Study of Cardiovascular System

Using Time Variance Elastance Model

Course No: ME 400

Submitted By-
Tasfin Ahmed
Student ID: 1510082
Mushfiq Ahmad Siddiqui
Student ID: 1510141

Submitted To-
Department of Mechanical Engineering
in partial fulfillment of the requirements for the degree of Bachelor of Science in Mechanical
Engineering.

Supervised by-
Dr. Sheikh Mohammad Shavik
Assistant Professor
Department of Mechanical Engineering

Bangladesh University of Engineering and Technology (BUET) Dhaka-

1000, Bangladesh
October 2021
CERTIFICATION

This is to certify that the work presented in the thesis is an outcome of the investigation
carried out by the authors under the supervision of Dr. Sheikh Mohammad Shavik,
Department of Mechanical Engineering, Dhaka. It is declared that this thesis has been
submitted only for the award of graduation.

Authors

Tasfin Ahmed Mushfiq Ahmad Siddiqui

Signature of the Supervisor

Dr. Sheikh Mohammad Shavik

Assistant Professor
Department of Mechanical Engineering
Bangladesh University of Engineering and Technology (BUET)
ACKNOWLEDGEMENT

We would like to express our deepest gratitude to our supervisor Dr. Sheikh Mohammad Shavik
for his guidance on this project showing us the path of conducting successful research and above all
for always being there as our mentor. He shared his wisdom with us in analyzing subject matters and
at the same time valued our thinking approach to synthesize those topics. His suggestions drove us
towards better ways of thinking, his reviews enriched us in solving problems, and his support gave us
strength at the time of our disappointment. We shall forever cherish the memories of working with
him. We deeply thank our friends and families for always believing in us even at the moment when
we were losing our confidence.
ABSTRACT

Cardiovascular system, including both pulmonary and systemic, is a closed loop system that is
solely responsible for the circulatory motion of blood and nutrients around the body. Being one of the
most important and sensitive system of human body, many studies have been performed about it,
although most of the studies only focused on the left ventricular motion and related vascular system.
The right ventricular myocardium along with pulmonary vascular system are severely understudied.
In this study, we have taken an approach to construct the modeling of the combined cardiovascular
system using MATLAB. We used time varying elastance model to compute and graphically explain
the mechanical properties of both left and right myocardium. The model parameters can be tuned to
simulate healthy and diseased heart.
 The following are the list of variables used in
this thesis: PA: Pulmonary Artery

LV: Left Ventricle MV: Mitral Valve

RV: Right Ventricle TV: Tricuspid Valve

RA: Right Atrium AV: Aortic Semilunar Valve

LA: Left Atrium
PV: Pulmonary Valve
Ao: Aorta
VLV: Volume of Left Ventricle (ml) PRA: Pressure of Right Atrium (mmHg)

VRV: Volume of Right Ventricle (ml) PLA: Pressure of Left Atrium (mmHg)

VRA: Volume of Right Atrium (ml) RMV: Mitral Valve Resistance (Pa ms ml-1)

VLA: Volume of Left Atrium (ml) RTV: Tricuspid Valve Resistance (Pa ms ml-1)

PLV: Pressure of Left Ventricle (mmHg) RAV: Aortic Valve Resistance (Pa ms ml-1)

PRV: Pressure of Right Ventricle (mmHg) RPV: Pulmonary Valve Resistance (Pa ms ml-1)
CVEN: Venous Compliance (ml Pa-1)
CAO: Compliance of Aorta (ml Pa-1)
CARTE: Arterial Compliance (ml Pa )
-1

e(t): time-varying activation function

CPA: Pulmonary Artery Compliance (ml Pa-1) (mmHgml−1)

E(t): time-varying elastance function

(mmHgml−1)

EES: end-systolic elastance (mmHgml−1)

Ea: Arterial Elastance

EDPVR: end-diastolic pressure–volume
relationship

ESPVR: end-systolic pressure–volume

relationship
TABLE OF CONTENTS

Page

1. Introduction
1.1. Cardiovascular System…………………………………………………………………….... 1
1.2. Pressure Volume Loop…………………………………………………………………….... 3
1.3. Time Varying Elastance Model……………………………………………………………... 4

2. Research Methodology…………………………………………………………………………. 6

3. Mathematical Formulation and Physical Modeling………………………………………….. 7

4. Computational Method & Results

4.1. Figure Generated from the Code……………………………………………………………. 11

5. Conclusion
5.1. Limitations……………………………………………………………………………….…. 15
5.2. Recommendations & Future Aspect

6. Bibliography ……………………………………………………………………………………. 16
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CHAPTER 1

I NTRODUCTION

1.1Cardiovascular System

The heart is a muscular pump connected to the systemic and pulmonary vascular systems. Working together,
the principal job of the heart and vasculature is to maintain an adequate supply of nutrients in the form of
oxygenated blood and metabolic substrates to all of the tissues of the body under a wide range of conditions.
It is a closed loop which has two main fluid pumps and a network of vascular tubes. It can be divided into the
pulmonary vascular system which contains the right ventricle, the pulmonary arteries, the pulmonary
capillaries and pulmonary veins and the systemic vascular system which contains the left ventricle, the
systemic arteries, the systemic capillaries and the systemic veins.

Figure 1.1: Block diagram of cardiovascular system

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1.1.1 Pulmonary Vascular System

Pulmonary Vascular System includes the right side of the heart. Here the circulation that happens is
called pulmonary circulation. In pulmonary circulation, there is vast network of a vast network of
arteries, veins, and lymphatics that function to exchange blood and other tissue fluids between the heart,
the lungs, and back. Pulmonary circulation has some unique functions, such as ventilation and gas
exchange. The circulation moves blood between the heart and the lungs. Transportation of deoxygenated
blood to the lungs to absorb oxygen and release of carbon dioxide. The oxygenated blood then flows back
to the heart.
In the pulmonary loop, deoxygenated blood exits the right ventricle of the heart and passes through the
pulmonary trunk. The pulmonary trunk splits into the right and left pulmonary arteries. These arteries
transport the deoxygenated blood to arterioles and capillary beds in the lungs. There, carbon dioxide is
released, and oxygen is absorbed. Oxygenated blood then passes from the capillary beds through venules
into the pulmonary veins. The pulmonary veins transport it to the left atrium of the heart. The pulmonary
arteries are the only arteries that carry deoxygenated blood, and the pulmonary veins are the only veins
that carry oxygenated blood.

Fig 1.2: Pulmonary Circulation

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1.1.2 Systemic Vascular System

Systemic vascular system includes the left side of the heart. Here systemic circulation happens. In
systemic circulation, blood moves between the heart and the rest of the body. It sends oxygenated blood
out to cells and returns deoxygenated blood to the heart. In the systemic loop, oxygenated blood is
pumped from the left ventricle of the heart through the aorta, the largest artery in the body. The blood
moves from the aorta through the systemic arteries, then to arterioles and capillary beds that supply body
tissues. Here, oxygen and nutrients are released and carbon dioxide and other waste substances are
absorbed. Deoxygenated blood then moves from the capillary beds through venules into the systemic
veins. The systemic veins feed into the inferior and superior venae cava, the largest veins in the body.
The venae cavae flow deoxygenated blood to the right atrium of the heart.

Figure 1.3: Systemic Circulation Flow Chart

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1.2 Pressure Volume Loop

To determine a considerable amount of cardiac performance P-V loops are used. Scientists have historically
relied on systemic blood pressure, blood flow, and ventricular pressure to report changes in heart
performance. These are all important parameters, but only form part of the picture of heart performance.
Pressure-Volume (PV) loops provide a range of hemodynamic parameters which are not readily measurable
by other methods, including changes in contractility, elastance, power, energetics and efficiency. What is
even more powerful about PV loops is that they provide quantitative measurements of parameters, not just
qualitative results.

Figure 1.4: Pressure Volume loop

1.2.1 End-Diastolic Pressure (EDP)

Pressure in the ventricle at the end of diastole.

1.2.2 End-Diastolic Volume (EDV)

Volume in the ventricle at the end of diastole

1.2.3 End-Diastolic Pressure Volume relationship (EDPVR)

The EDPVR describes the passive filling curve for the ventricle and thus the passive properties of the
myocardium. The slope of the EDPVR at any point along this curve is the reciprocal of ventricular
compliance (or ventricular stiffness).

1.2.4 End-Systolic Pressure (ESP)

Pressure in the ventricle at the end of systole

1.2.5 End-Systolic Volume (ESV)

Volume in the ventricle at the end of systole

1.2.6 ESPVR (End-Systolic Pressure Volume Relationship)

The ESPVR describes the maximal pressure that can be developed by the ventricle at any given cardiac
chamber volume. This implies that the PV loop cannot cross over the line defining ESPVR for any given
contractile state.
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1.3Time Varying Elastance Model

The time-varying elastance theory of Suga et al. is widely used to simulate left ventricular function in
mathematical models and in contemporary in vitro models. It states that the relation between pressure and
volume variation in the LV is described by an elastance curve according to the following formulation:

P(t)= E(t)[V(t) – V0] (1)

Where, P(t) is the time-varying pressure (mm Hg), V(t) is the time-varying volume (ml), E(t) is the time-
varying elastance (mmHg/ml), and V0 is the volume at which the LV can no longer generate pressure (ml).

The curve is independent of ventricular preload and afterload within a physiological range, and its maximum
(Ees, end-systolic elastance) has been used widely as a marker of the contractility of the LV. Because it is
independent of the cardiac load, each individual case has its own elastance curve that only changes when the
basic contractile function of the heart changes.
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CHAPTER2

RESEARCH METHODOLOGY

Characterizing circulatory dysfunction and choosing a suitable treatment is often difficult and
time consuming, and can result in a deterioration in patient condition, or unsuitable therapy
choices. A stable minimal model of the human cardiovascular system (CVS) is developed with
the ultimate specific aim of assisting medical staff for rapid, on site modelling to assist in
diagnosis and treatment. Models found in the literature simulate specific areas of the CVS with
limited direct usefulness to medical staff. The goal of this thesis was to study the modeling of
combined cardiovascular system using the time variance elastance model. We started the thesis
work by studying the system mechanics of left ventricular myocardium which is the most popular
research interest of Cardiovascular System. We then advanced to the understudied right
ventricular myocardium. We construct a combined model of left and right ventricular system
with the help of existing studies. Some simulation study has been done on MATLAB, to
understand the system behavior. A simulink model has been developed in MATLAB, for P-V
closed loop system and the system is analyzed for different circulatory values.

The difference in elasticity and fibre pressure of the various valves and ventricles of the cardio-
vascular system lead to unstable responses of the simulation, which was later fixed by adjusting the
model and code for new variable. This model was also used to evaluate vascular insufficiency
(Regurgitation).
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CHAPTER 3

MATHEMATICAL FORMULATION & PHYSICAL MODELING

Ventricular mechanics can be expressed by end diastolic (PED) and end-systolic (PES) pressure–volume (P–V)
curves. Formulas for LV end-systolic and end-diastolic P–V relationships are

PLVES(VRV) = a(FCON)ELVES(VLV - VD,LV) (3.1)

PLVED(VLV) = P0,LV(exp(λLV(VLV - V0,LV)) - 1) (3.2)

For the RV, they are:

PRVES(VRV) = a(FCON)ERVES(VRV - VD,RV) (3.3)

PRVED(VRV) = P0,RV(exp(λRV(VRV - V0,RV)) - 1) (3.4)

Where, VD and V0 are the abscissa intercepts of the ESPVR and the EDPVR, respectively. P0 and λ are constants
used to fit the end-diastolic P–V relationship, as described below.

ELVES and ERVES are the maximum end-systolic elastances of the left and right ventricles under control
conditions (a(FCON) = 1), and are the slopes of Eqs. (1) and (3). Their values are constant and were obtained
from published data (Segers et al., 2001; Slama et al., 2000). The effect of myocardial contractility on end-
systolic behavior is denoted by a(FCON). It is determined by sympathetic neural activity (FCON). When
baroreflex control is absent, it is assumed to be 1, which corresponds to nominal values for left and right
ventricular end-systolic elastance.
A time-varying ventricular activation function e(t) provides a smooth transition between the EDPVR and ESPVR
relationships and is defined as a weighted sum of Gaussian time curves:
N
− (1−Ci )2
e(t) = ∑ Ai exp ( 2
2 Bi
) (3.5)
i=1

Here, e(t) represents the time course of instantaneous ventricular elastance. It establishes instantaneous
ventricular
pressure, as follows:

PLV(t) = e(t)PLVES(VLV) + [1 - e(t)]PLVED(VLV) (3.6)

PRV(t) = e(t)PRVES(VRV) + [1 - e(t)]PRVED(VRV) (3.7)

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Figure 3.2B is used to plot the normalized activation function used in this study.

Figure 3.1. The equivalent hydraulic circuit of the heart model. The pressure-operated heart valves are modeled by a hydraulic diode-resistance pair. All
chambers are subject to intra-thoracic pressure. RA: right atrium, RV: right ventricle, LV: left ventricle, and LA: left atrium
 Page |9

Figure 3.2. Ventricular mechanics. (A) ESPVR and EDPVR curves for the left ventricle. (B) Normalized activation function of the ventricles (Segers et
al., 2001). (C) Resultant left ventricular P–V loop from ESPVR, EDPVR, and activation function. Points a, b, c, and d in Panels B, C, and D represent points
on the P–V loop corresponding to time points of the activation function. (D) Right ventricular ESPVR, EDPVR, and resultant P–V loop

Figure 3.3: Closed Loop of Cardiovascular System

Valves were assumed to open and close depending on weather the axial pressure gradient across the valves was
positive or negative. The rate of change in V was calculated assuming conservation of mass,

dV
=qin−qout ;
dt

Closed-Loop Systemic Circulatory Model

Models of the aorta and LV were coupled via a closed-loop modeling framework describing the systemic
circulatory system. Other components of the circulatory system were modeled using electrical analogs. Mass of
blood was conserved by the following equations relating the rate of volume change in each storage compartment
of the circulatory system to the inflow and outflow rate
dVLA (t )
= qven (t) - qmv (t); (3.8)
dt
dVLv(t)
= qmv (t) - qao (t); (3.9)
dt
dVart (t)
= qao (t) - qper (t); (3.10¿
dt
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dVven(t )
= qper(t) - qven(t); (3.11)
dt

Where, VLA, VLV, Vart, and Vven are volumes of each compartment, and qven, qmv, qao, and qper are flow rates
at different segments. Flow rate at different segments of the circulatory model depends on their resistance to flow
(Rao, Rper, Rven, and Rmv) and the pressure difference between the connecting storage compartments (i.e.,
pressure gradient). The
flow rates are given by,

{
PLV , cav ( t ) −Part , cav ( t )
; When , PLV , cav (t ) ≥ Part ,cav (t)
qao(t)= Rao ; (3.12)
0 ;When , PLV , cav ( t ) ≤ Part , cav (t )

Part , cav ( t )−Pven , cav ( t )

qper(t)= ; (3.13)
Rper

Pven ( t )−PLA ( t )
qven(t)= ; (3.14)
Rven

{
PLA ( t )−PLV , cav ( t )
; When , PLA ( t ) ≥ LV , cav (t)
qmv(t)= Rmv ; (3.15)
0 ; When , PLA ( t ) ≤ PLV , cav (t )

Pressure in each storage compartment is a function of its volume. A simplified pressure volume relationship,

Vven(t)−Vven , 0
Pven(t) =
Cven

Closed-Loop Pulmonary Circulatory Model

Models of the pulmonary and RV were coupled via a closed-loop modeling framework describing the pulmonary
circulatory system. Other components of the circulatory system were modeled using electrical analogs. Mass of
blood was conserved by the following equations relating the rate of volume change in each storage compartment
of the circulatory system to the inflow and outflow rate
dVRA (t)
= qvc(t) - qtv(t); (3.16)
dt
dVRv(t )
= qtv(t) - qpv(t); (3.17)
dt
dVPA (t)
= qpv(t) - qper(t); (3.18¿
dt
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dVvc( t)
= qper(t) - qvc(t); (3.19)
dt

Where, VRA, VRV, VPAt, and Vvc are volumes of each compartment, and qac, qtv, qpv, and qper are flow rates at
different segments. Flow rate at different segments of the circulatory model depends on their resistance to flow
(Rac, Rper, Rac, and Rtv) and the pressure difference between the connecting storage compartments (i.e.,
pressure gradient). The
flow rates are given by,

{
PRV , cav ( t )−Ppa, cav ( t )
; When , PRV , cav ( t ) ≥ Ppa , cav (t)
qpv(t)= Rpv ;
0 ;When , PRV , cav ( t ) ≤ Ppa , cav (t )

Ppa , cav ( t )−Pvc , cav ( t )

qper(t)= ;
Rper

Pvc ( t ) −PRA ( t )
qven(t)= ;
Rvc

{
PRA ( t )−PRV , cav (t )
; When , PRA ( t ) ≥ PRV , cav (t)
qtv(t)= Rtv
0 ;When , PRA ( t ) ≤ PRV , cav (t )

Pressure in each storage compartment is a function of its volume. A simplified pressure volume relationship,

Vac(t)−Vac ,0
Pac(t) =
Cac

CHAPTER 4

COMPUTATIONAL METHOD &

RESULTS

The model was constructed through using time varying elastance theory. We applied the theory to both of our
Pulmonary circulation and Systematic circulation. Then after getting the mathematical equations necessary to get
the desired values, we used MATLAB for our computational software.
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The goal of this study was to develop models for both systemic circulatory system and pulmonary circulatory
system. After generating the model we ran some analysis to get the graphs where it shows some data of the
different parts of the system.

4.1 Figure Generated from the Code

Figure 6.1: Pressure Volume Diagram of the Left Ventricle

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Figure 6.2: Pressure in LV, aorta, and LA during cardiac cycle

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Figure 6.3: Pressure Volume diagram of left artrium

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Figure 6.4: Pressure Volume Diagram of the right Ventricle

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Figure 6.5: Pressure in RV, Pulmonary artery, and RA during cardiac cycle
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Figure 6.6: Pressure Volume diagram of right atrium

From the code we generated some pressure volume diagrams and Pressure in parts of the system during cardiac
cycle. Normally P-V diagrams of the systemic cardiovascular system is common to see as most of the studies
occurred about the systemic circulation. Thus it is rare to find the model and data of pulmonary circulation. So we
had to estimate the data of the pulmonary systems to make the diagrams.
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CHAPTER 5

CONCLUSION

The goal of this study was to develop models for both systemic circulatory system and pulmonary
circulatory system. After generating the model, we ran some analysis to get the graphs where it shows the
pressure and volume of the circulation system parts. By analyzing those graphs, we can get some idea about
the model of our heart. The model parameters can be further tweaked to simulate heart in different
conditions.

5.1 Limitations

Some of the data that we needed for the variables of the model was hard to find and some further studies are
needed in order to find the precise data that the model requires. Some assumptions were

5.2 Recommendations and Future Aspect

Some data were hard to get hold of as the work done on the pulmonary system is very low. There weren’t
enough data so had to assume a lot of the data that we worked on. In the future this model can be more
precise if we could get hold of a real-life model and get the data from there so the results we get can get as
close to the actual results.
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