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POWERPOINT® LECTURE SLIDE PRESENTATION
by LYNN CIALDELLA, MA, MBA, The University of Texas at Austin
Additional Text by J Padilla Exclusively for physiology at ECC
UNIT 3
15
PART A
Blood Flow and the
Control
of Blood Pressure
HUMAN PHYSIOLOGY
AN INTEGRATED APPROACH
DEE UNGLAUB SILVERTHORN
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FOURTH EDITION
Overview: Cardiovascular System
Arteries take blood
away from the heart
and veins return it.
Arteries connect to
arterioles, that
connect to capillaries,
that connect to
venules, that connect
to veins
Two portal systems
shown here have two
sets of capillaries
connected
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Figure 14-1
Functional Model of the Cardiovascular System
Systemic
Arteries
maintain
pressure during
ventricular
relaxation by
changing
vessel diameter
Arteries and
veins are for
travel and
capillaries for
exchange
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 15-1
Blood Vessel Structure
Blood vessels vary in
diameter and wall
thickness.
Veins have a larger
diameter and thinner
walls than arteries.
Capillaries are thin
enough to allow for
diffusion and narrow
to restrict RBC to flow
in single file
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Figure 15-2
Metarterioles
Capillaries lack smooth muscle and elastic tissue
reinforcement which facilitates exchange
The walls are thin
enough to allow WBC
and plasma to scape.
Plasma that leaves the
capillaries and bathes
the tissues will be
called lymph and will
be collected by
lymphatic capillaries.
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Figure 15-3
Precapillary Sphincters
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Figure 15-15a
Capillaries: Exchange
 Plasma and cells exchange materials across thin
capillary wall
 Capillary density is related to metabolic activity of
cells
 Capillaries have the thinnest walls
 Single layer of flattened endothelial cells
 Supported by basal lamina
 Bone marrow, liver and spleen do not have typical
capillaries but sinusoids
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Two Types of Capillaries
Continous Capillary
Fenestrated Capillary
Sinusoidal Capillary
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Angiogenesis
 New blood vessel development- after birth, happens to
accommodate tissue growth like when one gains weight
 Necessary for normal development- growth needed during
childhood
 Wound healing and uterine lining growth- blood vessel
formation needed in adulhood
 Controlled by cytokines- chemical signal that induce mitosis
 Mitogens: VEGF and FGF- vascular endothelial growth factor
and fibroblast growth factor
 Inhibit: angiostatin and endostatin- these natural occuring
chemicals are being used to treat cancer and coronary disease
 Coronary heart disease
 Collateral circulation- natural formation of additional blood
vessels to supplement flow of blocked vessels
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Velocity of Blood Flow
Velocity of flow depends
on total cross-sectional
area of the vessels.
The greater the total
cross-sectional area
the slower the
velocity. Velocity is
slowest at the
capillaries. Although
the diameter of a
capillary is smaller
than any other vessel
its total cross-sectional
area is greater than
any other.
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Figure 15-17
Review of Blood Flow
Flow is inversely proportional to resistance. Resistance
is influenced by vessel diameter. The larger the diameter
the slower the speed as long as the flow rate is constant.
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Pressure Differences in Static
and Flowing Fluids
Pressure falls over distance as energy is lost because of friction. In
circulation the further away the blood is from the heart the
lower the pressure. Pressure is lower is veins than in arteries
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Figure 14-3a
Fluid Flow through a Tube
Flow  ∆P
Pressure
gradient
cause a
fluid to
flow .
Blood
vessels
create
pressure
gradients
by altering
diameter
size
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Figure 14-4
The Role of Radius in Determining
Resistance to Flow
A small change in diameter can use a great
change in resistance and flow. Thus blood
vessels can dramatically alter blood flow when
they vasoconstrict or vasodialate
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Figure 14-5
Fluid Rate Versus Velocity of Flow
The velocity of flow is influenced by cross-sectional
area. Although a large cross-sectional area may allow
more fluid to pass at one time, it also causes it to
slow down. Don’t think of cross-sectional area as the
diameter of the blood vessel.
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Figure 14-6
Pressure throughout the Systemic Circulation
Blood pressure is highest in the
arteries and decreases
continuously as it flows through
the circulatory system.
Systolic pressure is exerted on
vessel walls when the heart
contracts
Diastolic pressure is pressure
during heart relaxation.
Pulse pressure measures
strength of pressure wave
systolic P – diastolic P
Mean arterial pressure
measures driving pressure
diastole P + 1/3 pulse pressure.
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 15-5
Elastic Recoil in Arteries
This process explains how pressure is
transferred to blood vessels when the heart
contracts
(a) Ventricular contraction
Arterioles
1
2
3
1
Ventricle contracts.
3
2
Semilunar valve opens.
Aorta and arteries expand
and store pressure in
elastic walls.
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 15-4a
Elastic Recoil in Arteries
This process explains how pressure is
maintained in blood vessels while the heart
relaxes
(b) Ventricular relaxation
1
2
3
1
Isovolumic ventricular
relaxation occurs.
3
2
Semilunar valve shuts,
preventing flow back
into ventricle.
Elastic recoil of arteries
sends blood forward into
rest of circulatory system.
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 15-4b
Measurement of Arterial Blood Pressure
Pulse Pressure = systolic P – diastolic P
Valves ensure one-way flow in veins
MAP = diastolic P + 1/3(systolic P – diastolic P)
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 15-7
Pressure Change
 Pressure created by contracting muscles of the heart and blood
vessels is transferred to blood
 Driving pressure is created by the ventricle. Thus usually
blood pressure reading focus on left ventricular systole and
diastole and arterial pressure not venous pressure.
 If blood vessels constrict, blood pressure increases because the
diameter decreases and the muscle exerts more pressure on the
blood.
 If blood vessels dilate, blood pressure decreases because the
opposite happens.
 Blood volume changes are major factors for blood pressure in
CVS. Drinking a lot of fluid increases blood volume, blood
loss and dehydration decreases blood volume. The kidneys try
to regulate blood volume via fluid loss or retention. The CV
system cause changes in diameter to help compensate when
posible.
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Blood Pressure
Blood pressure control involves both the cardiovascular
system and the renal system
Increase or
decrease in
blood volume
is
compensated
by CV and
kidney
changes
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 15-9
Stroke Volume and Cardiac Output
 Stroke volume
 Amount of blood expelled by one ventricle during a contraction
 EDV – ESV = stroke volume
 Force of contraction
 Stroke volume increases of decreases based on contraction force
 Affected by length of muscle fiber and contractility of heart
 Frank-Starling law
 Stroke volume increase as EDV increases
 EDV determined by venous return
 Skeletal muscle pump
 Respiratory pump
 Sympathetic innervation
 Cardiac output
 Volume of blood pumped by one ventricle in a given period of time
 CO = HR  SV (heart rate times stroke volume)
 Average = 5 L/min
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Factors that Affect Cardiac Output
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Figure 14-31
Blood Pressure
Mean arterial pressure is a function of cardiac output
and resistance in the arterioles= the volume produced by
the heart times vessel radius (vasodilation/vasoconstriction)
Copyright © 2007 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 15-8
Arteriolar Resistance (vasoconstriction)
 Sympathetic reflexes- control blood distribution as needed to maintian
homeostasis such as body temperature
 Local control of arteriolar resistance- based on metabolism of tissue and tissue
needs for blood flow, can override CNS control in heart and muscle
 Hormones- those that bind to kidney cells and control salt and water levels.
 Myogenic autoregulation- increased blood flow causes increase pressure that
stretches the walls. The smooth muscle responds by contracting thus increasing
resistance and reducing flow. Therefore, no neural input is needed
 Paracrines –secreted by endothelium, allows for local control
 Active hyperemia- increase blood flow accompanies increased metabolic
activity. As more paracrines accumulate, they call for more blood.
 Reactive hyperemia- increase blood flow after a state of abnormally low
metabolic rate due local hypoxia. Nitric oxide is made for vasodilation
 Sympathetic control
 SNS: norepinephrine; tonic release maintains myogenic tone, increase release
causes vasoconstriction
 Adrenal medulla: epinephrine: heart, liver, and skeletal muscle vasodilate
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Hyperemia
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Figure 15-11a
Norepinephrine
Tonic control of arteriolar diameter
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Figure 15-12
Factors that Influence Mean Arterial Pressure
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Figure 15-10
Blood Pressure
Components of the baroreceptor reflex
KEY
Stimulus
Sensor/receptor
Integrating center
Efferent pathway
Effector
Medullary
cardiovascular
control
center
Change in
blood
pressure
Carotid and aortic
baroreceptors
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Figure 15-21
Blood Pressure
KEY
Medullary
cardiovascular
control
center
Stimulus
Sensor/receptor
Integrating center
Efferent pathway
Change in
blood
pressure
Effector
Parasympathetic
neurons
Carotid and aortic
baroreceptors
Sympathetic
neurons
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Figure 15-21 (5 of 10)
Blood Pressure
KEY
Medullary
cardiovascular
control
center
Stimulus
Sensor/receptor
Integrating center
Efferent pathway
Change in
blood
pressure
Effector
Parasympathetic
neurons
Sympathetic
neurons
Carotid and aortic
baroreceptors
SA node
Ventricles
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Figure 15-21 (8 of 10)
Blood Pressure
KEY
Medullary
cardiovascular
control
center
Stimulus
Sensor/receptor
Integrating center
Efferent pathway
Change in
blood
pressure
Effector
Parasympathetic
neurons
Sympathetic
neurons
Carotid and aortic
baroreceptors
SA node
Ventricles
Veins
Arterioles
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Figure 15-21 (10 of 10)
Blood Pressure
The
baroreceptor
reflex: the
response to
increased blood
pressure
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Figure 15-22
Blood Pressure
The baroreceptor
reflex: the response
to orthostatic
hypotension
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Figure 15-23
Distribution of Blood
Distribution of blood in the body at rest
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Figure 15-13
Cardiovascular disease (CVD): Risk Factors
 Risk factors that are not controllable
 Gender
 Age
 Family History
 Risk factors that are controllable




Smoking
Obesity
Sedentary lifestyle
Untreated hypertension
 Uncontrollable genetic but modifiable lifestyle
 Blood lipids
 Leads to atherosclerosis
 HDL-C versus LDL-C
 Diabetes mellitus
 Metabolic disorder contributes to development of atherosclerosis
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LDL and Plaque
The development of atherosclerotic plaques
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Figure 15-24
Hypertension
Graph shows the relationship between
blood pressure and the risk of
developing cardiovascular disease
Essential hypertension has no clear
cause other than hereditary
 Carotid and aortic baroreceptors
adapt
 Risk factor for atherosclerosis
 Heart muscle hypertrophies
 Pulmonary edema
 Congestive heart failure
 Treatment
 Calcium channel blockers,
diuretics, beta-blocking drugs, and
ACE inhibitors
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Figure 15-25