Volume 1 Track 01
Simulating Cardiovascular Haemodynamics by Bond Graph Technique
Kaiyong Dai, Gangmin Ning, Shuzhen Chen, Juan Du, Xiaoxiang Zheng
Dept. of Biomedical Engineering, Key Laboratory for Biomedical
Engineering of Education Ministry Zhejiang University, China
Abstract— A bond graph model for simulating cardiovas-
cular haemodynamics is proposed. The model is given by an
elastance variable description of heart, head and neck circula-
tion, pulmonary circulation, coronary circulation, abdomen
circulation and extremity circulation. Also, the carotid barore-
flex control mechanism for circulation is embeded. The model
responds to sympathetic and vagal activity by modifying sys-
temic peripheral resistance, heart rate and ventricular
end-systolic elastance. It is able to simulate the blood pressure
and blood flow wave on arbitrary segment of circulation sys-
tem, subsequently, the cardiovascular parameters such as
stroke volume, cardiac output and eject fraction of heart can be
computed. The simulation results under physiological condition
are in agreement with human physiological experimental data.
By modifying the arterial compliance and balance point of
barorecpter, the hypertension is simulated and the results are
consistent with the pathological features. In conclusion, the
model could simulate the performance the cardiovascular sys-
tem validly.
Keywords— cardiovascular system model, bond graph, barore-
flex, hypertension
I. INTRODUCTION
Mathematic model for entire cardiovascular system is one
of the frontiers in cardiovascular research. Since Frank de-
veloped Windkessel model of arterial system, various models
[1]-[6] for entire cardiovascular system have been published
for physiology research and education. These studies as-
sumed ventricle as an elastance variable and the vascular
network as lumped capacitance, resistance and inertial,
meanwhile, the simulation results have shown good agree-
ment with the experimental data and clinical observations.
However, the extendibility of the models in addressed pub-
lications is not satisfactory.
The bond graph is an explicit graphical tool for capturing
the common energy structure of systems by elements which
generate, store, dissipate, transmit or transform energy. It has
been used for physiological system modeling [4], [7]-[8], in
which the bond graph represents the store, dissipation and
transmission of blood flow. These studies demonstrated that
the bond graph technique is a valid tool for modeling the
physiological system.
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151
The aim of this paper is to build an extendable mathematic
model for cardiovascular system by bond graph. The model
is constituted of pulsating heart, vascular network, and the
interaction with carotid baroreflex system. The heart and
vascular network are represented by an elastance variable
description and segment description [1],[4], respectively,
while the interaction with carotid baroreflex is accomplished
by adjusting systemic peripheral resistance, heart rate and
ventricular end-systolic elastance [5].
The structure of this paper is as follow. First, the model
description and applied methods are presented. Subsequently,
the simulation results of healthy and hypertension are given.
Last, the behavior of baroreceptor in hypertension is dis-
cussed.
II. METHODS
The models of heart, vascular network and baroreflex
system are constructed respectively.
A. Heart
The heart, which is composed of atriums, ventricles and
valves, is described as a pulsatile pump. The atrium is as-
sumed to be with no contractility. The inlet and outlet valves
of each ventricle are emulated by modifying the resistance
corresponding to the blood flow direction [1]. The left and
right ventricles in diastolic and systolic phase are simulated
by two functions respectively. In the diastolic phase of heart,
the ventricular pressure is assumed to rise as an exponential
function of the ventricular volume which increases from the
end-systolic volume to end-diastolic volume [3]:
P (t ) a ˜ [exp( Ds ˜ V (t )) -1]  Po (1)
where P(t) and V(t) are ventricular pressure and volume
respectively, Ds is the ventricular diastolic stiffness, P0 is the
minimum diastolic ventricular pressure and a is constant.
While in the systolic phase, the relationship of ventricular
pressure and volume is assumed as:
dV
P(t)= E(t)¸ [V(t) -Vd ] + R(t) (2)
dt
where Vd is the unstressed volume of ventricle. P(t) and V(t)
are ventricular pressure and volume, respectively. R(t) is the
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source resistance. E(t) is ventricular elastance, which is the Pi+1. Meanwhile, the output of ith segment are the flow for
key parameter for determining the ventricular function and i+1th segment, denoted as Qi , and the pressure for i-1th
indicates the contractile state of ventricle. In general, E(t) segment, denoted as Pi (Fig.2). The bond graph model
could only be determined by experiments. By far, E(t) is equations of ith segment are deduced by
proposed to be expressed in various equations [5], [9]-[10]. dVi
In our model, E(t) is adopted according to experiment data Qi 1  Qi (3)
and the expression given by Ursino. dt
dOi
Head and neck circulation Pi  Pi 1  Ri ˜ Qi (4)
dt
Left upper extremity circulation where,
Qi Oi / I i (5)
Right upper extremity circulation
Pi Vi / Ci (6)
Pulmonary circulation Vi is the volume of Ci, and Ȝi is the pressure momentum
of Ii.
Heart Rejv Cejv Rivn Civn Rbrn Cici Rici Ceci Reci

I ejv I eci

Coronary circulation I ivn I brn Iici

Abdomen circulation
Rlav Clav Rlac Clra Rlra Claa Rlaa Clsa Rlsa
Left lower extremity circulation

Right lower extremity circulation I lav Ilra I laa Ilsa

Rrav CravCrra Rrac Craa Rrra Crsa Rraa Rrsa
Fig. 1 Structure of cardiovascular system model

Irav I rra I raa Irsa

B. Vascular network
Rpar Cpar Rpcl Cpvn Rpvn Clat
The vascular network is composed of circulation of head,
neck, pulmonary, coronary, abdomen and extremity. The
extremity circulation includes upper and lower extremity of I par I pvn Rlat
both sides (Fig. 1). Each circulation is divided into several Rpvv I pvv Rmvv I mvv
vessel segments, so the whole vascular network is con- Clvt
Crvt
structed of totally 30 vessel segments. Each segment is re- Rtvv Rcor
garded as a modified Windkessel model, composed of I tvv Ravv I avv
Rlat
capacitance (C), resistance (R) and inertial (I) elements. Ctvc+rat Ctat
Subsequently, the vessel segment is expressed by bond graph Rtvc
Icor
(Fig. 2). Itvc Racl Rtat I tat
Cavc Caat
Ii
Qi-1 Qi Ravc I avc I acl Raat I aat
Rlgv Clgv Rlgc Clga Rlga
Pi Pi+1
Ci Ri I lgv I lga
Rrgv Crgv Rrgc Crga Rrga
Fig. 2 Bond graph for ith vessel segment

I rgv I rga
For ith segment the input are the flow of i-1th segment,
denoted as Qi-1 and the pressure of i+1th segment, denoted as Fig. 3 Bond graph model for cardiovascular circulation system

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The complete model for cardiovascular circulation system

can be built after expressing the heart and all segments of 600

vascular network by bond graph (Fig. 3). Totally 54 equa-

500
tions construct the cardiovascular system model.
400

Q/mL.s-1
C. Carotid baroreflex
300
The carotid baroreflex is described as the afferent pathway,
the efferent sympathetic and parasympathetic pathway, and 200

the resulted actions [5], [11], like the regulation of systemic

100
peripheral resistance, heart rate and ventricular end-systolic
elastance. 0
The interaction of cardiovascular system and carotid 45 46 47
t/s
48 49 50

baroreflex is simulated by the method given in the literature b

[5], [11].
130

120
III. RESULTS 110

100
According to references [1],[5],[10],[11],[12], a group of

V/mL
90
parameters was chosen for cardiovascular model under
physiological condition. The model simulation was accom- 80

plished using MATLAB 7.01 (Mathworks, Inc.). It starts with 70

an initial state and runs for 60 seconds until a steady state is 60

reached. Numerical integration of differential equations is 50
performed using the fifth-order Runge-Kutta method with a 40
step length of 0.001s. 45 46 47
t/s
48 49 50

The simulation results under normal physiological condi- c

tion are shown in Fig.4. The numerical values of sys-
tolic/diastolic blood pressure (SBP/DBP), stroke volume 125

(SV), cardiac output (CO) and eject fraction (EF) are

achieved and shown in Tab.1. 115
P/mmHg

Table 1 The numerical results under physiological condition 105

Parameter (SBP/DBP)/mmHg SV/mL CO/L EF/% 95

Value 115/79 75 5.4 62.0
85

120
75
45 46 47 t/s 48 49 50
100 d
80
Fig. 4 The simulation results under physiological condition (a) Blood
pressure in left ventricle (dashed line) and aorta (solid line); (b) Flow wave
P/mmHg

in left ventricle; (c) Volume in left ventricle; (d) Blood pressure at left arm
60

40 Hypertension is simulated by reducing the compliance of

arterial 25% [13] and resetting the balance point of cardio
20
baroreceptor from 93mmHg to 107mmHg, Fig.5 shows the
blood pressure in left ventricle (dashed line) and aorta (solid
0
45 46 47
t/s
48 49 50 line) of hypertensive. The numerical results are given in
a Tab.2.

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140
120
100
P/mmHg
80
60
40
20
0
45 46 47 48 49
t/s
Fig. 5 Blood pressure in left ventricle (dashed line) and aorta (solid line)
under hypertension
Table 2 The numerical results under hypertension
Parameter (SBP/DBP)/mmHg SV/mL CO/L
Value 132/96 75
IV. DISCUSSION
The typical values of systolic/diastolic blood pressure,
stroke volume, cardiac output and eject fraction under
physiological condition are achieved as 115/79mmHg, 75ml,
5.40L and 62.0%, respectively. The blood pressure in left
ventricle and aorta (Fig.4.a), flow wave in left ventricle
(Fig.4.b.), volume in left ventricle (Fig.4 .c) and pressure at
left arm (Fig.4.d) were obtained. The systolic blood pressure
at left arm is higher than that in aorta, while the diastolic
blood pressure is lower. All simulation results are in good
agreement with human physiological features [14],[15], thus
the validity of the model is verified.
In case of hypertension, the compliance of arterial and the
balance point of cardio baroreceptor are modified. The
simulation results demonstrate that the systolic and diastolic
blood pressures are increased by about 14.78% and 17.71%
respectively.
V. CONCLUSIONS
Mathematical models are useful tools for a deep under-
standing of complex process of cardiovascular system in the
physiological and pathological state. The presented model is
able to simulate the physiological state and hypertension and
the results are in good agreement with the clinical observa-
tions. Due to the advantage of bond graph technique identic
structure design of functional components, the model is
flexible to be extended if necessary.
In conclusion, the present work provides a useful model to
study the law of cardiovascular system. Owing to its flexi-
bility, the model can be further developed for educational,
research and clinical purpose.
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ACKNOWLEDGMENT
This work is supported by the National Nature Science
Foundation of China (Grant 30570483).
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Address of the corresponding author:
Author: Gangmin Ning
Institute: Dept. of Biomedical Engineering, Zhejiang University
Street: Zheda Road 38, 310027
City: Hangzhou
Country: China
Ema il: ninggm@mail.bme.zju.edu.
IFMBE Proceedings Vol. 14/1