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List of abbreviations 4
Introduction 5
References 62
3
LIST OF ABBREVIATIONS
4
INTRODUCTION
5
There are many different methods of numerical simulation in hemody-
namics. They are based on the finite element analysis. In the last time the
models of two-phase hemodynamics are used for investigation of microcircu-
lation [2, 14, 30, 31]. Most often the continuous phase corresponds to plasma
and discret phase is determinated by characteristics of the red blood cells. In
microvessels the rheological features of the blood are becoming significance,
namely: correlation between vessel size and blood viscosity, Fahraeus and
Fahraeus-Lindqvist effects and existence of the cell-free layer [10, 20, 55]. Nev-
ertheless, the single-phase flow models of viscous incompressible liquid are well
adapted for numerical simulation of blood flow in big vessels. In case of steno-
sis the narrowing parts of vessel appear and non-Newtonian rheological features
of blood may be hemodynamic significance. In these conditions, the using of
two-phase hemodynamics is of interest to the study.
Taken into account all above mentioned the construction of the two-phase
non-stationary hemodynamics model is relevant for the study of the coronary
artery stenosis influence to blood flow.
The purpose of this study is to develop a model of non-stationary two-
phase hemodynamics in stenosis based on the rheology of the non-Newtonian
liquid. During the work, the following tasks are solved:
receiving of two-phase hemodynamic equations in cylindricaly-symmetric
coordinate system,
construction of an axially symmetrical collisionless model of two-phase
hemodynamics in Comsol Multiphysics,
construction of axially symmetrical models of single-phase and two-phase
mixture flows in case of stenosis and without it in Comsol Multiphysics,
comparison of numerical calculations results for different models.
6
1 Computational models of blood flow
The results of many researchers of XVI – XIX centuries lie in the base of
modern hemodynamics. For example, the Hagen–Poiseuille law [56,61] gives the
velocity in case of laminar stationary liquid flow through cylinder. As known it
has the parabolic profile. Herewith Yong and Weber [23] studied a wave motion
in elastic tubes. In result Moens and Korteweg received the known formula
s
Eh
v= .
2ρR
It set the dependence of the wave velocity v from such parameters as the Young
modulus E, a thickness of tube wall h, a radius of tube R and density of tube
wall ρ.
It was be mentioned that the motion equations of hemodynamics are
Navier–Stokes equations. Herewith the modern scientific results admit to di-
vided all hemodynamic models to single-phase and multiphase models. In first
the single-phase models appeared.
The one of the first blood flow model is, so named, Frank model. It is based
on the conceptions of Windkessel theory [11]. Frank suggested that artery is an
elastic tube, herewith pulse flow runs in the vessel and stationary flow runs out
the vessel. In the systole phase blood flows in a vessel and in the diastole phase
it flows out. The Frank model uses the finite velocity of wave propagation.
Opposite to Frank suggestions Hamilton assumed that pressure wave have
infinite velocity in an aorta but in peripheral vessels it is finite too [23].
In [62] Womersley solved the linearized Navier–Stokes equation for a rigid
vessel. It was considered that a vessel is an infinite cylinder for which a wall’s
thickness is more smaller then its radius. Further [63] elastic features of vessels
were taken into consideration. In the next researches a pulse wave reflection [64]
7
and a variable viscosity [65] were taken into account too. There are many models
which are based on the Womersley model. The description of such models is
presented in [7].
One of many classes of hemodynamics models is a set of analogous or
lumped-parameter models [22,23,27,51]. These models are based on the analogy
between blood and electric current flow. In this case a heart corresponds to
power element with alternating electromotive force and vascular network is
replaced by set of resistances and capacitances. Herewith voltage relates to
pressure and current relates to blood flow. Then these characteristics satisfy
an equation similar to the Ohm’s law. As known hemodynamic parameters of
blood flow do not calculate well enough for lumped-parameter models [8]. So
it is a disadvantage of the corresponding simulations.
The next big class of hemodynamics models connects with hydrodynamic
equations considered in 1d, 2d or 3d modelling. One dimensional models ad-
mit to calculate blood flow parameters for all vascular network which is rep-
resented by one dimensional graph. These models are described by average
Navier–Stokes equation [23, 34, 42]. Two and three dimensional hemodynam-
ics models admit to simulate a curved and branched network of vessels more
exactly. They are described by Navier–Stokes equation and require more com-
puting resources. These models is often used for numerical investigation of
different vascular anomaly or curved and bifurcated vessels [4, 48]. It must be
marked the study [6] which defines a correlation between bifurcation angle at
the left coronary artery and hemodynamics.
In the last time there are numerical simulations which are used different
approaches in one model. It may be either combination of lumped-parameter
model and 2d or 3d modelling either combination of 1d-model and 2d or 3d
simulation. In these cases lumped-parameter models or 1d simulations are used
for calculating of boundary conditions for 2d or 3d modeling which are described
a blood flow in a fixed vessel. For example, in [43] a lumped parameter coronary
8
vascular bed model calculates inlet and outlet conditions for three-dimensional
vessel. In result blood flow in this vessel was simulated.
9
considered. The analogy task is presented in [60] but here erythrocyte’s layer
is defined as non-Newtonian liquid with constant viscosity. In both studies it
is considered that the cell depleted layer and hematocrit are depends on vessel
radius.
In [30, 31] a blood plasma fills the entire volume of vessel, the red blood
cells are distributed at vessel with exception of the cell depleted layer. Herewith
the blood viscosity depends on radius of vessel. The motion equations are
equations of inertionless motion of two-phase system with incompressible phases
and constant pressure gradient. The velocities of erythrocytes and plasma are
calculated, it is received that the red blood cells move more quickly than the
blood plasma. The dependence of blood viscosity and hematocrit on vessel
radius is researched. In case of the radius in interval from 5 to 50 µm the
relative viscosity experimental data are bad correlated with model results if
the flow average of hematocrit grows. In other cases the experimental and the
numerical data are well correlated.
The two-phase system without interphase interaction forces is consid-
ered [57] in case of stenosis. The hemodynamic equations are the equations
of magnetohydrodynamics. The influence of temperature is taken into account,
herewith the pressure gradient depends on time according to the harmonic law.
It was interesting the investigation [1] at which a dependence of Reynolds
number from red blood cells was received. In this case a blood flow in micro-
tubes was considered in framework of mixture model [29].
The all above considering multiphase models correspond to hemodynamics
in microvessels. In [5, 16, 21, 33] coronary blood flow simulation was studied.
Herewith four different non-Newtonian viscosity models are compared in case
of two-phase Eulerian–Eulerian method [21,33]. The simulation was performed
for curved coronary artery with the diameter 4,37 mm and the curvature radius
4,15 cm. A pulsatile inlet velocity and an outlet constant pressure were used
for both phases. Moreover, it was received that the mixture viscosity for the
10
two-phase case is some what higher than the single-phase model on the inside
and the outside curvatures. The red blood cells volume fraction is higher on
the inside curvature. The cases with stenosis were not considered. But the
corresponding vessel geometries were considered in [5, 16]. The high and low
hematocrit region were calculated near stenosis but this variation of hematocrit
was sufficiently small.
11
2 Physiological bases of coronary blood flow
12
significance [37–39, 59].
If particles have spherical shapes or their concentration is small then these
particles move in own layer without moving to a neighboring layers. If particles
have not spherical shapes or their concentration is high then the they get to
neighboring layer. In result, the difference appears between the velocities of the
layers. Additional resistance to movement of layer is consequence the velocity
mismatch. If particles have adhesion to each other they are formed to the stacks
of erythrocytes, rouleaux. This case corresponds to the system with particles
of non-spherical forms.
Plasma is the main part of the blood (about 60%) and about 99% from
the all blood cells are erythrocytes. So, the blood may be considered as two-
phase disperse medium It must be marked that red blood cells (pic. 2.2) have
Figure 2.2 — Red blood cells. The figure taken from [49]
the shape of a biconcave disk. Its diameter is about 7 − 8 µm, they may
be deformated and coagulated. The flow of erythrocyte through capillaries1
is explained by the erythrocyte ability to deform [12, 45, 52]. The process of
erythrocyte deformation is presented2 on the figure 2.3. On the figure 2.4
receiving in [40] experimental and numerical results3 are presented.
1
The red blood cells is squeezed if they flow through vessels with diametr more smaller than their equilibrium
diametr. For example the capillary diameter my have size about 2-3 microns.
2
The figure taken from publication [52]
3
The figure taken from publication [40]
13
Figure 2.3 — The modelling result of erythrocyte deformation in case of its
flowing through small channel. This confirms that the erythrocyte membrane
bend to a concave form [52]
Figure 2.4 — The experimental results are marked by letter (b) and (e). The
numerical results are marked by another letters
14
also defined as flow average hematocrit. Let also there is another channel which
connects the above considering channels, a hematocrit in this middle channel
is named the tube hematocrit. It can be calculated by expression
Z Z
1
Ht = Hds,
S
S
Arteries consist of three tunicas, see figure 2.5. An internal tunica is named
intima, it contents endothelium cells. An external tunica is named adventitia, it
consists of fibrous connective tissue. A tunica media is a middle layer of vessel,
it consists of muscle and elastic fibers. In different vessels there are various
correlations between muscle and elastic fibers. This defines a building type of
an artery. It may be elastic, muscle or muscular-elastic type [19].
Coronary arteries are arteries covering the heart. They are arteries of
muscle type [19] which bring oxygenated blood to the myocardium. The arteries
locating on the external tissue of the heart are named epicardium arteries.
Herewith the arteries locating on the internal tissue of the heart are named
endocardium or microvascular arteries.
There are two main coronary arteries (see pic. 2.6). The left coronary
artery (LCA) begins at the left aortic sinus. It start from the main stem of the
15
Figure 2.5 — The structure of an artery wall [50]
left coronary artery (LMCA) which is bifurcated5 to the left anterior descending
artery (LAD) and the circumflex artery (Cx).
The right coronary artery (RCA) begins at the right aortic sinus. It goes
to lower part of the heart. RCA ends with the posterior descending artery
(PDA) for more number of patients.
Numerical modelling of coronary blood flow is a non-invasive method for
determination of the cardiovascular system state. One of the reason of coronary
flow injury is a formation of narrowing parts in the arteries. Such part of the
vessel is named as stenosis. Stenotic injuries of the coronary vessels are usually
observed in certain parts of the coronary tree. The LCA stenosis often appear
in the bifurcation region which divided LCA to the left anterior descending
artery and the circumflex artery. The RCA is often narrowed in the proximal
segments [17].
Determination of the hemodynamic significance of the stenosis is provided
by complex of different methods. There are coronary angiography, intravascular
ultrasound, MRI, determination of fractional flow reserve. The last diagnostic
method is based on the calculation of the ratio of maximum blood flow distal
5
Some times there is a trifuracation [36].
16
Figure 2.6 — The coronary arteries tree [32]
17
problem appears when there two consequently placed stenosis. It is impossible
to determine which of them is more significance [17]. Sometimes it is enough to
stent only one of the stenosis for hemodynamics improvement. The numerical
simulations can to solve both of them problem.
To correct set boundary conditions for hemodynamics simulation must be
mentioned the following features. The coronary blood flow is defined by vessel
resistance which depends from a changing of intramiocardial and intra-cavity
pressure. At the systole there is a powerful contraction of the left ventricle which
leds to compression of small coronary arteries. As result in the left coronary
artery the blood flow dominates in the diastole phase. In the right coronary
artery the extravessel compression is low and the systolic blood flow is defined
too [17].
18
3 Basics of the multiphase disperse media theory
The different hydrodynamics models [24, 37, 38, 44, 59] are used for blood
flow modelling because the blood is a liquid. The multiphase theory is applied
to describe suspension and emulsion flows [37, 38, 59]. This theory can be con-
sidered in case of hemodynamics modelling as the blood consists of two phases:
plasma and cell component.
The disperse system motion equations are based on the continuity equation
∂ρ
+ div(ρv) = 0
∂t
∂v r (v ϕ )2 vr 2 ∂v ϕ
r 1 ∂p r
+ (v∇) v − = − + ν 4v − 2 − 2 ,
∂t r ρ ∂r r r ∂ϕ
∂v ϕ ϕ r ϕ r
v v 1 ∂p v 2 ∂v
+ (v∇) v ϕ + = − + ν 4v ϕ − 2 + 2 , (3.1)
∂t r ρr ∂ϕ r r ∂ϕ
∂v z 1 ∂p
+ (v∇) v z = − + ν4v z ,
∂t ρ ∂z
v = (v r , v ϕ , v z )
19
In cylindrical coordinate system the continuity equation of incompressible viscid
fluid is
1 ∂rv r 1 ∂v ϕ ∂v z
+ + = 0.
r ∂r r ∂ϕ ∂z
For multiphase disperse system the next restrictions [37, 38] are used:
Every phase occupies the entire volume of space and it is described by the
hydrodynamics equations.
Phase features (a density, a pressure, a phase energy and other) jump on
the boundary.
Related equations of system must to take into account phase interactions.
In the multiphase theory a true density2 ρ◦k is a density of the corresponding
phase as a self-contained continuum system. They are related by the expressions
X X
ρ= ρk , ρk = αk ρ◦k , αk = 1 (3.2)
k k
with a density of the all system ρ. Herewith αk is a volume fraction for k-th
phase, ρk is a density for k-th phase.
The velocities are defined by
X
ρv = ρk vk . (3.3)
k
In case of suspension of viscid fluid with particle the viscosity of the system is
defined by Einstein relation [3]
µ = µ1 (1 + C · α2 ),
µ
η=
µ1
20
In case of collisionless disperse two-phase system there are the next sug-
gestion [37].
The sizes of inhomogeneities in the mixture are more larger than the sizes
of molecules and less than the distances at which the parameters variations
are significance.
In every elementary macrovolume the particles of the disperse phase are
spherical and have the same radius.
Disperse phase volume fraction is very small: α22 1.
Effects of chaotic and internal movement of the dispersed phase particles
are negleted.
Direct collisions and processes of the dispersed phase particle coagulation
are neglected too.
Mass equation have the form [37, 38]
∂ρk ∂ρk vki
+ = njmk , (3.4)
∂t ∂xi
∂n ∂nv2i
+ = 0,
∂t ∂xi
here m corresponds to the disperse phase, jmk – velosity of phase transitions in
the direction from m to k. The particle number in a mixture volume unit is
3α2
n=
4πa3
where a is the particle radius.
Let there are no direct interaction between the particles and ρ◦k are con-
stants. Herewith let a pulse of the mixture volume unit equals to the sum of
phase pulses. In these assumptions the phase pulse equations are [37, p. 72]
d1 v 1 ∂σ k1
ρ1 = k
− nf 12 + ρ◦1 α1 g,
dt ∂x
d2 v 2
ρ2 = nf 12 + ρ◦2 α2 g, (3.5)
dt
here
dk v k ∂v k
= + (v k ∇)v k ,
dt ∂t
21
the stress tensor is [37, p. 70]
kl Σ
σ1 = − α1 p1 + α2 p2 − 2 δ kl + α2 Πkl + σµkl ,
2a
1
σµkl = 2µ ekl − em mδ
kl
, (3.6)
3
1
ekl = ∇k V l + ∇l V k ,
2
V = α1 v1k + α2 v2k ,
k
k l
kl ◦ 2 kl w12 w12
Π = −ρ1 (ω1a ) δ +
2
and σµkl is a viscous stress tensor, ekl is a strain tensor, Πkl is a pulse transfer,
a
w12 = v 1 − v2 , ω1a = divV ,
3α2
a is a particle radius, Σ is a coefficient of particle’s surface stress and µ – effec-
tive viscosity defined by Einstein formula. Herewith the interactions between
particles are absent. The particle radius is constant and the phase transmissions
are absent too (jmk = 0).
The interphase interaction force f12 is a sum of the buoyant force fA , the
added mass force fm and the force of viscous friction fµ :
f12 = fA + fm + fµ ,
2πa3 0 d1 v 1 d2 v 2 3 d2 a
fm = ρ − + w12 ,
3 1 dt dt a dt
fµ = 6πaµ1 ψa w12 , ψa = α1pw ,
22
and in case of spherical particles
3α2
n= .
4πa3
Take into account that the first term of the right part of the second equa-
tion of (3.7) is the buoyant force.
1
h1 = h3 = h1 = h3 = 1, h2 = r, h2 = .
r
In such transformation tensors are not changed by the tensor law in case of
transformation from one curved coordinate system to another.
The gradient operator in cylindrical coordinate system [24] is
∂ 1 ∂ ∂
∇= , , , (3.8)
∂r r ∂ϕ ∂z
here γ = (h1 h2 h3 )2 .
23
As result, in the axially symmetric case3 the system’s components not
depend from ϕ so the equations (3.4) are transformed to
∂αk
+ div(αk v k ) = 0. (3.11)
∂t
∂α1 ∂α2
=− .
∂t ∂t
divV = 0. (3.12)
In fist we rewrite the viscous stress tensor σµkl considered in the equation
(3.6) in cylindrical coordinate system. It has the form
2
σµkl = 2µekl − (µ + 2µ1 )divV δ kl , (3.13)
3
1 ∂V ϕ V r
ϕ z ϕ
1 ∂V 1 ∂V V
eϕϕ = + , eϕz = + − , (3.14)
r ∂ϕ r 2 ∂z r ∂ϕ r
z
z r
∂V 1 ∂V ∂V
ezz = , ezr = + .
∂z 2 ∂r ∂z
Further, taken into account (3.12) we write viscous stress tensor (3.13) as
Now, substituting the relation (3.15) to the equation (3.10) we receive the
3
Here k = 1, 2
24
next equalities:
V ϕ ∂µ µ
1 ∂V 2 ∂
∇k σµkϕ = 4µ V ϕ + ·∇ µ− + + 2 (µV r ) ,
r ∂ϕ r ∂r r r ∂ϕ
µ ∂V ϕ
∂V 1 ∂ µ
∇k σµkr = 4µ V + r
·∇ µ− 2 ϕ
(µV ) − 2 − 2 V r , (3.16)
∂r r ∂ϕ r ∂ϕ r
∇k σµkz = 4µ V z ,
1 ∂ ∂ 1 ∂ ∂ ∂ ∂
4µ = µr + µ + µ (3.17)
r ∂r ∂r r ∂ϕ ∂ϕ ∂z ∂z
herewith
∂V r ∂ 1 ∂V ϕ ∂ ∂V z ∂
1 ∂V 1
·∇ = + +
r ∂ϕ r ∂ϕ ∂r r ∂ϕ ∂ϕ ∂ϕ ∂z
and
∂V r ∂ 1 ∂V ϕ ∂ ∂V z ∂
∂V
·∇ = + + .
∂r ∂r ∂r r ∂r ∂ϕ ∂r ∂z
Further we assume
∇k α2Πkl = 0
then taken into consideration the relation (3.16) we have that in the cylindrical
coordinate system the equation (3.7) is defined by
∂v k divΩ V
ρk + (v k · ∇) v k = −αk ∇p − + 4µ V + ∇ µ −
∂t 2 (3.18)
−αk χ + (−1)k fm + fµ + ρk g k ,
25
where (v k · ∇) is a scalar product of vectors and
The mixture model equations are the equations which are used in the
Comsol Multiphysics in case of mixture model. These model can be chosen
for two-phase model with continuum and disperse phase. The last may be
presented by liquid droplets, gas bubbles or solid particles. The equations of
the model were considered with the different points of view, the review of the
corresponding methods is presented in [28]. In the Comsol Multiphysics the
next assumption are used.
The basic theory of the mixture model originates on the two-phase hydrody-
namics equations, see the section 3.1, namely the equations (3.4) and (3.5)
and the above presented theory. The next motion equation of the mixture is
26
received from (3.5) after some transformations, it is
∂v α2 ρ2
ρ + ρ(v · ∇)v = −∇p − ∇ · (ρ − α2 ρ2 )vslip vslip +
∂t ρ (3.25)
+∇ · (∇v + ∇v T ) + ρg + F
where
α1 ρ◦1 v1 + α2 ρ◦2 v2
v= ,
ρ
the index 2 corresponds to disperse phase and 1 corresponds to the continuum
phase. Herewith the relations (3.2) and (3.3) were used. The relative velocity
between the phases vslip in the laminar conditions have the form
vslip = v2 − v1 .
28
4 Two-phase vascular blood flow models
29
disperse phase volume fraction is very small,
it is possible to neglect the energy and effects of the chaotic and internal
movement of particles of the disperse phase,
direct collision and coagulation of the disperse phase particles are not
considered,
the pressure is is the same in both phases and particle radius is constant,
the densities ρ◦1 and ρ◦2 are constant too.
For the model construction the assumption
µ α1−0.8 − 1
η= = 1 + 2.2 . (4.2)
µ1 (1 − 0.45)−0.8 − 1
In this case η(0) = 1.
For numerical simulation the following parameters are used. The plasma
viscosity is
µ1 = 1, 5 · 103 g/(s · mm),
30
the red blood cells density is
where
pmax −pmin
p
min + 2 (1 + cos(2πt − π)), t ≤ 0, 7T,
p0 (t) = (4.3)
pmin , 0, 7T < t ≤ T,
31
4.1.1 The first case of hematocrit function
In this case the numerical simulation results were received, we have that
the velocities of the red blood cells and the plasma are equal.
So the blood velocity V can be calculated from the relation
ρ1 v1 + ρ2 v2
V = .
ρ
Taken into account the equations (3.2) and (3.3) we have that the blood velocity
equals to the plasma and red blood cells velocity, as v1 = v2 . So, the maximum
value of blood velocity is shown at the figure 4.3.
Let us increase the pressure gradient putting now
p = (1 − 0, 2z)p0 (t).
2
It equals to hematocrit.
32
Figure 4.3 — The simulation result for the velocity at the moment t = 0.62T ,
here the period equals to 1 second and p = (1 − 0, 1z)p0 (t). The velocity is
measured in m/s
Figure 4.4 — The velocity at the moment t = 0.62T , here the period T = 1 s
and p = (1 − 0, 2z)p0 (t). The velocity is measured in m/s
33
In this case the blood velocity will increase too. The corresponding results may
be seen at the figure 4.4.
Further consider a volumetric flow rate of blood3 Q, which is
ZR
Q = 2π V (r)rdr.
0
In case of constant blood flux we decrease a radius of the vessel and compare it
with value of the pressure gradient. It was received that the pressure gradient
− 14
∂p
Figure 4.5 — The ordinate axis shows ∂z , and the abscissa axis shows
the radius of the artery. The pressure is measured in Torr and the radius is
measured in mm. The result was received in case of constant blood flow
is inversely proportional to fourth power of the vessel radius (see figure 4.5):
∂p 1
= .
∂z (1, 09r + 0, 02)4
The absolute error of velocity estimation is about 0,025 m/s.
In the considering case the cell depleted layer was not done by inlet model
parameters and don’t appear as a simulation result. In [30, 31] this layer was
done as inlet function. Thus we do this too in the next construction.
3
It is also named the blood flux.
34
4.1.2 The second case of hematocrit function
Here h determinates a thickness of the cell depleted layer. The similar function
was chosen in [30,31] for value of hematocrit too. We also use the next function
for pressure: p = (1 − 0, 2z)p0 (t). The velocity of the plasma v1 is presented on
the figure 4.6. It have the same profile as the erythrocyte velocity v2 and the
35
Figure 4.7 — The red blood cells velocity at the moment t = T = 1 s in case
of step function of hematocrit, p = (1 − 0, 2z)p0 (t)
equals to zero. It is seen that the velocity profile is different from Poiseuille
profile.
In this simulation the dependence of hematocrit and viscosity on vessel
radius is a constructive feature of the model. All known multiphase blood
flow simulations use different rheological models for viscosity determination.
In our case the blood viscosity is described by Einstein equation with specific
parameters which were suggested in [30, 31]. Our results are coordinated with
36
Figure 4.9 — The difference v2 − v1 in m/s, at the moment t = T = 1 s and in
case of step function of hematocrit, p = (1 − 0, 2z)p0 (t). Here v2 is RBCs
velocity and v1 is plasma velocity
results of other authors [30, 31, 47, 53, 60] in that the hematocrit and viscosity
are depend on vessel radius. In the studies of author [30,31] there is a difference
between plasma and erythrocytes velocities. In our model these velocities do
not differ in case of first hematocrit function and very small differ in case of step
hematocrit function. This difference is about 7-8 RBC diameter per second.
The principle feature of the constructed model consists in the using of
non-stationary equations and a pulse wave. Herewith the results were received
not for small vessels. The authors [30, 31, 47, 53, 60] considered the stationary
blood flow.
37
by Navier-Stocks equations (3.1) above presented. Calculations were received
in Comsol Multiphisics.
The rigid vessel with radius 1.62 mm and length 10 mm is constructed in
axially symmetric geometry. The initial values are
v r = 0, m/s v z = 0, 2 m/s
Figure 4.10 — The pressure function using in the simulation at the inlet
where
ρ◦1 = 1, 03 · 10−3 g/mm3
38
Figure 4.11 — The ordinate axis shows vout (t) in m/s, and the abciiss axis
shows the time in seconds
and hematocrit equals to 0.4. The red blood cells radius is a = 4 µm.
Figure 4.12 — The pressure of the single-phase laminar flow in the rigid vessel
It was received that the pressure is the same at all points of the vessel,
corresponding time dependence is done on the figure 4.12. The velocity has a
39
Figure 4.13 — The velocity of the single-phase laminar flow in the rigid vessel,
it is time dependence
radial distribution (see pic. 4.14) and ts time dependence is presented on the
figure 4.13.
Now we construct a two-phase model of hemodynamics.
Let us consider the equations of mixture model (3.25), the gravity force ρg
and the added force F are not taken into account. The numerical simulations
based on the mixture model will be performed in the Comsol Multiphysics.
The two-phase simulation in the same rigid vessel as in the single-phase
case was realized in the Comsol Multiphysics. So, in new conditions, the model
equations consist from the motion equations
dv α2 ρ2
ρ = −∇p − ∇ · (ρ − α2 ρ2 )vslip vslip + ∇ · (∇v + ∇v T ) (4.5)
dt ρ
and the continuity equations for the mixture and the disperse phase
∂ρ
+ div(ρv) = 0,
∂t (4.6)
∂α2 ρ◦2
+ div(α2 ρ◦2 v2 ) = 0.
∂t
40
Figure 4.14 — The velocity of the single-phase laminar flow in the rigid vessel,
the vertical axis shows v(t) in m/s, at t = 1 s
dv ∂v
= + (v · ∇)v.
dt ∂t
41
The mixture model requires to choose a slip velocity determination (see the
section 4.5). We use the Hadamard-Rubczynski slip model for liquid droplets
or bubbles:
µ1
!
2a2 (ρ − ρ2 )µ1 1+ µ2
vslip =− 2µ1 ∇p.
9ρµ 1+ 3µ2
and the red blood cells viscosity is defined by relation µ2 = 1, 5µ1 , we used the
study [54] for RBCs viscosity estimation. The plasma density ρ◦1 and the red
blood cells density ρ02 are the same as at the above considered models.
These model conditions are identical for case of normal and stenotic vessels.
The models are different not only by geometry. The viscosity construction will
be calculated by different ways too.
In first, consider a case of normal vessel.
42
Figure 4.15 — The mixture velocity of the two-phase laminar flow in the rigid
vessel, the vertical axis shows v in m/s at the time t = 0, 62 s
Figure 4.16 — The time dependence of the mixture velocity of the two-phase
laminar flow in the rigid vessel, the vertical axis shows v(t) in m/s at the
point with r = 0 and z = 5 mm
43
Figure 4.17 — The red blood cells velocity of the two-phase laminar flow in
the rigid vessel, the vertical axis shows v2 in m/s at time 0, 62 s
Comparing the slip velocity with RBC diameter we receive that erythrocytes
move faster than plasma by 2-3 own diameters per second. It is three to four
times less than in the previous collisionless two-phase model.
At the figure 4.19 you can see a pressure dependence on z-coordinate.
Obviously, the difference between the pressure around the vessel axis and the
pressure near the vessel wall appears due to boundary condition influence. The
last one would end on 2 mm after the inlet and before the outlet of the vessel.
So it can be concluded that the pressure does not depend on vessel radius in
the region of vanishing influence of boundary conditions. The pressure gradient
in this vessel part equals to value about 0,03 Torr/mm.
It must be marked, a time-dependence of the pressure is done on the
figure 4.20. Its time profile corresponds to the using inlet pulse wave.
As a result of the simulation a RBCs volume fraction was received too.
The hematocrit small depends on time and depends on the vessel radius, see
figures 4.21–4.23. Near the vessel wall a minimal erythrocytes volume fraction
takes place at the peak of the blood flow velocity, see figures 4.16 and 4.23.
Herewith at the vessel axis a hematocrit has minimum a little before the time
44
Figure 4.18 — The slip velocity between RBCs and plasma in case of the
two-phase laminar flow in the rigid vessel, the vertical axis shows vslip in m/s
at the point r = 0 and z about 5 mm
45
Figure 4.20 — The pressure at the point r = 0 and z about 5 mm
at which it appears near the wall. This moment corresponds to the beginning
of a systole.
At the period about 0,8-0,9 seconds an increasing of the slip velocity leads
to a decreasing of the RBCs volume fraction at the center of vessel, see fig-
ures 4.18 and 4.22. It is apparent. If particles velocity is growing relative
to plasma flow then number of particles per unit volume drops. Taking into
consideration the plot 4.20 we can conclude that a pressure boost leads to an
increasing of the RBCs volume fraction at the vessel axis and only after this its
growth appears near the vessel wall.
Considering presented on the figure 4.24 plot we can see an appearance of
46
Figure 4.22 — The RBCs volume fraction at the point r = 0 and z about 5
mm
Figure 4.24 — The RBCs distribution in case of laminar flow near the wall.
There is a cell depleted layer
47
a cell depleted layer. It is so despite constant hematocrit at the beginning, see
figure 4.24. At a distance of 20 micrometers from the vessel wall a hematocrit
has a value about 0,25 but at a distance of 10 micrometers from the vessel wall
it drops twice.
Now we include a stenosis to the considering vessel.
There are two types of stenotic wall was constructed. They are presented
at the figures 4.25 and 4.26. The vessel radius equals to 1,62 mm too.
A degree of the first stenosis (see pic. 4.25) is about 31% and a degree of
the second stenosis is about 49% (see pic. 4.26).
These simulations differ from the case of normal vessel by blood viscosity
determination. In this case we admit that µ is defined by (4.2) in points with
r < 0, 9R, where R is the vessel radius. For other values of radial coordinate
we have µ = µ1 where µ1 = 1, 5 · 103 g/mm3 . Herewith α1 equals to 0.6 The
erythrocyte distribution is calculated at the model too.
48
The boundary and initial conditions are described above in this section.
In first we describe a pressure which was calculated for both stenotic ves-
sels. A diastolic pressure is presented on the figures 4.27 and 4.28. A receiving
systolic pressure you can see on the figures 4.29 and 4.30 correspondingly. To
note, the high pressure zones at the ends of the vessels appear due to boundary
conditions and ones must be ignored.
As you can see, a decreasing of pressure behind stenosis is more significant
in a vessel with a greater degree of narrowing.
At the figure 4.31 a time dependence of a pressure is ploted for both cases of
stenosis at the point r = 0 and z = 5 mm, it corresponds to center of stenosis.
Blue line corresponds to a stenotic vessel with degree of narrow about 31%,
and a red line corresponds to a stenosis of 49% degree of narrow. Comparing
the both curves we can conclude that a diastole phase lengthens as the vessel
narrows.
Receiving values of the mixture velocities are presented on the figures 4.32
49
Figure 4.29 — A systolic Figure 4.30 — A systolic
pressure in case of 31% stenosis pressure in case of 49% stenosis
Figure 4.31 — A systolic preassure for 31% stenosis and 49% stenosis
and 4.33 correspondingly. Its time dependence you can see at the figures 4.34
and 4.35. The blue and red lines on these plots determinate the mixture
velocities at the vessel axis before stenosis and at the points of maximum vessel
narrowing. The green and yellow lines correspond to these velocities at the
vessel axis too but only behind the stenosis.
50
Figure 4.32 — The velocity at Figure 4.33 — The velocity at
the 31% stenosis is done in the 49% stenosis is done in
mm/s mm/s
figures 4.36 and 4.37. The yellow lines determinate it at the vessel axis in the
center of stenosis. As you can see, these values drop sharply to zero near the
stenotic wall.
To compare RBCs and plasma velocities we constructed plots of slip ve-
locities which are presented at the figures 4.38 and 4.39. As you can see, the
slip velocity at the figure 4.39 is greater then one at the figure 4.38. The order
of these values is comparable to the erythrocytes diameter.
It is not hard to notice, there is a small peak of the mixture velocity behind
the stenosis near the wall, see figures 4.36 and 4.37. This is due to a specific
red blood cells distribution which is presented at the figure 4.40 for the 31%
stenosis and at the figure 4.41 for the 49% stenosis too.
We can see that a cell depleted layer is appear as in above considering
cases, see figure 4.42. Behind stenosis it have a more complex structure then
before stenosis.
51
Figure 4.34 — The velocity at the 31% stenosis is done about the vessel center
Herewith behind stenosis the low hematocrit layer is appeared and it de-
creases when removed from the stenotic part of vessel. But in this layer there
is a high RBCs volume fraction zone, see figures 4.43 and 4.44.
52
Figure 4.35 — The velocity at the 49% stenosis is done about the vessel center
53
Figure 4.38 — It is a slip velocity dependence on r for the 31% stenosis
54
Figure 4.40 — It is a volume fraction of red blood cells at the 31% stenosis
Figure 4.41 — It is a volume fraction of red blood cells at the 49% stenosis
55
Figure 4.42 — There are cell depleted layers, results is done at points behind
stenosis
Figure 4.43 — RBCs volume fraction (or hematocrit) dependence on r for the
31% stenosis
Figure 4.44 — RBCs volume fraction (or hematocrit) dependence on r for the
49% stenosis
56
publications (see for example [9, 30, 31, 53, 60]) the cell depleted layer is defined
by some function. At this model the hematocrit was done only at the inlet and
outlet boundary. The influence of these boundary conditions is vanished on the
some distance from the boundaries. The initial conditions not influence on the
solution after one period of pulse wave too.
At the all known articles the RBC distribution is a some function of the
model. Our result shows that the cell depleted layer appears as a result of inter-
phase interactions. The RBC distribution is calculated during the simulation.
Figure 4.45 — The red blood cells distribution in case of second stenosis. The
zone of high hematocrit near the wall. Time of 0.62 of period
57
Figure 4.46 — The red blood cells distribution in case of second stenosis. The
zone of high hematocrit near the wall. Time of 0.68 of period
Figure 4.47 — The red blood cells distribution in case of second stenosis. The
zone of high hematocrit near the wall. Time of 0.78 of period
then at other times. See figures 4.45 – 4.47. When pressure is decreased the
high RBC zone grows away from stenosis.
58
the red blood cells can accumulate in the zone.
These result requires clarification and further research because of this effect
may be a consequence of inappropriate mesh choosing during a simulation.
Despite this, the study [66] should be considered in the context of the
our results. An in vitro investigation of a dynamics of mixture of platelet-
sized fluorescent particles and RBC suspension was studied. A narrowing glass
microchannel was constructed. The dynamics of the receiving particles mixture
in this microchannel was investigated. It was received that there is a high
platelet-sized particles zone which is located several microns away from the
wall. Moreover in the cell depleted layer RBCs recirculate and confluent to the
main flow. It is consistent with our results.
Also in the study [66] was received that before or behind narrow part of
microchannel the cell depleted zone appear too. I our study there is a little cell
depleted zone in considering parts of stenosis.
Thus our results are consistent with both theoretical studies and experi-
mental ones.
59
CONCLUSION
During the study all planed tasks were solved. As a consequence the
following results were obtained:
rheological properties of blood and basic features of the theory of multi-
phase disperse systems were studied;
two-phase collisionless hemodynamic equations in cylindricaly-symmetric
coordinate system were received;
an axially-symmetric collisionless model of two-phase hemodynamics was
constructed;
an axially-symmetric mixture model of two-phase blood flow and a single
phase hemodynamics model were constructed in Comsol Multiphysics;
axially-symmetric mixture model was adapted to numerical simulation of
blood flow in stenotic vessels in Comsol Multiphysics.
Using of rheological properties of blood to provide a numerical simulations
of blood flow is a perspective direction in modern studies. In case of different
models of microcirculation this approach is widely adopted. But insufficient
number of studies are used features of blood rheology in case of big vessel.
More over the corresponding approach is used in few cases only.
During this investigation the basic features of the theory of multiphase
hydrodynamics were studied. Receiving two-phase collisionless hemodynamic
equations in cylindricaly-symmetric coordinate system was adopted to construct
a collisionless axially-symmetric model of two-phase hemodynamics. A numer-
ical simulation was performed in Comsol Multiphysics. The main results cor-
responds to other researchers but a difference of this model consists in using
of time-dependent calculations. There is a disadvantage of the result which
consists in suggestion that velocity not depends on z-coordinate. We assume
the next development of constructing model.
The next receiving model is an axially symmetrical 2d mixture model. We
60
adapted these equations to construct of the corresponding model which describe
the blood flow in arteries. The simulations were done in Comsol Multiphysics
too as in normal as in stenotic vessels. It was shown that
a volume fraction of the RBCs depends on radius and a geometry of vessel
and small depends on the initial and boundary distribution,
a cell depleted layer appear near the vessel wall and near a stenosis,
there is a high hematocrit zone in region behind stenosis.
In common all results are agreement with data obtained by other authors.
The result about the existence of a high hematocrit zone was not found in
literature. We think that the high hematocrit zone can influence to the progress
of the stenotic injury. This result requires clarification and further research. For
this investigation it is necessary to take into account the elastic properties of
the vascular wall.
The results of the study were reported and discussed at the scientific sem-
inars of the General and experimental physics department of TSU.
61
REFERENCES
11. Frank O. The basic shape of the arterial pulse. First treatise: mathematical
analysis.// Journal of Molecular and Cellular Cardiology. — 1990. — Vol.
22, iss. 3. — P. 255–277.
12. Freund J. B. The flow of red blood cells through a narrow spleen-like slit
// Phys. Fluids. – 2013. – Vol.25. – 110807
14. Gould I.G. Hematocrit distribution and tissue oxygenation in large micro-
circulatory networks / I.G. Gould, A.A. Linninger // Microcirculation. –
2015. – Vol. 22. P. 1-18
15. Hariprasad D.S. Two-dimensional simulation of red blood cell motion near
a wall under a lateral force / D.S. Hariprasad, T.W. Secomb // Phys. Rev.
E Stat. – Nonlin Soft. Matter. Phys. – 2014. – Vol.90. – 053014.
16. Huang J. Pulsatile flow in a coronary artery using multiphase kinetic the-
ory / J. Huang, R. W. Lyczkowski, D. Gidaspow // Journal of Biome-
chanics. – 2009. – Vol. 42. – P. 743-754
63
19. Kayumov F.A. Cardiovascular system. Its importance for surgical practice:
student tutorial / F.A. Kayumov, M.A. Nartaylakov, Ufa: Publishing of
Bashkir State Medical University, 2013. – 69 p.
20. Kim S. The cell-free layer in microvascular blood flow / S. Kim [et al] //
Biorheology. – 2009. – Vol.46. P. 181-189.
22. Kokalari I. Review on lumped parameter method for modeling the blood
flow in systemic arteries / I. Kokalari, T. Karaja, M. Guerrisi // J. Biomed-
ical Science and Engineering. – 2013. – V. 6. – P. 92-99.
29. Massoudi M. Modeling and numerical simulation of blood flow using the
theory of interacting continua. / M. Massoudi, J. Kim, J.F. Antaki //
64
International Journal of Non-Linear Mechanics. – 2012. – Vol. 47. – P.
506-520.
30. Medvedev A.E. Two-phase blood flow model in large and small blood
vessels // Mathematical biology and bioinformatics. – 2011. – Vol.6, 2.
P.228-249
31. Medvedev A.E. Empirical two-phase model of blood flow in vessels less
than 1000 microns // The XI All-Russian Congress on Fundamental Prob-
lems of Theoretical and Applied Mechanics”, Uchenye Zapiski Kazanskogo
Universiteta. Seriya Fiziko-Matematicheskie Nauki, V.157, no. 3, Kazan
University, Kazan, 2015, P.2515-2517.
36. Nekrasov A.S. Successful endovascular treatment for LCA trunk trifurca-
tion lesion / A.S. Nekrasov, A.A. Grechishkin, S.V. Mayngart // Innova-
tive medicine of Kuban – 2017. – Vol.2. – P.28-33.
65
37. Nigmatulin R.I. Dynamics of multiphase media, V. I/ R.I. Nigmatulin –
M.: Nauka, 1987
41. Numerical methods for simulating blood flow at macro, micro, and multi
scales/ Y. Imai [et al] // J. Biomech. – 2016. – Vol.49. – P.2221–2228.
44. Pedley T. J. The fluid mechanics of large blood vessels /T.J. Pedley –
Cambridge: Cambridge University Press, 1980.
45. Picot J. A biomimetic microfluidic chip to study the circulation and me-
chanical retention of red blood cells in the spleen /J. Picot [et al] // Am.
J. Hematol. – 2015. Vol.90. – 339
47. Pries A.R. Generalization of the Fahraeus principle for microvessel net-
works / A.R. Pries, K. Ley, and P. Gaehtgens // American Journal of
66
Physiology-Heart and Circulatory Physiology. – 1986. Vol.251, N.6, P.
H1324-H1332
49. Renal hematuria: the cause of blood in the urine needs to be clarified [Elec-
tronic resource] //Medical atlas. – URL: https://med-atlas.ru/vnutrennie-
organy/gematuriya-chto-eto-takoe.html (access date: 17.05.2021).
53. Sharan M. A two-phase model for flow of blood in narrow tubes with
increased effective viscosity near the wall /M. Sharan , A.S. Popel //
Biorheology. – 2001. – Vol. 38. – P. 15-428.
67
// Microcirculation. – 2014. – Vol. 21. – P. 628-639
57. Tripathi B. MHD pulsatile two-phase blood flow through a stenosed artery
with heat and mass transfer [Electronic resource]/ B. Tripathi, B.K.
Sharma, M. Sharma //arXivLabs, URL:https://arxiv.org/abs/1705.09794
(access date: 17.05.2021)
60. Verma S.R., Srivastava A., Analitical study of a two-phase model for
steady flow of blood in a circular tube /S.R. Verma, A. Srivastava //
Int. Journal of Engineering Research and Applications. – 2014. – Vol.4,
12. – P.1-10.
61. Volarovich M. P. Poiseuil’s work on the flow of liquid in pipes (To the
centenary since publication) // Izzvestiya Acad. Sci. USSR, Physics Series.
– 1947. – Vol. 11, 1.
62. Womersley J.R. Method for the calculation of velocity, rate of flow and vis-
cous drag in arteries when the pressure gradient is known // J. Physiology.
– 1955. – Vol.127, N3. P. 553–563.
68
64. Womersley J. R. Oscillatory flow in arteries II: the reflection of the pulse
wave at junctions and rigid inserts in the arterial system // Physics in
Medicine andBiology. – 1958. – V. 2. P. 313–323.
65. Womersley J. R. Oscillatory flow in arteries III: flow and pulse velocity
formulae for a liquid whose viscosity varies with frequency // Physics in
Medicine andBiology. – 1959. – V. 2. P. 374–382.
69