Nothing is a waste of time if you use the experience wisely --- Rodin
BIOFLUID DYNAMICS OF THE HUMAN CIRCULATORY SYSTEM1
<Human Arjomandi> harjo001@fiu.edu <Stephanie S. Barcelona> sbarc002@fiu.edu
<Siobhain L. Gallocher> siobhain.gallocher@fiu.edu and <Martha Vallejo> mvalle02@fiu.edu 2
AbstractThe human circulatory system, consisting of
the cardiovascular and lymphatic systems, is a complex
network of branching vessels. The non-Newtonian
behavior of blood makes it a unique fluid. An analysis
of the fluid dynamics of the arteries is not an easy task
due to the many variables: fluid properties, vessel
properties, and Poiseuille flow was adapted to take into
account the pulsatility of flow in the large vessels.
Finally, wave propagation speeds were derived which
took into account the compliant nature of the vessels.
Analog models of blood flow, such as the Windkessel
model and Kirchoffs electrical model are presented. In
the venous system, veins have less well-developed intima
and media than comparable sized arteries. They
represent a large distensible sink or reservoir for blood
volume such that 50% of the circulating blood volume is
in the systemic venous system at rest. In addition to
viscosity of blood, the main determinants in finding the
resistance and flow are the vessel diameter and length.
The capillaries are the most important part of the
cardiovascular system because they are the only part of
the system in which exchange between blood and
interstitial fluid occurs. The rate of fluid exchange in
the capillaries is determined by hydrostatic pressure
and by oncotic pressure. The Starling hypothesis shows
their relationship to each other. The coronary
circulation supplies the heart with blood.
Hemodynamics and the interaction of blood cells with
vessel wall helps to understand blood flow behavior
within the heart.
Key wordsBlood, non-Newtonian, Hagen-Poiseuilles
Law, Reynolds number, Navier-Stokes, Bessel
functions, Womersly parameter, Windkessel model,
electrical analog model, CFD, Starling hypothesis,
Ficks First Law of diffusion.
The numbers in parenthesis refer to bibliographical
references with cited pages.
1 The body has three types of fluids. These include the
This review article was prepared for the Congress on
Biofluid Dynamics of Human Body Systems. Biomedical
Engineering Institute, Florida International University,
10555 West Flagler Streeet, Miami FL 33174,
organized on April 17, 2003. For details contact <Dr.
Megh R. Goyal> m_goyal@ece.uprm.edu or <Dr. Richard
T. Schoephoerster> schoepho@fiu.edu
2
Contributors are in the alphabetical order.
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL
INTRODUCTION
The human circulatory system consists of both the
cardiovascular and lymphatic systems. Together, they help
to maintain the normal functioning of all the cells within
the body. The cardiovascular system functions in
transportation, regulation, and protection, while the
lymphatic system transports excess, accumulated fluid from
the interstitial spaces to the blood and plays an
immunological role [1; 2; 3 and 7-8]. The purpose of this
study was to present a conceptual model, explain the fluid
mechanics, investigate the computational fluid dynamics,
and discuss research advances of the circulatory system.
DESCRIPTION OF THE SYSTEM
The cardiovascular system is comprised of the heart, blood,
and blood vessels. It can be seen from Figure 1 that the
heart, the muscular organ responsible for driving the blood
through the vessels, acts as two pumps in series. The right
side of the heart receives blood from the venous system and
is responsible for pumping it through the pulmonary circuit.
The oxygenated blood returns to the left side of the heart
where it is pumped into the systemic circuit. Each different
blood vessel type is responsible for performing a specific
function. Under normal resting conditions, 70% of the
blood is located in the venous system, and only 17% is
located in the arterial system [1; 12; and 23].
As is shown in figure 2, the cardiovascular and lymphatic
systems are intertwined, and they function in unison. The
lymphatic system transports capillary ultrafiltrate,
combined with proteins, bacteria, fat micelles, and immune
cells, from the interstitial spaces back to the cardiovascular
circulation. The lymphatic system consists of lymph, a
network of lymphatic vessels, specialized cells called
lymphocytes, and lymphoid tissues and organs [1; 12; 19;
and 23].
FUNCTIONS OF THE BIOFLUIDS
extracellular, intracellular and transcellular fluids. Table 1
reveals that these fluids form 60% of the body weight for
an average 70-kg male, which results in a total fluid
volume of about 40 liters. The intracellular fluid makes up
36% of the body weight, this fluid consists of the fluid
found within the cells. Extracellular fluid consists of
A-1

Figure 1. Schematic diagram of the circulatory system
[4].
b If the body temperature rises, the blood is directed to the
a c
Figure 2. Overview of the lymphatic system [12, 753].
interstitial fluid that accounts for 17% of the body weight,
and the blood plasma that comprises around 4% of the body
weight [4].
Here we shall consider lymphatic fluid and natural blood.
The blood, the fluid portion of the cardiovascular system,
has numerous functions, without which, the body would
cease to function. Table 2 shows the constituents and
functions of the blood.
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL
Table 1. Body fluids [4].
Fluid volume
Fluid % of Body Weight
(liters)
Intracellular 25 36
Extracellular 15 21
Interstitial 12 17
Plasma 4
Transcellular ------- ------
Total 40 57
At the alveoli capillaries, the blood picks up oxygen and
releases carbon dioxide. When the oxygenated blood
reaches the capillaries within the tissues, the oxygen is
released, and carbon dioxide, the by-product of cellular
respiration, is picked up for transporting it back to the
lungs.
The blood collects and releases nutrients and hormones for
distribution to target cells throughout the body, and waste
products are transferred to the kidneys for excretion in the
same manner. The blood regulates pH and ion
compositions of interstitial fluids. The capillary walls are
permeable to ions and water, so a diffusion gradient
between the interstitial fluid and the blood results in the
diffusion of water and ions down their concentration
gradient until normal physiologic conditions persist.
Excess ions become excreted by the kidneys and in
perspiration. Within the blood, a buffering system exists,
so if the pH drops, the blood accepts hydrogen ions and
vice versa. In this manner, the blood is capable of
regulating the pH. The blood prevents excessive fluid loss
at sites of injury by inducing a cascade of events that leads
to the formation of a clot to temporarily plug the injury site.
The blood contains leukocytes and antibodies that defend
against any toxins and pathogens that enter the system.
Finally, the blood regulates overall body temperature by
absorbing excess heat that is generated and redistributing it.
surface of the skin where the heat can be lost to the
environment. If the body temperature is low, the blood is
redirected to the brain and other temperature-sensitive
organs [1; 12; and 23].
The lymphatic system plays an essential part in maintaining
a healthy body. The lymph consists of fluid and solutes
from the interstitial spaces. There is an imbalance in the
amount of fluid the capillaries add to and remove from the
tissues, so the lymphatic system removes this fluid
containing solutes as lymph for return to the venous
system. Many substances from the tissues that are not
capable of entering the bloodstream directly through the
capillaries enter it through the lymphatic system. It is in
this fashion that the lymph transports hormones, nutrients,
waste products, and dietary lipids. The lymphatic system
produces, maintains, and distributes lymphocytes within the
lymph. The lymphocytes are part of the immune response
and react to the presence of invading pathogens (viruses
and bacteria), abnormal body cells, and foreign proteins by
eliminating them or adapting them [1; 12; and 23].
A-2
Table 2. Constituents and functions of the blood cells [3]. Table 3. Blood flow to different organs and tissues under
basal conditions [10, 176].
Organ Percent ml/min ml/min/100g
Constituents Main functions
Brain 14 700 50
Formed elements (37-54%) Heart 4 200 70
Erythrocytes (RBC) Bronchial 2 100 25
CO2 and O2 transport
(99.9 %) Kidneys 22 1100 360
Leukocytes Neutrophil
Phagocytosis of bacteria Liver 27 1350 95
(WBC) (50-70%)
(<0.1%) Eosinophil Defense against parasitic Muscle (inactive
15 750 4
(2-4%) helminthes; modulation of state)
inflammatory processes Bone 5 250 3
Basophil Release of histamine and Skin (cool weather) 6 300 3
(<1%) other inflammation
mediators Thyroid gland 1 50 160
Monocyte Generation of monuclear- Adrenal glands 0.5 25 300
(2-8%) phagocyte system cells in Other tissues 3.5 175 1.3
tissues.
Lymphocytes T cells kill virus-infected Total 100.0 5000 ---
(20-30%) cells; B cells generate
antibody-producing terminal Table 3 summarizes the blood distribution to the different
cells; Natural killer cells kill organs and tissues in the human body. Table 4 summarizes
tumor and virus-infected the blood distribution by volume and flow. From these
cells
tables it can be seen that the greater the metabolism in an
Thrombocytes (Platelets)
Clotting of blood organ, the greater the blood flow.
(<0.1%)
Plasma (46-63%) PHYSICAL PROPERTIES OF THE BIOFLUIDS
Plasma Albumins Contributes to the osmotic
proteins (60%) pressure of plasma; The physical characteristics of blood remain the same for
(7%) transports fatty acids, all the different sources of blood (venous blood, arterial
thyroid hormones, and some blood, etc). Blood temperature is roughly 38 C (100.4 F),
steroid hormones. pH is between 7.35 and 7.45, and viscosity is five times
Globulins Immunoglobulins attack
greater than that of water. Table 5 lists the physical
(35%) foreign proteins and
pathogens; transport properties of an adult human blood. s the blood flows
globulins bind ions, through the body, materials are constantly being added and
hormones, and other removed, so the variations occur continuously. There are
compounds that might be differences among normal persons in every measurable
lost at kidneys or have very constituent. The composition of the blood is affected by
low solubility in water. age, sex, genetic factors, environmental conditions,
Fibrinogen Converted to fibrin, which physiological state of the individual, and disease [4].
(4%) provide the basic framework Lymph is derived from interstitial fluid that flows into the
for a blood clot.
lymphatics. It is a clear, watery fluid found in the
Regulatory Catalyze specific
proteins biochemical reactions and lymphatic vessels. There are several factors that affect
(<1%) regulate activities of other lymph flow, but essentially the primary factors that
cells. determine lymph flow are: (1) The interstitial fluid pressure
Other Electrolytes Maintain normal and (2) The activity of the lymphatic pump. Thus it can be
solutes extracellular fluid ion said that the rate of lymph flow is determined by the
(1%) composition essential for product of interstitial fluid pressure times the activity of the
cellular activities; contribute lymphatic pump [10].
to osmotic pressure of body
fluids.
Organic Needed for ATP production,
CHEMICAL AND BIOLOGICAL
nutrients growth, and cell COMPOSITION OF THE BIOFLUIDS
maintenance.
Organic Carried to sites of Blood is a fluid connective tissue that is composed of a
wastes breakdown or excretion. fluid matrix, plasma, with suspended formed elements.
Water Transports organic and inorganic molecules, The formed elements, whose percentage volume or
(92%) formed elements, and heat. hematocrit in blood is 37-54%, consist of three basic cell
types, namely, erythrocytes (red blood cells), leukocytes
(white blood cells), and thrombocytes (platelets).

2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-3
 formed elements, are involved in the bodys clotting
Table 4. Blood distribution by volume and flow [3, 513]. process [3 and 15].

Physiologic Typical Typical Plasma makes up 46-63% of the volume of whole blood. It
structure volume flow rate, is an aqueous, saline suspension medium that is 92% water
% mL mL/min by volume. The composition of the plasma closely
Aorta 4.5 156 5345 resembles that of the interstitial fluid, with the major
Arteries, larger 5.4 187 695 plasma ions being those similar to the interstitial fluid. The
distributing two major differences between the plasma and interstitial
Brain, cerebral 2.3 78 - fluids exist in the concentrations of dissolved proteins and
circulation the presence of respiratory gases. There is a continuous
Heart chambers 9.8 338 - exchange of water and ions across the capillary membrane,
so an equilibrium results in similar concentrations of ions.
Coronary circulation 2.3 78 267
The capillary membrane is impermeable to the plasma
Renal circulation 1.5 52 1149
proteins, resulting in the marked difference in
Lungs 15 520 5185
concentrations across the membrane. Plasma proteins
Lymphatic 0.4 15 5 make up approximately 6.5-8% by weight of the plasma.
circulation The three major plasma proteins are albumins, globulins,
Muscle, inactive 21 728 802 and fibrinogens. Albumins contribute to the osmotic
skeletal pressure of plasma and transport lipids and steroid
Skin 7.5 260 428 hormones. Globulins transport ions, hormones, and lipids,
Veins, large 26.7 925 - and participate in the immune response. Fibrinogen is a
collecting vital component of the clotting system. The remaining 2%
Vena cava 3.6 125 5185 of the plasma consists of mineral, trace elements, and
Total 100 3462 5345 electrolytes, some required by the cells for normal
functioning while the others contribute to the acid-base
Table 5. Physical properties of adult human blood. balance of the blood [3 and 15]. Table 6 shows a
laboratory analysis of blood for a healthy 20-year-old
Value female along with the normal ranges [2].
Property Ref
Range Normal
Lymph is considered to be a part of the extracellular fluid
Density (g/cm ) 3
1.050-1.064 1.057 [5, 475] system, and it is in many ways similar to plasma. Lymph
differs from plasma in that it contains a significantly lower
Viscosity (cP) 2.18-3.59 3.0 [5, 475] percentage of suspended proteins. In terms of the common
ions found in both the intracellular and extracellular
pH 7.35-7.45 7.4 [5, 475] compartments of the body, the difference in concentrations
of these ions between the lymph and plasma is not
Specific gravity 1.0501-1.0619 1.057 [5, 475] significant. Lymphocytes are the most abundant cells
found in lymph, accounting for 83% of the cells.
Refractive index 16.2-18.5 17.4 [2, 12]
Neutrophils, eosinophils, and erythrocytes are also found in
the lymph contributing to 0.9, 0.2, and 15% of the total
Specific heat (g/cal) - 0.92 [2, 12] number of cells respectively [15 and 19]. In Table 7, the
lymph components of a healthy male are given.
Surface tension
55.5-61.2 - [2, 12]
(dynes/cm) RHEOLOGY OF THE BLOOD
Colloid osmotic
Many factors govern pressure and flow in the circulation,
pressure: plasma 280-480 330 [2, 12]
and their interaction is complex. Blood is a non-
(mmHg)
homogenous, ionic, anisotropic, composite fluid, which is
formed of a mixture of blood cells and plasma. carried in a
The erythrocytes contribute to approximately 95% of the liquid that contains high molecular weight, long- chain
formed elements, and these cells are specialized for the polymers that behave in a complex way under shear stress
transportation of oxygen in the blood. The leukocytes are [3]. Thus blood exhibits a non-Newtonian, viscoelastic
far less numerous than the erythrocytes, accounting for less flow. In contrast, for a Newtonian fluid the shear-stress rate
than 0.15% of the formed elements. The leukocytes are an relationship is linear with the slope equal to the viscosity of
integral part of the bodys defense mechanism as they are the fluid [4]. For the non - Newtonian fluids, the slope of
capable of identifying and removing foreign substances the line at a given value of the shear rate is the apparent
from the body. The agranulocytes, the monocytes and viscosity. Blood can behave both as Newtonian and non-
lymphocytes, identify foreign matter, and the granulocytes, Newtonian fluid depending on the shear rate.
the neutrophils, eosinophils, and basophils, dispose of it.
The thrombocytes, accounting for approximately 5% of the
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-4
Table 6. Laboratory analysis of blood for a healthy 20- Table 7. Lymph components of a healthy male [2].
year-old female [2].
Component Units Average Range Thoracic duct
Constituent Units
lymph
Glucose mg/dl 91 65 - 115
Electrolytes
Sodium mEq/L 142 134 - 147
Chloride mEq/L 87 103
Potassium mEq/L 4.1 3.5 - 5.5
Phosphorous mEq/L 2.0 3.6
Chloride mEq/L 105 95 - 110
Potassium mEq/L 3.9 5.6
Carbon dioxide mEq/L 23.3 23.0 - 32.0
Sodium mEq/L 118 - 132
Urea nitrogen mg/dl 10 6.0 - 22.0
Nitrogenous substances
Creatinine mg/d 0.9 0.5 - 1.4
Protein, Total g/100mL 2.91 7.33
Bun/Creatinine ratio ------ 11.1 7 - 23 Albumin g/100mL 1.50 2.67
Uric Acid mg/dl 4.2 1.7 - 7.4 Globulin g/100mL 1.50 - 4.80
Phosphate mg/dl 3.7 2.4 - 4.9 Bilirubin g/100mL 0.8
Calcium mg/dl 9.5 8.5 - 10.5 Creatinine g/100mL 0.8 - 8.9
Protein, total g/dl 8.2 6.2 - 8.4 Uric Acid g/100mL 1.7 - 10.8
Albumin g/dl 4.6 3.4 - 5.1 Nitrogen, non-
g/100mL 13.4 - 139.0
Globulin, protein
g/dl 3.6 2.2 - 3.7
(Calculated) Lipids, carbohydrates
A/G ratio ------ 1.3 1.0 - 1.9 Cholesterol, Total mg/100mL 34 - 106
Bilirubin: Total mg/dl 0.5 0.2 - 1.3 Free mg/100mL 15 - 51
Bilirubin: Direct mg/dl 0.14 0.00 - 0.40 Fat, Total mg/100mL 1.1
Alkaline Glucose mg/100mL 136
U/L 76 20 - 150
phosphatase Enzymes
GGT U/L 11 1 - 70 Aldolase units/mL 10
AST U/L 14 1 - 45 Phosphatase units/mL 0.7
ALT U/L 8 1 - 45 Alkaline units/mL 1.9
LD U/L 126 80 - 235 Transaminase units/mL 12
Tryglycerides mg/dl 94 40 - 200
Cholesterol mg/dl 141 120 - 200 At low shear rates, the apparent viscosity of the blood is
Iron mg/dl 83 40 - 180 quite high due to the presence of rouleaux and aggregates,
TIBC mg/dl 357 250 - 390 thus blood behaves as non-Newtonian fluid. However, at
Trans. Sat. percent % 23 15.0 - 50.0 shear rates above 100/sec, only individual cells subsist, and
PBG mg/gm 0.73 0.00 - 1.20 blood behaves as if were a Newtonian fluid [4].
HDL Cholesterol mg/dl 53 35 - 95
Cholesterol/HDL
ratio
------------ 2.7 2.9 - 4.3 Blood flow in arteries, veins, and the smaller vessels is
LDL Cholesterol Newtonian near the vessel wall, and non-Newtonian as the
mg/dl 69 50 - 130 flow approaches the centerline of the vessel [4]. The
(Calculated)
CBC anomalies in the viscous behavior of blood result partly
WBC 103/mm3 6.3 3.9 - 11.4 from the presence and orientation of the cells suspended in
RBC 106/mm3 4.11 3.80 - 5.10 plasma and partly from the accumulation of RBCs in the
Hemoglobin, Hb g/dl 12.5 11.6 - 15.1 axial portion of the bloodstream. The result of this is a
Hematocrit, Hct % 37.2 34.0 - 45.0 decrease in apparent viscosity with increasing velocity of
MCV fl 90.5 80.0 - 96.0 flow and with decreasing vessel radius [17]. As blood
MCH PG 30.4 26.8 - 33.2 leaves the aorta and flows into capillaries, the velocity of
MCHC % 33.6 32.0 - 36.0 the blood decreases. The average velocity of blood in the
RDW % 11.9 11.0-15.0 aorta is approximately 0.3 m/s while the average velocity of
Platelet count 103/mm3 277 150 - 400
blood in a capillary is about 10-3 m/s. Blood velocity is
MPV fl 7.3 7.5 - 11.5
inversely related to the total cross-sectional area of the
Segmented
103/mm3 4.17 1.70 - 8.50 vessels carrying the blood as shown in figure 3 [21].
Neutrophils, ABS
Lymphocytes, ABS 103/mm3 1.61 1.10 - 3.50
Monocytes, ABS 103/mm3 0.40 0.04 - 0.90 The velocity of blood at the center of the vessel is greater
Eosinophil, ABS 103/mm3 0.06 0.03 0.55 than the velocity near the walls (Figure 4). This affects the
Basophils, ABS 103/mm3 0.05 0.00 - 0.13 distribution of RBCs in the circulatory system. It implies
Segmented that the distribution of RBCs is not uniform so that there
% 66.2 40.0 - 75.0
Neutrophils are more in the center than at the edges. The effect of this
Total lymphocytes % 25.6 15.0 50.0 is two-fold. First, as blood enters a small vessel branching
Monocytes % 6.3 0.0 10.0 from the side of a main vessel, the hematocrit (percentage
Eosinophils % 1.0 0.0 6.0 of red blood cells in blood) will be less than that of the
Basophils % 0.8 0.0 2.0 main vessel. Second, extremities have a greater percentage
ESR, westergreen mm/hr 17 0 - 20 of RBCs than blood from the heart [21].

2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-5
 Figure 6. The viscosity-shear rate relations in whole
blood (), defibrinated blood (x----x), and washed
cells in Ringer solution (-----), at 45% and 90% red cell
colume concentrations.
Figure 3. Velocity of blood (solid line) decreases as total
cross-sectional area increases (dashed line) [21]. The rheology of blood can be significantly affected by the
hematocrit and the plasma protein concentration. Increasing
the hematocrit increases the viscosity of blood (Figure 5).
The same effect is also seen when the fibrinogen
concentration increases. Fibrinogen is the primarily
responsible for the non-Newtonian fluid behavior of the
blood. Other plasma proteins like albumin, do not
contribute to the non-Newtonian behavior of blood [7].

Blood is a nonhomogeneous, anisotropic, ionized fluid

containing a suspension of viscoelastic particles, and it
displays non-Newtonian, viscoelastic deformation
characteristics that can be modeled by the Power Law:
n
du /1/
= k + y
dy
Figure 4. (a) Velocity profile of blood flow. (b) Non-
uniform distribution of blood cells [21]. Where: is the time dependent stress, du/dy is the time
dependent strain, K is a material dependent constitutive
parameter which reduces to the real dynamic coefficient of
viscosity for a Newtonian fluid, n is the material-dependent
non-linearity index that is > 0, and y is the yield stress. y,
for blood, in dynes per square centimeter, can be calculated
using the equation:

y = ( H 0.1)( C F + 0.5 )
/2/

Where: H is the hematocrit expressed as a fraction, and CF

is the plasma concentration of fibrinogen, expressed in
grams per 100 mL. Typical values for K and n are
0.1352x10-1 Pa-s and 0.7844 respectively [3, 482].

It has been determined that the deformation properties of

RBC suspensions is influenced by shear rate, hematocrit,
Figure 5. Viscosity versus Hematocrit percentage [10]. degree of cellular aggregation, and the mechanical
properties of each of the cells themselves [3, 477].

2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-6
Figure 6 reveals that an increase in shear rate leads to a
decrease in viscosity, and an increase in hematocrit leads to
an increase in viscosity. In Figure 7, the effects of shear
rate and temperature are observed. Again, viscosity is
shown to decrease with increasing shear rate, and a
decrease in temperature led to an increase in viscosity.

Deformability is a term used to describe the structural

response of a body or cell to applied forces. The effect of
RBC deformability in influencing general fluidity of whole
blood is clearly revealed in Figure 8. This figure shows the
relative viscosity of blood at a shear rate >100 s-1 (at which
particle aggregation is negligible, isolating RBC
deformability) compared with that of suspensions with
rigid spheres. At 50% concentration, the viscosity of a
suspension of rigid spheres reaches almost infinity so that
the suspension is not able to flow. On the contrary, normal
blood remains fluid even at a hematocrit of 98%, on
Figure 7. The variation of the viscosity of human blood with shear
account of the deformability of its RBCs [32]. rate and temperature for a male donor with a hematocrit of 44.8 %
[6, 68].
Cassons equation is another method used to describe the
shear stress of whole blood:
du
= y +
dy /3/

Where: the shear stress, yield stress, and shear rate are
defined by equation /1/ and /2/, and is a constant.
Experimental data of whole blood at 37C and a hematocrit
of 51.7% are shown in Figure 9. It is observed that
Cassons equation can be fitted to the experimental data.

In Figure 10, the impact of hematocrit on the yield stress of

whole blood is represented. As is expected, the yield stress
increases with increasing hematocrit.
Figure 8. Variation of relative viscosity of blood and
Figure 11 shows the impact of shear rate on shear stress. It suspension with rigid spheres at a shear rate < 100 s-1 [32].
can be seen that at low shear rates, the blood behaves like a
non-Newtonian, Casson fluid, but as the shear rate
increases, the blood begins to act more and more like a
Newtonian fluid.. In the figure, the data to the right of the
dashed curve represents the Newtonian nature of the fluid,
whereas the non-Newtonian region is located on the left
hand side of the dashed curve.

The most contributing factor in making blood non-

Newtonian is RBC aggregation. Human RBCs have the
ability to form aggregates known as rouleaux. Rouleaux
formation is highly dependent on the concentration of
fibrinogen and globulin in plasma. As RBCs form
rouleaux, they will tumble while flowing in large vessels.
The tumbling disturbs the flow and requires the
consumption of energy, thus increasing blood viscosity at
low shear. As shear rate increases, blood aggregates tend
to be broken up resulting in drop in blood viscosity. In
short, rouleaux formation increases blood viscosity,
whereas breaking up rouleaux decreases blood viscosity Figure 9. Casson plot for whole blood at a hematocrit of
[32]. 51.7% and at a temperature of 37C [6, 69].

2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-7

Figure 10. Variation of the yield stress of blood with
hematocrit [8, 70].
Figure 11. Casson plot for a higher shear rate rheological data
for blood [6, 71].
Figure 12. Elevated blood viscosity at low shear rates
indicates RBC aggregation (rouleaux formation). Blood
viscosity decreases with increasing shear rates as RBC
aggregations breaks up to individual RBCs [32].
For blood flowing through a cylindrical vessel, such as is
found in the human circulatory system, the apparent
viscosity decreases with decreasing vessel diameter when
all other parameters are kept constant. This effect, known
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL
as the Fahreus-Linqvist effect is shown clearly in Figure
12. While the blood is flowing through the vessels, the
RBCs drift towards the centerline and equilibrate and align
themselves at a particular radial location in order to
decrease the amount of profile drag in the direction of flow.
With this arrangement of RBCs, a cell free layer persists at
the walls of the vessel, so fluid flowing along the walls of
the vessels consists only of plasma. The cell free layer is
what leads to a decrease in the hematocrit with decreasing
vessel diameter, as the size of the cell free layer remains
constant in all sized vessels. What this means is that with
decreasing vessel size, the cell free layer occupies a greater
volume of the vessel leading to decreased apparent
viscosity. A phenomenon called plasma skimming occurs
in the body, as small branching vessels draw the majority
of their fluid from the cell free layer, thereby decreasing the
hematocrit in the smaller vessels [3 and 6]. Figure 13
shows the effect of the size of the blood vessel on the
relative viscosity of the blood.
Figure 13. The change of relative viscosity of blood with the size
of blood vessel [6, 172].
Lymph is thought to behave like a Newtonian fluid and it
obeys Newtons law of viscosity:
du
= /4/
dy
Where: is the dynamic coefficient of viscosity [3 and 6].
CONCEPTUAL MODEL OF THE
CIRCULATORY SYSTEM
The Figure 14 shows an analog model of the human
cardiovascular system, but it provides a basic idea of how it
functions. In this model, the Oxygen Plant represents the
lungs where oxygen is absorbed and carbon dioxide is
removed from the blood. The pipeline leading from the
plant to pump 1 represents the pulmonary veins, pump 1
represents the left hand side of the heart, and the pipeline
leading from pump 1 to the factory represents the systemic
arterial circulation. The factory represents the capillaries
bed where oxygen and nutrients diffuse into the tissues.
The pipeline leading from the factory to the inlet valve
represent the systemic venous system, pump 2 represents
A-8
the right hand side of the heart, and the pipeline leading
from pump 2 to the plant represents the pulmonary arteries
[36, 1-2].
Figure 14. Circulatory system analogy using industrial
system [36, 1].
FLUID MECHANICS
The description of any flow problem requires the
determination of the three major component equations of
motion and pressure as functions of position and time.
However, the problem of treating the pulsatile flow of
blood through the cardiovascular system in precise
mathematical terms is overwhelming. This can be reasoned
as blood is non-Newtonian; flow is not steady but pulsatile;
vessels are elastic, multi branched conduits of constantly
changing diameter and shape. Therefore, a precise
calculation of blood is required in each segment of the
cardiovascular system [33, 35].
Blood flow through an organ or any vascular network is
driven by a pressure gradient or perfusion pressure that is
normally represented by the difference between the arterial
and venous pressures across the organ. The actual blood
flow at any given pressure gradient is determined by the
resistance to blood flow [14, 80-86].
Blood flow can be either laminar or turbulent. Flow is
laminar when the fluid travels smoothly or in regular paths.
The velocity, pressure, and other flow properties at each
point in the fluid remain constant. Turbulent flow occurs
when the fluid undergoes irregular fluctuations or mixing.
The speed of the fluid at a point is continuously undergoing
changes in magnitude and direction, which results in
swirling and eddying as the bulk of the fluid moves in a
specific direction. Reynolds number can be used to find if
the flow is laminar or turbulent [8, 84-99]:
um d
Re = /5/
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL
There are three primary factors that determine the
resistance to blood flow within a single vessel: diameter (or
radius), length, and viscosity of the blood. Other factors
are the organization of the vascular network (series and
parallel arrangements), and extravascular mechanical
forces acting upon the vasculature [36].
If only the primary factors are considered, Poiseuilles law
can be used to find the resistance and flow. In Poiseuilles
law, vessel resistance R is directly proportional to the
length (l) of the vessel and the viscosity () of the blood,
and inversely proportional to the radius to the fourth power
a4, [36].
8. .l
R= /6/
4
.a
Flow, then, can be related to the resistance as follows:
P
Q = /7/
R
Where: P= Pressure difference between two points and Q
is the volume flow rate.
In the body, however, flow does not conform quantitatively
to this relationship because this relationship assumes long,
straight tubes (blood vessels), a Newtonian fluid (e.g.,
water, not blood which is non-Newtonian), and steady,
laminar flow conditions. Nevertheless, the relationship
clearly shows the dominant influence of vessel radius on
resistance and flow and therefore serves as an important
concept to understand how physiological and pathological
changes in vessel radius affect flow [22, 2].
In Figure 15, the relationship between flow and radius for a
single vessel is shown. Laminar flow conditions are
assumed at pressure, viscosity, and vessel length. As vessel
radius decreases, there is a dramatic fall in flow because
flow is directly related to radius to the fourth
power. Therefore very small changes in vessel radius can
have dramatic effects on flow [35].
Within a given organ, the vascular arrangement is a
combination of series and parallel elements. For example,
in the Figure 16, the vascular segments labeled A (large
artery), a (arterioles), c (capillaries), v (venules), and V
(large vein) are in-series with each other. All of the blood
that flows through the large artery (A), also flows through
each of the other segments. Within each of the series
segments, there may be many parallel components (e.g.,
several parallel capillaries may arise from a single
arteriole). Each vascular segment will have a resistance
value (Rx) that is determined by the length and radius of
each of the individual parallel vessels [35].
A-9

Figure 15. Change in radius with flow [35].
Figure 16. Veins in series [35]
For the in-series resistance network, the total resistance
(RT) equals the sum of the individual resistances [35]:
R = R A + R a + R c + R v + RV /8/
For the parallel resistance network, with 3 parallel vessels,
total resistance is used [35]:
1 1 1 1
= + + /9/
R R1 R2 R3
The total resistance of a network of parallel vessels is less
than the resistance of the vessel having the lowest
resistance. Therefore, a parallel arrangement of vessels
greatly reduces resistance to blood flow. That is why
capillaries, which have the highest resistance of individual
vessels because of their small diameter, constitute only a
small portion of the total vascular resistance of an organ or
microvascular network [35].
CORONARY CIRCULATION
Since the heart works continuously, cardiac muscle cells
need reliable supplies of oxygen and nutrients. The
coronary circulation supplies the heart with blood while the
heart pumps the blood into the systemic circulation.
During maximum exertion, oxygen demand rises and blood
flow to the heart increases nine times that of resting levels.
Coronary artery disease (CAD) is the partial or complete
blockage of coronary circulation. CAD is one of the
leading causes of mortality and morbidity in western
society. Reduced circulatory supply, or coronary ischemia,
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL
results from partial or complete blockage of the coronary
arteries due to the formation of a fatty deposit, or plaque, in
the wall of a coronary vessel. Blood flow is reduced as a
result of the narrowing of the passageway [28].
During maximum exertion, oxygen demand rises and blood
flow to the heart increases nine times that of resting levels.
Coronary artery disease (CAD) is the partial or complete
blockage of coronary circulation. CAD is one of the
leading causes of mortality and morbidity in western
society. CAD results from atherosclerotic lesions
(narrowing) in the main branches or from diffuse disease in
the microvascular bed. Both lead to reduced blood flow
where the oxygen demand of the heart muscles is not met
resulting in myocardial ischemia and angina pectoris [28;
13, 415].
Complex hemodynamics plays a critical role in the
development of atherosclerosis. It is important to
understand not only the forces and movement of blood cells
and whole blood but also the interaction between blood
cells and the vessel wall. Geometry and elasticity of vessel
walls help determine the flow behavior. High velocity
fluctuations that disturb flow should be avoided. The
following dynamic factors are responsible for the deposit of
blood cells and lipids, a leading cause of atherosclerosis:
1. Flow rate ratio.
2. Pressure and velocity gradients.
3. Flow behavior, velocity distribution, and shear stress
on the wall and on blood cells.
Interaction between blood cells and vessel wall leads to the
formation of plaques and agglomeration. These deposits
are found predominantly at arterial bends or wherever
blood flow is disturbed such as bifurcations, wherever a
secondary flow is created, and wherever flow separation
regions can be found [13, 415].
CORONARY ARTERY FLOW
The following factors are important to wall adaptation and
to the development of atherosclerosis in coronary arteries:
local wall shear stress induced by coronary artery flow and
local wall stress (or strain) induced by wall deformation.
The wall shear stress induced by coronary artery flow is
dependent on the following: (1) Vessel geometry which is
three-dimensional, non-planar, and time-dependent as a
result of wall motion induced by pressure pulse acting on a
distensible wall and movements of the heart (Figure 17);
(2) Flow, a time-dependent pulsatile (Figure 18); and (3)
Rheological properties of blood that is exhibiting shear
thinning behavior as a result of RBC deformation (Figure
19).
The wall stress induced by wall deformation is dependent
on the following: (1) Vessel geometry which is three-
dimensional and time-dependent exhibiting a non-uniform
wall thickness (Figure 14); (2) Motion of the heart (Figure
17); (3) Pressure wave in coronary arteries (Figure 18); and
(4) Material properties of the arterial wall [24, 17-15].
A-10
 Figure 20. Laminar flow in a round tube.

Blood flow in the arteries is pulsatile, and the pulsatility

Figure 17. Systolic and diastolic geometry of the right
coronary artery [24, 17].
decreases with distance from the heart. In order to
investigate the flow of blood through the arteries, a
simplified model is needed, and its complexity must then
be increased in order to give an accurate representation of
blood flow [5, 108-112; 18, 1-8].

Laminar Flow in a Tube

The vessels of the arterial system are for the most part
circular, therefore the laws governing the flow of liquids in
in a long straight tube were considered for steady state,
laminar flow and Newtonian fluid. In Figure 20, the radius
of a tube is a. The velocities in the x, y, and z directions
are: u = u(y, z); v = 0; w = 0.

In order to perform the analysis, flow of an incompressible

The fluid entering the system does not accumulate, so we
can use following the continuity equation:

u v w
+ + =0 /10/
x y z

The Navier-Stokes equation for flow through a cylindrical

Figure 18. Relevant pressure and flow waves [24, 15]. tube is:

2 2
u u 1 dp
+ = /11/
y
2
z
2 dx

dp/dx is a pressure gradient. The Navier-Stokes equation in

cylindrical coordinates (x, r, ) is as follows:

2
1 u 1 u 1 dp
r + 2 2
= /12/
r r r r dx

If the flow is assumed symmetrical, the equation reduces

to:

1 d du 1 dp
r = /13/
r dr dr dx

No-slip condition at the tube wall at r = a and the symmetry

Figure 19. Shear thinning behavior of blood [24, 15]. at the center line yield following boundary conditions:
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-11
 2
u = 0 at r = a u 1 u 1 p 1 u
+ + = /18/
2 r r x t
r
du
= 0 at r = 0 For the case of pulsatile flow, the pressure gradient is
dr
assumed to be a simple harmonic motion:
On integrating equation /13/, we get:
p * i t
= A e /19/
u=
1
4
(a 2
r
2 dp
) dx /14/
x

Where: A* is the complex conjugate of A, and =2f, the

angular frequency in radians per second. Substituting
The equation /14/ shows is a parabolic velocity profile for equation /18/ into equation /19/, we get:
the Hagen-Poiseuille flow. Volume flow rate is defined as:
2 *
a u 1 u 1 u A i t
Q = 2 0 urdr /15/ + = e /20/
2 r r t
r
Equations /14/ and /15/ result in the following Hagen- Equation /20/ can be simplified by substituting
Poiseuille formula: U = ue it , and by canceling out the exponential term
throughout the equation. We get:
4 4
a dp a p p
Q = = = /16/ 2 *
8 dx 8 L R d U 1 dU i A
+ U = /21/
2 r dr
dr
Where: p is the pressure drop in a segment of vessel of
length L, and R is the resistance. The shear stress at the Equation /21/ is a form of the Bessels equation. The
vessel wall, (u/r) at r = a is as follows: solution with appropriate boundary conditions is as
follows:
a dp a p 4

w
=
2 dx
=
2 L
= Q /17/
a3 A 0 r
* [ ( / )i ]
3/ 2

As was shown in Figure 15, the most important factor

U =
i
1
0 R [ ( / )i ]
3/ 2
/22/

controlling blood flow through and artery is the radius of

the vessel. If the size of the vessel is halved, the flow rate
decreases by a factor of 16, and if the vessel size is
The equation /22/ contains the Bessel function. The
doubled, the flow rate increases by a factor of 16. A
decrease in vessel size by a factor of 2 would require an quantity, R ( / ) , is a non-dimensional parameter
increase in pressure by a factor of 16 in order to maintain referred as Womersly number (). It is a ratio of unsteady
the constant flow rate, and vice versa. Physiologically
to viscous effects. When becomes large, the velocity
speaking, a successful way to adjust blood pressures is by
profile becomes blunt, and this can be seen in Figure 21.
changing vessel diameters.
The volume flow can be calculated in the same manner as
Hagen-Poiseuilles equation is not applicable to large
Poiseuille flow rate. The Bessel function provides a
arteries with turbulent, pulsatile flow. Another requirement
solution to the Navier-Stokes equation for pulsatile,
for equation /16/ is that the tube should be rigid and long
unsteady flow, and this more closely approximates what is
enough to avoid entrance effects. Thus many of the
happening in the arteries [5, 130-134; 18, 35-39; 25, 137-
assumptions are not applicable under actual physiological
161].
conditions. Therefore, Hagen-Poiseuilles formula can
only be used for blood flow under very specific conditions
Wave Propagation in Arteries
[5, 114-120; 18, 12-17; 31].
The arterial walls are highly elastic. Therefore, when a
Pulsatile Flow in a Tube pressure waveform traverses the artery, a certain amount of
stretch is observed in the arterial wall. This stretch is
The Navier-Stokes equation for unsteady, laminar flow and
proportional to the pressure at the specific location.
an incompressible liquid is given by:

2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-12

Figure 21. Theoretical velocity flow profiles of an
oscillating flow [12, 3.9].
Figure 22. Cross-section of artery showing change of
volume and volume flow rate [12, 3.7].
Figure 23. Steepening of a pressure pulse with distance
along the artery [12, 3.8].
To explain wave propagation, we assumed an ideal case
with an infinitely long, straight, isolated, circular,
cylindrical, elastic tube containing a homogeneous,
incompressible, and nonviscous fluid (Figure 22).
If this tube is disturbed, a wave will propagate along the
tube. Our aim is to determine the speed of wave
propagation. For one-dimensional flow, the conservation
of mass is defined by:
A proximity of arterial pulses gives the venous system
+ ( Au ) = 0 , /23/
t z
The conservation of momentum equation is as follows:
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL
u u 1 p
+u + = 0, /24/
t z z
Where: A is the tube cross sectional area, u is the uniform
axial velocity of blood, p is the pressure in the tube, is the
fluid density, z is the axial coordinate, and t is time. It is
assumed that the elasticity of the wall is given by a
relationship between pressure and cross-sectional area. It is
assumed that the wavelength is large compared with the
tube radius, so the conservation of mass and momentum
equations reduce to:
A u
= A /25/
t z
u 1 p
= /26/
t z
Equation /25/ is differentiated with respect to time, and
equation /26/ is differentiated with respect to z. We obtain:
2 2 2
p A p 2 p
= =c /27/
2 A p t 2 2
z t
We can solve for the wave speed (c) to obtain:
A p
c= /28/
A
The solution to this equation states that waves are
propagated at speed, c, from the heart to the distal
circulation. The high-pressure portion of the pressure wave
will tend to travel at a higher speed than the low-pressure
portion of the wave, resulting in a steepening of the
pressure wave as it travels from the heart to the distal
circulation. This is represented in figure 23. It can be
observed that wave speed varies with age due to the
ultimate stiffening or loss of elasticity in the vessel walls.
An assumption was made that the vessels were infinitely
long, but in reality, this is not true, so it is possible for the
wave to reflect backwards up the artery and add to new
wave forms being generated [5, 140-150; 12, 3.6-3.8].
VENOUS SYSTEM
The main characteristic of the venous system is having
walls that are thinner than arteries. This gives the venous
system a lower pressure than in arteries, and a possibility of
collapsing. Furthermore, presence of valves and anatomical
pressure fluctuations [35]. In the venous system, the
Reynolds number does not exceed 3,300. Table 8
illustrates Reynolds numbers in various part of the venous
system.
A-13
Table 8. Some properties of the venous system [34].

Vessel Velocity Diameter

Re #
(cm/sec) (cm)
Venule
0.2 0.002 0.01
Vein
10 0.5 140
Vena
Cava 38 3.0 3300

MICROCIRCULATION

Physically blood in the capillaries can be viewed as a two-

phase fluid consisting a liquid plasma phase and an
elastically deformable solid phase filled with blood cells.
Before going into the actual mechanics in the capillaries it
is necessary to explain the different forces that act upon the
capillaries. The first force and probably the most relevant is
pressure. In the cardiovascular system the pressure gradient Figure 24. Vessel diameter, total cross sectional area,
is the circulatory pressure that averages100 mm Hg. This average blood pressure and velocity of blood flow in the
is value is so high in part because this pressure is needed to blood vessels [15, 704].
force blood through the arterioles and the peripheral
capillaries. The circulatory pressure is often separated in
three classes: (1) Blood pressure: capillary blood flow is
directly proportional to blood pressure, (2) Capillary
hydrostatic pressure (CHP): it normally ranges from 35 mm
Hg to about 18 mm Hg, and (3) Venous pressure: this
pressure is very low.

The resistance should also be considered. The flow is

directly proportional to the pressure gradient, and inversely
proportional to the resistance. The resistance of the
cardiovascular system opposes the movement of blood.
The greater the peripheral resistance, the slower the blood
flow. Peripheral resistance comes from different sources
such as vascular resistance, viscosity and turbulence.
Vascular resistance is the resistance of the blood vessels Figure 25. Forces acting across capillary walls [15, 709].
and depends both on the vessel length and the vessel
diameter. Viscosity is the resistance to flow caused by the If on the other hand both numbers are larger than 1, fluid
interactions of molecules and suspended materials in a viscosity is ignored, and the flow is said to be
liquid. And finally turbulence is causes the flow to slow macrocirculation. These numbers are dimensionless [15,
and the resistance to increase. The variation of pressure 196]:
through the different blood vessels and the variation in
cross sectional area, diameter, and velocity are shown in
D
figure 24.. It can be seen that pressure and the speed of =N = /30/
blood flow are proportional to the cross-sectional area of w 2
the vessels involved, also blood flow velocity decreases in
velocity as the total cross sectional area of the vessel
Where: D is the blood vessel diameter, is the kinematic
increases [6, 702-703].
viscosity of the blood, and is the circular frequency of
oscillation of the blood velocity fluctuations.
Capillary blood flow is often identified with the
microcirculation. The microcirculation also includes blood
flow to the arterioles, and venules. In order to distinguish VD
Re = /31/
between macrocirculation and microcirculation, two basic

parameters are taken into account: Womersley number (),
and the Reynolds number (Re). If the Womersley number
Where: V is the mean velocity of flow in the vessel, D is
and the Reynolds number are both smaller than 1, then
the diameter of the vessel and is the kinematic viscosity
inertial force is not taken into account, and flow is said to
of the blood. It should be mentioned that Equation /5/ and
be microcirculation.
/31/ are the same. Some of the general features of the
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-14
microcirculation are: hematocrit is lower in the blood that
in the heart, apparent viscosity of blood decreases due to
the declining concentration of red blood cells, and activated
white blood cells have a greater chance to stick to the wall
vessel because of closer contact with the endothelium [6,
179 and 196].
The velocity and hematocrit distribution in any capillary
bed fluctuates constantly. One of the most important
features of the microcirculation is the appearance of
RBCs. In small blood vessels (capillaries) RBCs are so
big that they fill the vessel from wall to wall. The non-
uniform RBC distribution results in the Fahraeus effect that
emerges when the microvessel hematocrit is smaller than
the feed or discharge hematocrit; due to the fact that RBCs
move with a higher velocity than blood plasma, and the
Fahraeus-Lindqvist effect in which the apparent viscosity
of blood is less than the bulk viscosity. The apparent
viscosity of a fluid through a cylindrical vessel under a
pressure diffference is known as the Poiseuilles law,
equation /11/.
This law states that the rate of blood flow is directly
proportional to the fourth power of the radius of the vessel,
which demonstrates that that the diameter of a blood vessel
is the most important factor in determining the rate of blood
flow to a vessel. The units of this equation are kg /m sec [3,
31-33].
The exchange of materials between blood and interstitial
fluid across the capillary membrane is regulated by three
specific mechanisms: (1) Hydrostatic pressure on each side
of the capillary wall, (2) Osmotic pressure in the plasma
and in the tissue fluid, and (3) The characteristics of the
capillary wall (Figure 25). The pressure outside the
capillary wall plays an important role in mass transport; the
flow of fluid across the capillary wall is driven by a
difference in pressure across this capillary wall. This
difference takes place due to the hydrodynamic effects, and
the difference in osmotic pressure between the fluids
separated by the membrane [4, 8-9].
The following Starling equation represents the fluid flow
across the capillary membrane, and it can also be used to
describe the flow across any permeable membrane. The
units of this equation are mm Hg.
J
LpS
[( )(
= Pc Pif c if )] = P /32/
In this equation: Lp stands for hydraulic conductance, J
represents the volumetric fluid transfer rate, S is the total
circumferential surface area of the capillary wall, and P is
the effective pressure. The first term in brackets is the
difference between hydrodynamic pressure between the
capillaries and the interstitial fluid. If this term is positive
fluid will leave the capillary, if it is negative it fluid will
flow from the interstitial fluid into the capillary.
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL
The second term is the osmotic pressure difference between
the capillary and the interstitial fluid. If this term is
positive osmotic flow of water into the capillary will occur,
and if it is negative, the opposite will occur. If the first
term in brackets is positive, this net osmotic pressure flows
opposite to the flow induced by the hydrodynamic pressure
difference. From equation /32/, if the value in brackets is
positive, then there is a net flow from the capillary to the
interstitial fluid, on the other hand if this term is negative,
the fluid will go into the opposite way (interstitial to
capillary) [4, 8-9].
Also from the Starling equation, the filtration coefficient
can be defined as the ratio of J and P. This coefficient is a
constant and represents the properties of the pore. Lp for
blood, in m2 sec/ kg can be calculated using equation:
Ap r 2
lp = /33/
S 8tm
The stokes equation for the plasma, which states the
pressure-flow relationship in a capillary blood vessel:
1 p 2
0= + u i /34/
xi
Since this is flow in the capillaries, it can be assumed that
the Reynolds number and the Womersley number are less
than 1, thus the acceleration term on the left side of the
equation can be set to zero. Here ui is the velocity vector. In
order to compute the flow in the vessel the pressure
distribution and other stresses at the entry and exit sections
need to be specified [6, 203].
Flow through a vessel is based on two factors: (1) Pressure
difference and (2) Vascular resistance. Equation /11/
shows that blood flow is directly proportional to the
pressure difference and inversely proportional to the
resistance [10, 146].
Another phenomenon that takes place in the capillaries and
that is important to mention is diffusion. Diffusion is the
most important mechanism for transferring nutrients and
waste products between blood and tissues. Lipid-soluble
substances such as oxygen and carbon dioxide diffuse
rapidly down their concentration gradients across the
lipophilic membranes. Water and water-soluble substances
(figure 26) such as ions and glucose pass through the
capillary wall at a slower rate, mainly through intercellular
clefts and fenestrae [10, 164].
MECHANISMS OF CAPILLARY EXCHANGE
Fluid, electrolytes, gases, and other substances transverse
the capillaries by different mechanisms: (1) Diffusion; (2)
bulk flow; (3) Vesicular transport; and (4) Active
transport. Diffusion is important for O2, CO2, and lipid-
soluble substances (a in Figure 27).
A-15
Figure 26. Diffusion of fluid molecules and dissolved Figure 29. Hydrostatic forces within the capillaries [29].
substances between the capillary and interstitial fluid
spaces [10, 164].
Capillary Fluid Exchange

Water, electrolytes, and small molecules are feely

Figure 27. Mechanisms of capillary exchange [27].
exchanged between the intravascular and extravascular
compartments of the body. The primary site for this
exchange is the capillary. Several mechanisms are
involved in this exchange with bulk flow and diffusion
being the most important ones. The rate of exchange
(Figure 28), however, is determined by physical factors
such as hydrostatic pressure and oncotic pressure [38].

HYDROSTATIC PRESSURE

The hydrostatic pressure is the principal force in filtration

across capillary walls. It consists of two opposing forces:
Capillary Hydrostatic Pressure (PC) and Tissue (Interstitial)
Hydrostatic Pressure (PT). Since PC >>PT, the net
hydrostatic pressure gradient across the capillary is positive
Figure 28. Forces that affect the rate of fluid exchange and fluid flows from the capillary into the interstitium [38].
across the capillary [38].
Capillary Hydrostatic Pressure, Pc
Ficks First Law of diffusion describes movement (or flux)
across capillaries: Capillary hydrostatic pressure is dependent on the arterial
pressure, the venous pressure, precapillary (artery and
dn = DA C arteriolar) resistance, and postcapillary (venules and small
dt X /35/ veins) resistance (Figure 29).

dn An increase in arterial or venous pressure results in an

Where: = flux (moles/sec) increase in capillary hydrostatic pressure while a decrease
dt
D = diffusion constant in each has the opposite effect. Likewise, an increase in
A = surface area arteriolar resistance results in a decrease in capillary
C = concentration difference pressure while an increase in venous resistance results in an
increase in capillary pressure. Thus, since the capillary
X = thickness of barrier to diffusion.
hydrostatic pressure is highest at the arteriolar end of the
capillary and lowest at the venular end, filtration is favored
Bulk flow of fluid and electrolytes occurs through the pores
at the arteriolar end and reabsorption is favored at the
and intercellular clefts (d,e,f in Figure 27). Vesicles can
venular end [29; 38; and 39]. Capillary hydrostatic
also fuse together creating pores across endothelial cells to
pressure [29] is determined by:
allow bulk flow of fluid across the capillary (c in Figure
25). Unlike bulk flow, vesicular transport involves the
Rv
translocation of macromolecules across capillary Pa + Pv
endothelium (b in Figure 27). Finally, in active transport, Ra
Pc = /36/
vascular endothelial cells take up molecules such as ions, Rv
1+
glucose, and amino acids by transport mechanisms [27]. Ra
Where: Pc = Capillary hydrostatic pressure.
Pa = Arterial pressure.

2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-16
 Pv = Venous pressure.
Ra = Precapillary resistance (on the arterial side).
Rv = Postcapillary resistance (on the venous
side).
Tissue (Interstitial) Hydrostatic Pressure, PT
This pressure is dependent on the interstitial fluid volume
and by tissue compliance. Normal value for PT is nearly
zero. However, during enhance filtration or lymphatic
blockage, PT dramatically increases as a result of increased
interstitial fluid volume. It results in a decrease in the
hydrostatic gradient across the capillary thereby limiting
filtration [38; 39].
ONCOTIC PRESSURE
There are also two opposing oncotic pressures influencing
fluid exchange: capillary plasma oncotic pressure (C) and
tissue (interstitial) oncotic pressure (T).
Capillary Plasma Oncotic Pressure
Since the capillary barrier is permeable to ions, the osmotic
pressure within the capillary is determined by plasma
proteins that are impermeable. This pressure, which is
generated by colloids, is referred to as capillary plasma
oncotic pressure. Albumin is responsible for about 70% of
the oncotic pressure, which is typically at 25-30 mm Hg.
Along the length of the capillary especially along
capillaries with high net filtration, C increases along its
length because the filtering fluid leaves behind proteins
thereby increasing concentration of these proteins.
Tissue (Interstitial) Oncotic Pressure
This pressure depends on the interstitial protein
concentration and the reflection coefficient of the capillary
wall such that increased permeability of the capillary
barrier to proteins has a positive effect on T. This pressure
is also dependent on the amount of fluid filtered into the
interstitium such that an increase in capillary filtration
decreases interstitial protein concentration and reduces T
[29; 38; and 39].
Oncotic pressure difference, = C - T, is determined by
the following equation:
= ( )RT (Ci Co ) /37/
Where: = Oncotic pressure difference.
= Reflection coefficient.
R = Gas constant.
T = Absolute temperature.
Ci = Solute concentration inside the capillary.
Co = Solute concentration outside the capillary.
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL
Since C >> T, then the oncotic pressure difference, = C
- T, if unopposed by hydrostatic forces, would reabsorb
fluid from the interstitium into the capillary [29].
BALANCE OF HYDROSTATIC AND ONCOTIC
PRESSURESTARLING HYPOTHESIS
The Starling hypothesis expounds on the relationship
between hydrostatic pressure and oncotic pressure and their
role in regulating fluid passage across the capillaries. This
relationship can be expressed by the following equations:
J = k (P ) /38/
[( ) (
J = k Pc Pi p i )] /39/
J = k (Pc Po ) /40/
Where: J = Rate of fluid movement.
k = Filtration constant for the capillary
endothelium.
Pc = Capillary hydrostatic pressure.
Pi = Interstitial fluid hydrostatic pressure.
= Reflection coefficient.
p = Plasma protein oncotic pressure.
i = Intersititial fluid oncotic pressure.
( )
Po = p i + Pi
Filtration occurs when the algebraic sum of the hydrostatic
and oncotic pressures is positive while absorption occurs
when it is negative. In an idealized capillary, filtration
occurs at the arterial end while absorption occurs at the
venous end. However, this is not the case in most
capillaries, such as in the renal glomerulus, where filtration
has been observed over their entire lengths (Figure 30). In
other capillaries, such as in the intestinal mucosa, Starling
forces change when intestinal epithelium actively pumps
water from the intestinal lumen into the interstitium,
thereby promoting absorption of fluid (Figure 31).
Rate of fluid movement across the capillary (J) also
depends on the filtration constant of the capillary
endothelium (k):
k = Lp A /41/
Where: k = Capillary filtration constant.
Lp = Hydraulic conductivity of the endothelium.
A = Area of the capillary wall available for
Filtration.
Hydraulic conductivity of the endothelium is not affected
by arteriolar dilation nor is it affected by capillary
distension. However, capillary injury such as those due to
toxins and severe burns increases capillary permeability
such that large amounts of fluid and protein leaks out of the
capillaries into the interstitial space. Total capillary surface
available for filtration is dependent on the number of open
capillaries in a capillary bed [29].
A-17
 Windkessel Model

The heart beats rhythmically and creates pressure and flow

wave forms within the arteries. When the heart contracts,
pressure within the left ventricle increases until it is greater
than the pressure in the aorta, leading to the opening of the
aortic valve. Blood flows out of the ventricle into the aorta,
and through the contraction cycle, both flow and pressure
decrease until pressure within the aorta becomes higher
than in the ventricle, leading to the closing of the aortic
valve. The pressure in the ventricle decreases rapidly as
the muscle relaxes; however, the decrease in pressure in the
aorta occurs at a much slower rate as the elastic vessel acts
as a reservoir. The Windkessel model (Figure 32) is a
linear mechanical model of circulatory system. The aorta
and large vessels are modeled as a compliant chamber,
while the peripheral vessels are modeled as rigid tubes.
According to the model:

P
V =CP and Qout = , /42/
R

Where: V, P, and C are the volume, pressure, and

Figure 30. When PC > PO, capillaries exhibit filtration over compliance in the compliant chamber; Qout is the outflow
their entire lengths [29]. of the chamber; R is the linear resistance of the rigid tube;
and Pvenous is assumed to be zero. Law of Conservation of
Mass requires:
dP P
Qin = C + /43/
dt R

Figure 32. (a) The Windkessel model of the aorta and

peropheral circulation. (b) Electrical analog of the
Windkessel model [12, 3.21].

Figure 31. When PC < PO, absorption of fluid occurs [29].

ANALOG MODELS OF BLOOD FLOW

The circulatory system consists of a complex network of

branching tubes, and it is capable of adjusting itself in
response to certain stimuli from different systems within
the body. Analog models provide a means to analyze Figure 33. Electrical analog for blood flow in a
single vessels, or even the entire cardiovascular system. compliant vessel [12, 3.22].

2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-18
It is possible to solve equation /46/ analytically with
specific boundary conditions. Therefore, this equation can
be used to determine flow, pressure, compliance, or
resistance in the cardiovascular system [5, 170; 12, 3.21-
3.22; and 18, 125].
Electrical Analog Models
Electrical analogs are used to estimate blood flow trends,
and they result in the derivation of linear differential
equations. In the electrical models, the vessels resistance
to blood flow is represented by a resistor, the tube
compliance by a capacitor, and the blood inertia by
inductance. An electrical current can represent the blood
flow and the voltage can represent the blood pressure. The
system can be modeled as shown in Figure 33. Using
Kirchoffs law of currents, the governing differential
equation for the system becomes:
2 fluid particle model that can accurately measure scales
d P dP dQ
+ RC +P=L + RQ /44/
2 dt dt
dt
use of systems of algebraic equations that replace the
governing partial differential equations used normally to
solve fluid dynamics problems. CFD creates a solution
based on these algebraic equations by using iterations, due
to the non-linearity of the governing equations [9]. By
using a process of discretization the algebraic equations are
linked to the values of the dependent variables at the
adjacent point. One obstacle that is present in this type of
computational models is the generation of computational
meshes that accurately resolve both the complex geometry
and the physiologically flow features. Various studies have
been conducted in the field of circulatory system by using
CFD this is due to the fact that the equations that are used
to model the blood flow are non linear, complex and not
well constrained. Some of the studies done include: the
mechanism of aggregation of red blood cells in capillary
vessels. A discrete-particle model in 3D was used to model
the flow of plasma and red blood cells inside a capillary
tube. This particular work did not use classical CFD, but a
from 0.001 to 100 m. Different models were done such as
sickle cell and normal [26]. Examples are shown in figures
35 to 38.

The next study is based on arterial stenosis, a new method

of calculating coronary flow reserve (CFR) and fractional
flow reserve (FFR) based on pressure measurements
around the stenosed region was developed. In vitro studies
using CFD method was tested. The blood vessel was
modeled as a rigid tube, and the vascular bed as a porous
media. The blood was assumed to be a Newtonian fluid,
Figure 34. Lumped-parameter electrical analog and Navier-Stokes equations were solved by using the CFD
model of a multicompartment arterial segment. package FLUENT [20].
When vessels are attached in series as shown in Figure 34,
a more complex model is required to explain the system Now we shall present frequency dependence of dynamic
that is composed of numerous compartments, i = 1, 2, curvature effects on flow through coronary arteries. The
3etc. Kirchoffs law can be applied to each loop, entry to the tube was fixed but the radius of curvature was
resulting in: varied sinusoidally in time at two different frequencies (1
or 5 Hz). Computational studies were done on the flow
through a curved tube model of a coronary artery (Figure
dQi 35). From this model different studies on the time varying
Pi Pi 1 = Ri Qi + Li /45/
dt curvature on flow patterns that have been related to
arteriosclerosis were done. CFD software was used to
model this particular curved tube [16].
Vi
Pi = /46/ FLOW IN THE ASCENDING AORTA
Ci
Flow in the ascending aorta is complex, pulsatile, and
dVi three-dimensional. Kilner et al. (1993) and Bogren and
Qi Qi 1 = /47/ Bounocore (1999) visualized aortic flow patterns with a
dt Magnetic Resonance Velocity Mapping technique. They
found that the right-handed helical flow through the
Again, the system can be solved with the appropriate ascending aorta to the aortic arch was unstable.
boundary conditions. The RCL characteristics can be
derived from the specific properties of the blood and They attributed the skewed pattern to flow in a curved tube.
vessels [12, 3.22-3.23]. Both groups also noticed a retrograde flow in the inner
curvature of the ascending aorta during late systole and
COMPUTATIONAL FLUID DYNAMICS (CFD) diastole but could not speculate on the cause [11, 13]. A
combination of magnetic resonance imaging (MRI) and
Computational techniques are widely used for studying CFD was used by Jin et al (2001) to simulate flow patterns
hemodynamics in the circulatory system CFD involve the in the ascending aorta.
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-19
Figure 35. (a) Fluid particle model, (b) RBC model made
of flexible particles, (c) RBC model after volume Figure 37. Color-encoded wall shear rate in a curved
rendering, and (d) real image of deformed RBC [26]. bifurcation model of a coronary artery whose curvature is
being varied in time [16].

Figure 36. Computational flow model for a stenosed

vessel [20].

Their results revealed the following: (1) in contrast to the

previously reported retrograde flow in the inner curvature
of the ascending aorta by Kilner et al. (1993) and Bogren
and Bounocore (1999), a relatively steady, large vortex
during late systole and most of diastole was discovered and
(2) the skewing flow pattern seemed to be formed as a
Figure 38. Effects of the unsteady movement of the lumen
result of the acceleration movement of the ascending aorta
on flow patterns [11, 14].
rather than the geometric influence of curvature as
previously thought [11, 13-14].
RESEARCH ADVANCES
Unsteady movement of the lumen had a strong effect on the
Biologists at the California Institute of Technology have
flow patterns. Figure 38a shows velocity contours of MRI
uncovered an unsuspected but fundamental genetic rule
data at middle systole; 38b shows computed velocity
governing the formation of the cardiovascular system. The
contours of the moving wall model at same time and same
cells destined to form arteries and veins are already
location as 38a; 38c shows computed contours with the
genetically distinct at the earliest stages of blood vessel
wall radial expansion-contraction model; and 36d shows
formation in the embryo. It is likely that arteries and veins
contours of a rigid wall model. While Figures 36a and 36b
will differ in their expression of many other genes that have
show similar peak flow velocity positions during systole,
yet to be discovered. Such genes may lead to the
Figures 38c and 38d provide evidence of different pattern
development of new artery- or vein-specific drugs, or may
behavior [11, 14].
help to target known drugs specifically to either arteries or
veins. Such advances could potentially enhance the efficacy
or specificity of blood vessel-directed anticancer drugs
[30].
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-20
 CONLUSIONS
The cardiovascular and lymphatic systems work in unison
to form the human bodys circulatory system. Blood, the
biofluid of the cardiovascular system, can be broken down
into two constituents, namely formed elements and plasma.
Fluid, electrolytes, respiratory gases, and leukocytes leave
and enter the blood at the level of the capillaries, and some
of these excess components accumulate in the interstitial
fluid. It is the job of the lymphatic system to constantly
drain the excess interstitial fluid and return it to the venous
blood, thereby maintaining the fluid balance within the
human body. It is because of this that the composition of
lymph closely resembles that of plasma, except for the
abundance of proteins and lipids. Lymph has a lower
concentration of proteins and a higher concentration of
lipids than the blood plasma.
Blood is nonhomogeneous and anisotropic, and it contains
a suspension of particles that display viscoelastic
properties. All of this contributes to why blood does not
obey Newtons linearized law of viscosity. Instead, bloods
viscoelastic deformation can be modeled by the power law
or by its manipulation, the Casson equation. Many trends
in the deformation properties of blood have been witnessed.
It has been found that increasing shear rate, decreasing
hematocrit, decreasing vessel size, and increasing
temperature all lead to a decrease in the apparent viscosity
of blood. The Casson equation could be fitted to the
experimental data between shear rate and shear stress;
however, at high shear rates, blood tended to display more
linear, Newtonian qualities. In addition, increasing
hematocrit percent led to increases in yield stress.
The flow in the venous system is dependent on the diameter
(or radius), length, and viscosity of the blood. Other
factors are the organization of the vascular network (series
and parallel arrangements), and extravascular mechanical
forces acting upon the vasculature. In the venous system,
veins have less well-developed intima and media than
comparable sized arteries. They represent a large
distensible sink or reservoir for blood volume such that
50% of the circulating blood volume is in the systemic
venous system at rest. Most veins are 1-9 mm in diameter
with a well-developed adventitia. Small and medium sized
veins have valves to prevent backflow within their lumens.
The valves consist of two folds of the tunica intima
composed of elastic tissue and covered with endothelium
that project into the lumen.
To understand capillary fluid exchange requires knowledge
of the capillary. There are three different types of
capillaries: (1) Continuous with the lowest permeability
consists of a basement membrane that is continuous and
intercellular clefts that are tight; (2) Fenestrated with
relatively high permeability consists of perforations in the
endothelium; and (3) Discontinuous with extremely high
permeability consists of large intercellular gaps and gaps in
the basement membrane.
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL
Fluid, electrolytes, gases, and other substances transverse
the capillaries by different mechanisms: (1) Diffusion; (2)
Bulk flow; (3) Vesicular transport; and (4) Active
transport. The rate of exchange, however, is determined by
physical factors such as hydrostatic pressure and oncotic
pressure. The hydrostatic pressure is the principal force in
filtration across capillary walls. It consists of two opposing
forces: capillary hydrostatic pressure and tissue
(interstitial) hydrostatic pressure. There are also two
opposing oncotic pressures influencing fluid exchange:
capillary plasma oncotic pressure and tissue (interstitial)
oncotic pressure. The Starling hypothesis expounds on the
relationship between hydrostatic pressure and oncotic
pressure and their role in regulating fluid passage across the
capillaries. Filtration occurs when the algebraic sum of the
hydrostatic and oncotic pressures is positive while
absorption occurs when it is negative.
The human circulatory system is a complex network of
branching arteries, each with a different compliant nature
and flow characteristics. The pressure and flow in the
circulatory system is under the autonomic control, so
certain vessels can dilate and constrict, and the properties
of the fluid can change over time. It is almost impossible
to accurately model the circulatory system as it is not
possible to include all known variables in a single model.
If all the known variables were included, the model would
become complex and difficult to solve. Due to this, the
approach adopted included a simplified model whose
complexity was increased in order to provide a better
understanding of blood flow within the arteries. Initially,
laminar flow in a rigid, cylindrical tube was investigated,
and this gave rise to Poiseuilles formula for flow rate. The
results showed an inverse relationship between pressure
and vessel radius and the direct relationship between flow
rate and radius.
Pulsatile flow, as is observed in the aorta and other large
arteries, was also considered. It was seen that as the
Womersly parameter was increased, the velocity profile
became more blunt. Wave propagation in elastic arteries
was calculated, and it was found that the speed of
propagation was dependent on the pressure change with
area.
Analog models were used to understand the blood flow. In
a mechanical model, the Windkessel model, the flow was
found to be dependent of the pressure change with time, the
compliance of the elastic vessel, and the resistance of the
peripheral vessels. In an electrical model using Kirchoffs
law of currents: pressure, flow, compliance, resistance, and
fluid inertial effects were each given electrical analogs.
Although it was possible to describe blood flow in the
arteries using mathematical, mechanical, and electrical
models, none of the models, however, could encompass all
properties of the arteries and blood.
A-21
 ACKNOWLEDGEMENTS
This study was aided in part by the teachings of Dr. James
E. Moore Jr, Florida International University, Fluid
Mechanics Applications in Physiologic Systems. Our
thanks to Megh R. Goyal, University of Peurto Rico for
reviewing this article.
REFERENCES
1. Aaronson, P.I. 1999. The Cardiovascular System at a
Glance. Massachusetts: Blackwell Science.
2. Altman, P.L. 1961. Blood and Other Body Fluids.
Washington, D.C.: Federation of American Societies
of Experimental Biology, 1961.
3. Enderle, J.D., Blanchard, S.M. and Bronzino, J.D.
2000. Introduction to Biomedical Engineering. San
Diego: Academic Press.
4. Fournier, R.L. 1998. Basic Transport Phenomena in
Biomedical Engineering. Pennsylvania: Taylor &
Francis.
5. Fung, Y.C. 1997. Biomechanics: Circulation. New
York: Springer-Verlag
6. Fung, Y.C. 1993. Biomechanics: Mechanical
Properties of Living Tissues. New York: Springer-
Verlag.
7. Fung, Y.C. 1990. Biomechanics- Motion, Flow, Stress,
and Growth. New York: Springer-Verlag.
8. Geankoplis, C. J. 1993 Transport Processes and Unit
Operations 3rd Edition, New Jersey: Prentice Hall
9. Gutierrez, Ronald. 2003. Personal communication.
Miami-Fl: Tissue and Bioengineering Lab, Florida
International University.
10. Guyton, A.C. and Hall, J.E. 2000. Medical
Physiology. 10th edition. Philadelphia, PA: W.B.
Saunders Company.
11. Jin, S., Oshinki, J. and Giddens, D. 2001. Effects of
inflow conditions and wall motion on flow in the
ascending aorta. 2001 Bioengineering Conference.
12. Kutz, M. 2003. Standard Handbook of Biomedical
Engineering Design. New York: McGraw-Hill.
13. Liepsh, D. 2002. An introduction to biofluid
mechanicsbasic models and applications. Journal
of Biomechanics.
14. Lightfoot, E. N. 1974 Transport Phenomena and
Living Systems. New York: John Wiley & Sons Inc.
15. Martini, F.H. 2001. Fundamentals of Anatomy and
Physiology. New Jersey: Prentice Hall.
16. Moore, J.E. 2001. Frequency dependence of dynamic
curvature effects on flow through coronary arteries.
Journal of biomechanical engineering.
17. MountCastle, V.B. 1974. Medical Physiology. 13th
edition, Saint Louis,MO: C. V. Mosby Company.
18. Nichols, W.W. and ORourke, M.F. 1990.
McDonalds Blood Flow in Arteries: Theoretical,
Experimental, and Clinical Principles. London:
Hodder and Stoughton.
19. Nieweg, O.E., Essner, R., Reintgen, D.S. and
Thompaon, J.F. 2000. Lymphatic Mapping and Probe
Applications in Oncology. New York: Marcel Dekker
Inc.
2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL
20. Shalman, E. 2001. Pressure-based simultaneous CFR
and FFR measurements: understanding the physiology
of a stenosed vessel. Computers in biology and
medicine.
21. Skofronich, J.G., Cameron J.R., and Grant, R.M.
1999. Physics of the Body. 2nd edition.. Wisconsin :
Medical Physics Publishing.
22. Stanely, A. B., Stroud, J.S. and Rayz, V.
Hemodynamic Simulations of Flow in Veins. 2001.
ASME International Mechanical Engineering
Congress and Exposition Journal.
23. Tortora, G.J. and Grabowski, R.R. 1996. Principles of
Anatomy and Physiology. New York: Harper Collins.
24. Van de Vosse, F. N., Gijsen, F. J. H., and Wolters, B.
J. B. M. 2001. Numerical analysis of coronary artery
flow. 2001 Bioengineering Conference.
25. Wood, N.B. 1999. Aspects of Fluid Dynamics
Applied to Larger Arteries Journal of Theoretical
Biology, 199:137-161.
26. Yuen, D.A. 2003. A discrete-particle model of blood
dynamics in capillary vessels. Journal of colloid and
interface science.
27. http://cvphysiology.com/Microcirculation/M016.htm
28. http://cwx.prenhall.com/bookbind/pubbooks/martini7/
chapter20/medialib/CH20/html/ch2036.html.
The Heart.
29. http://human.physiol.arizona.edu/SCHED/CV/Baldwi
n/Bald19/Baldwin.L19.html. Transcapillary Fluid
Exchange: Starling Forces.
30. http://pr.caltech.edu/media/lead/052998DA.html.
Tinidol, R. May 1998.
31. http://scienceworld.wolfram.com/physics/Navier-
StokesEquations.html. Navier-Stokes Equations.
Wolfram Research: Scienceworld
32. http://thesis.library.drexel.edu/archive/00000084
33. http://thesis.library.drexel.edu/view/subjects/Non-
Newtonian%20fluids.html. Drexel University
Sangho, K. 2002. Study of Non-Newtonian viscosity
and yield stress of blood in a scanning capillary-tube
rheometer.
34. http://www.coheadquarters.com/PennLibr/MyPhysiolo
g/lect5/Tables5.01.htm. Hemodynamics
35. http://www.cvphysiology.com/Hemodynamics/H001.h
tm. Hemodynamics.
36. http://.www.cvrti.utah.edu/~macleod/bioen/be6010/no
tes/hemo-bw.pdf
37. http://www.jdaross.cwc.net/heart2. The Circulatory
System. John Ross
38. http://www.oucom.ohiou.edu/cvphysiology/
M011.htm. Cardiovascular Physiology Concepts:
Capillary Fluid Exchange.
39. http://www.oucom.ohiou.edu/cvphysiology/
M012.htm. Cardiovascular Physiology Concepts:
Hydrostatic and Oncotic Pressures.
A-22
 GLOSSARY OF TERMS
Abdominal aorta - The portion of the aorta in the
abdomen.
Alveoli - Air sacs in the lungs where oxygen and carbon
dioxide are exchanged.
Aorta - The largest artery in the body and the initial blood-
supply vessel from the heart
Aortic valve - The valve that regulates blood flow from the
heart into the aorta.
Arterioles - Small, muscular branches of arteries. When
they contract, they increase resistance to blood flow, and
blood pressure in the arteries increases.
Artery - A vessel that carries oxygen-rich blood to the
body.
Vein Any one of a series of blood vessels of the vascular
system that carries blood from various parts of the body
back to the heart; returns oxygen-depleted blood to the
heart.
Ventricle (right and left) One of the two lower
chambers of the heart, either on the left or right.
Ventricular fibrillation A condition, in which the
ventricles contract in a rapid, unsynchronized fashion.
When fibrillation occurs, the ventricles cannot pump blood
throughout the body.

Blood Pressure The force or pressure exerted by the

heart in pumping blood; the pressure of blood in the arteries

Cardiac Pertaining to the heart

Cardiac output - The amount of blood the heart pumps
through the circulatory system in one minute.
Cardiology The study of the heart and its function in
health and disease
Cardiovascular (CV) Pertaining to the heart and blood
vessels. The circulatory system of the heart and blood
vessels is the cardiovascular system.
Circulatory System Pertaining to the heart, blood
vessels and the circulation of blood.
Coronary arteries - Two arteries arising from the aorta
that arch down over the top of the heart and divide into
branches. They provide blood to the heart muscle.

Inferior vena cava - The large vein returning blood from

the legs and abdomen to the heart.

Lipid - A fatty substance insoluble in blood.

Platelets One of the three types of cells found in blood;

they aid in the clotting of the blood

Pulmonary Referring to the lungs and respiratory system

Pulmonary valve The heart valve between the right
ventricle and the pulmonary artery. It controls blood flow
from the heart into the lungs.
Pulmonary vein The blood vessels that carry newly
oxygenated blood from the lungs back to the left atrium of
the heart.

Sodium - A mineral essential to life found in nearly all

plant and animal tissue. Table salt (sodium chloride) is
nearly half sodium.
Stenosis - The narrowing or constriction of an opening,
such as a blood vessel or heart valve.
Superior vena cava - The large vein that returns blood
from the head and arms to the heart.

Thrombosis - A blood clot that forms inside the blood

vessel or cavity of the heart.

Vascular - Pertaining to the blood vessels.

2003 Congress on Biofluid Dynamics of Human Body Systems at Biomedical Engineering - FIU, Miami - FL A-23