University in Ljubljana

Faculty of Mathematics and Physics

POSTGRADUATE SEMINAR
Blood Flow
Barbara Grobelnik
advisor: doc. dr. Igor Sersa
The Jozef Stefan Institute
Ljubljana, January 2008
Abstract
The understanding of blood ow dynamics is of a major importance in the study of
the vascular diseases development and in the design of the prosthetic or extra-corporeal
ow devices. The mathematical description of blood ow can be very complicated, yet
some simplied models provide quite good understanding of the behavior of blood when
owing through the vessels.
Contents
1 Introduction 3
2 Cardiovascular Physiology 3
3 Physical properties of Blood 4
3.1 Viscosity of plasma and of whole blood . . . . . . . . . . . . . . . . . . . . . . . 4
3.2 Fahraeus-Lindqvist Eect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
4 Steady Blood Flow 6
4.1 Poiseuilles equation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
4.2 Entrance length . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
4.3 Bernoullis equation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
4.4 The vascular resistance and branching . . . . . . . . . . . . . . . . . . . . . . . 10
4.5 Turbulent ow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
5 Oscillatory Blood Flow 12
5.1 Windkessel Theory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
5.2 Wommersley Equations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
6 Conclusion 16
2
1 Introduction
The study of the behavior of blood ow in the blood vessels provides understanding on con-
nection between ow and the development of dieseases such as atherosclerosis, thrombosis,
aneurysms etc. and how the ow dynamics is changed under these conditions. The under-
standing of the ow dynamics past prosthetic devices such as heart valves, vascular grafts
and articial hearts will help improving the design of the implants. The functioning of several
extra-corporeal ow devices such as blood oxygenators and dialysis machines, which are com-
monly used in modern medicine, can be improved if blood ow behavior through the devices
is well understood.
This seminar consists of a short review of cardiovascular physiology and a description of
blood physical properties, mainly of blood viscosity and its behavior in blood ow through
vessels. The following chapter deals with the steady blood ow. The Poiseuille equation,
which describes the laminar ow in a rigid straight circular tube, is applied to explain the
entrance eects and branching in the blood ow in vessels, whereas in ow through constric-
tions and aneurysms can be described well by the Bernoulli equation. In the nal part of the
seminar a brief introduction into the oscillatory blood ow is given.
2 Cardiovascular Physiology
The cardiovascular system includes the heart, blood
and blood vessels of the systemic and pulmonary cir-
culation. The ow of blood from the left ventricle into
the aorta then to the peripheral regions of the body
and back to the right atrium is dened as the sys-
temic circulation. The arteries and arterioles carry the
oxygenated blood to the capillaries in the tissues and
the deoxygenated blood returns to the right atrium
through the venules and the veins. Blood ow from
the right ventricle into the lungs and back to the left
atrium is dened as the pulmonary circulation.
Blood receives oxygen in the lungs and nutrients in the
intestine and delivers them to the cells in all parts of
the body. The circulating blood also removes cellular
wastes and carbon dioxide from the cells for excetion
through the kidneys and the lung. It maintains the
visceral organs (brain, kidney, liver...) at a constant
temperature by convecting the heat generated and dis-
sipating the same through transfer across the skin. It
stabilizes the body temperature and pH.
Fundamental requirements of the circulatory system are to provide adequate blood ow with-
out interruption and to regulate blood ow according to the various demands of the body.
The contracting heart supplies the energy required to maintain the blood ow through the
vessels. The pressure gradient developed between the arterial and the venous end of the
circulation is the driving force causing blood ow through the vessels.
3
3 Physical properties of Blood
The whole blood consists of formed elements that are suspensed in plasma. The plasma is a
dilute electrolyte solution containing about 8% by weight of proteins. About 45% by volume
of whole blood consist of formed elements and about 55% of plasma in the normal human
blood. The formed elements of blood are red blood cells (95%), white blood cells (0.13%) and
platelets (4.9%). The diameter of red blood cell is about 8.5 m at the thickest portion and
about 1 m at the thinnest portion. Its membrane is exible and the cell can pass through
capillaries of diameter as small as 5 m assuming a bent shape.
3.1 Viscosity of plasma and of whole blood
The viscosity of blood and plasma varies with samples due to the variations in species as well
as in various constituents like protein and red blood cells between samples. The viscosity
of a uid is also strongly dependent upon its temperature. In general, viscosity of liquids
decreases with increasing temperature.
Human plasma has a density of about 1035 kg/m
3
and its viscosity coecient ranges be-
tween 1.1 and 1.610
3
Pa s (the viscosity of water is 110
3
Pa s). The presence of plasma
proteins results in the higher viscosity compared to water.
Whole blood has a density of about 1056 kg/m
3
. From experimental measurements it has
been determined that blood behaves as a Newtonian uid
1
only at high shear rates (v/y
100 s
1
). For ow in large arteries where the shear rate is well above 100 s
1
, a value of
3.5 10
3
Pa s is often used as an estimate for the viscosity of blood. In smaller arteries and
in the capillaries, where the shear rate is very low, blood must be treated as a non-Newtonian
uid. At low rates of shear, the red blood cells tend to aggregate and thus exhibit an increase
in viscosity. As the shear rate increases, the aggregates break up. At shear rates higher than
50 s
1
, the viscosity approaches the above mentioned asymptotic value.
The whole blood follows the non-linear relationship between the shear stress and the strain
in the form of Cassons equation

0
+ K
c

dv
dy
The high shear stress can destroy or activate red blood cells and plateletes. Hemolysis of red
blood cells will result in the release of hemoglobin into the plasma, a possible consequence
is then anemia where the blood cannot transport a sucient amount of oxygen to tissues.
Platelet activation can trigger the formation of thrombus within a vessel.
3.2 Fahraeus-Lindqvist Eect
It was observed that in very small diameter tubes the apparent viscosity of blood has a very
low value. The viscosity increases with the increase in tube diameter and approaches an
asymptotic value at tube diameters larger than about 0.5 mm. This phenomenon is reered
to as the Fahraeus-Lindqvist eect. As the blood ows through a tube, the blood cells tend to
1
A Newtonian uid is the one in which the viscosity is constant. In reality, many uids do not follow
the ideal linear relationship between the viscous shear stress and the shear rate. Here, the viscosity is not a
constant, but depends on the shear rate at which it is measured.
4
Figure 1: The variation of the blood viscosity with the tube diameter, illustrating the Fahraeus-Lindqvist
eect. The blood viscosity increases along with the tube diameter above about 9.0 m and also varies with
changes in hematocrit (this is a measure of the proportion of blood volume that is occupied by red blood cells).
When the tube diameter is comparable to the size of blood cells (8 m), the blood viscosity has its minimum
and begins to increase with further decreasing of the vessels diameter.[1]
rotate and move towards the center of a tube. Hence, a cell-free layer exists near the wall. In
tubes with small diameter, the area of the cell-free zone is comparable to the central core. The
net eect of the cell-free zone with a lower viscosity (viscosity of plasma alone) is to reduce
the apparent viscosity of ow through the tube. As the tube diameter increases, the eect of
the cell-free zone reduces and the viscosity coecient approaches the asymptotic value. Two
mathematical models have been developed to describe the Fahraeus-Lindqvist eect and are
considered in the next subsection.
Cell-free marginal layer model
The tube cross-section can be divided into a core region and a cell-free plasma region near
the wall. The governing equations for both the regions are

p
L
=
1
r
d
dr
(
c
r
dv
c
dr
), 0 r R

p
L
=
1
r
d
dr
(
p
r
dv
p
dr
), R r R
The boundary conditions to obtain the solution for the two dierential equations are that the
velocity gradient is zero in the tube center, no slip occurs at the tube wall and the velocity
and the shear stress are continuous at the interface between the two zones. The expression
for the volume ow is therefore equal to
Q =
R
4
p
8L
1

p
_
1 (1

R
)
4
(1

p

c
)
_
Comparison with the viscosity which applies in the Poiseuille law (Q = R
4
p/8L) yields
eective viscosity
=

p
1 (1

R
)
4
(1

p

c
)
The Sigma eect theory is based on a hypothesis that when blood ows through a small
5
diameter tube, the assumption of continuum is not valid. Assume that the tube diameter is
so small that there is room only for N red blood cells to move abreast. Then the velocity
prole will not be continuous and will consist of concentric laminae. The expression for the
volume ow can be rewritten as
Q = 2
_
R
0
v(r)rdr =
_
R
0
d[v(r)r
2
]
_
R
0
r
2
dv
dr
dr
Applying no slip condition at the wall, rst integral is identically equal to zero. The expression
for the velocity gradient is given by
dv
dr
=
pr
2L
so
Q =
p
2L
_
R
0
r
3
dr
If we assume that the ow occurs in N concentric laminae, each of thickness , the integral
can be replaced by summation as
Q =
p
2L
N

n=1
(n
3
) =
pR
4
8L
(1 +

R
)
2
Thus, the apparent viscosity can be given by the formula

app
=

(1 +

R
)
2
4 Steady Blood Flow
In this section we will discuss some applications of hydrostatics and steady ow models to
describe blood ow in arteries. Although the ow in the human circulatory system is unsteady,
particulary at the precapillary level, steady ow models provide some insight into the aspects
of ow through the arteries. As can be expected, steady ow models are simpler to use because
of the absence of time variations in the governing equations. They also avoid the complexity
of the moving interface between the blood and the vessel wall as the artery distends with the
pulse pressure.
4.1 Poiseuilles equation
In considering a vascular system with its contained blood, we are naturally concerned with
the physical laws governing the ow of liquids through solid tubes. The simplest example is
that of a straight, uniform, rigid tube with a steady rate of non-turbulent liquid ow through
it. To maintain such a steady ow, there must be a constant head of pressure applied to
the liquid because of its viscosity. Steady ow in a rigid cylindrical tube is described by the
Poiseuille equation, its derivation is given below.
Consider a thin cylindrical liquid shell of thickness r, inner radius r and length L; its axis z
is coincident with the tube axis, and the velocity v is parallel to the axis everywhere, and is
a function of the distance r from this axis. The force exerted by the pressure on the end of
the cylindrical shell is the pressure multiplied by the cross-sectional area minus the force on
the distal end, so that
F
p
= (p
1
p
2
)2r r
6
Figure 2: 1. A thin cylindrical liquid shell of thickness r, inner radius r and length L for the derivation of
the Poiseuille equation. 2. The velocity prole in steady laminar ow.[1]
The retarding viscous force on the inner surface can be written as
F
visc
=

r
(
v
r
2rL)r
Equating these, we obtain

2
v
r
2
+
1
r
v
r
+
(p
1
p
2
)
L
= 0
The solution of the upper equation can be written in the form of
v(r) = r
2
(p
1
p
2
)
4L
+ Alnr + B
Since the velocity of the liquid must be nite at the axis, A = 0. The solution for B, due to
zero velocity at the wall, is B = R
2
(p
1
p
2
)
4L
. Finally, the expression for veloctiy prole is
v(r) =
(p
1
p
2
)
4L
(R
2
r
2
)
This is the equation for the parabola, where v = 0 when r = R and v is maximum at the axis
of the tube, when r = 0. To obtain the volume ow, it is necessary to determine the volume
of the paraboloid which has this parabola as its prole. The volume ow is
Q =
_
R
0
2v(r)rdr = R
4
(p
1
p
2
)
8L
This is commonly reered to as the Poiseuille equation. The volume ow is related to the
fourth power of radius, therefore, ow increases exponentially with increase in internal radius.
The average velocity v of the liquid across the tube is obtained by dividing the volume ow
Q by the cross-sectional area R
2
, so that
v =
Q
R
2
= R
2
(p
1
p
2
)
8L
=
1
2
v
r=0
=
v
max
2
Thus the average velocity is half the axial velocity.
Several assumptions in deriving the Poiseuille law were made and the validity of these as-
sumptions in models describing blood ow should be critically examined. The conditions
under which Poiseuilles equation applies are the following:
7
1. The liquid is homogeneous with constant viscosity. Blood is a suspension of particles,
but, in tubes in which the internal diameter is large compared with the size of the red
blood cells, it behaves as a Newtonian liquid. In small vessels with an internal radius
less than 0.5 mm, changes in viscosity occur (compare Section 3.1).
2. The liquid does not slip at the wall. This is the assumption that velocity is zero when
r = R. The inner most lining of the arterial wall in contact with the blood is a layer of
endothelial cells and it is reasonable to assume no slip at the interface.
3. The ow is laminar (the liquid is moving parallel to the walls of the tube). There is no
experimental evidence of sustained turbulence in the human circulation in the absence
of diseased states.
4. The rate of ow is steady. As the ow in all large arteries is markedly pulsatile, it is
clear that Poiseuilles equation cannot be applied in these vessels.
5. The tube is long compared with the region being studied. Close to the inlet (or entrance)
of a tube, ow has not yet become established with the parabolic velocity prole (Section
4.2). Similarly, the ow passes through branching points and curved sections, where the
ow is appropriately altered. Clearly, the assumption of fully developed ow is not
valid.
6. The tube is cylindrical in shape. Most arteries of the systemic circulation are circular
in cross-section, but many veins and the pulmonary arteries tend to be elliptical. The
requirement of parallel walls is probably never exactly met in blood vessels because
individual arteries taper (i.e. become narrower) as they progress toward the periphery.
7. The tube is rigid; the diameter does not vary with the internal pressure. Blood vessels
are viscoelastic structures, and their diameter is a function of pressure. The interaction
between the distensible arterial wall and the owing blood is an important factor in the
description of the ow dynamics.
4.2 Entrance length
As uid enters a pipe from a reservoir, the velocity prole will be relatively at and the uid
must pass through a nite length in the tube before the velocity prole will attain a parabolic
shape. At the entrance, the uid coming in contact with the tube wall will be forced to have
zero velocity due to the no slip condition and the velocity gradient is established in the radial
direction. As the uid moves downstream, more and more uid is retarded due to shearing
of uid adjacent to the wall, meanwhile the uid in the core region is accelerated to maintain
the same ow rate, resulting in a parabolic velocity prole further downstream. Very near
the entrance, the radial distance in the uid in which the viscous eects are present, is very
thin (the thickness to which this diusion has occured is referred to as the boundary layer).
As we proceed downstream the viscous eects have diused further in the radial direction.
The ow becomes fully developed,when the boundary layer has grown to the centerline of the
tube. An estimation of the length along the tube beyond which the ow is fully developed
(entrance or inlet length) is given below. A small uid element within the boundary layer is
considered in Fig. 3.
8
Figure 3: Flowing blood that enters the ow channel has initially at velocity prole. After the distance
from the entrance known as the entrance length (z
0
) a parabolic velocity prole is established.[8]
The net viscous force on the area will be the area times the change in stress with the distance
r from the wall and will be given by
F
visc
=
d
dr
(
dv
dr
)A(r
2
r
1
)
A solution of the governing equations in the boundary layer is too complicated to be solved
analytically. To obtain an estimate of the viscous forces, the boundary layer thickness at
the distance z from the entrance and the free stream velocity U are used.
F
visc
=
U

2
A(r
2
r
1
)
The viscous forces must be balanced by the inertial forces on the element.
F
i
= aV =
U
2
z
A(r
2
r
1
)
If the boundary layer thickness is considered at a distance z from the entrance of the tube,
then the time scale for the uid to reach that distance is z/U. The acceleration at this location
is then proportional to U/(z/U) or U
2
/z. Equating these two scaled forces, we obtain

U
2
z
= k
U

2
,
where k is the proportionality constant that can be derived from the experiments. The
boundary layer thickness at any axial location can be written as

_
z
U
From the above relationship can be seen that the boundary layer is proportional to the square
root of the entrance distance. The boundary layer extends over the whole tube and the ow
becomes fully developed when the boundary layer thickness is equal to D/2, where D is the
diameter of the tube. The entrance length is be given by
z
0
= kD
2
U

= kD
_
UD

_
= kDR
e
where the term in the parenthesis represent the Reynolds number. The magnitude for the
constant k has been determined experimentally to be approximately 0.06.
9
4.3 Bernoullis equation
The Poiseulle equation derived previously considered only the force due to the pressure gra-
dient and viscous forces. In ow through constrictions and across orices, the application of
Bernoullis equation is useful. With the assumption of steady ow of incompressible inviscid
uid, the Bernoullis equation is given by the relationship
p + gz +
1
2
v
2
= constant
Constriction in the circulatory system
If a cross-section of a vessel is narrowed, from the principle of conservation of mass
A
1
v
1
= A
2
v
2
follows, that the velocity through a narrow segment will increase. If the
cross-sections under consideration are relatively near to each other, we can neglect the
eect of the viscous dissipation and apply the Bernoulli equation. Since the gravitational
forces are also negligible, the relationship reduces to
p
1
+
v
2
1
2
= p
2
+
v
2
2
2
In the considered case, the pressure at the narrowed part will be substantially lower,
which may result in caving in or even completely closening of the vessel. Then the
ow velocity will slow down due to the frictional resistance, the kinetic energy will be
converted to pressure and the vessel will reopen. This phenomenon will repeat itself
causing the uttering of the vessel.
Pressure rise in an aneurysm
An aneurysm is caused by the weakening of the arterial wall where a bulge occurs and
the cross-section of a vessel increases considerably. An analysis as before will show that
the ow velocity will be reduced at the cross-section of an aneurysm and the pressure
will increase. The higher pressure may cause further expansion of the cross-section,
which can lead to the bursting of the vessel at that site.
4.4 The vascular resistance and branching
The vascular resistence is given as the pressure dierence over the volume ow.
R
v
=
p
Q
From the Poiseuille expression for the volume ow through a tube we obtain a relationship
R
v
=
8L
R
4
A small change in the radius of the wessel will aect the resistance to ow considerably.
The mean arterial pressure is normally about 100 mmHg and has fallen very little in the
smallest arteries. In the capillaries it is generally agreed to be about 30 mmHg at the arterial
end and about 15 mmHg at the venous end. The pressure in large veins will only be a few
mmHg. Most of the fall (up to 60 mmHg) will occur in arterioles less than 200 m in diam-
eter. As the resistance is proportional to the drop in mean pressure, it is apparent that the
resistance of the arterioles constitutes the largest proportion of whole. With the alteration of
muscle tension, which is controlled by the autonomic nervous system, the arterioles can be
10
distended or contracted selectively to vary the amount of ow into the various segments of
the body.
Changes in the lumen of arteries are virtually all associated with the occurence of branches.
These branches are narrower than the parent trunk, but the total cross-section area nearly
always increases with succesive branching. A change in the size of a channel will aect the
ow rate, the Reynolds number and the pressure gradient
2
.
Figure 4: A junction with two branches of equal radii (R
2
, R
3
) and velocity (v
1
, v
2
).[1]
Take a main vessel, cross-sectional area A
1
, that divides into n branches of equal size and
each of cross-sectional area A
1
. The total cross-section area changes by a factor d so that
dA
1
= nA
2
, d 1. The volume ow Q = vR
2
into and out of the system must be equal, so
v
1
v
2
=
nR
2
2
R
2
1
= d,
where v
1
and v
2
are the mean velocities. The mean velocity of ow in the branches will be
less by a factor of d whatever the numbers of branches
3
. In addition, the Reynolds number
in the branches will be less that in the main artery.
Comparing the pressure gradients (Q = R
4
p/8) in the main trunk and the branches we
obtain
p
1
p
2
=
nR
4
2
R
4
1
=
d
2
n
from which we see that for steady ow the pressure gradient remains the same only if d = n
1/2
.
The average value for d that is often quoted is 1.26 and the minimum value of n is 2, so the
pressure gradient increases.
2
Following simple derivation applies generally in the venous system and approximately in small arteries,
whereas in the larger arterias pressure-ow relationships are quite dierent due to the pulsatile nature of the
ow.
3
For example, in the dog the mean blood ow velocity in the aorta is 15-20 cm/s, in the femoral artery
about 10-12 cm/s and in the capillaries about 0.05 cm/s, which implies that the cross-section area in femoral
artery level has increased by about 50% and in the capillaries the increase is 300-400 times that of the aorta
(such generalizations are only approximate).
11
4.5 Turbulent ow
The critical point where the ow becomes turbulent can be expressed by a dimensionless
quantity known as Reynolds number, which, when applied to liquid ow in a circular tube, is
Re =
vD

where v is the mean velocity of ow, D is the diameter of the tube, is the density of the
liquid and its dynamic viscosity. The critical value of Reynolds number is usually stated as
about 2000. It should be emphasized that ow in the circulatory system is normally laminar,
although ow in the aorta can destabilize briey during the deceleration phase of late systole;
however, this time period is generally too short for ow to become fully turbulent. Turbulent
ow may occur in large blood vessels, but the distensible vessel wall and arterial narrowing
diminish the disturbances in ow. Certain disease conditions can produce turbulent blood
ow, particularly downstream of a vessel narrowing or distal to defective heart valves. Such
a ow can damage the vessel wall and contribute to the further progression of a disease.
5 Oscillatory Blood Flow
The steady ow models considered in previous section provided some insight on the ow
through the vessels, however, more realistic models need to be taken into account due to the
unsteady nature of ow through the arteries. The pressure pulse, generated by the contraction
of the left ventricle travels with a nite speed through the arterial wall, which is much greater
than the blood velocity in vessels. The speed of transmission is dependent on the wall elastic
properties as well as on the interaction between the wall and blood. The pressure pulse also
changes shape as it travels downstream due to the interaction between the forward moving
waves and the waves reected at discontinuities in the arterial system such as branching
and curvature sites. The governing equations for oscillatory blood ow considering all above
mentioned characteristics can be very complicated. The detailed knowledge of pulsatile ow
through the vessels is beyond our interest, therefore we will consider only two simplied
models.
5.1 Windkessel Theory
Early theories to describe the blood ow in circulation described the arterial system to be
elastic storage vessels, which transformed the discontinous ow due to the pumping of the
heart into steady ow in the peripheral organs. The windkessel theory considers the arteries as
a system of interconnected tubes with a storage capacity. The uid is pumped into windkessel
chamber by the ventricular injection and the outow at the other end is based on the pressure
gradient and the resistance to ow. The storage capacity of the elastic blood vessels is given
by the distensibility D
i
= dV/dp, where V is the volume and p is the pressure. The rate of
storage of volume in the elastic chamber can be written as
dV
dt
=
_
dV
dp
_
dp
dt
= D
i
dp
dt
A mass balance for the uid in the elastic chamber (Inow - Outow = Rate of Storage) is
given by
Q(t)
p p
V
R
V
= D
i
dp
dt
12
The outow is represented by the drop in pressure (p p
V
) over the peripheral vascular
resistance R
V
and when the venous pressure, p
V
, is neglected, reduces to p/R
V
. The simplest
assumption on the inow is
Q(t) =
_
Q
0
, 0 t t
s
0, t
s
t T
where t
s
is the time at the end of systole and T is the duration of the cardiac cycle. Then
the equation for systole can be written as
dp
dt
+
p
R
s
D
i
=
Q
0
D
i
with the inital condition p = p
0
at t = 0. Integrating the above equation, we obtain
p(t) = R
s
Q
0
(R
s
Q
0
p
0
)e
(t/R
s
D
i
)
During diastole, the equation reduces to the form,
dp
dt
=
p
R
s
D
i
with the condition that the pressure at the end of diastole is equal to p
T
(p = p
T
at t = T),
which yields
p(t) = p
T
e
(Tt)/R
s
D
i
Figure 5: 1. A typical pressure pulse curve assuming constant volume ow Q
0
at t 1.43 s and no ow at
1.43 s 3 s. The duration of the cycle is 3 s, the length of systole is 1.43 s, and the maximum pressure is p
0
.
2. A ow velocity pulse (Q) and the arterial pressure pulse (P) recorded simultaneously in the femoral artery
of a dog.[1]
The pressure pulse curve obtained in Windkessel model is far from the actual pulse shape
(Fig. 5.1). A ow velocity pulse and the arterial pressure pulse are similar in shape when
plotted on a comparable scale, but the fact, that the peak ow occurs before the pressure
peak, shows that there is no simple relation between these two curves. The ow is, in fact,
determined by the pressure gradient.
13
5.2 Wommersley Equations
The equation for the motion of a viscous liquid in laminar ow in a tube of circular cross-
section with radius R in its general form for an incompressible liquid is

2
w
r
2
+
1
r
w
r
+
1

p
z
=

w
t
Following common convention, the axis of the tube is taken as the z axis and the velocity in
the direction of that axis is w (the velocities in the x and y axes for a rigid tube are both
zero). The coecient of viscosity is and the density of the liquid is . The form of the
pressure gradient is taken as a simple harmonic motion
4
and written in complex form.
p
z
= A

e
it
With this substitution and w = ue
it
we obtain
d
2
u
dr
2
+
1
r
du
dr

i

u =
A

This is a form of Bessels equation, and its solution, appropriate to the boundary conditions,
can be written as
u =
A

i
_
1
J
0
[r
_
(/)i
3/2
]
J
0
[R
_
(/)i
3/2
]
_
where an expression of the form J
0
(xi
3/2
) is a Bessel function of the rst kind of order
zero and complex argument. The quantity R
_
(/) is a non-dimensional parameter that
characterizes kinematic similarities in the liquid motion and it is written as the symbol .
The radius is also made non-dimensional by substituting the fractional radius, y = r/R. The
solution for the velocity w is then
w =
A

R
2
i
2
_
1
J
0
(yi
3/2
)
J
0
(i
3/2
)
_
e
it
The Womersley number, , in unsteady ow has a signicance similar to that of Reynolds
number in steady ow. It provides a comparison between unsteady inertial forces and viscous
forces. In the human circulatory system, ranges from 10
3
in capillaries to 18 in aorta in
rest. When 1, viscous forces dominate in every region in the tube (known as quasi-steady
ow). As increases, the inertial forces become more important and start to dominate,
initially at the center of the tube. As a result, a delay with respect to the driving pressure
gradient can be observed in the bulk ow, and the velocity prole becomes at in the central
region of the tube.
The forms of the velocity prole created by a pressure which oscillates sinusoidally are pre-
sented in Fig. 6. The pressure gradient is assumed to be in form cos t. The angular frequency
t is respectively in the ratio 1,2,3 and 4, which gives the values in the ratios of the square
roots (1,

2,

3 and 2). The actual values used were taken from an experiment on the
femoral artery of a dog in which the pulse rate was 2.8 Hz. It can be seen from the illustra-
tions that, even at the lowest frequency shown, a true parabolic prole is not formed at any
4
Any periodic function, such as the arterial pulse, can be represented with the aid of the Fourier series.
14
Figure 6: The velocity proles, at intervals of 15

, of the ow resulting from a sinusoidal pressure gradient

(cos t) for the rst four harmonics of the ow curve (:3.34, 4.72, 5.78 and 6.67). Only half a cycle is
illustrated because with simple harmonic motion the second half is inverted form of the rst half.[1]
time. There is a phase lag between the applied pressure and the movement of the liquid: the
amplitude of the pressure gradient is a maximum at 0

, while the maximum for the total ow

integrated across the tube is about 60

in example 1.A, and about 77

in example 1.D. The

laminae that move rst are those nearest the wall; since they always have a low velocity owing
to the eect of viscosity, they can reverse easily. As we move towards the axis of the tube,
the momentum becomes progressively higher relative to viscous drag, so there is a greater lag
between the pressure gradient and the movement of the liquid. The liquid begins to behave
rather like a solid mass sliding inside a thin layer of viscous liquid surrounding it.
As the frequency increases, increases and the velocity prole becomes very attened. An
increase in diameter will also cause an increase in and produce a similar alteration in the
prole. The eects of the larger are seen to be a attening of the prole of the central
region, a reduction of amplitude of the ow and the rate of reversal of ow increases close to
the wall.
In order to visualize the velocity proles in an artery, it is necessary to sum the proles
of the main harmonic components, with their appropriate amplitudes and phases, together
with a parabolic prole representing the steady-ow component (the mean forward ow).
It can be seen in Fig. 6.2 that in the fast systolic rush a prole that approaches the form of
parabola is created. The reversal of ow begins in the peripheral laminae and progressively
involves those towars the axis. During back ow, the harmonics are considerably out of phase,
and the prole is very much attened. The maximum retrograde velocity occurs in the lami-
nae with the fractional radius of between 0.3 and 0.4. The point of ow reversal in the most
peripheral lamina (r/R=0.95) is about 25

later than pressure gradient reversal, in the axial

lamina reversal occurs abot 40

later still.
It can be seen that the ow of liquid near the wall follows the pressure gradient most closely
and that the phase lag increases to a maximum at the axis. The peak mean forward velocity
was 105 cm/s at 75

and the peak mean backward velocity was 25 cm/s at 165

.
15
Figure 7: 1. Velocity proles calculated from the measured pressure gradient in the femoral artery of the
dog. The rst four harmonic components with the same values of as in Fig. 62. are summed together with
a parabola (axial velocity 30 cm/s) representing the steady forward ow.2. The velocity of pulsatile ow in
the dog femoral artery displayed in terms of individual laminae in the stream (y=r/R) corresponding to the
proles shown in the left. The measure pressure gradient from which the curves were computed is displayed
below.[1]
6 Conclusion
Blood ow phenomena are often too complex that it would be possible to decribe them
entirely analytically, although simple models, such as Poiseuille model, can still provide some
insight into blood ow. The understanding of governing laws that apply in the pulsatile
blood ow is crucial for my future work. For the planned experiment of dissolving blood clots
under physiological conditions of pulsatile ow and for building a model to describe such ow
through the clot channel the pulsatile ow dynamics and entrance eects should be studied
thoroughly.
16
References
[1] W. W. Nichols, M. F. ORourke. McDonalds Blood Flow in Arteries. Theoretical, exper-
imental and clinical principles. Fifth Edition. Hodder & Arnold, London, 2005
[2] D. O. Cooney. Biomedical Engineering Principles. An Introduction to Fluid, Heat and
Mass Transport Processes. Marcel Dekker, New York, 1976
[3] R. L. Whitmore. Rheology of Circulation. Pergamon Press, New York, 1968
[4] C. G. Caro, T. J. Pedley, R. C. Scroter, W. A. Seed. The Mechanics of Circulation.
Oxford Medical Publications, Oxford, 1978
[5] Y. C. Fung. Biodynamics: Circulation. Springer-Verlag, New York, 1984
[6] W. R. Milnor. Hemodynamics. Second Edition. Williams and Wilkins, Baltimore, 1989
[7] R. F. Rushmer. Cardiovascular Dynamics. W. B. Saunders Company, Philadelphia, 1976
[8] I. Sersa et al. Modelling the eect of laminar axially directed blood ow on the dissolution
of non-occlusive blood clots. Phys. Med. Biol., 2007, vol. 52, p. 2969-2985.
[9] Circulatory System (Fig. on the page 3) http://www.nstlearning.com/~km/?p=1645
17