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Blood Newtonian Fluid Large Arteries
Blood Newtonian Fluid Large Arteries
by
MASTER OF SCIENCE
in the subject
APPLIED MATHEMATICS
at the
SUPERVISOR: DR J M W MUNGANGA
NOVEMBER 2005
******************
i
SAMUEL OUKOUOMI.
ii
ACKNOWLEDGEMENTS
1 Introduction 1
1.1 Background . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
3.1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
iii
CONTENTS iv
3.1.3 Preliminaries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
4 Conclusion 45
CONTENTS v
A appendix 47
References 57
Chapter 1
Introduction
1.1 Background
The physiology of the cardiovascular system has been elucidated only gradually, over
many centuries. Among the major actors in the lengthy process have been some of the
central characters in human history.
Aristote (384-322 B.C.), for example, identified the role of blood vessels in transferring
“ animal heat” from the heart to the periphery of the body (although he ignored blood
circulation).
In the third century B.C., Praxagoras realized that arteries and veins have different roles
(believing that arteries transported air while veins transported blood). Galen was the
first to observe the presence of blood in the arteries. Much later, in the 17th century, Sir
William Harvey inaugurated modern cardiovascular research with his De Motu Cardis
and Sanguinis Animalibus, in which he wrote, “ When I turned to vivisection I found the
task so hard I was about to think that only God could understand the heart motion”.
Harvey observed that the morphology of veins is such that they are effective only if blood
is flowing toward the heart. His conclusion: “ I began privately to consider if it (the
blood) had a movement, as it is, it would be in a circle”.
In the 18th century, the Reverend S. Hales introduced quantitative studies of blood pres-
sure (Hemostatics, 1773). Later, Euler and D. Bernoulli both made great contributions
to fluid dynamic research. Bernoulli in particular as a Professor of anatomy at the Uni-
versity of Basel in Switzerland, investigated the laws governing blood and formulated
his famous law relating pressure, density, and velocity: p + 12 ρ| u |2 = const (vis viva
equation, 1730).
In the 19th century, J.P. Poiseuille, medical doctor and physicist, was studying the flow
of blood in arteries when he derived the first simplified mathematical model of flow in a
cylindrical pipe, a model that still bears his name today.
T. Young later made fundamental contributions to research on elastic properties of ar-
terial tissues and on the propagation of pressure: “ The inquiry in what manner and at
1
CHAPTER 1. INTRODUCTION 2
what degree the circulation of the blood depends on the muscular and the elastic power
of the heart and the arteries, supposing the nature of these powers to be known, must
become simply a question belonging to the most renowned department of the theory of
hydraulics” (From a lesson given by Young at the Royal Society of London in 1809 ).
At the beginning of the 20th century, O. Franck introduced the idea that the circulatory
system is analogous to an electric network. In 1955, J. Womersley, studying vascular
flows, found the analytical counterpart of Poiseuille flow in pressure gradients that vary
periodically in time, a situation that more closely describes actual pressure variations
during the cardiac cycle.
In the second half of the 20th century, developments in mathematical modeling were lim-
ited to basic paradigms, such as flow in morphologically simple regions (e.g., Poiseuille or
Womersley solutions), or to models based on electric network analogies. Exact solutions
are very difficult to obtain in more general situations, because of the strong nonlinear
interactions among different parts of the system and the geometric complexities of indi-
vidual vascular morphologies.
The historical details in this section is extracted from Modeling the Cardiovascular
System-A Mathematical Adventure: Part I by Alfio Quarteroni [13].
Blood is a circulating tissue composed of fluid plasma and cells (red blood cells, white
blood cells, platelets). The main function of blood is to supply nutrients to the tissues
and to remove waste products. Blood also enables cells (leukocytes, abnormal tumor
cells) and different substances (lipids, hormones, amino acids) to be transported between
tissues and organs [8].
1. Red blood cells or erythrocytes (96%). In mammals, mature red blood cells lack
a nucleus and organelles. They contain the blood’s hemoglobin and distribute
oxygen. The red blood cells (together with endothelial vessel cells and some other
cells) are also marked by proteins that define different blood types.
2. White blood cells or leukocytes (3.0%), are part of the immune system; they destroy
infectious agents.
3
CHAPTER 2. CARDIOVASCULAR PHYSIOLOGY AND EQUATIONS 4
Q = vA. (2.1)
In the left ventricle, the blood flow is described by the cardiac output Q (i.e. flux, blood
flow per unit of time), so that the equation reads:
∆P
Q= , (2.2)
R
where R is the total peripheral vascular resistance. R is directly related to the blood
viscosity µ and to the length L of the vascular system, and inversely related to its radius
to the 4th power:
8µL
R= [9]. (2.3)
πr4
Doubling the length of the system only doubles the resistance, where halving the radius
increases the resistance sixteen-fold.
voltage of the source (battery or power supply) in that loop (or zero if there is no source
in that loop). This is essentially the conservation of energy. In the cardiovascular case,
the flow into a branch is equal to the sum of the flows out; in the electrical case, the same
is true for currents at a junction of conductors: conservation of charge. In the electrical
parlance, these principles are known as Kirchoff’s laws. These laws lead to the following
rules for treating voltages and currents in series and parallel configurations:
1. The voltage drop across two components in series is equal to the sum of the voltage
drops across each component. We think of the pressure drops in the arteries and
in the arterioles.
2. The currents flowing through two components in series are equal. If an arteriole
and a venule were joined by a single capillary, the fluid flow through them all would
be the same.
3. The voltage drops across two components in parallel are equal. This corresponds
to a branching of an artery into different arterioles.
4. The current flowing through two components in parallel is equal to the sum of
the currents flowing through each component. This implies that the resistances
through alternate paths determine how much current flows through each of them:
electricity tends to the path of least resistance ([9]).
Chapter 3
3.1 Introduction
This chapter provides a model for blood flow in the large arteries and addresses the
analysis of the Navier-Stokes problem, having provided boundary conditions which can
be considered as a generalization of the mean pressure drop problem investigated in
[7], as they arise in bioengineering applications. Our purpose is to consider both the
stationary case and the nonstationary case. In this regard, we will prove the existence
of a weak solution for the stationary case based on Brouwer’s fixed point theorem and
afterward, we will establish a well-posedness analysis for the nonstationary case based on
a suitable energy estimate that we are going to derive as well as a well-known compactness
argument.
8
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 9
particularly significant when the particle size becomes appreciably large in comparison
to the dimension of the channel in which the fluid is flowing. This situation happens in
the microcirculation (small arterioles and capillaries).
Consider a suspension in which the suspending fluid has a Newtonian behavior. If the
suspended particles are spherical and have the same density as the suspending fluid,
then for any motion the shear stress will be proportional to the rate of shear and the
suspension will behave as a Newtonian fluid. This rule applies as long as the concen-
tration of spheres is low, less than 30%. This rule was arrived at through experiments
performed under steady state conditions with suspensions of rigid spheres. These exper-
iments showed that the viscosity of the suspensions, was independent of the shear rate
for volume concentrations of suspended spheres up to 30%. However, if the suspended
particles are not spherical or are deformable in any way, then the shear stress is not
proportional to the shear rate unless the concentration is much less than 30%.
The cells suspended in blood are not rigid spheres, and the volume fraction of erythro-
cytes is about 40 to 45%. Therefore, one should expect that the behavior of blood is
non-Newtonian. But it has been shown that human blood is Newtonian at all rates of
shear for hematocrits up to about 12% [11]. In general blood has a higher viscosity
than plasma, and as the hematocrit rises, the viscosity of the suspension increases and
non-Newtonian behavior is observed, being detectable first at very low rates of shear.
Studies with human blood show that viscosity is independent of shear rate when the
shear rate is high. With a reduction of shear rate the viscosity increases slowly until a
shear rate less than 1s−1 , where it rises extremely steeply [2]. The shear stresses can be
divided into two groups according to the effect of the shear rate:
1. At low shear rates, the viscosity increases markedly. The reason for this increase is
that at low shear rates a tangled network of aggregated cell structures (Rouleaux)
can be formed [11]. If blood is subjected to shear stress less than a critical value,
these aggregated structures form. As a result, they exhibit a yield stress. This
behavior is, however, only present if the hematocrit is high. If the hematocrit
falls below a critical value, there are not enough cells to produce the aggregated
structures and no yield stresses will be found.
2. At high shear rates, the viscosity in small vessels is lower than it is in larger vessels.
The progressive diminution with the size of the vessels is detectable in vessels with
an internal diameter less than 1 mm. It is even more pronounced in vessels with a
diameter of 0.1 mm to 0.2 mm. The decreased viscosity with vessel size is known
as the Fȧhraeus and Lindqvist effect. Experiments were performed at high enough
shear rates for the erythrocytes not to aggregate. It was found that the viscosity
was approximately constant in vessels larger than 1 mm, but when the radius
dropped below that, there was a substantial decrease in viscosity.
In the larger vessels it is reasonable to assume blood has a constant viscosity, because
the vessel diameters are large compared with the individual cell diameters and because
shear rates are high enough for viscosity to be independent of them. Hence in these
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 10
vessels the non-Newtonian behavior becomes insignificant and blood can be considered
to be a Newtonian fluid.
In the microcirculation, it is no longer possible to think of the blood as a homogeneous
fluid; it is essential to treat it as a suspension of red cells in plasma. The reason for this
is that even the largest vessels of the microcirculation are only approximately 15 red cell
widths in diameter.
In summary, we can conclude that blood is generally a non-Newtonian fluid, but it is
reasonable to regard it as a Newtonian fluid when modelling arteries with diameters
larger than 1 mm. For very small vessels it is not easy to reach conclusions as to the
Newtonian nature of blood because some effects tend to decrease the viscosity and others
to increase it. The latter influence on viscosity is due to a small flow, which increases the
viscosity significantly, as well as to the fact that cells often become stuck at constrictions
in small vessels (see [2, 11, 12]).
X 3
∂ui ∂vi
∇u : ∇v = ( )( ).
i,j=1
∂x j ∂xj
∂p ∂p ∂p
∇p = ( , , ).
∂x1 ∂x2 ∂x3
X3 3 3
∂ 2 u1 X ∂ 2 u2 X ∂ 2 u3
∆u = ( , , ).
j=1
∂x2j j=1 ∂x2j j=1 ∂x2j
3
X 3 3
∂v1 X ∂v2 X ∂v3
(∇v)u = (u · ∇)v = ( uj , uj , uj ).
j=1
∂xj j=1 ∂xj j=1 ∂xj
The spaces C(Ω), C k (Ω), C0k (Ω), C0∞ (Ω) and their vector-valued analogues C(Ω), Ck (Ω),
Ck0 (Ω), C∞
0 (Ω) are defined as usual, the superscript indicating continuous derivatives to
a certain order and the subscript zero indicating functions with compact support.
C(Ω) = {u : Ω → R | u is continuous}.
L2 (Ω) is a Hilbert space. We denote by (·, ·) and k · k the associated inner product and
norm in L2 (Ω) respectively,
Z Z
2
(u, v) = uv dx and kuk = u2 dx .
Ω Ω
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 12
The corresponding vector space (Lp (Ω))3 will be denoted by Lp (Ω). We still denote by
(·, ·) and k · k the inner product and norm in L2 (Ω) respectively.
Sobolev spaces Wpk (Ω) (1 ≤ p < ∞) consists of all locally summable functions u : Ω →
R such that for each multiindex α with |α| ≤ k, Dα u exists in the weak sense and belong
to Lp (Ω). It is endowed with the norm denoted by k · kWpk (Ω) ;
XZ 1
kukWpk (Ω) = ( |Dα u|p dx) p ,
|α|≤k Ω
where D0 u = u. The corresponding vector space (Wpk (Ω))3 will be denoted by Wkp (Ω).
If p = 2, we write
H k (Ω) is a Hilbert space. the associated inner product (·, ·)k is defined by
XZ
(u, v)k = Dα u : Dα v dx.
|α|≤k Ω
3
Correspondingly, we set Hk (Ω)=(H k (Ω)) and we still denote its norm by k · kk and its
inner product by (·, ·)k .
We denote by Hk0 (Ω) the completion of C∞ k
0 (Ω) in H (Ω).
For functions depending on space and time, for a given space V of space dependent
functions, we define (for some T > 0)
Z T
2
L (0, T ; V) = {v : (0, T ) → V | v is measurable and kv(t)k2V dt < ∞}
0
RT
with norm kvkL2 (0,T ;V ) =( 0 kv(t)k2V dt)1/2 and
Lp (0, T ; Y)
for 1 ≤ p < ∞.
The space
C(0, T ; Y)
comprises all continuous functions u : [0, T ] → Y with
3.1.3 Preliminaries
In this subsection, we recall some assumptions used in [7, 14], and we are going to make
use of them throughout our analysis. In what follows, Ω is a bounded domain of R3 with
a boundary Γ sufficiently smooth. Γ consists of the artery wall denoted by Γwall and
some artificial sections (see Fig 3.1). The velocity is required to be zero on the artery
wall. To account for homogeneous Dirichlet boundary conditions on the artery wall, we
define
X ≡ {ϕ∈H1 (Ω) : ϕ|Γwall = 0}.
Poincaré’s inequality
kϕk ≤ CΩ k∇ϕk (3.1)
holds for ϕ∈X ([4, 7, 14]). The artificial sections consist of the upstream section on
the side of the heart and the downstream sections on the side of the peripheral vessels.
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 14
Rather than giving serious thought to the artificial sections boundary conditions, in
seeking a variational formulation, the test space is left free on these portions of the
boundary. In this regard, we introduce
as the test space. To prove an existence theorem for a Navier-Stokes problem, either
steady or non-steady, it is convenient to construct the solution as a limit of Galerkin ap-
proximations in terms of the eigenfunctions of the corresponding steady Stokes problem.
This use of the Stokes eigenfunctions originated with Prodi and was further developed
by Heywood [6]. To define the corresponding Stokes operator, we introduce V? as the
completion of V with respect to the norm of L2 (Ω). Then for every f ∈ V? , there exists
exactly one v ∈ V satisfying
Moreover, for each v ∈ V, there exist at most one f ∈ V? , such that (3.3) holds. In this
way, a one-to-one correspondence can be defined between elements f of V? and functions
v belonging to a suitable subspace of V that we denote by D(∆).e The Stokes operator
e : D(∆)
∆ e → V? (3.4)
is defined setting
e =f
− ∆v (3.5)
so that (3.3) is satisfied.
The inverse operator ∆ e −1 is completely continuous and self-adjoint. Therefore it pos-
sesses a sequence of eigenfunctions {ak }∞ k=1 , which are complete and orthogonal in both
V and V? .
In what follows, ci (i = 1, 2, ..) will denote generic constants, not necessarily the same at
different places. The inequalities
1
e 12
sup|v| ≤ c1 k∇vk 2 k∆vk (3.6)
Ω
e
k∇vk ≤ c2 k∆vk (3.7)
e provided that Ω is a bounded domain (see [14] page
are satisfied for every v ∈ D(∆),
178).
Γ2
Γwall
Γ1 Ω
Γ3
Figure 3.1: Artery portion.
Let Ω ⊂ R3 be the artery portion where we aim at providing a detailed flow analy-
sis. For each x ∈ Ω, and any time t > 0, we denote by u(x, t) and p(x, t) the blood
velocity and pressure respectively. The blood density ρ and the blood viscosity µ are all
assumed to be constant. Under these previous assumptions, blood flow can be described
by the Navier-Stokes equations
(
∂u
ρ + ρ(u · ∇)u + ∇ · T = 0
∂t x ∈ Ω, t > 0 (3.8)
∇·u=0
where T is the Cauchy stress tensor, which in the case of a Newtonian fluid reads
T = pI − µ(∇u + (∇u)T )
where I denotes the identity tensor. The equations are expressions of balance of lin-
ear momentum and incompressibility. We are neglecting the presence of any external
forces. Then (3.9) is obtained by substitution of the divergence-free constraint into the
expression for the stress in (3.8)1 .
(
∂u
ρ + ρ(u · ∇)u − µ∆u + ∇p = 0
∂t x ∈ Ω, t > 0 (3.9)
∇·u=0
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 16
In fact
we set
3
X Z
c(t, v) = − Pi (t) n · v ds for each v ∈ H1 (Ω). (3.16)
i=1 Γi
Furthermore, if we define
3
X
Pe = sup |Pi |, K = max Ki , (3.17)
t≥0 1≤i≤3
i=1
where c4 depends on the trace inequality (A.13) and the Poincaré’s inequality (3.1).
The former is a consequence of the trace inequality for solenoidal functions (A.13) and
the proof of (3.19) is given in [14].
and
Z X 3 X3
∂ 2 ui
(∆u, ϕ) = ϕi 2
dx
Ω i=1 j=1
∂x j
Z X 3 Z X 3 X3
∂ϕi ∂ui ∂ui
= − dx + ϕi nj ds
Ω i,j=1 ∂xj ∂xj Γ i=1 j=1
∂xj
Z Z X 3
= − (∇ϕ) · (∇u)dx + ϕi (n · ∇ui )ds
Ω Γ
Z Z i=1
= − (∇ϕ) · (∇u)dx + (n · ∇)u · ϕ ds
Ω Γ
X3 Z
= −(∇ϕ, ∇u) + (n · ∇)u · ϕds.
i=1 Γi
Then we have
((u · ∇)u, ϕ) − (µ∆u, ϕ) + (∇p, ϕ)
X3 Z X3 Z
= ((u · ∇)u, ϕ) − µ(−(∇ϕ, ∇u) + (n · ∇)u · ϕds) + (Pi n) · ϕds
i=1 Γi i=1 Γi
X3 Z X3 Z
+µ (n · ∇)u · ϕds + Ki (u · n)n · ϕds
i=1 Γi i=1 Γi
X3 Z X3 Z
= ((u · ∇)u, ϕ) + µ(∇ϕ, ∇u) + (Pi n) · ϕds + Ki (u · n)n · ϕds
i=1 Γi i=1 Γi
X3 Z X3 Z
= ((u · ∇)u, ϕ) + µ(∇ϕ, ∇u) + Ki (u · n)n · ϕds + Pi n · ϕds.
i=1 Γi i=1 Γi
It follows that
X3 Z X3 Z
((u · ∇)u, ϕ) + µ(∇u, ∇ϕ) = − Ki (u · n)n · ϕds − Pi n · ϕds, (3.25)
i=1 Γi i=1 Γi
since
((u · ∇)u, ϕ) − µ(∆u, ϕ) + (∇p, ϕ) = 0
from (3.24)1 .
We notice that (3.25) does not depend on the pressure p. Therefore the weak formulation
of the problem reads as follow:
Thus
¯X Z ¯ ¯X Z ¯
¯ 3 ¯ ¯ 3 ¯
µk∇un k ≤ |((un · ∇)un , un )| + ¯¯
2
Ki (un · n)n · un ds¯¯ + ¯¯ Pi n · un ds¯¯ .
i=1 Γi i=1 Γi
(3.30)
Together with (3.1), we make use of (3.18) to obtain that
¯ Z ¯
¯X3 ¯
¯ ¯
¯ Pi (t) n · (un )ds¯ ≤ c3 Pekun k
¯ Γi ¯
i=1
≤ c3 CΩ Pek∇un k
≤ c5 Pek∇un k.
Likewise, from (3.19), we have that
¯ 3 ¯
¯X Z ¯
¯ ¯
¯ Ki (un · n)n · un ds¯ ≤ c4 Kk∇un kkun k
¯ Γi ¯
i=1
≤ c4 CΩ Kk∇un kk∇un k
≤ c6 Kk∇un k2 .
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 21
Proof.
Owing to Poincaré’s inequality (3.1), k∇ϕk is a norm equivalent to kϕk1 for all ϕ ∈ V,
therefore (3.32) defines a closed ball in span {a1 , ..., an }. To prove the solvability of the
finite-dimensional problem (3.28), we follow Fujita [3] in using Brouwer’s fixed point
theorem (see Appendix, theorem A.1), applying it to the continuous mapping v → w
defined by the linear problem (k=1,...,n):
X3 Z X3 Z
((v·∇)w, ak )+µ(∇w, ∇ak ) = − Ki (w·n)n·ak ds− Pi n·ak ds. (3.33)
i=1 Γi i=1 Γi
(3.33) is a system of n linear equations. These linear equations are uniquely solvable
if v lies in the ball defined by (3.32), because then w = 0 is the only solution of the
corresponding homogeneous equation (Ki = Pi = 0, 1 ≤ i ≤ 3). In fact, if v satisfies
(3.32) and w satisfies (3.33) with Ki = Pi = 0, we have that
ξk∇wk2 ≤ c7 k∇vkk∇wk2
s
ξ e
4c5 c7 P
≤ c7 1 − (1 − ) k∇wk2
2c7 ξ2
ξ
≤ k∇wk2 .
2
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 22
Together with Poincaré’s inequality (3.1), this imply that w = 0. To see that the
mapping v → w takes the ball defined by (3.32) into itself, suppose that v satisfies
(3.32). Then, similarly to (3.31), we obtain that
c Pe
≤ q 5
ξ 4c5 c7 Pe
2
+ 2ξ (1 − ξ2
)
q
ξ ξ 4c5 c7 Pe
cPe 2
− 2
(1 − ξ2
)
= q 5 q
ξ e 4c5 c7 Pe
2
+ 2ξ (1 − 4c5ξc27 P ) 2ξ − 2ξ (1 − ξ2
)
s
ξ 4c5 c7 Pe
= 1 − (1 − ) .
2c7 ξ2
into itself. The map has at least one fixed point, and any such fixed point is a solution
of (3.28). un is chosen to be any one of these fixed points. Hence Brouwer’s fixed point
has been applied and has given the existence of Galerkin approximations
n
X
un = dkn ak
k=1
satisfying s
ξ e
4c5 c7 P
k∇un k ≤ 1− (1 − ) .
2c7 ξ2
uk j * u.
In other words, bounded sequences in a reflexive Banach space are weakly precompact.
In particular, a bounded sequence in a Hilbert space contains a weakly convergent sub-
sequence.
Together with Poincaré’s inequality (3.1), the fact that the sequence {k∇un k}∞ n=1 is
∞
bounded imply that the sequence {un }n=1 is bounded in V. Therefore we make use of
lemma 3.1 to find that there exists a subsequence {unq }∞ ∞
q=1 ⊂ {un }n=1 , such that
Then we show that the weak limit u is in fact a weak solution. In this respect, we are
going to show that
X3 Z X3 Z
((u · ∇)u, ϕ) + µ(∇u, ∇ϕ) = − Ki (u · n)n · ϕds − Pi n · ϕds
i=1 Γi i=1 Γi
for each ϕ ∈ V.
Fix an integer k, (k = 1, 2, ...). From (3.28), we have the identity
X3 Z X3 Z
((un · ∇)un , ak ) + µ(∇un , ∇ak ) = − Ki (un · n)n · ak ds − Pi n · ak ds.
i=1 Γi i=1 Γi
(3.35)
We recall (3.34), to find upon passing to weak limits that
X3 Z X3 Z
((u·∇)u, ak )+µ(∇u, ∇ak ) = − Ki (u·n)n·ak ds− Pi n·ak ds. (3.36)
i=1 Γi i=1 Γi
Since {ak }∞
k=1 is a basis of V, it follows that
X3 Z X3 Z
((u · ∇)u, ϕ) + µ(∇u, ∇ϕ) = − Ki (u · n)n · ϕds − Pi n · ϕds
i=1 Γi i=1 Γi
for each ϕ ∈ V.
(unq ·∇)unq − (u·∇)u = (unq ·∇)unq + (unq ·∇)u − (unq ·∇)u − (u·∇)u
= (unq ·∇)(unq − u) + ((unq − u)·∇)u.
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 24
and
X3 Z
(∆u, ϕ) = −(∇ϕ, ∇u) + (n · ∇)u · ϕds.
i=1 Γi
Thus
∂u
( , ϕ) + ((u · ∇)u, ϕ) − µ(∆u, ϕ) + (∇p, ϕ)
∂t
∂u X3 Z X3 Z
= ( , ϕ) + ((u · ∇)u, ϕ) + µ(∇ϕ, ∇u) + Ki (u · n)n · ϕds + Pi n · ϕds
∂t i=1 Γi i=1 Γi
∂u
= ( , ϕ) + b(u, u, ϕ) + a(u, ϕ) − c(t, ϕ).
∂t
It follows that
∂u
( , ϕ) + b(u, u, ϕ) + a(u, ϕ) = c(t, ϕ), (3.39)
∂t
where the a, b and c are defined by (3.14), (3.15) and (3.16) respectively, since
∂u
( , ϕ) + ((u · ∇)u, ϕ) − µ(∆u, ϕ) + (∇p, ϕ) = 0
∂t
from (3.38)1 .
We notice that (3.39) does not depend on the pressure p. Therefore the weak formulation
of the problem reads as follow:
where
V = {ϕ∈H1 (Ω) : ϕ|Γwall = 0, ∇ · ϕ = 0}
is the space of test functions.
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 26
and
∂un
( , ak ) + a(un , ak ) + b(un , un , ak ) = c(t, ak ). (3.43)
∂t
Proof.
Assume that un is given by (3.41), we observe using the fact that {ak }∞k=1 is an ortho-
2
normal basis of L (Ω) that
∂un
( , ak ) = (dkn )0 (t), (3.44)
∂t
where (dkn )0 (t) is the derivative of dkn (t) with respect of t.
Furthermore, from (3.14) and the fact that a is a bilinear form, we have
n
X
a(un , ak ) = a( din (t)ai , ak )
i=1
Xn
= din (t)a(ai , ak )
i=1
Xn
= Aki din (t),
i=1
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 27
k
where Bi,j = b(ai , aj , ak ).
Moreover, we set
f k (t) := c(t, ak ).
It follows that (3.43) becomes the system of ODE’s
n
X n
X
0
dkn (t) + k i
Ai dn (t) + k i
Bi,j dn (t)djn (t) = f k (t) (k = 1, ..., n) (3.45)
i=1 i,j=1
subject to the initial condition (3.42). According to standard existence theory for or-
dinary differential equations, there exists a unique function dn (t) = (d1n (t), ..., dnn (t))
satisfying (3.42) and (3.45) for a.e. 0 ≤ t ≤ T . And then un defined by (3.41) solves
(3.43) for a.e. 0 ≤ t ≤ T . ¨
Proof.
We denote by λk the eigenvalue associated to the eigenfunction ak . Multiplying (3.39)
through by −λk dkn and summing over k = 1, ..., n, one obtains that
∂un e e n ) + a(un , −∆u
e n ) = c(t, −∆u
e n ).
( , −∆un ) + b(un , un , −∆u
∂t
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 28
Now
µ ¶
∂un e ∂un
( , −∆un ) = ∇( ), ∇un
∂t ∂t
µ ¶
∂
= (∇un ), ∇un
∂t
1d
= k∇un k2 ,
2 dt
also
3
X Z
e n ) = µ(∇un , ∇(−∆u
a(un , −∆u e n )) + e n )ds
Ki (un · n)n · (−∆u
i=1 Γi
3
X Z
2
e nk −
= µk∆u Ki e n )ds,
(un · n)n · (∆u
i=1 Γi
and
e n ) = −((un · ∇)un , ∆u
b(un , un , −∆u e n ),
furthermore
3
X Z
e n) = −
c(t, −∆u e n )ds
Pi (t) n · (−∆u
i=1 Γi
3
X Z
= e n ds.
Pi (t) n · ∆u
i=1 Γi
It follows that
X3 Z
1d 2 e 2 e e n )ds
k∇un k + µk∆un k = ((un · ∇)un , ∆un ) + Pi (t) n · (∆u (3.47)
2 dt i=1 Γ i
3
X Z
e n ds.
+ Ki (un · n)n · ∆u
i=1 Γi
Furthermore,
e n )≤ sup |un |k∇un kk∆u
((un · ∇)un , ∆u e n k.
Ω
so that
e n k≤Kc2 c4 k∆u
c4 Kk∇un kk∆u e n k2 .
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 30
Lemma 3.2
Let Y be a nonnegative function satisfying the inequality
Y 0 ≤ ηY 3 + ζ
and Y (0) = M0 be a strictly positive real number, then there exists a time interval (0, T ? )
where Y (t) is bounded by a positive constant M and M depends only on M0 , η and ζ
([5]).
Proof.
We have
Y 0 ≤ ηY 3 + ζ
µ ¶3
ζ 1
≤ η Y + ( )3
η
ζ 1
= η(Y + τ )3 where τ = ( ) 3 .
η
We set Z = Y + τ . It follows that
Z 0 ≤ηZ 3 ,
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 31
and so
Z0
≤η.
Z3
We integrate over (0, t), with 0≤t≤T
Z t Z t
Z0
3
dι≤ ηdι,
0Z 0
?
(M0 + ( ηζ ) 3 )−2 − ( ηζ ) 3
T > .
2η
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 32
Proof.
Considering (3.51), the energy estimates (3.46) now reads as:
4 2 e2
d e n k2 ≤ 16c1 k∇un k6 + 2c3 P .
k∇un k2 + κk∆u (3.52)
dt µ3 µ
Since κ>0, (3.52) implies that
d 16c4 2c2 Pe2
k∇un k2 ≤ 3 1 k∇un k6 + 3 . (3.53)
dt µ µ
Defining
Yn (t) = k∇un k2 ,
we see that inequality (3.53) has the following form:
Yn 0 ≤ ηYn 3 + ζ, (3.54)
where η > 0 and ζ > 0 are some constants depending on the data.
Remark 3.2
For each integer n, the function Yn (t) = k∇un k2 verifies the requirements of lemma
3.2 with Yn (0) = k∇u0 k2 because the initial condition is the same for all functions
un , n = 0, 1, 2, ... Consequently, the sequence {k∇un k2 }∞
n=1 is bounded by a real num-
ber M which depends only on the initial data. We make use of Poincaré’s inequality
(3.1) to find that for each integer n,
kun k21 = kun k2 + k∇un k2
≤ CΩ 2 k∇un k2 + k∇un k2
≤ (1 + CΩ2 )k∇un k2
≤ (1 + CΩ2 )M,
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 33
and
Z T?
kun k2L2 (0,T ? ;V) = kun k21 dt
0
≤ (1 + CΩ2 )M T ? , since kun k21 ≤ (1 + CΩ2 )M .
Remark 3.3
The space L2 (0, T ? ; V) being a Hilbert space, lemma 3.1 can be applied to the sequence
∞
{kun kL2 (0,T ? ;V) }∞ 2 ?
n=1 . In fact, the sequence {un }n=1 is bounded in L (0, T ; V). Conse-
∞ ∞
quently, there exists a subsequence {unq }q=1 ⊂ {un }n=1 , such that
We next show that the weak limit u is in fact a weak solution. In this respect, we are
going to show at first that
∂u
( , ϕ) + b(u, u, ϕ) + a(u, ϕ) = c(t, ϕ) for all ϕ ∈ V,
∂t
and thereafter
(u(0), ϕ) = (u0 , ϕ) for all ϕ ∈ V.
where {dk }Nk=1 are given functions and {ak } is the basis of V. We choose n ≥ N ,
multiply (3.43) by dk (t), sum k = 1, ..., N , and then integrate with respect to t to
find that
Z T? Z T?
∂unq
[( , w) + a(unq , w) + b(unq , unq , w)] dt = c(t, w)dt. (3.57)
0 ∂t 0
We recall (3.55), to find upon passing to weak limits (see remark 3.1 and [6]) that
Z T? Z T?
∂u
[( , w) + a(u, w) + b(u, u, w)] dt = c(t, w)dt. (3.58)
0 ∂t 0
Equality (3.58) then holds for all functions w ∈ L2 (0, T ; V) as functions of the
form (3.56) are dense in this space [6]. Hence in particular
∂u
( , ϕ) + b(u, u, ϕ) + a(u, ϕ) = c(t, ϕ)
∂t
for each ϕ ∈ V and a.e. t ≥ 0 .
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 34
2. In order to prove that (u(0), ϕ) = (u0 , ϕ) for every ϕ ∈ V, we first note from (3.58)
that
Z T? Z T?
∂w
[−(u, ) + a(u, w) + b(u, u, w)] dt = c(t, w)dt + (u(0), w(0)). (3.59)
0 ∂t 0
since unq (0)→u0 . As w(0) is arbitrary, comparing (3.59) and (3.61), we conclude
that (u(0), ϕ) = (u0 , ϕ) for each ϕ ∈ V.
Therefore u is a local weak solution of problem 3.1. ¨
Lemma 3.3
Let Y be a nonnegative, absolutely continuous function satisfying inequality
Y 0 + λY ≤ηY 3 + ζ, (3.62)
³ ´ 12
λ
let a real number M be such that 0 < M < 2η ,
λM
If Y (0) ≤ M , and ζ ≤ 2
, then Y (t) is bounded by M for all t > 0 [5] .
Proof.
This result is proven by contradiction. Suppose that there exists a t such that Y (t) > M ,
and define
t? = inf{t∈R+ , Y (t) > M },
we have Y (t? ) = M and Y 0 (t? ) > 0.
and so t? − ² doesn’t belong to the set I. It follows that Y (t? − ²)≤M , and this is
true for each ²>0, hence
Y (t? )≤M.
At the other hand, for each natural number n, we have t? + n1 >t? . We make use of
the fact that t? = inf(I) to see that there exists φn ∈I such that
1
t? ≤φn ≤t? + ,
n
φn is not necessarily unique. We choose one value that φn may take and we denote
it by tn . This defines a real sequence {tn }∞
n=1 .
For each natural number n, since tn ∈I, we have that Y (tn )>M . The fact that
t? ≤tn ≤t? + n1 implies that the sequence {tn }∞ ?
n=1 converges to t . We make use of
the continuity of Y to see that the sequence
{Y (tn )}∞ ?
n=1 converges to Y (t ).
Since tn ∈I for each n, we have Y (tn )>M , and then Y (tn )→Y (t? ) implies that
Y (t? ) ≥ M.
Y (t? ) = M.
Y 0 (t? ) > 0.
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 36
Finally we show that Y 0 (t? ) ≤ 0 and this contradicts the result obtained in (2.).
From (3.62), we have
♦
Theorem 3.5 (Global existence.)
Assume that the initial and boundary data are sufficiently small, precisely
µ ¶ 14 µ ¶ 41
κµ3 µ κ3 µ
k∇u0 k ≤ and Pe < , (3.63)
64c2 c41 4c1 c3 4c32
then for all T ≥ 0, there exists a weak solution u ∈ L2 (0, T ; V) of problem 3.1 and it
satisfies the inequality
µ ¶ 41
κµ3
k∇uk ≤ . (3.64)
64c2 c41
Proof
We recall the energy estimate (3.46)
4 2 e2
d e n k2 ≤ 16c1 k∇un k6 + 2c3 P ,
k∇un k2 + (µ − 2Kc2 c4 )k∆u
dt µ3 µ
κ = µ − 2Kc2 c4 >0.
Set
Yn = k∇un k2 ,
the energy estimate (3.65) takes the form
where
κ 16c41 2c23 Pe2
λ = , η = 3 and ζ = .
c2 µ µ
Also we have
Yn (0) = k∇u0 k2 for each integer n.
Set µ ¶ 12 µ ¶ 12
λ κµ3
M0 = = .
2η 32c2 c41
We choose µ ¶ 12
κµ3 M0
M= =√ ,
64c2 c41 2
it follows that
0 < M < M0 .
According to the hypothesis, we have
µ ¶ 21
κµ3
Yn (0) = k∇u0 k2 ≤ = M,
64c2 c41
³ ´ 14
and from the fact that Pe < µ
4c1 c3
κ3 µ
4c32
, we obtain that
µ ¶ 21
2c2 Pe2 κ κµ3 λM
ζ= 3 ≤ = .
µ 2c2 64c2 c41 2
Remark 3.4
We make use of lemma 3.3 to find that Yn = k∇un k2 is bounded by M for all t > 0 and
the bound doesn’t depend on n. Poincaré’s inequality (3.1) implies that
Proof.
Assume that there exist two solutions u(1) and u(2) associated with the same data. Set
w = u(1) − u(2) . Consider (3.39) with ϕ = w. We have
∂u(1)
( , w) + b(u(1) , u(1) , w) + a(u(1) , w) = c(t, w),
∂t
and
∂u(2)
( , w) + b(u(2) , u(2) , w) + a(u(2) , w) = c(t, w).
∂t
By substraction, we obtain that
∂w
( , w) + a(w, w) = b(u(2) , u(2) , w) − b(u(1) , u(1) , w). (3.66)
∂t
We recall that a is a bilinear form, b is a trilinear form and c is a linear form described
by (3.14), (3.15) and (3.16) respectively. We evaluate every term of (3.66):
∂w 1d
( , w) = kwk2 ,
∂t 2 dt
CHAPTER 3. BLOOD FLOW IN LARGE ARTERIES 39
also
3
X Z
2
a(w, w) = µk∇wk + Ki |w · n|2 ds,
i=1 Γi
and
b(u(2) , u(2) , w) − b(u(1) , u(1) , w)
= b(u(2) , u(2) , w) − b(u(2) + w, u(2) + w, w)
= b(u(2) , u(2) , w) − b(u(2) , u(2) + w, w) − b(w, u(2) + w, w)
= b(u(2) , u(2) , w) − b(u(2) , u(2) , w) − b(u(2) , w, w) − b(w, u(2) , w) − b(w, w, w)
= −b(w, w, w) − b(u(2) , w, w) − b(w, u(2) , w).
It follows that
X 3 Z
1d
kwk2 + µk∇wk2 + Ki |w · n|2 ds = −b(w, w, w) − b(u(2) , w, w) − b(w, u(2) , w).
2 dt i=1 Γi
(3.67)
We now make use of some classical estimates to evaluate the righthand side of (3.67) as
follow:
b(w, w, w) = ((w · ∇)w, w)
Z X 3
à 3 !
X ∂wi
= wj wi dx
Ω i=1 j=1
∂x j
Z X 3
à 3 ! Z
X ∂(wi wj )
= − wi dx + (w · w)(w · n)ds
Ω i=1 j=1
∂xj Γ
Z Z
= − ((w · ∇)w, w) − (w · w)(∇ · w)dx + (w · w)(w · n)ds
Z Ω Γ
and
|b(w, u(2) , w)| ≤ sup |∇u(2) |kwk2 .
Ω
It follows that
µ 1
|b(u(2) , w, w) + b(w, u(2) , w)| ≤ k∇wk2 + (sup |u(2) |)2 kwk2 + sup |∇u(2) |kwk2 .
2 2µ Ω Ω
X 3 Z
1d µ 1
kwk2 + µk∇wk2 + Ki |w · n|2 ds ≤ k∇wk2 + (sup |u(2) |)2 kwk2
2 dt i=1 Γi 2 2µ Ω
+ sup |∇u(2) |kwk2 + c6 kwkk∇wk2 .
Ω
Thus
1d µ 1
kwk2 +µk∇wk2 ≤ k∇wk2 + (sup |u(2) |)2 kwk2 + sup |∇u(2) |kwk2 + c6 kwkk∇wk2 ,
2 dt 2 2µ Ω Ω
Since w(0, x) = 0, there exists T1 > 0 such that kwk ≤ 2cµ6 with 0 < T1 < T ? . On the
interval (0, T1 ), we have
d
kwk2 ≤ ϑ(t)kwk2 , (3.68)
dt
where µ ¶
1 (2) 2 (2)
ϑ(t) = (sup |u |) + 2(sup |∇u |)
µ Ω Ω
Theorem 3.7
There exists a time interval where the solution of problem 3.1 depends continuously on
the prescribed data as the real functions Pi , (i = 1, 2, 3) are varied.
Proof.
(1)
Denote by u(1) the solution associated with the data Pi (i=1,2,3) and, correspondingly,
(2)
by u(2) the solution associated with Pi (i=1,2,3).
Set ¯ ¯
¯ (1) (2) ¯
w = u(1) − u(2) , P = max ¯Pi − Pi ¯ .
i=1,2,3
We make use of (3.39) for u(1) and u(2) with ϕ = w. We obtain that
∂u(1)
( , w) + b(u(1) , u(1) , w) + a(u(1) , w) = c1 (t, w),
∂t
and
∂u(2)
( , w) + b(u(2) , u(2) , w) + a(u(2) , w) = c2 (t, w),
∂t
where
3
X Z
(1)
c1 (t, v) = − Pi (t) n · v ds for each v ∈ H1 (Ω),
i=1 Γi
and
3
X Z
(2)
c2 (t, v) = − Pi (t) n · v ds for each v ∈ H1 (Ω).
i=1 Γi
This gives us
X 3 Z
1d
kwk2 + µk∇wk2 + Ki |w · n|2 ds = −b(w, w, w) − b(u(2) , w, w) − b(w, u(2) , w)
2 dt i=1 Γi
3
X Z
(2) (1)
+ (Pi − Pi ) w · n ds.
i=1 Γi
Also
3
X Z 3
X Z
(2) (1)
(Pi − Pi ) w · n ds ≤ P |w · n| ds
i=1 Γi i=1 Γi
X3 µZ ¶ 21 µZ ¶ 21
2
≤ ci P |w · n| ds where ci = ds
i=1 Γi Γi
3
à 2 Z !
X c2 P
i
≤ + ²i |w · n|2 ds for each ²i ∈ R (A.4)
i=1
4²i Γi
3
X Z
2
≤ c7 P + Ki |w · n|2 ds, where ²i = Ki .
i=1 Γi
It follows that
1d µ 1
kwk2 + µk∇wk2 ≤ k∇wk2 + (sup |u(2) |)2 kwk2 + sup |∇u(2) |kwk2
2 dt 2 2µ Ω Ω
2
+c6 kwkk∇wk2 + c7 P .
Thus
µ ¶
d 1 2
kwk2 +(µ−2c6 kwk)k∇wk2 ≤ (sup |u |) + 2(sup |∇u |) kwk2 +2c7 P . (3.70)
(2) 2 (2)
dt µ Ω Ω
Since w(0, x) = 0, there exists T1 > 0 such that kwk ≤ 2cµ6 with 0 < T1 < T ? . On the
interval (0, T1 ), we have that
µ ¶
d 2 1 2
kwk ≤ (sup |u |) + 2(sup |∇u |) kwk2 + 2c7 P .
(2) 2 (2)
(3.71)
dt µ Ω Ω
It follows that
d 2
kwk2 ≤ c8 kwk2 + 2c7 P ,
dt
where ·µ ¶¸
1 (2) 2 (2)
c8 = sup (sup |u |) + 2(sup |∇u |) .
(0,T1 ) µ Ω Ω
Hence a small change in the given data produces a correspondingly small change in the
solution.
Therefore the solution of problem 3.1 is stable in the interval (0, T1 ) as the real functions
Pi , (i = 1, 2, 3) are varied. ¨
Theorem 3.8
There exists a time interval where the solution of problem 3.1 depends continuously on
the prescribed data as the initial condition u0 (x) is varied.
Proof.
(1)
Denote by u(1) the solution associated with the initial data u0 and, correspondingly,
(2)
by u(2) the solution associated with the initial data u0 .
Set w = u(1) − u(2) .
Consider (3.39) with ϕ = w. We have that
∂u(1)
( , w) + b(u(1) , u(1) , w) + a(u(1) , w) = c(t, w),
∂t
and
∂u(2)
( , w) + b(u(2) , u(2) , w) + a(u(2) , w) = c(t, w).
∂t
By substraction, we obtain that
∂w
( , w) + a(w, w) = b(u(2) , u(2) , w) − b(u(1) , u(1) , w), (3.73)
∂t
and this gives us
X 3 Z
1d
kwk2 + µk∇wk2 + Ki |w · n|2 ds = −b(w, w, w) − b(u(2) , w, w) − b(w, u(2) , w).
2 dt i=1 Γi
(3.74)
We estimate the righthand side of this equality like we did in the case of uniqueness and
we obtain that
X 3 Z
1d 2 2 µ 1
kwk + µk∇wk + Ki |w · n|2 ds ≤ k∇wk2 + (sup |u(2) |)2 kwk2
2 dt i=1 Γi 2 2µ Ω
Thus,
µ ¶
d 1
kwk2 + (µ − 2c6 kwk)k∇wk2 ≤ (sup |u |) + 2(sup |∇u |) kwk2 .
(2) 2 (2)
(3.75)
dt µ Ω Ω
µ
Therefore, on any interval during which kwk ≤ 4c6
, Poincaré’s inequality (3.1)
kwk ≤ CΩ k∇wk
gives that
µ ¶
d µ 1
kwk2 + − (sup |u |) − 2(sup |∇u |) kwk2 ≤0.
(2) 2 (2)
(3.76)
dt 2CΩ2 µ Ω Ω
It follows that
d
kwk2 ≤ −c7 kwk2 ,
dt
where µ ¶
µ 1 (2) 2 (2)
c7 = sup − (sup |u |) − 2(sup |∇u |) ,
J 2CΩ2 µ Ω Ω
Hence a small change in the given data produces a correspondingly small change in the
solution.
Therefore, the solution of problem 3.1 is stable in the interval J as the initial condition
u(x, 0) = u0 (x), x ∈ Ω
is varied. ¨
Chapter 4
Conclusion
This work has reviewed the basic physiology of the cardiovascular system, and described
the anatomy of blood and some cardiovascular equations. The main emphasis was placed
on the blood circulation through the large arteries. The problem of modelling blood
flow as well as some simplifying assumptions were discussed. We established the weak
formulation of the considered boundary value problem for both stationary case and
nonstationary case. Then we showed that the weak formulation did not depend on the
blood pressure. Rather than giving serious thought to the artificial sections boundary
conditions, in seeking a variational formulation, the test space was left free on these
portions of the boundary. For this purpose, we introduced
V ≡ {ϕ∈H1 (Ω) : ϕ|Γwall = 0, ∇ · ϕ = 0}
as the test space. The Stoke’s operator ∆e was defined, we made use of the fact that its
inverse ∆e is self adjoint and possesses a sequence of eigenfunctions which is orthogo-
−1
nal in the space of test functions V and orthonormal in L2 (Ω), to derive some helpful
estimates. We employed galerkin’s method by first solving the problem in some finite
dimensional spaces, then we were able to construct a sequence of finite dimensional so-
lutions, and showed that this sequence weakly converged by considering a compactness
argument. In this regard, we made use of Brouwer’s fixed point theorem in the case of
the stationary problem to prove the existence of Galerkin approximations. When con-
sidering nonstationary problem, we made use of an existence theorem from the theory of
ordinary differential equations. An energy estimate was derived as well, this helped us to
prove the local existence of a weak solution. Later on, we proved that the weak limit of
the Galerkin approximantions was indeed a weak solution of the initial/boundary value
problem.
We moved on to prove the uniqueness of a local solution and its continuous dependence
upon the data. Gronwall’s inequality was useful in the proof of the uniqueness and the
stability of the results.
Blood is a very complex fluid in its nature. It is not homogeneous and consists of plasma
and corpuscules. Its flow properties are uniquely adapted to the architecture of the blood
45
CHAPTER 4. CONCLUSION 46
vessels. In the large arteries, whole blood can be approximated as a Newtonian fluid. In
the future, we are going to consider the shear thinning viscoelastic nature of blood for
more accuracy and this will lead us to the reformulation of the initial boundary value
problem described in this dissertation.
Appendix A
appendix
In this section, we gather in one place the results that are continually employed through-
out the dissertation.
uk → u,
if
limk→∞ kuk − uk = 0.
Definitions.
A sequence {uk }∞
k=1 ⊂ X is called a Cauchy’s sequence provided for each ² > 0 there
exists N > 0 such that
kuk − ul k < ² for all k, l ≥N.
47
APPENDIX A. APPENDIX 48
is continuous, where B(0, 1) denotes the closed unit ball in X. Then u has a fixed point;
that is, there exists a point x ∈ B(0, 1) with
u(x) = x.
Definition. A Hilbert space H is a Banach space endowed with an inner product which
generates the norm.
Definitions. (i) Two elements u, v ∈ H are orthogonal if (u, v) = 0.
(ii) A comptable basis {wk }∞ k=1 ⊂ H is called orthonormal if
(wk , wl ) = 0 (k, l = 1, ...; k 6= l) and kwk k = 1 (k = 1, ...).
If u ∈ H and {wk }∞
k=1 ⊂ H is an orthonormal basis, we can write
∞
X
u= (u, wk )wk ,
k=1
< u? , u >
to denote the real number u? (u). The symbol < , > denotes the pairing of X ? and X.
We define
ku? k := sup{< u? , u > | kuk ≤1}.
A Banach space is reflexive if (X ? )? = X. More precisely, there exists u ∈ X such that
uk * u,
if
< u? , uk >→ < u? , u >
for each bounded linear functional u? ∈ X ? .
uk → u implies that uk * u.
Any weakly convergent sequence is bounded. In addition, if uk * u, then
2 b2
ab ≤ ²a + (a, b ∈ R, ² > 0). (A.4)
4²
Proof.
b b2
0 ≤ (²a − )2 ≤ ²2 a2 − ²ab + .
2 4
APPENDIX A. APPENDIX 51
Then
b2
²ab ≤ ²2 a2 + .
4
Hence
2 b2
ab ≤ ²a + .
4²
♦
ap bq
ab ≤ + (a, b > 0). (A.5)
p q
Consequently
1 ²
±(x, y)X ≤ kxk2X + kyk2X .
2² 2
kxkX
Minimize the right hand side by setting ² = kykX
, provided y 6= 0. ♦
APPENDIX A. APPENDIX 52
Proof.
By homogeneity, we may assume kukLp (U ) = kvkLq (U ) = 1. Then Young’s inequality
implies that for 1 < p, q < ∞
Z Z Z
1 p 1
|uv|dx ≤ |u| dx + |v|q dx = 1 = kukLp (U ) kvkLq (U ) .
U p U q U
T : W 1,p (U ) → Lp (∂U )
such that \
(i) T u = u|∂(U ) if u ∈ W 1,p (U ) C(U )
and
(ii) kT ukLp (∂U ) ≤ CkukW 1,p (U ) , (A.12)
for each u ∈ W 1,p (U ), with the constant C depending only on P and U .
Definition. T u is called the trace of u on ∂U .
1. If
n
k < ,
p
then u ∈ Lq (U ), where
1 1 k
= − .
q p n
We have in addition the estimate
kukLq (U ) ≤ C kukWpk (U ) ,
H 2 (U ) ⊂ C(U ). (A.16)
f −1 (U ) ∈ M
fk → f a.e. on A,
where A ⊂ Rn is measurable, |A| < ∞. Then for each ² > 0 there exists a measurable
subset E ⊂ A such that
(i) |A − E| ≤ ²
and
(ii) fk → f uniformly on E.
provided at list one of the terms on the right hand side is finite. In this case, we say f
is integrable.
Definition.
A measurable function f is summable if
Z
|f | dx < ∞.
Rn
APPENDIX A. APPENDIX 56
f : [0, T ] → X
and Z Z
T T
?
<u , f(t) dt > = < u? , f(t) > dt
0 0
? ?
for each u ∈ X .
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