Cardiovasc Eng (2010) 10:45–51
DOI 10.1007/s10558-010-9093-0
ORIGINAL PAPER
Mathematical Modelling and Electrical Analog Equivalent
of the Human Cardiovascular System
Mona Abdolrazaghi • Mahdi Navidbakhsh •
Kamran Hassani
Published online: 9 March 2010
Ó Springer Science+Business Media, LLC 2010
Abstract The objective of this study is to develop a
model of the cardiovascular system capable of simulating
the normal operation of the systemic and pulmonary cir-
culation, starts from aorta, and follows by upper and lower
extremities vessels, finally ends with pulmonary veins. The
model consists of a closed loop lumped elements with 43
compartments representing the cardiovascular system. The
model parameters have been extracted from the literature.
Using MATLAB software, the mathematical model has
been simulated for the cardiovascular system. Each com-
partment includes a Resistor-Inductor-Capacitor (RLC)
segment. The normal cardiovascular operation is charac-
terised by the pressure–volume curves in different parts of
the system. Model verification is performed by comparing
the simulation results with the clinical observation reported
in the literature. The described model is a useful tool in
studying the physiology of cardiovascular system, and the
related diseases. Also, it could be a great tool to investigate
the effects of the pathologies of the cardiovascular system.
M. Abdolrazaghi, M. Navidbakhsh and K. Hassani contributed
equally to this work.
M. Abdolrazaghi  M. Navidbakhsh
Mechanical Engineering Department, Iran University of Science
and Technology, Tehran, Iran
e-mail: Mona.Abdolrazaghi@gmail.com
M. Navidbakhsh
e-mail: m.navid@iust.ac.ir
K. Hassani (&)
Biomedical Engineering Deaprtment, Science and Research
Branch of Islamic Azad University, Tehran, Iran
e-mail: K.Hasani@srbiau.ac.ir
Keywords Modelling  Cardiovascular system 
Hemodynamics  Electrical equivalent
Introduction
Diseases of the human cardiovascular system are one of the
main problems in contemporary health care in the industrial
countries. These diseases cause the majority of deaths and
also often afflict people in their most productive age. In this
context different approaches have been used with the aim of
providing better understanding and modelling of the arterial
tree and heart mechanism in the human cardiovascular sys-
tem. Several mathematical and electrical models dedicated
particularly to simulate the operation of cardiovascular
system over the past decade by many scientists such as
Beeler and Reuter (1977), Stergiopulos and Young (1992),
Nebot et al. (1998), Mukkamala and Cotton (2001),
Migliavacca and Pennati (2001), Heldet and Shim (2002),
Darovic and Stratton (2002), Urquiza and Blanco (2003),
Manoliu (2004), Liang and Liu (2005) and Waite (2006). In
an early effort to model the cardiovascular system, Wester-
hof et al. (1969) developed the Windkessel model to describe
the blood flow in the heart. The model included only four
compartments. In later study, he studied the analogue mod-
elling of the human systemic arterial tree. Croston et al.
(1974) devised a 28-compartment lumped-parameter model.
They modelled arterial, venous, and cardiac compartments
in terms of coupled ordinary differential equations that
describe the dynamics of the system. In a subsequent
extension of modelling the cardiovascular system, Rupnic
et al. (Rupnic and Runvovc 2002) designed an electronic
circuit to analyze the operation of cardiovascular system in
steady-state and transient phenomena. Their model was
useful in teaching physiology and pathophysiology but the
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arterial system was not detailed. Olufsen and Nadim (2004) can be either linear or time variant. The analogue circuit of
derived a lumped model for the blood flow and pressure in each compartment is actually presented by three-element
the systemic arteries using the equations of fluid dynamics. Windkessel model in Fig. 2a, b. The description of viscous
They started with the one-dimensional Navier–Stokes resistance (R1) (R2) defined according to the following rela-
equations describing time-dependent flow and pressure in a tions (Olufsen and Nadim 2004):
rigid vessel and derived first and second–order lumped  
models using Laplace transform. The resulting lumped kq 8lL 8lL
R1 ¼ 1 ; R2 ¼ ð1Þ
model can be represented by electrical circuits. Hassani et al. kp p:r 4 p:r 4
(2006) presented a new model for normal operation of car-
The values of blood density (q) and viscosity (l) as well as
diovascular system and implemented a 42-compartment
length of artery (L), radius (r), thickness (h) and Young
steady state model of the system connected to models of left
modulus (E) have been extracted from literature (Wang and
and right ventricles. Each compartment included a resistor,
Parker 2004). The inertance (L1), due to blood inertia, was
capacitor and inductor. The model described the arterial
described as follows (Olufsen and Nadim 2004):
system in details and was used to simulate the cardiovascular
system using an equivalent electronic system. Using OR- 8qL
L1 ¼ ðkq  kp Þ ð2Þ
CAD software, we designed a circuit for the operation of the p  r2
system in normal condition. Despite the fact that we tried as The elastic behaviour of the artery was described by the
much as possible to avoid a passive arterial model, we compliance (C), determined under the following relation
acknowledge that our previous model is not active. In an (Rideout 1991):
attempt to overcome the limitation of passive cardiovascular
3p  r 3 L
models, we have taken a different approach to the modelling C¼ ð3Þ
2Eh
of the system and tried to improve our previous model by
investigating the stiffness of the ventricles and presenting The input flow is represented by blood flow (q) through the
precise pressure–volume graphs for different parts of the left ventricle which was described by (Olufsen and Nadim
cardiovascular system. Also, we have extracted a new 2004):
pressure-flow mathematical model describing the flow in    
1 1 dq 1 L1 dp
vessels based on a vessel diameter. The system has been L1 þ þq¼ þp ð4Þ
simulated by MATLAB software, and all the results R1 R2 dt R2 R1 dt
including the pressure–time and volume-time graphs of the Note that the pressure (p) actually represents the pressure
system segments have been compared with the relevant difference between the inlet and outlet of the artery. The
clinical data. Moreover, these results were verified by values of time-scale kp and kq depend on the radius of the
physiological and experimental data. artery (r). If the radius of the artery is less than 0.2 cm, the
compartment has only one resistor and there are two resistors
in the compartment for the arteries with the radius of more
Methods than 0.2 cm. Furthermore, the value of time-scale is
determined according to the following relations (Olufsen
We have extended our previous model to facilitate represen- and Nadim 2004):If radius of the artery is less than 0.2 cm
tation of cardiovascular system operation in normal condition then:
and presented a mathematical model with active elements.
kq ¼ 0:1729; kp ¼ 0:0075
The model is mathematically formulated in terms of an elec-
tric circuit. Figure 1 describes the block diagram of the car- If radius of the artery is more than 0.2 cm then:
diovascular system staring from ascending aorta and ends with
kq ¼ 0:2057; kp ¼ 0:0392
pulmonary veins. This model can be divided into two main
parts: the heart (left and right), including atriums and ventri- The values of the hemodynamic parameters for ventricles,
cles, and the arterial system. To facilitate the understanding of pulmonary artery, veins, arterioles, capillaries, and atriums
the system, we have depicted the anatomic structures into the have been extracted from the literatures (Rideout 1991).
diagram. The peripheral circulation is divided into upper body The entire electrical equivalent of the model is shown in
(including Carotid and Subclavian arteries), Aorta artery, Fig. 3. The electronic parameters are correlated to their
Gastric, Hepatic, Splenetic, Renal, Mesenteric branches and mechanical parameters as follows: voltage (volt) is analo-
lower extremely sections. Arterioles and Capillaries and veins gous to pressure (mmHg), capacitance (lF) to compliance
are separately identified. The model consists of 43 compart- (ml/Pa), resistance (kX) to resistance (1 Pa.s/ml), and
ments, each of the compartments is represented by one or two inductance (1lH) to inertance (1 Pa.s2/ml). The heart rate is
linear resistances, one linear inductor and one capacitor that considered 75 beats per minute and the length of cardiac

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Fig. 1 Block diagram of the cardiovascular system including 43 compartments

Fig. 2 The elements of each

artery including one or two
resistor, an inducer and a
capacitor. Figure (a) belongs to
the arteries with the radius of
less than 0.2 cm and figure (b)
belongs to the rest of the arteries

   
cycle is 0.8 s. The pumping action of the heart is realized by 2p
varying the right and left ventricular capacitors according to SRV ¼ 1=CRV ¼ SRS sin þ SRD  UðtÞ ð6Þ
T
a step-function U(t) with unit amplitude. The function has a
pulse width of 35.5% indicating the ratio of the systolic SRS, SRD represent the right ventricle stiffness in systole
duration to the cardiac cycle (0.3 s/0.8 s). The defined unit- and diastole. CRV denotes the compliance of right ventricle.
step function is a time dependent function for the ventricles We considered (Rideout 1991) the atrium pressure
to show that the heart signals are pulsated. We have calcu- (PAT) = 4.5 mmHg, left ventricle pressure in systole
lated the left ventricle stiffness in our model using the fol- (PES = 90 mmHg), maximum left ventricle volume
lowing relation: (QLVmax ¼ 120 ml) and minimum left ventricle volume
    (QLVmin ¼ 48 ml); to calculate the left ventricle systolic and
1 2p
SLV ¼ =CLV ¼ SLS sin þ SLD  UðtÞ ð5Þ diastolic stiffness as follows:
T
SLD ¼ PAT  1332=QLVmax ¼ 4:5  1332=120
SLV denotes the total left ventricle stiffness, SLS and SLD ¼ 49:5 gm=cm4 s2 ð7Þ
represent the left ventricle stiffness in systole and diastole. CLV
expresses the compliance of left ventricle. In a similar method, SLS ¼ PES  1332=QLVmin ¼ 90  1332=48
we calculated the total right ventricle stiffness (SRV): ¼ 2497:5 gm=cm4 s2 ð8Þ

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Fig. 3 The lumped model of the cardiovascular system. The anatomical name of each element has been included

Fig. 4 The graph of left ventricle stiffness versus time

Using the same method, we have calculated the right

ventricle stiffness in systole and diastole: SRS = 350
gm/cm4s2, SRD = 67 gm/cm4s2. The values of the stiffness
have been set by Rideout (1991) are SLS = 2500 gm/cm4s2,
SLD = 67 gm/cm4s2, SRD = 63 gm/cm4s2 and SRS = 341
gm/cm4s2. After the above relations determined were
introduced into the program, various simulations were done
Fig. 5 The pressure graph of the left ventricle (PLV), Left atrium
(PLA), Ascending aorta (PASC) and Left ventricle volume (QLV)
and the outputs were obtained and plotted using the cardiac
cycle of 0.8 s. We have shown the variation of left ven-
tricle stiffness versus time in Fig. 4.

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Fig. 6 The pressure graph of the arterioles (PARTERIOL), capillar-

ies (PCAP), systemic vein I (PSYSVEIN1), and systemic vein II Fig. 8 The pressure graph of right ventricle (PRV) and pulmonary
(PSYSVEIN2) pressures artery II (PPULART2)

Results and Discussions

4.6 mmHg. The second variable of interest is the left
ventricle volume (QLV), shown in Fig. 5. Note that the
Representative simulated pressure/volume curves are
volume pumped out of the ventricle per beat is 60 ml
shown in Figs. 5, 6, 7, 8 and 9. The pressure in Left ven-
which means that the cardiac output is 60/0.8 = 72 ml/s.
tricle pressure (PLV), left atrium (PLA), and ascending
Peak volume is approximately 120 ml and thus the ejection
aorta (PASC) is shown in Fig. 5. It can be seen that the
fraction of the ventricle is 60/120 = 0.5. Figure 6 shows
pressure within the ventricle reaches to the highest value of
plots of the systemic veins pressure (PSYSVEIN1, PSYS-
120 mmHg, and at the end of diastole decreases to
VEIN2), together with the arterioles (PARTERIOL) and
7 mmHg. The aortic pressure (PASC) follows (PLV) dur-
capillaries (PCAP) pressure. The arterioles pressure varies
ing the systole but it varies between 70 and 125 mmHg.
between 70 and 90 mmHg. Although in this figure has been
The left atrium pressure (PLA) also varies between 2.4 and

Fig. 7 The pressure graph of right atrium (PRA) and systemic vein II Fig. 9 The pressure graph of left atrium (PLA) and pulmonary vein
(PSYSVEIN2) II (PPULVEIN2)

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Fig. 10 The graph of pressure/volume variations for aorta artery and
left ventricle extracted from Guyton’s text book of medical physi-
ology (1996)
shown that the pressure of systemic veins and capillaries
are almost constant, they have pulsated pressure curves
with small amplitude which could be shown by depicting
each pressure individually. Furthermore, the pressure in the
capillaries is normally between the ranges 15–40 mm Hg
(Guyton 1996), it changes due to the size of the capillary.
We decided to adjust the pressure of capillaries in
40 mmHg constant because the variation of the pressure is
not pulsated in the very small arteries like capillaries. The
detailed pressure curves of systemic vein II as well as right
atrium graph have been shown in Fig. 7. The pressure of
systemic vein (PSYSVEIN2) varies between 7.45 and
7.6 mmHg. Furthermore, the figure shows the pressure of
right atrium (PRA) varies between 6.6 and 7.2 mmHg.
Figures 8 and 9 show the vital pressure plots for the right
ventricle (PRV), pulmonary artery II (PPULART2), pul-
monary vein II (PPULVEIN2), and left atrium pressure
Fig. 11 The graph of pressure
variation for different parts of
cardiovascular system including
the arteries and veins extracted
from Guyton’s text book of
medical physiology (1996)
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Cardiovasc Eng (2010) 10:45–51
(PLA). Note that the amplitude of the right ventricular
pressure is close to an expected peak value of 30 mmHg,
whereas the pulmonary artery peak is somewhat higher
than the normal 25 mmHg. This could be somewhat cor-
rected by lowering the systolic stiffness of the heart. The
pressure variation in pulmonary veins and right atrium vary
between (2.5–3 mmHg) and (5–5.5 mmHg). Figures 10
and 11, which have been directly extracted from Guyton’s
text book of medical physiology, demonstrate that all
major pressure/volume curves generated by the model are
within the range ones observed in physiological studies
(Guyton 1996). Comparing the model outputs with the
literature, we found out the outputs resulted in physiological
values for pressure/volume curves in the compartments.
Mathematical models show our level of understanding of
the behaviour of the cardiovascular system under consid-
eration. This model helps us to probe the system and
investigate the cause of a particular observation. The
research presented in this article is an effort to improve
mathematical models in the investigation of the cardio-
vascular operation in normal and diseased conditions.
Besides, we compared the model outputs with the relevant
clinical data.It needs to be pointed out that our previous
model was passive due to its voltage sources. It was not
capable of studying all the hemodynamic features of the
cardiovascular system. Therefore, we introduced this
model with active elements which is sensitive to the vari-
ation of RLC values of each compartment and can be used
for investigation of the pathologies in future.
Conclusions
This model has expressed a deeper study on cardiovascular
system hemodynamics. The novelty of this study is in
Cardiovasc Eng (2010) 10:45–51
describing the system based on the vessel diameters, and
simulating the mathematical equations with active electri-
cal elements. We have outlined the use of the model as a
tool to better understand the physiology of the system and
study the related diseases.
Acknowledgments The authors would like to acknowledge all the
help and support of their colleagues at Iran University of science and
technology and Chagalesh Consulting Engineers Company.
References
Beeler GW, Reuter H. Reconstruction of the action potential of the
ventricular myocardial fibers. J Physiol. 1977;268:177–210.
Croston RC, Fitzjerrell DG. Cardiovascular model for the simulation
of exercise, lower body negative pressure, and tilt table
experiments. In: Proceedings 5th Annual Pittsburgh conference
modeling simulation, 1974, pp 471–476.
Darovic OG, Stratton KL. Hemodynamic monitoring, invasive and
non invasive clinical application. 3rd ed. Saunders: Philadelphia;
2002. p. 306–39.
Guyton AC. Overview of circulation; medical physics of pressure,
flow, and resistance. In: Hall JE, editor. Textbook of medical
physiology. 9th ed. Pennsylvania: WB Saunders; 1996. p. 107–
19.
Hassani K, Navidbakhsh M, Rostami M (2006) Simulation of the
cardiovascular system using equivalent electronic system, J
biomedical Papers of the medical faculty of the University
Palacky, Olomouc, 150(1): 105–112.
Heldet T, Shim E. Modeling of cardiovascular response to orthostatic
stress. J Appl Physiol. 2002;92:1239–54.
Liang F, Liu H. A closed-loop lumped parameter computational
model for human cardiovascular system. JSME Int J.
2005;48(4):484. Series C.
51
Manoliu V (2004) Consideration about the lumped parameter
windkessel model applicativity in the cardiovascular system
structure, National symposium of theoretical electrical engineer-
ing, 22–23, Burcharest, UPB, pp 428–437.
Migliavacca F, Pennati G. Modeling of the Norwood circulation
effects of shunt size, vascular resistance and heart rate. Am J
Physiol Heart Circ Physiol, Am J Physiol Heart Circ Physiol.
2001;280:457–70.
Mukkamala R, Cotton RJ. A forward model based validation of
cardiovascular system identification. Am J Physiol Heart Circ
Physiol, Am J Physiol Heart Circ Physiol. 2001;281:2714–30.
Nebot A, Cellier FE, Vallverdu M. Mixed quantitative/qualitive
modeling of the cardiovascular system and simulation of it. J
Comput Methods Programs Biomed. 1998;55:127–55.
Olufsen MS, Nadim A. On deriving lumped models for blood flow
and pressure in the systemic arteries. J Math Biosci Eng.
2004;1(1):61.
Rideout VC. Mathematical and computer modeling of physiological
system. New Jersey: Printice-Hall Inc; 1991. p. 27–66.
Rupnic M, Runvovc F. Simulation of steady state and transient
phenomena by using the equivalent electronic circuit. J Comput
Methods Programs Biomed. 2002;67:1–12.
Stergiopulos N, Young D. F Computer simulation of arterial flow with
applications to arterial and aortic stenosis. J Biomed.
1992;25:1477–88.
Urquiza S, Blanco P. Coupling multidimensional compliant model for
carotid artery blood flow. J Mecánica Computacional.
2003;XXII:232–43.
Waite L. Biofluid mechanics in cardiovascular system. Mc Graw-Hill,
2006.
Wang JJ, Parker KH. Wave propagation in a model of arterial
circulation. J Biomech. 2004;37:457.
Westerhof N, Bosman F, DeVries CJ, Noordergraaf A. Analogue
studies of the human systemic arterial tree. J Biomech.
1969;2:121–43.
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