaxation as seen, for example, during
RV ischemia.13 Third, the RV is functionally divided
into sinus (inflow) and conus (outflow) regions.14 In
the sinus, myocytes are disposed longitudinally and
are therefore sensitive to meridional wall stress,
whereas the circumvascular myocytes of the conus
are more sensitive to circumferential wall stress.
Fourth, the complex collagen and elastic network of
the RV may play an important role in the wall
stress-sarcomere length relationship, acting as series
and parallel viscoelastic elements.15,16 Last, RV
shape often undergoes major alterations, independent of the extramural RV filling pressure, as a result
of local scarring, pericardial stretching,17,18 left ventricle overfilling,19 or lung hyperinflation.20 Thus, for
a given patient, at a given point in time, sarcomeres
may be stretched in some parts of the RV but
relatively unstressed in other parts. Finally, there is
no proof that averaging sarcomere lengths is relevant
or that transmural filling pressure, wall stress, or
EDV accurately reflect average RV diastolic sarcomere length.
This suggests a different approach for assessing
filling of the intact RV. The driving force for RV
filling is provided by the venous return. The hydraulic energy of venous return is transferred to the RV
as internal energy via changes in both RV pressure
and RV volume during diastole. Thus, RV filling can
be formulated according to the law of energy conservation and can be represented by the area under
the passive RV pressure-volume curve.
D (energy)50(kinetic1gravitational
1internal energy)5heat1work
Ignoring kinetic energy, gravitational energy, and
heat, we have:
DEi5DEL5

end diastole

P z dV

(1)

Ei5internal energy, EL5elastic energy, P5ventricular distending pressure, V5ventricular volume.


Thus, the hydraulic energy of venous return is
changed to a ventricular elastic energy, which promotes complex fiber interactions and lengthening,
creating not only preload but also overall RV filling
effects that include stretching of nonmuscular tissues
and surrounding structures. We undertook this study
to develop and validate EL as an index of RV filling.

Materials and Methods


Study Design
Our objectives were to develop a simple method for assessing
EL at the bedside and to compare EL with conventional RV
filling-related indexes in patients meeting conventional criteria
for right heart catheterization. Our gold standard for RV filling
assessment was Starlings law of the heart. Starlings law of the
heart, as illustrated experimentally by the preload-total tension
curve,21 may be relevantly formulated for the intact RV, at the
bedside, by the relation between filling and cardiac contraction.22
Then, each RV filling index was evaluated according to its relation
to RV ejection and RV mechanical efficiency.
Calculation of Hemodynamic Variables
During filling, RV pressure and volume result from complex
interactions between stretching of elastic elements, relaxation of
contractile elements, and RV morphologic features.23,24 However, the potential energy of contractile elements is entirely lost
during relaxation and, based on the law of energy conservation,
EL at the end of filling integrates all energetics interactions,
including atrial systole and external influences. In both experimental and mathematical models, only a small hysteresis in the
pressure-volume relationship of diastolic left ventricles has been
found, indicating that most of the elastic energy at the end of
filling is available to perform mechanical work during ejection.16,25 In this study, we assumed that this is also the case for the
RV, and that EL was available for mechanical work during RV
ejection. Then, available energy is simply represented by the
amount of EL acquired during filling. Calculating this amount of
EL requires construction of the diastolic pressure-volume relationship (ventricular compliance [Cv] curve) followed by determination of its specific volume intercept (V 90) and by measurement of EDV (Fig 1). Four additional assumptions were made to
simplify EL evaluation at the bedside:
First, V 90 was determined by the volume axis intercept of the
regression line of all available Pra-EDV couples of measurements
during the RV filling.26 When calculated values of V 90 were
below 60 mL/m2, we assigned to V 90 a fixed value560 mL/m2,
which was the lowest acceptable V 90 value based on the literature.26,27 A reasonable hypothesis was that lower values were due
to inaccurate measurements in the flat segment of the Cv curve.
Second, we assumed that the Cv curve between V 90 and the
EDV point was linear instead of curvilinear. In most situations,
the linearity of the diastolic pressure volume relationship has
been verified.7,28 This assumption is not likely to provide significant error except in the event of sharp increases in RV volume
and pressure. In this case, the area under Cv curve may be
overestimated, although this is partly compensated by a proportional overestimation of V 90.
Third, to calculate EL, it is necessary to average the RV filling

352

Clinical Investigations

Downloaded from chestjournals.org on April 30, 2007


Copyright 1997 by American College of Chest Physicians

Figure 1. RV function curve (focused on filling energetics).


Ev5ventricular elastance; Ea5arterial elastance; Cv5ventricular
compliance; EDP5end-diastolic pressure. End-systole (time of
maximal elastance) occurs after the RV pressure peak and before
the end of ejection. The area limited by the Cv curve between
V 90 and EDV represents EL. This area can be evaluated by the
triangular gray area using variables that are easily available at the
bedside (Pra, EDV, ESV).

pressure between two points in the volume axis (V 90 and EDV).


However, bedside automatic integrators provide us with a time
average of pressure, and it has been established that the diastolic
time-volume relationship is not linear.29 Nevertheless, we made
the assumption that the volume average RV filling pressure is
consistently close to the time average RV filling pressure.
Fourth, mean transmural Pra was taken as the mean value of
the RV filling pressure. This assumption is valid provided the
tricuspid valve is intact.
The area under the Cv curve was calculated by solving two
equations, as shown in Figure 1. The first equation was mean
(Pra2Pem)/m5EDP/(EDV-V 90), where Pra2Pem was used to
assess the mean RV transmural filling pressure and where m was
the arithmetic mean between end-systolic volume (ESV) and
EDV. The second equation was EL5EDP3(EDV2V 90)/2. By
replacing EDP in the second equation by its value on the first
equation, the equation can be solved as follows:

another and it is unlikely that the cumulative error would be


important. Thus, we are confident that assessing EL at the
bedside is acceptable and as reliable as Pra or EDV assessments.
Assessing ventricular performance using energetics is clinically
relevant.30-32 Previous studies have described the energetics of
the contractile process as systolic energy (energy expenditure
between end-diastole and end-systole) and potential energy
(residual ventricular amount of energy at the end-systole).33
However, traditional assessment of RV energetics is limited to
RV stroke work (RVSW) derivation using a simplified formula:
RVSW5(PAPm2Pra)3SV, where PAPm is the mean pulmonary
pressure, and SV is the stroke volume.
In this study, we distinguished mechanical ejection energy
(EM) represented by the area under the RV pressure volume
loop, from the nonmechanical energy (ENM) represented by the
area limited by the left side of the RV pressure-volume loop, the
ventricular elastance line, and the volume axis (Fig 2). To
evaluate EM and ENM at the bedside, we needed to evaluate
mean ejection pulmonary artery pressure (PAPe). This parameter
is not usually assessed and was derived from the systolic (PAPs)
and diastolic (PAPd) pulmonary artery pressures using a previously validated formula: PAPe5(2PAPs1PAPd)/3.34 EM and
ENM are different from energetics that assess contractile process, since the dividing point between systolic energy and
potential energy is the time of maximum elastance (end-systole
point) instead of end-ejection. However, the sum EM1ENM is
equal to the sum systolic energy1potential energy and to the
total energy expenditure of contraction (ET).
ET5EM1ENM

(2)

EM5SV3~PAPe2Pem!

(3)

(4)
ENM5~ESV2V 0 !3~PAPe2Pem!/ 2
During systole, kinetic energy is low compared to mechanical
energy (,2%) and can be neglected. The volume intercept for
the end-systolic pressure-volume relationship (V0) could not be
calculated exactly and was assumed to be zero.35 Pra and Pem are
measured in mm Hg and volumes in mL; EM, ENM, and ET are
given in g/m using a transformation constant50.01428.
RV pressure-volume loops have more triangular shape than left
ventricular loops as long as pulmonary resistance remains low.
However, in critical care patients, pulmonary vascular resistance
often increases and the RV pressure-volume loops become more

EL5(Pra2Pem)3(EDV2V 90)2/(EDV1ESV22V 90)


(1a)
when ESV.V 90
when ESV,V 90: (1b)
EL5(Pra2Pem)3(EDV2V 90)
EL50
when EDV,V 90: (1c)
Pem5extramural RV pressure. Kinetic energy was neglected.
When Pra and Pem are measured in mm Hg and volumes in mL,
EL is given in g.m using a transformation constant50.01428.
In a hypothetic population with Gaussian distribution for
hemodynamic variables, Pra5863 mm Hg, Pem50,
EDV5175650 mL, ESV5120650 mL, and V 90575610 mL;
formulas 1a through c show that a 1-mm Hg systematic error in
Pra measurements (error in Pra517617%) leads to an error of
similar magnitude in EL estimation. A 10-mL isolated systematic
error in EDV assessment (error in EDV5661%) leads to an
error in EL estimation51065%. However, an isolated error in a
single volume assessment is not likely to occur, and the formula
shows that a systematic error in the assessment of all RV volumes
(EDV, ESV, and V 90) does not change the EL value. Moreover,
the other assumptions used to evaluate EL are not likely to
introduce significant errors. Since these assumptions are based
on independent parameters, one error may compensate for

Figure 2. RV function curve (focused on ejection energetics).


The area under the pressure-volume loop represents EM (gray
quadrangular area). The area limited by the left side of the loop
and the Ev curve represents ENM (dotted triangular area).
CHEST / 111 / 2 / FEBRUARY, 1997

Downloaded from chestjournals.org on April 30, 2007


Copyright 1997 by American College of Chest Physicians

353

Table 1Ranges of RV Filling Variables*

Pra, mm Hg
EDV, mL
EL, g/m

First
Quartile

Second
Quartile

Third
Quartile

Fourth
Quartile

,5
,145
,1.5

5-7
145-175
1.5-3.6

8-9
175-185
3.6-7

.9
.185
.7

*Values indicate the range of each quartile.

quadrangular. However, independent from the shape of RV


pressure-volume loop during ejection, accurate measurements of
EDV, ESV, and PAPe lead to accurate assessment of EM. Using
the reported method,34 the error in assessing PAPe was ,7%.
Formulas 3 and 4 show that a 10% error in PAPe measurement
leads to an equivalent error in EM estimation. Similarly, an
isolated error in a single volume measurement leads to an error
of similar magnitude in EM, ENM, SV, cardiac output (CO), or
RVSW assessment. Systematic error in both ESV and EDV
assessment has no consequence except on ENM calculation. In
this situation, a 10-mL isolated error introduced an error in ENM
of 962% and in ET of 562% in the hypothetical population
described. Thus, assessment of EM and ENM at the bedside is
acceptable and as reliable as conventional RV ejection indexes.
Last, global RV mechanical efficiency can be assessed at the
bedside using ejection fraction (EF).36 The same mechanism can
be evaluated using the ratio EM/ET.

tor was injected at the end of an inspiration to ensure homogeneous computation of CO and RV volumes during the endexpiration phase.6,7 Patients with significant tricuspid
regurgitation (v peak pressure .5 mm Hg on the Pra pressure
curve [v5the v part of the right atrial pressure curve]) were
excluded from the study, as were patients with decompensated
COPD and intrinsic positive end-expiratory pressure .5 cm
H2O. No guidelines for therapy were given to clinicians, but
treatment was maintained during the study.
Data Analysis
RV filling indexes were Pra, EDV, and EL. Indexes of RV
ejection were SV, RVSW, EM, and ET. Indexes of RV mechanical efficiency were EF and the EM/ET ratio. We first compared
the R (regression coefficient), F (analysis of variance), and p
(significance) values of the linear regressions between each
change in filling index and each change in ejection or mechanical
efficiency index. After a univariate analysis, forward stepwise
multiple regression analyses were performed to identify the
major RV filling index for each index of ejection and mechanical
efficiency. All continuous data were tested for normal distribution using the Kolmogorov-Smirnov test (SPSS Inc; Chicago). All
normally distributed data are reported as means6SDs. The
remaining variables are expressed as median values (minimummaximum); p values ,0.05 were considered indicative of absence
of type I error.

Patients and Protocol

Results

After approval of our protocol by our institutions ethics


committee, we studied 26 postoperative patients who required a
rapid fluid challenge after cardiovascular surgery. These 26
patients did not have sepsis. The decision to perform a rapid
filling test was taken by a senior intensivist to adjust filling
conditions when CO was judged insufficient and possibly fillingdependent. All patients were sedated and mechanically ventilated. To minimize the effect of extramural pressure, no positive
end-expiratory pressure was used and pressure values were
measured at the end of expiration. We performed two sets of
hemodynamic measurements before and after a rapid infusion of
500 mL of colloid. Each hemodynamic evaluation included
conventional right heart catheterization with beat-to-beat dilution of cool dextrose water to derive CO and EF, which, together
with heart rate, yielded SV, EDV, and ESV of the RV (Refox
Swan Ganz catheter; Baxter Edwards; Irvine Calif). Cool indica-

Median age was 66 years (range, 30 to 82 years).


CO was usually within the normal range at basal
metabolism (CO55.461.7 L/min). Initial RV filling
index values were as follows: Pra56.262.3 mm Hg;
EDV5166633 mL; and EL53.762.9 g.m. Quartile
ranges of RV filling variables in the study patients are
given in Table 1. EL appeared as the most sensitive
indicator, since the ratio of the fourth quartile lower
limit over the first quartile upper limit was 4.6 vs 1.3
for EDV and 1.8 for Pra.
Three important results were obtained (Table 2).
First, among RV ejection indexes, those that correlated best with RV filling indexes were EM and ET.

Table 2Relation Between Changes in RV Filling and Changes in RV Ejection*

Univariate analyses
DPra
DEDV
DEL
Multivariate analyses
DPra
DEDV
DEL

DSV

DRVSW

DEM

DET

DEF

DEM/ET

1.51
14.8
24.5

2.56
12.4
18.6

0.01
18.5
47.6

0.02
29.4
41.6

1.97
3.05
6.74

1.01
4.69
8.67

NIM
NIM
24.5

21.2
NIM
38.1

NIM
NIM
47.6

NIM
4.57
17.6

NIM
NIM
6.47

NIM
NIM
8.67

*For univariate analyses, numbers5F values of analysis of variance tables between variables. For multivariate analyses, numbers5F values to
remove the model. D5variation of value after rapid fluid challenge; NIM5not in model.

p,0.01.

p,0.0001.

p,0.05.
354

Clinical Investigations

Downloaded from chestjournals.org on April 30, 2007


Copyright 1997 by American College of Chest Physicians

usefulness for predicting the result of the fluid


challenge. We therefore assessed the clinical usefulness of filling indexes by comparing the values in
these indexes in the 10 patients with the greatest
improvements and in the 10 patients with the smallest improvements in RV ejection or mechanical
efficiency (good and poor responders, respectively).
For all RV ejection indexes (SV, RVSW, EM, ET)
and all RV mechanical efficiency indexes (EF, EM/
ET), the largest significant differences between the
two groups were found using EL (Table 3).

Discussion
Since RV failure is a frequent abnormality that
limits left ventricular filling and output, increasing
RV filling to an optimal value is essential to
improve RV performance. We found that derivation
of RV filling elastic energy can improve the assessment of Starlings law of the heart for the RV
compared with EDV and Pra. In most ICUs, microcomputers are available for calculating hemodynamic parameters at the bedside. Our method for
deriving EL can be easily included using a short
program. Using these tools, EL assessment is simple
and only requires two traditional sets of Pra, EDV,
and ESV measurements.

Figure 3. Relationship between EL and RV ejection (SV


and EM).

Second, we found significant linear relationships


between improved RV filling, as assessed based on
changes in EDV and EL, and improvement in RV
ejection, as assessed based on changes in SV, RVSW,
EM, or ET. Third, changes in EDV and EL also
predicted improved mechanical efficiency, as assessed by changes in EF or the EM/ET ratio.
In all situations, changes in EL yielded the strongest correlations (Table 2 and Fig 3). In contrast,
improved Pra did not correlate significantly with any
of the study parameters. Multiple regression analyses
consistently identified the change in EL as an independent predictor of both RV ejection and mechanical efficiency. EDV was an additional independent
predictor of ET.
Unfortunately, for none of the RV filling indexes
were we able to identify a threshold of potential

Limitations of the Method


EL evaluation at the bedside requires five assumptions. Despite these limitations, the accuracy of EL
value can be estimated at 620%. The value of
bedside derivation of EDV and ESV using right
heart catheterization has been challenged on the
grounds that the commercially available black box
does not specify the accuracy with which EF is
derived. However, this method has been tested

Table 3Results of a Rapid Fluid Challenge


Good Responders

End point: changes in SV


SV, mL
Pra, mm Hg
EDV, mL
EL, g/m
End point: changes in EF
EF, %
Pra, mm Hg
EDV, mL
EL, g/m

Poor Responders

Before Fluid

After Fluid

% Increase

Before Fluid

After Fluid

% Increase

p Value*

59 6 17
6.6 6 1.7
177 6 31
3.9 6 2.2

82 6 15
7.6 6 1.6
190 6 30
6.1 6 3.5

40
15
7
56

53 6 16
5.9 6 3.1
159 6 33
4.0 6 3.8

59 6 15
6.3 6 3.0
164 6 32
4.7 6 4.0

13
7
3
18

0.0001
NS
0.03
0.0006

35 6 11
7.0 6 1.1
169 6 8
3.9 6 1.8

45 6 10
7.9 6 1.0
181 6 13
6.0 6 2.9

29
15
13
54

33 6 7
6.0 6 3.2
159 6 39
4.4 6 3.9

36 1 6
6.5 6 2.9
168 6 37
5.4 6 4.0

9
8
6
22

0.01
NS
NS
0.0006

*p values are for differences between good responders and poor responders. NS5not significant.

CHEST / 111 / 2 / FEBRUARY, 1997

Downloaded from chestjournals.org on April 30, 2007


Copyright 1997 by American College of Chest Physicians

355

extensively under the conditions of our study 6,7,37,38:


moreover, no alternative is available for routine
repeated evaluation of RV volumes at the bedside.
Review of Results
During a rapid fluid challenge, improved RV
filling was related to increased ejection and mechanical efficiency. The fact that EL was the best RV
filling index, ie, showed the closest correlations with
RV performance indexes, was not surprising since
available elastic energy at the end of filling can
represent up to 30% of the mechanical energy
expended during ejection. However, stretching myocardial fibers increases elastic energy but first of all
increases the number of biochemical sites of active
contraction.39,40 Although biochemical recruitment
is obviously less closely related to the increase in EL
than to the increase in fiber length, to our knowledge, no means of assessing average fiber lengthening in clinical settings are available. EL was the best
method for assessing all effects of filling (elastic and
biochemical) on RV ejection. Neither is it surprising
that EM and ET were the best indexes of RV
ejection, since they take into consideration the pressure work, which is neglected when CO or SV is used
or roughly evaluated when RVSW is used. Pressure
work can contribute substantially to RV mechanical
work in pathologic situations such as acute respiratory failure.14
EDV was also an independent predictor for ET.
During a rapid fluid challenge, we found that ET was
not better than EM for assessing ejection. The
proportion of EM and ENM in total energy of
contraction (ET) varies with ventricular contractility,
afterload, and relaxation. Our findings are in keeping
with theory. Figure 2 shows that when the RV
function loop expands toward the right after a fluid
challenge, RV mechanical efficiency increases as a
result of a selective increase in SV or EM. In
contrast, ENM cannot change substantially since
ventricular contractility, afterload, and relaxation
usually remain unchanged during the short time
needed for a rapid fluid challenge. The improvement
in ET was therefore primarily due to the improvement in EM and explains why EL was strongly and
positively correlated with EM, ET, EF, and EM/ET
in our study. However, a corollary of our hypothesis
that V050 is that larger EDV values are associated
with larger ENM and ET values. This explains why
the multivariate analysis identified EDV as independently linked to ET. Since a reasonable assumption
is that the true V0 does not vary substantially around
zero in most situations, EDV may be more closely
linked to RV dilation than to RV filling.
The stronger correlation between RV perfor-

mance (ejection and mechanical efficiency) and


EL compared with Pra and EDV cannot be ascribed to chance or bias. EL was derived from Pra
and EDV values using an associative function.
However, when a specific phenomenon is related
to several measured elementary variables, combination of these variables to create a new complex
variable often weakens the correlation. This may
be due to several mechanisms. Two elementary
variables used to calculate a complex variable may
be interrelated and may therefore assess the same
information. Alternatively, when the elementary
variables are independent from each other, the
loss of information may be due to independent
distributions of patients according to each variable. Last, complex variables may lose predictive
value because of either accumulation of measurement errors or opposite-direction physiologic
changes in the elementary variables used to calculate the complex variable. Thus, the correlation of
a calculated variable can exceed that of the measured elementary variables used in the formula
only if the information provided by the associative
function offsets the cumulative loss of information
due to the three above-listed mechanisms. In
other words, although measurement of a specific
biological variable that directly reflects a given
physiologic mechanism may be unfeasible, it may
be possible, using an appropriate model, to derive
with acceptable accuracy the original indicator
from other related variables accessible to direct
measurement.
The loss of information when assessing RV
filling using Pra or EDV has been discussed above.
In bedside evaluation of EL, the loss of information is due to the assumptions made to simplify
calculations. In our study, we demonstrated that
the power of the model offset the cumulative
errors due to our assumptions. In all associative
functions, mathematical coupling is a possible
cause of bias, but mathematical coupling is also
usually a component of the physiologic information. For example, the strong mathematical coupling between EDV and SV (SV5EDV2ESV)
does not abolish the clinical usefulness of both
variables. In addition, mathematical coupling does
not necessarily tighten the correlation between
two variables. In fact, all hemodynamic variables
are dependent and are composed of many shared
hidden variables that are not accessible to the
clinician. Mathematical coupling is only one of the
factors that can affect correlations between data
and should not be given undue emphasis. After a
rapid fluid challenge, one might expect mathematical coupling to be most marked between EDV
and SV, as seen above. However, we found a closer

356

Clinical Investigations

Downloaded from chestjournals.org on April 30, 2007


Copyright 1997 by American College of Chest Physicians

correlation between EL and SV. Thus, evaluation


of EL is the best means of taking into account all
accessible and hidden variables at the bedside and
of improving the physiologic information at our
disposal.
From a given value of RV filling, it was not
possible to predict the result of rapid fluid infusion.
This is not surprising since many parameters contribute to the result of fluid therapy. However, both
RV ejection and mechanical efficiency increased
only when the rapid fluid infusion increased EL, and
vice versa. This was not observed using Pra and was
rarely observed using EDV. These findings may have
clinical implications. When a filling test is decided to
improve RV function, it should probably be prolonged until significant increase in EL is obtained.
Then EL derivation may allow better RV filling
optimization in clinical situations where hidden hypovolemia and RV overload coexist, including the
following: postoperative states, especially after cardiac surgery; pulmonary embolism; RV infarction;
septic shock; and ARDS.
Thus, derivation of EL significantly improved RV
filling assessment at the bedside. In contrast, EDV
seemed to reflect RV dilation rather than RV filling.
Our model may provide insights into the relationships among physiology, pathology, and clinical investigation, and may benefit in the future from
improvements in measurement accuracy.
ACKNOWLEDGMENTS: We thank Dr. Dominique Denjean
and Dr. Dany Goldgrand-Toledano for their help in collecting
data; Prof. Guy Thomas for his help with the statistical analysis;
and Dr. Herve Mentec, Prof. Yves Le Carpentier, and Prof. Alain
Nittenberg for their critical review of the manuscript.

9
10
11
12
13
14
15
16
17
18

19

20
21

References
1 Glower D, Spratt J, Snow N, et al. Linearity of the FranckStarling relationship in the intact heart: the concept of
preload recruitable stroke work. Circulation 1985; 71:9941009
2 Sarnoff S, Berglund E. Starlings law of the heart studied by
means of simultaneous right and left ventricle function curves
in the dog. Circulation 1954; 9:706-14
3 Sonnenblick E. Force velocity relations in mammalian heart
muscle. Am J Physiol 1962; 202:931-40
4 Feneley M, Elberry J, Gaynor J, et al. Ellipsoidal shell
subtraction model of right ventricular volume: comparison
with regional free wall dimensions as indexes of right ventricular function. Circ Res 1990; 67:1427-36
5 Braunwald E. Assessment of cardiac performance. In: Braunwald E, ed. Heart diseases. Philadelphia: WB Saunders, 1988;
472-92
6 Jardin F, Gueret P, Dubourg O, et al. Right ventricle volumes
by thermodilution in the adult respiratory distress syndrome:
a comparative study using two dimensional echography as a
reference method. Chest 1985; 88:34-9
7 Pinsky M, Desmet J, Vincent J. Effects of positive end-

22
23
24
25
26
27
28
29

expiratory pressure on right ventricular function in humans.


Am Rev Respir Dis 1992; 146:681-87
Weber K, Janicki J, Shroff S, et al. The right ventricle:
physiologic and pathophysiologic considerations. Crit Care
Med 1983; 11:323-28
Ryan T, Petrovic O, Dillon J, et al. An echocardiographic
index for separation of right ventricular volume and pressure
overload. J Am Coll Cardiol 1985; 5:918-24
Feneley M, Gavaghan T. Paradoxical and pseudoparadoxical
interventricular septal motion in patients with right ventricular volume overload. Circulation 1986; 74:230-38
Stool E, Mullins C, Leshin S, et al. Dimensional changes of
the left ventricle during acute pulmonary arterial hypertension in dogs. Am J Cardiol 1974; 33:498-504
Brinker J, Weiss J, Lappe D, et al. Leftward septal displacement during right ventricular loading in man. Circulation
1980; 61:626-32
Schulman D, Biondi J, Zohbgi S, et al. Coronary flow limits
right ventricular performance during positive end-expiratory
pressure. Am Rev Respir Dis 1990; 141:1531-37
Hurford W, Zapol W. The right ventricle and critical illness:
a review of anatomy, physiology and clinical evaluation of
function. Intensive Care Med 1988; 14:448-57
Sato S, Ashrof M, Milliard R. Connective tissue change in
early ischemia of porcine myocardium. J Mol Cell Cardiol
1983; 15:261-69
Shroff S, Janicki J, Weber K. Left ventricular systolic dynamics in terms of its chamber mechanical properties. Am J
Physiol 1983; 245:H110-24
Calvin J. Optimal right ventricular filling pressures and the
role of pericardial constraint in right ventricular infarction in
dogs. Circulation 1991; 84:852-61
Goldstein J, Vlahaker G, Verrier E, et al. The role of right
ventricle systolic dysfunction and elevated intra-pericardial
pressure in the genesis of low output in experimental right
ventricle infarction. Circulation 1982; 65:513-22
Biondi J, Schulman D, Souffer R, et al. The effect of
incremental positive end expiratory pressure on right ventricle hemodynamics and ejection fraction. Anesth Analg 1988;
84:144-51
Takata M, Robotham J. Ventricular external constraint by the
lung and pericardium during positive end expiratory pressure.
Am Rev Respir Dis 1991; 143:872-75
Starling E. Linacre lecture on the law of the heart. In:
Longmans, ed. London: Green; 1918
Guyton A. Determination of cardiac output by equating
venous return curves with cardiac response curves. Physiol
Rev 1955; 35:123-29
Sabbah H, Stein P. Negative diastolic pressure in the intact
canine right ventricle: evidence of a diastolic suction. Circ Res
1981; 49:108-13
Stein P, Sabbah H, Anbe D, et al. Performance of the failing
and nonfailing right ventricle of patients with pulmonary
hypertension. Am J Cardiol 1979; 44:1050-55
Rankin J, Arentzen C, McHale P, et al. Viscoelastic properties
of the diastolic left ventricle in the conscious dog. Circ Res
1977; 41:37-45
Dhainaut J, Brunet F, Monsallier J, et al. Bedside evaluation
of RV performance using a rapid computerized thermodilution method. Crit Care Med 1987; 15:148-54
Dhainaut J, Lanore J, De Gournay J, et al. Right ventricular
dysfunction in patients with septic shock. Circ Shock 1987;
21:335-36
Tyberg J, Taichman G, Smith E, et al. The relationship
between pericardial pressure and right atrial pressure: an
intra-operative study. Circulation 1986; 73:428-32
Woodward J, Bertram C, Gow B. Right ventricular volumetry
CHEST / 111 / 2 / FEBRUARY, 1997

Downloaded from chestjournals.org on April 30, 2007


Copyright 1997 by American College of Chest Physicians

357

30
31
32
33
34

by catheter measurement of conductance. Pace 1987; 10:


862-70
Suga H. External mechanical work from relaxing ventricle.
Am J Physiol 1979; 236:H494-97
Suga H. Total mechanical energy of a ventricle model and
cardiac oxygen consumption. Am J Physiol 1979; 236:494-97
Squara P, Journois D, Formela F, et al. Value of elementary,
calculated and modeled hemodynamic variables. J Crit Care
1994; 9:223-35
Suga H, Hayashi T, Shirahata M. Ventricular systolic pressure
volume area as a predictor of cardiac oxygen consumption.
Am J Physiol 1981; 240:H39-44
Squara P, Golgrand-Toledano D, Mentec H, et al. Validation
of a simple formula to evaluate the mean systolic pulmonary
artery pressure (PAPsm). Am Rev Respir Dis 1994; 149:
A1061

35 Brown K, Ditchey R. Human RV end-systolic pressurevolume relation defined by maximal elastance. Circulation
1988; 78:81-91
36 Robotham J, Takata M, Berman M, et al. Ejection fraction
revisited. Anesthesiology 1991; 74:172-83
37 Boldt J, Kling D, Hempelman G. Right ventricular function
and cardiac surgery. Intensive Care Med 1988; 14(suppl
2):496-99
38 Dhainaut J, Aouate P, Monsallier J, et al. Improvement of
right ventricle performance by continuous positive airway
pressure in ARDS. J Crit Care 1987; 2:15-21
39 Yoran C, Covell J, Ross JJ. Structural basis for the ascending
limb of left ventricular function. Circ Res 1973; 21:33-39
40 Leyton R, Spotnitz H, Sonnenblick E. Cardiac ultrastructure
and function: sarcomeres in the right ventricle. Am J Physiol
1971; 221:902-10

358

Clinical Investigations

Downloaded from chestjournals.org on April 30, 2007


Copyright 1997 by American College of Chest Physicians

Elastic energy as an index of right ventricular filling


P Squara, D Journois, P Estagnasie, M Wysocki, A Brusset, D Dreyfuss and
JL Teboul
Chest 1997;111;351-358
This information is current as of April 30, 2007
Updated Information
& Services

Updated information and services, including high-resolution


figures, can be found at:
http://chestjournals.org

Citations

This article has been cited by 1 HighWire-hosted articles:


http://chestjournals.org

Permissions & Licensing

Information about reproducing this article in parts (figures,


tables) or in its entirety can be found online at:
http://chestjournals.org/misc/reprints.shtml

Reprints

Information about ordering reprints can be found online:


http://chestjournals.org/misc/reprints.shtml

Email alerting service

Receive free email alerts when new articles cite this article
sign up in the box at the top right corner of the online
article.

Images in PowerPoint format Figures that appear in CHEST articles can be downloaded
for teaching purposes in PowerPoint slide format. See any
online article figure for directions.

Downloaded from chestjournals.org on April 30, 2007


Copyright 1997 by American College of Chest Physicians

You might also like