Modeling and Simulation of the Human Cardiovascular System
with Bond Graph: a Basic Development
Mireya Diaz-Insua, Marisol Delgado
Department of Processes and Systems, Sim6n Bolivar University, Venezuela
Abstract
A bond graph model of the cardiovascular system has
been developed. With the model, changes in the blood
pressure waveform are studied at different points in the
systemic and pulmonary circulations when exposed to a
normal ventricular function. The waveforms such obtained
show a good model performance which reflects actual
waves when compared with physiological human data.
Wave reflection phenomena effects, capability in handling
elements, addition of new compartments, and obtention of
numerical data for spectral analysis are among the model
features. These results and facilities offered by the
"intuitive" and simple bond graph approach suggest its use,
especially for life scientists, in the development of more
detailed models for educational, research and clinical
purposes.
1. Introduction
In the eighteenth century Otto Frank formally developed
Hales' Windkessel theory, basis of the first modern
cardiovascular models. Since then, models of various
degrees of complexity based on transmission lines or
segments have been developed for educational, research and
clinical purposes.
The modeling of such systems generally entails a high
degree of complexity due to the fact that they show
multiple domain mechanisms being, simultaneously, non-
linear and time-varying. This complex nature has led to a
search for modeling tools which would enable users from
the life sciences to describe the systems through more
familiar diagrams and graphs, and avoid in this way the
formulation of a large differential equation set which
normally describes this type of systems.
The bond graph method [ l ] is an alternative, being its
main asset the fact that it provides for a unified description
of various types of physical systems as it is based on the
universal concept of energy. Furthermore, it shows the
topological structure of the physical system and includes
its mathematical description also. The use of this
"intuitive" method for multienergy systems has been
proposed in 121.
The technique is centered in the description of the system
by elements which generate, store, dissipate, transmit or
transform energy. It has been used in the clinical-research
0276-6547196$5.000 1996 IEEE
environment for the developement of an optimal controller
for the Penn State EVAD (ventricular assist device) [3], in
which the bond graph represents the motor, the coupler and
a small circulatory system. It has also been used as a
transparent internal representation of a cardiovascular model
builder library [4].
This paper shows the applicability of the bond graph
method in the modeling and simulation of physiological
systems. It addresses the development of a cardiovascular
model using a segmental description of the blood vessels
based on [5, $1 which allows, among other things, to study
the modifications endured by the blood piressure along the
vascular tree -a variable which reveals the mechanical
properties of vessels- when exposed to a nlormal ventricular
driving pressure. The model highlights this most important
blocks of the systemic and pulmonary circulations, such as
the cardiac chambers and valves, main arteries and the
remaining vessels included in arteries, veins and periphery.
2. Model Description
A combination of two models, one electric [5] and one
hydraulic [6], was used in order to build the bond graph
model shown in Fig. la. The most important assumptions
made to reach a certain degree of simplicity in the mod'el
were: each blood vessel was represented by a linear-element
lumped description; closed loop configur,ation; absence of
external influences; absence of venous valving mechanism.
Each blood vessel (Fig. 1b) was represented by a parallel
capacitance (C) and resistant-inertial (]<-I) elements :in
series. The capacitances, resistances and inertances represent
the vessel wall elasticity, the vessel opposition to blood
flow and the inertial blood movement, respectively. These
three elements are linked by the energy transmission
points: 0-junction (same blood pressure) ,and 1-junction
(same blood flow) respectively.
The non-linear pressure-volume relationship and
pulsatile behaviour of ventricles are concentrated in two
effort sources (SE) which are ,connected with its
correspondent atrium, a constant compliance (circled area in
Fig. 1c). The representation of the heart valves introduce a
problem related to transitions between diifflerent modes of
operation; i.e. non-linearities. The modulated R-element
presented by [7] was used as a solution (lower section in
Fig. IC). This modulated R-element was decomposed, as
in [7], into a fixed R and a modulated transfoimer
(MTF), representing the non-ideal conduction and the
393 Computers in Cardiology 1996
 . .
Fig.1: Bond graph of the (a) cardiovascular system (b) blood vessel (c) cardiac chamber and valve
switching behavior, respectively. The transfoming module
m is a logic variable with values 1 or 0 depending upon
whether the valve (switch) is open or closed.
Human data for vessels and heart valves were obtained
from [5] and [8] respectively, in order to complete the
model.
3. Results
The model was simulated with the Enport 5.2 software
[9], starting from a zero initial state and running for 9
seconds until an end-diastolic steady state was reached. The
final state thus obtained was used as the initial state in any
subsequent simulation. A stiff numerical integration
method was selected, since the boundary time constants are
separated by four orders of magnitude being the smaller
0.41 msec and the larger 1.68 sec.
Figures 2a) through 2n) show the pressure curves (in
steady state) at different sites in the systemic and
pulmonary circulations when exposed to normal
ventricular driving pressure: half-sinusoid, 0.75 sec (80
beatdmin), and systolic/diastolic values of 120/5 and 21/2
mmHg for left ( F i g . 2 ~ )and right (Fig.2d) ventricles. The
systolic and diastolic values obtained are within the normal
range reported in physiology textbooks.
In the graphs, both the peak systolic and the end-
diastolic pressure values are shown. A dicrotic notch is
observed in the aortic (Fig.2e) and pulmonary (Fig.20
artery pressures. Capital letters used in Fig. 2a), 2b), 2e),
and 2f) represent the moment of atrioventricular (mitral-
MV, tricuspid-TV) and semilunar (aortic-AV, pulmonic-
PV) valve opening (0)and closing (C) respectively. The
valve states were as follows:
Valve 0 (sec) C (sec) Valve O(sec) C(sec)
0.077 0.250 Mitral 0.374 0.001
Aortic
Pulmonary 0.035 0.296 Tricuspid 0.361 0.001
394
4. Discussion
The model developed shows features of physiological
interest. During systole, the driving ventricle transmits its
strength to the arterial subsystem through its main artery,
therefore the arterial pressure follows the ventricular
pressure. But in diastole, when the heart and the arterial
subsystem are isolated, the great arteries serve as second
pressure sources and therefore, the arterial compartments
follow that pressure. This is made evident observing the
diastolic value which is greater than the one in the
associated ventricle.
This large diastolic value, which limits the fall of the
arterial pressure during this phase, is also explained as a
wave propagation phenomena effect. This consists in the
addition of forward and backward waves through the arterial
system caused by multiple reflection sites in it.
Another wave propagation phenomena effects are the
diminished pressure values in arteries (Fig.2g, 2h) and
periphery (Fig.2i, 2j), and the dicrotic notch present in the
main arteries (Fig.2e, 2 0 .
The reduction in pressure amplitude is explained by the
viscous-elastic properties of blood vessels included in the
impedance of the segments. This characteristic smooths
the pulsatile pressure generated by the heart when it arrives
to the capillaries. Additionally, the viscous-elastic
behavior introduces a phase lag in the pressure wave in its
travel along the arterial tree.
The dicrotic notch is a matter of controversy. So far, it
has not been completely determined whether it is an effect
of the valve closure or, as a result of the reflection
phenomena in the arterial tree, the notch forces the valve
closure, The exhibition of this feature by the model
suggests that it could be used to elucidate this issue.
As it may be noticed, this bond graph version of a
lumped model can represent changes in the blood pressure
waveforms associated with reflection phenomena, even
 7.5
* 2,-, .
MVQ MVC
TV Q TV C
0 0.3 TIME [ s e c ] 1.2 1.5 0 0.3 TIME ( s e c ] 1.2 1.5

p [ m m H 41 Left Ventricle dl P [ m m H4 1 hght Ventricle

140
3 0 r 1

-
70

0 0.3 TIME ( S e c ] 1.2 1.5 0 0.3 TlME(SQC1 1.2 1.58

1' P ( m m Hg I Aorta 'P(mmHg1 Pulmonary Artely

140
30

70 . PVQ 5 ~

I I I . - I B . . I I

0 0.3 TIME (Sec) 1.2 1.5 0 0.3 TIME ( S I C ] 1.2 1.5

'P(mmHg1 Systemic Arteries

125

0i 0.3 TIME [ s e c ] 1.2 1.5

P- 63.4
i - 9.4

0 0.3 TIME [Sec] 1.2 1.5 0 0.3 TIME ( s e c ) 1.2 1.5

- 5 5

3,7

-10

.. .
-1301 . * 1 -301
0 0.3 TIME [ s e c ) 1.2 1.5 0 0.3 TIME [ s e c ) 1.2 1.5

Fig. 3: a> - n> Pressure waveforms at Merent sites in systemic and pulmonary circulations.

395
though in [lo] is referred that a lumped structure has
proven inadequate for this purpose.
Lower pressure values are also found in pulmonary
compartments (Fig.2f, 2h, 2j) with respect to their
systemic (Fig.2e, 2g, 2i) counterparts. This is due to the
fact that pulmonary vessels have a larger caliber than the
corresponding systemic vessels, thus offering a lower
resistance to blood flow. The pulmonary veins (Fig.21) are
the exception, in view of the higher pressures that the left
heart transmits to them in comparison with the lesser
pressures that the right heart transmits to the systemic
veins (Fig.2k).
The atrial pressures (Fig.2a, 2b) show the "v" wave and
the "y" descent, proper of the atrial filling with the atrio-
ventricular valve closed and the fast diastolic ventricular
filling when this valve opens, respectively. But, the "a"
and "c" curves, resulting from atrial contraction and
begining of the ventricular systole, did not showed up. It
could be explained by the constant atrial compliance used
which does not represent completely the contraction-
relaxation mechanism of this cardiac chamber. The absence
of this characteristic curves can lead to wrong conclusions;
for example, infer an atrial fibrillation when it actually
does not occur.
With respect to the cardiac valves, two features arose.
First, valvular events according to the cardiac cycle are
displayed in Fig. 2a), 2b), 2e), and 2f). Systole lasts one-
third of the beat, and right heart valves labor begins first
and are opened longer than the correspondent left heart
valve. The latter happens due to the greater pressure levels
present in the left heart -which are more difficult to reach
and to descend from them- and also because of the
differences in the conduction system anatomy.
Second, the valves (Fig.2m, 2n) experience extreme
cyclic loading conditions during each cardiac cycle. During
the open state a very low gradient, almost zero, is present;
but, when the valves are closed, the negative pressure
value shows a large pressure gradient between the adjacent
compartments, which acts upon the corresponding valve.
5. Conclusions
The simulations of the model developed in this paper
present good quantitative and qualitative results, similar to
other cardiovascular model simulations and to
physiological actual data. Aside from the satisfactory
results described above, there are practical issues
concerning the modularity of the model developed and the
capability of the Enport in handling elements. These
advantages show that the bond graph approach is a suitable
tool for the modeling of non-linear, multi-energy and time-
varying systems, such as the physiological ones and,
among them, the cardiovascular system.
We suggest as future work the development of enhanced
models in order to study normal and pathological
conditions of the system by:
- Performing a signal analysis over the numerical
results, to correlate harmonic contents with the
normal and pathological states.
396
Changing parameters, which also allows to test the
model robustness.
Adding more vessels and non-linear characteristics to
them, to explore regional circulation features and
represent system dynamics more accurately.
Introducing compartments of other domains, external
influences and neural control schemes, to describe
more aspects of the system.
Acknowledgements
We deeply appreciate the words of praise received from
Professors G. Dauphin-Tanguy and J. LeFbvre which
made the effort worthwhile, and to Prof. G. Saidel who
took his time to review this paper.
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Address for correspondence:
Mireya Diaz-Insua
c/o Bamco CCS-053-00
P.O.Box 05322
Miami, FL 33102-5322
e-mail: mcd8@po.cwru.edu