Abstract— A nonlinear lumped parameter model of the Recently, mathematical models of the human circulation
cardiovascular system coupled with a rotary blood pump is pre- have been developed also for studying its interaction with
sented. The blood pump is a mechanical assist device typically assist devices. Bai et al [4] presented a cardiovascular system
interposed from the left ventricle to the aorta in patients with
heart failure. The cardiovascular part of the model (consisting model which includes a simulation of a cardiac assist device
of the left heart atrium and ventricle), and the systemic by external counterpulsation. It includes the left and right
circulatory system are implemented as an RLC circuit with two heart and the pulmonary circulation. De Lazzari et al [5]
diodes. The diodes represent the mitral and aortic valves in the studied the interaction between a pneumatic left ventricle
left heart. The cardiovascular model has been validated with assist device (LVAD) and the cardiovascular system, by using
clinical data from a patient suffering from cardiomyopathy.
The pump model is a first order differential equation relating energy variables, such us external work, oxygen consumption
pressure difference across the pump to flow rate and pump and cardiac mechanical efficiency for both fixed and variable
speed. The combined cardiovascular-pump model has been heart rates. Computer models [6], [7] have been useful for
represented as a fifth order nonlinear dynamical system in simulating the interaction between the human cardiovascular
state space form with pump speed as the control variable. system and assist devices, prior to in vitro and in vivo
This model was used to simulate the hemodynamic variables to
different values of afterload and a linearly increasing (ramp) experiments. However, control strategies derived from such
pump speed. Because of its small dimensionality, the model is complex models have not been implemented due to the
suitable for both parameter identification and the application many state variables that are not observable in practice.
of modern control theory. For the same reason, on-line identification of cardiovascular
parameters remains a difficult task.
I. INTRODUCTION To apply modern control techniques the cardiovascular-
The human cardiovascular system is a time-varying dis- pump model must be formulated in terms of state-space
tributed parameter nonlinear system. Nevertheless, lumped- description. Thus, our main purpose in this paper is to
parameter mathematical models of the cardiovascular system describe the nonlinear cardiovascular-pump model in a state-
have been developed for many years for a variety of pur- space form, suitable for the direct application of modern
poses. These include estimation and study of cardiovascular control techniques.
parameters difficult to measure in practical situations and The paper is organized as follows: Section II describes the
analysis and development of new medical products. heart model, its parameters and the left ventricular pressure-
Zacek et al [1] modeled the human cardiovascular system volume relationship. Section III presents the cardiovascular-
as 15 elements (tubes) connected in series representing the pump model and its state space description. Section IV
main parts of the system, with rigid and elastic reservoir shows how the heart model was validated and shows the
components. This model provided reasonable results, even hemodynamic tests performed with both models. Finally,
at higher and varying heart rates. Voytik et al [2] developed results are discussed and further improvements are suggested.
an electrical model of the human circulatory system to
investigate a variety of designs for an accessory skeletal II. C ARDIOVASCULAR MODEL
muscle ventricle (SVM). Three different configurations of
the SVM were simulated as counterpulsatile assist devices One advantage in representing the cardiovascular model
for both normal and congestive heart failure. Avanzolini et as a lumped circuit is that Kirchoff’s laws for node currents
al [3] use computer aided design of control system (CADCS) and loop voltages can be applied. In doing so, we can
to simulate the human cardiovascular system steady-state re- relate current with flow and voltage with pressure. Moreover,
sponse. Transients were introduced by varying the peripheral components like resistors, capacitors and inductors can be
resistance. associated with hydraulic resistance, compliance and iner-
tance, respectively. The cardiovascular model can therefore
This research was supported in part by NSF under contract ECS-0300097 be represented as a lumped parameter electric circuit [8],[9]
and NIH/NHLBI under contract 1R43HL66656-01
A. Ferreira and S. Chen are graduate students at the Department of as shown in Figure 1. Preload and pulmonary circulation are
Electrical Engineering, University of Pittsburgh, PA, USA. represented by a single compliance and afterload by a four-
M. A. Simaan and J. R. Boston are with the Department of Electrical element Windkessel model. Table I lists the state variables
Engineering, University of Pittsburgh, PA, 15261 USA.
J. F. Antaki is with the Department of Biomedical Engineering, Carnegie employed, and Table II provides the system parameters and
Mellon University, Pittsburgh, PA 15213 USA. their associated values.
E(t) (mmHg/ml)
Resistances (mmHg.sec/ml)
R1 variable Systemic Vascular Resistance 1
898
TABLE III
4) Isovolumic phase:
P HASES OF THE CARDIAC CYCLE
⎡ ⎤
0 0 0 0
Modes Valves Phases ⎢ ⎥
D1 D2 ⎢ ⎥
⎢ 0
⎢ − R 1C 1
R1 C2
0 ⎥
⎥
1 closed closed Isovolumic contraction 1 2
A2 (t) = ⎢
⎢
⎥
⎥ (10)
2 closed open Ejection ⎢ 0
⎢
1
− R 1C 0 ⎥
⎥
1 closed closed Isovolumic relaxation ⎣
R1 C3 1 3
⎦
3 open closed Filling
0 0 0 0
- open open Not feasible
5) Ejection phase:
B. State equations ⎡ ⎤
0 0 0 −1
We will now write the state equations in terms of the x ⎢ ⎥
⎢ ⎥
⎢ 0 − R 1C 1
0 ⎥
state vector (i.e derive the A1 (t) matrix) for each of these ⎢
⎢
1 2 R1 C2 ⎥
⎥
three phases. The A2 (t) matrix can be derived using equation A2 (t) = ⎢
⎢ 0 1
− R 1C 1 ⎥
⎥ (11)
⎢ R1 C3 1 3 C3 ⎥
(6). ⎢ ⎥
⎢ ⎥
1) Isovolumic phase: In this phase, the aortic and mitral ⎣ E(t)
0 1
−L −
(R3 +R4 ) ⎦
L L
valve are closed, which means D1 and D2 are both open-
circuit. Moreover, x4 (t) = 0. In this case, we have
6) Filling phase:
⎡ ˙ ⎤ ⎡ ⎤
E(t) E(t) E(t)
E(t)
0 0 0 − 0 0
⎢ ⎥ ⎢ R2 R2
⎥
⎢ ⎥ ⎢ ⎥
⎢ ⎥ ⎢ ⎥
⎢
⎢ 0 − R 1C 1
R1 C2
0 ⎥
⎥ ⎢ E(t) −(R1 +R2 ) 1
0 ⎥
A1 (t) = ⎢
1 2
⎥ (7) ⎢ R2 C2 C2 R1 R2 R1 C2 ⎥
⎢ ⎥ A2 (t) = ⎢ ⎥ (12)
⎢ ⎢ ⎥
⎢ 0 1
R1 C3
− R 1C 0 ⎥
⎥ ⎢ 0 1 −1
0 ⎥
⎣ 1 3
⎦ ⎢ R1 C3 R1 C3 ⎥
⎣ ⎦
0 0 0 0 0 0 0 0
899
Resistor R6 is pressure dependent and simulates the suction for the z vector. Also
phenomena [13].
b2 = [0 0 0 − β2 /(L + L)]T (22)
0 if x1 > Pth ;
R6 = (13)
−3.5x1 + 3.5Pth otherwise where
where Pth = 1 mmHg is a threshold. H represents the L = L1 + L0 + β1 (23)
pressure difference across the pump and is defined by the and
following characteristic equation, relating pump flow and R = R 5 + R 0 + R6 + β 0 (24)
speed [12]
dQP 2) Ejection phase: As in the previous model, D2 is short-
H = β0 QP + β1 + β2 ω 2 (14) circuit and D1 is open-circuit. In this case, we have two flows
dt
going into the circulatory system, one from the aorta and the
where β0 = −0.1707, β1 = −0.02177 and β2 = 0.0000903
other from the pump. The matrix Â1 (t) is given by
are the pump model parameters in this case. Notice that the
resulting model is a forced system, where the primary control ⎡ ⎤
0 0 0 −1 0
variable is the pump speed. ⎢ ⎥
⎢ 0 −1 1
0 0 ⎥
A. State equations ⎢ R1 C2 R1 C2 ⎥
⎢ ⎥
⎢ ⎥
⎢ 1 −1 1 ⎥
Now there is an external source of energy in the A2 (t) = ⎢ 0 0 ⎥ (25)
⎢ R1 C3 R1 C3 C3 ⎥
cardiovascular-pump model. Thus this system is forced, and ⎢ ⎥
⎢ ⎥
⎢ E(t)
0 −1 −(R3 +R4 ) R3 ⎥
can be written as ⎢ L L L L ⎥
⎣ ⎦
ż = Â1 (t)z + b1 u(t) (15) 0 0 0 −R3
L
R−R3
L
where u(t) = w2 (t) is the control variable and Â1 (t) can be for the z vector and
either a (4 × 4) or (5 × 5) time varying matrix, depending on
the modes of D1 and D2 . The dimension of the scalar vector b2 = [0 0 0 0 − β2 /L]T (26)
b1 , changes accordingly, i.e, it can be (4 × 1) or (5 × 1). The 3) Filling phase: In this phase of the cardiac cycle, D1 is
state-vector z is defined as short-circui and D2 = 0 is open-circuit, which again implies
T T
x = [x1 , . . . , x5 ] = [LV P, LAP, AP, QT , QP ] (16) x5 (t) = x4 (t). Therefore, we have
where, QT is total flow and QP is pump flow. As in the ⎡ E(t) 1 ⎤
− R2 R2
0 −1
cardiovascular model, it is also possible to define the states ⎢ ⎥
⎢ ⎥
of the system as ⎢ E(t) −(R1 +R2 ) 1 ⎥
⎢ R2 C2 C2 R1 R2 R1 C2
0 ⎥
⎢ ⎥
A2 (t) = ⎢ ⎥ (27)
z = [z1 , . . . , z5 ]T = [(LV V − V0 ), LAP, AP, QT , QP ]T ⎢ 1 −1 1 ⎥
(17) ⎢ 0 ⎥
⎢ R1 C3 R1 C3 C3 ⎥
⎣ ⎦
and the state vectors x and z are related by the nonlinear E(t) −1 −(R+R4 )
0
transformation x = Sz, where the matrix S is L +L L +L L +L
⎡ ⎤ for the z vector and
..
⎢ E(t) . 0 ⎥
S(t) = ⎢ ··· ⎥ b2 = [0 0 0 − β2 /(L + L)]T
⎣ ··· (18) (28)
⎦
..
0 . I n
900
120 800
Figure 6 shows an example of curve fitting to human
AoP clinical data, using the heart model. We estimated the pa-
rameters for a patient suffering from cardiomyopathy, from
LVP, AoP and LAP (mmHg)
90 600
0
work (area of the pv-loop, SW) of the patient with that
0 0.5 1 1.5
time (sec)
2 2.5 3 0 0.5 1 1.5
time (sec)
2 2.5 3
generated by the model. The first was 10, 690 mmHg.ml and
(a) (b) the second 10, 201 mmHg.ml, which represents a difference
Fig. 4. Simulated hemodynamic waveforms for a normal subject of 4.5%.
A. Cardiovascular-pump model response
180
ESPVR
150 Once the cardiovascular model was validated, tests
ESPVR
R1 = 2.0
R2 = 0.005
were performed to assess the open-loop response of the
120
R1 = 1.5
100
R2 = 0.05
cardiovascular-pump model shown in Figure 3. As the pump
speed is increased (see Figure 7(a)), the amplitude of oscil-
LVP (mmHg)
LVP (mmHg)
R1 = 1.0
R2 = 0.2
R1 = 0.5 R2 = 1.0
lation gradually decreases, while net flow increases. Beyond
60 50
the point of maximum flow, the waveform exhibits sudden
negative spikes, indicative of suction. (See Figure 7(c)).
0 0
0 50 100 150 0 50 100 150
200
LVV (ml) LVV (ml)
(a) (b) 16
AoP
150
100
12
volume of the ventricle are depicted in the form of pressure- (a) (b)
volume (pv)-loops. The pv-loops in Figure 5a, represent the 100 300
0
in Figure 5b depict the result of altering preload conditions
QP (ml/s)
150
by changing the mitral valve resistance (R2 ). The slope of the -50
100
onset of suction
ESPVR (Emax ) for the loading data in Figure 5a was 2.49 -100
50
onset of suction
for the ESPVR, since the correlation coefficient between (c) (d)
those two variables was 0.99. As for preload changes (Figure
Fig. 7. (a) Speed profile, (b) AoP and LVP pressures, (c) Pump Inlet
5b), the slope of ESPVR was 2.45 mmHg/ml for ESPVR, Pressure and (d) Pump Flow
V0 was 10.45ml, and a correlation coefficient of 0.99.
During ejection, theoretically, there are two paths for the
120 120 flow out the ventricle, either through the aortic valve or
Measured Measured
Model Model through the pump. However, the aortic valve does not open if
100 100
the left ventricular pressure is lower than the aortic pressure.
80 80
This is usually the case, since the pump decreases the internal
pressure in the ventricle. Whether the aortic valve will open
LVP (mmHg)
LVP (mmHg)
(a) (b)
Another test investigated how hemodynamic variables
were affected as systemic vascular resistance changes. To
Fig. 6. Curve fitting using human clinical data simulate a “weak” heart, the value of Emax was set to 0.7,
901
120
VI. ACKNOWLEDGMENTS
100 R1 = 2.0
Antonio Ferreira gratefully acknowledges the Alcoa Foun-
R1 = 1.5 dation Maranhao, Brazil Engineering Fellowship Program
80 R1 = 1.0
and the Foundation of Research of the State of Maran-
LVP (mmHg)
R1 = 0.5
0
R EFERENCES
80 100 120 140 160 180 200
LVV (ml) [1] M. Zacek and E. Krause, “Numerical simulation of the blood flow in
the human cardiovascular system,” J. Biomechanics, vol. 29, no. 1, pp.
Fig. 8. PV-loops for model validation 13–20, 1996.
[2] S. Voytik, C. Babbs, and S. Badylak, “Simple electrical model of the
circulation to explore design paramters foa a skeletal muscle ventricle,”
TABLE IV Journal of Heart Transp., vol. 9, no. 2, pp. 160–174, 1990.
H EMODYNAMIC PARAMETERS FOR Emax = 0.7 [3] G. Avanzolini et al., “Cadcs simulation of the closed-loop cardiovas-
cular system,” Int. J. Biomed. Comput., vol. 18, pp. 39–49, 1988.
R1 SV CO AoP (mmHg) LAP (mmHg) [4] J. Bai, K. Ying, and D. Jaron, “Cardiovascular responses to external
(ml) (l/min) Sys / Dia / Mean Max / Mean / Min counterpulsation: a computer simulation,” Journal of Heart Transp.,
0.5 68.67 5.1 101 / 69 / 88 22 / 15 / 9 vol. 30, pp. 317–323, 1992.
1.0 49.01 3.6 114 / 85 / 100 17 / 11 / 9 [5] C. D. Lazzari, G. Ferrari, R. Mimmo, G. Tosti, and D. Ambrosi,
1.5 39.89 2.99 120 / 87 / 107 15 / 10 / 8 “A desktop computer model of the circulatory system for assistance
2.0 35.20 2.64 124 / 88 / 110 13 / 10 / 8 simulation: effect of an lvad on energetic realtionships inside the left
ventricle,” Med. Eng. Phys., vol. 16, pp. 97–103, 1994.
[6] L. Xu and M. Fu, “Computer modeling of interactions of an electric
motor, circulatory system and rotary blood pump,” ASAIO J, vol. 46,
no. 5, pp. 604–611, 2000.
approximately 1/3 of its nominal value (Emax = 2.0). In [7] M. Vollkron, H. Schima, L. Hubber, and G. Wieselthler, “Interactions
of the cardiovascular system with an implanted rotary assist device:
all simulations, we ran the cardiovascular-pump model by Simulation study with a refined computer model,” Intern. Soc. for Art.
incrementing the speed as a ramp from 9,000 rpm to 10,000 Organs, vol. 26, no. 4, pp. 349–359, 2002.
rpm in 20 seconds. Table IV shows the hemodynamic values [8] D. S. Breitenstein, “Cardiovascular modeling: the mathematical ex-
pression of blood circulation,” Master’s thesis, University of Pitts-
found at steady state in those tests and Figure 8 shows the burgh, PA, 1993.
PV loops. [9] Y.C Yu, J. Boston, M. Simaan, and J. Antaki, “Estimation of systemic
vascular bed parameters for artificial heart control,” IEEE Trans.
Automat. Contr., vol. 43, pp. 765–777, June 1998.
V. CONCLUSION [10] H. Suga and K. Sagawa, “Instantaneous pressure-volume relationships
and their ratio in the excised, supported canine left ventricle,” Circ Res,
vol. 35, no. 1, pp. 117–126, 1974.
We presented a nonlinear coupled cardiovascular-pump [11] N. Stergiopulos, J. Meister, and N.Westerhof, “Determinants of stroke
model and its characterization in state space form. That volume and systolic and diastolic aortic pressure,” Am J Physiol., vol.
particular representation is suitable for the design of pump 270, no. 6 Pt 2, pp. H2050–2059, 1996.
[12] S. Choi, “Modeling and control of left ventricular assist system,” Ph.D.
speed controllers using modern control techniques. The suc- dissertation, University of Pittsburgh, Pittsburgh, PA, May 1998.
tion phenomena, due to overpumping, can also be studied [13] H. Shima, J. Honigschnable, W. Trubel, and H.Thoma, “Computer
by using this model. A simple capacitance represents the simulation of the circulatory system during support with a rotary blood
pump,” Tran Am Soc Artif Intern Org, vol. 36, pp. M252–M254, 1990.
pulmonary circulation and left atrium in our proposed model. [14] A. Guyton and J. E. Hall, Textbook of Medical Physiology. Philadel-
It is difficult to obtain reliable measurements for the high phia, PA: W. B. Saunders Co., 1996.
pressure system (left ventricle), and is even harder to measure [15] A. Ferreira, S. Chen, D. Galati, M.A. Simaan, and J.F. Antaki, “A
dinamic state space representation and performance analysis of a
those variables (pressures and flows) in the right side of feedback controlled rotary left ventricular assist device,” To appear in
the human heart. Since this model is univentricular, it may the Proc. of the ASME 2005 - International Mechanical Engineering
be suitable for studying physiological phenomena associated Congress and Exposition, Orlando, USA, November 5-11, 2005.
with hypoplastic heart syndrome (univentricular heart).
A more accurate model for the elastance function, which
takes into account the nonlinear behavior of EDPVR is
currently being developed as well as a baroreflex system to
accommodate variations in heart rate and systemic vascular
resistance due to MAP changes. Moreover, a gradient based
feedback controller has been developed to automatically
adjust the pump speed to meet the patient’s blood flow
requirements up to the point where suction may occur [15].
At that point the controller will maintain a constant pump
speed keeping the gradient of the minimum pump flow at
zero. Simulation results have shown the feasibility of this
approach.
902