Human Anatomy & PhysiologyNinth Edition
PowerPoint® Lecture Slides
prepared by
Barbara Heard,
Atlantic Cape Community
College
C H A P T E R
© 2013 Pearson Education, Inc.© Annie Leibovitz/Contact Press Images
The CardiovascularSystem: BloodVessels: Part A
19
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Structure of Blood Vessel Walls
• Lumen
– Central blood-containing space
• Three wall layers in arteries and veins
– Tunica intima, tunica media, and tunica
externa
• Capillaries
– Endothelium with sparse basal lamina
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Tunica intima
• Endothelium• Subendothelial layer• Internal elastic membrane
Tunica media
(smooth muscle and elastic fibers)• External elastic membrane
Valve
Tunica externa
(collagen fibers)
Lumen
Artery Capillary network
Lumen
Vein
Endothelial cells
Capillary
Basement membrane
• Vasa vasorum
Figure 19.1b Generalized structure of arteries, veins, and capillaries.
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Tunics
• Tunica intima
– Endothelium lines lumen of all vessels
• Continuous with endocardium
• Slick surface reduces friction
– Subendothelial layer in vessels larger than
1 mm; connective tissue basement membrane
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Tunics
• Tunica media
– Smooth muscle and sheets of elastin
– Sympathetic vasomotor nerve fibers control
vasoconstriction and vasodilation of
vessels
• Influence blood flow and blood pressure
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Tunics
• Tunica externa (tunica adventitia)
– Collagen fibers protect and reinforce; anchor
to surrounding structures
– Contains nerve fibers, lymphatic vessels
– Vasa vasorum of larger vessels nourishes
external layer
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Figure 19.2 The relationship of blood vessels to each other and to lymphatic vessels.
Venous system Arterial system
Large veins(capacitancevessels)
Largelymphaticvessels
Elasticarteries(conductingarteries)
Musculararteries(distributingarteries)
Lymphnode
Lymphaticsystem
Small veins(capacitancevessels)
Arteriovenousanastomosis
Lymphaticcapillaries
Sinusoid
Arterioles(resistancevessels)
Terminalarteriole
MetarteriolePrecapillarysphincter
Capillaries(exchangevessels)
Thoroughfarechannel
Postcapillaryvenule
Heart
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Arterial System: Elastic Arteries
• Large thick-walled arteries with elastin in
all three tunics
• Aorta and its major branches
• Large lumen offers low resistance
• Inactive in vasoconstriction
• Act as pressure reservoirs—expand and
recoil as blood ejected from heart
– Smooth pressure downstream
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Arterial System: Muscular Arteries
• Distal to elastic arteries
– Deliver blood to body organs
• Thick tunica media with more smooth
muscle
• Active in vasoconstriction
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Arterial System: Arterioles
• Smallest arteries
• Lead to capillary beds
• Control flow into capillary beds via
vasodilation and vasoconstriction
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Table 19.1 Summary of Blood Vessel Anatomy (1 of 2)
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Capillaries
• Microscopic blood vessels
• Walls of thin tunica intima
– In smallest one cell forms entire
circumference
• Pericytes help stabilize their walls and
control permeability
• Diameter allows only single RBC to pass
at a time
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Capillaries
• In all tissues except for cartilage, epithelia,
cornea and lens of eye
• Provide direct access to almost every cell
• Functions
– Exchange of gases, nutrients, wastes,
hormones, etc., between blood and interstitial
fluid
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Capillaries
• Three structural types
1. Continuous capillaries
2. Fenestrated capillaries
3. Sinusoid capillaries (sinusoids)
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Continuous Capillaries
• Abundant in skin and muscles
– Tight junctions connect endothelial cells
– Intercellular clefts allow passage of fluids and
small solutes
• Continuous capillaries of brain unique
– Tight junctions complete, forming blood brain
barrier
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Figure 19.3a Capillary structure.
Pericyte
Red bloodcell in lumen
Intercellularcleft
Endothelialcell
Basementmembrane
Tight junction
Endothelialnucleus
Pinocytoticvesicles
Continuous capillary. Least permeable, and mostcommon (e.g., skin, muscle).
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Fenestrated Capillaries
• Some endothelial cells contain pores
(fenestrations)
• More permeable than continuous
capillaries
• Function in absorption or filtrate formation
(small intestines, endocrine glands, and
kidneys)
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Figure 19.3b Capillary structure.
Pinocytoticvesicles
Red bloodcell in lumen
Fenestrations(pores)
Intercellularcleft
Endothelialcell
Endothelialnucleus
Basement membrane
Tight junction
Fenestrated capillary. Large fenestrations (pores)increase permeability. Occurs in areas of activeabsorption or filtration (e.g., kidney, small intestine).
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Sinusoid Capillaries
• Fewer tight junctions; usually fenestrated;
larger intercellular clefts; large lumens
• Blood flow sluggish – allows modification
– Large molecules and blood cells pass
between blood and surrounding tissues
• Found only in the liver, bone marrow,
spleen, adrenal medulla
• Macrophages in lining to destroy bacteria
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Figure 19.3c Capillary structure.
Endothelialcell
Red bloodcell in lumen
Largeintercellularcleft
Nucleus ofendothelialcell
Incompletebasementmembrane
Sinusoid capillary. Most permeable. Occurs in speciallocations (e.g., liver, bone marrow, spleen).
Tight junction
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Capillary Beds
• Microcirculation
– Interwoven networks of capillaries between
arterioles and venules
– Terminal arteriole metarteriole
– Metarteriole continuous with thoroughfare
channel (intermediate between capillary and
venule)
– Thoroughfare channel postcapillary
venule that drains bed
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Capillary Beds: Two Types of Vessels
• Vascular shunt (metarteriole—
thoroughfare channel)
– Directly connects terminal arteriole and
postcapillary venule
• True capillaries
– 10 to 100 exchange vessels per capillary bed
– Branch off metarteriole or terminal arteriole
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Blood Flow Through Capillary Beds
• True capillaries normally branch from
metarteriole and return to thoroughfare
channel
• Precapillary sphincters regulate blood
flow into true capillaries
– Blood may go into true capillaries or to shunt
• Regulated by local chemical conditions
and vasomotor nerves
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Vascular shunt
Precapillary sphinctersMetarteriole Thoroughfare
channel
Terminal arteriole
True
capillaries
Postcapillary venule
Sphincters open—blood flows through true capillaries.
Terminal arteriole Postcapillary venule
Sphincters closed—blood flows through metarteriole – thoroughfare
channel and bypasses true capillaries.
Figure 19.4 Anatomy of a capillary bed.
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Venous System: Venules
• Formed when capillary beds unite
– Smallest postcapillary venules
– Very porous; allow fluids and WBCs into
tissues
– Consist of endothelium and a few pericytes
• Larger venules have one or two layers of
smooth muscle cells
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Figure 19.5 Relative proportion of blood volume throughout the cardiovascular system.
Pulmonary bloodvessels 12%
Systemic arteriesand arterioles 15% Heart 8%
Capillaries 5%
Systemic veinsand venules 60%
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Veins
• Adaptations ensure return of blood to
heart despite low pressure
– Large-diameter lumens offer little resistance
– Venous valves prevent backflow of blood
• Most abundant in veins of limbs
– Venous sinuses: flattened veins with
extremely thin walls (e.g., coronary sinus of
the heart and dural sinuses of the brain)
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Table 19.1 Summary of Blood Vessel Anatomy (2 of 2)
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Figure 19.1a Generalized structure of arteries, veins, and capillaries.
Artery
Vein
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Vascular Anastomoses
• Interconnections of blood vessels
• Arterial anastomoses provide alternate
pathways (collateral channels) to given
body region
– Common at joints, in abdominal organs, brain,
and heart; none in retina, kidneys, spleen
• Vascular shunts of capillaries are
examples of arteriovenous anastomoses
• Venous anastomoses are common
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Physiology of Circulation: Definition of
Terms
• Blood flow
– Volume of blood flowing through vessel,
organ, or entire circulation in given period
• Measured as ml/min
• Equivalent to cardiac output (CO) for entire
vascular system
• Relatively constant when at rest
• Varies widely through individual organs, based on
needs
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Physiology of Circulation: Definition of
Terms
• Blood pressure (BP)
– Force per unit area exerted on wall of blood
vessel by blood
• Expressed in mm Hg
• Measured as systemic arterial BP in large arteries
near heart
– Pressure gradient provides driving force that
keeps blood moving from higher to lower
pressure areas
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Physiology of Circulation: Definition of
Terms
• Resistance (peripheral resistance)
– Opposition to flow
– Measure of amount of friction blood
encounters with vessel walls, generally in
peripheral (systemic) circulation
• Three important sources of resistance
– Blood viscosity
– Total blood vessel length
– Blood vessel diameter
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Resistance
• Factors that remain relatively constant:
– Blood viscosity
• The "stickiness" of blood due to formed elements
and plasma proteins
• Increased viscosity = increased resistance
– Blood vessel length
• Longer vessel = greater resistance encountered
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Resistance
• Blood vessel diameter
– Greatest influence on resistance
• Frequent changes alter peripheral
resistance
• Varies inversely with fourth power of
vessel radius
– E.g., if radius is doubled, the resistance is
1/16 as much
– E.g., Vasoconstriction increased resistance
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Resistance
• Small-diameter arterioles major
determinants of peripheral resistance
• Abrupt changes in diameter or fatty
plaques from atherosclerosis dramatically
increase resistance
– Disrupt laminar flow and cause turbulent flow
• Irregular fluid motion increased resistance
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Relationship Between Blood Flow, Blood
Pressure, and Resistance
• Blood flow (F) directly proportional to blood pressure gradient ( P)
– If P increases, blood flow speeds up
• Blood flow inversely proportional to peripheral resistance (R)
– If R increases, blood flow decreases:
F = P/R
• R more important in influencing local blood flow because easily changed by altering blood vessel diameter
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Systemic Blood Pressure
• Pumping action of heart generates blood
flow
• Pressure results when flow is opposed by
resistance
• Systemic pressure
– Highest in aorta
– Declines throughout pathway
– 0 mm Hg in right atrium
• Steepest drop occurs in arterioles
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Systolic pressure
Mean pressure
Diastolic
pressure
120
100
80
60
40
20
0
Figure 19.6 Blood pressure in various blood vessels of the systemic circulation.
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Arterial Blood Pressure
• Reflects two factors of arteries close to
heart
– Elasticity (compliance or distensibility)
– Volume of blood forced into them at any time
• Blood pressure near heart is pulsatile
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Arterial Blood Pressure
• Systolic pressure: pressure exerted in
aorta during ventricular contraction
– Averages 120 mm Hg in normal adult
• Diastolic pressure: lowest level of aortic
pressure
• Pulse pressure = difference between
systolic and diastolic pressure
– Throbbing of arteries (pulse)
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Arterial Blood Pressure
• Mean arterial pressure (MAP): pressure
that propels blood to tissues
• MAP = diastolic pressure + 1/3 pulse
pressure
• Pulse pressure and MAP both decline with
increasing distance from heart
• Ex. BP = 120/80; MAP = 93 mm Hg
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Capillary Blood Pressure
• Ranges from 17 to 35 mm Hg
• Low capillary pressure is desirable
– High BP would rupture fragile, thin-walled
capillaries
– Most very permeable, so low pressure forces
filtrate into interstitial spaces
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Venous Blood Pressure
• Changes little during cardiac cycle
• Small pressure gradient; about 15 mm Hg
• Low pressure due to cumulative effects of
peripheral resistance
– Energy of blood pressure lost as heat during
each circuit
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Factors Aiding Venous Return
1. Muscular pump: contraction of skeletal
muscles "milks" blood toward heart;
valves prevent backflow
2. Respiratory pump: pressure changes
during breathing move blood toward
heart by squeezing abdominal veins as
thoracic veins expand
3. Venoconstriction under sympathetic
control pushes blood toward heart
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Venous valve (open)
Contracted skeletalmuscle
Venous valve(closed)
Vein
Direction of blood flow
Figure 19.7 The muscular pump.
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Maintaining Blood Pressure
• Requires
– Cooperation of heart, blood vessels, and
kidneys
– Supervision by brain
• Main factors influencing blood pressure
– Cardiac output (CO)
– Peripheral resistance (PR)
– Blood volume
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Maintaining Blood Pressure
• F = P/R; CO = P/R; P = CO × R
• Blood pressure = CO × PR (and CO
depends on blood volume)
• Blood pressure varies directly with CO,
PR, and blood volume
• Changes in one variable quickly
compensated for by changes in other
variables
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Cardiac Output (CO)
• CO = SV × HR; normal = 5.0-5.5 L/min
• Determined by venous return, and neural
and hormonal controls
• Resting heart rate maintained by
cardioinhibitory center via parasympathetic
vagus nerves
• Stroke volume controlled by venous return
(EDV)
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Cardiac Output (CO)
• During stress, cardioacceleratory center
increases heart rate and stroke volume via
sympathetic stimulation
– ESV decreases and MAP increases
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Figure 19.8 Major factors enhancing cardiac output.
Exercise BP activates cardiac centers in medulla
Activity of respiratory pump
(ventral body cavity pressure)
Activity of muscular pump
(skeletal muscles)
Sympathetic venoconstriction
Sympathetic activity Parasympathetic activity
Venous return Contractility of cardiac muscle
Epinephrine in blood
EDV ESV
Stroke volume (SV) Heart rate (HR)
Cardiac output (CO = SV x HR)
Initial stimulus
Physiological response
Result
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Control of Blood Pressure
• Short-term neural and hormonal controls
– Counteract fluctuations in blood pressure by
altering peripheral resistance and CO
• Long-term renal regulation
– Counteracts fluctuations in blood pressure by
altering blood volume
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Short-term Mechanisms: Neural Controls
• Neural controls of peripheral resistance
– Maintain MAP by altering blood vessel
diameter
• If low blood volume all vessels constricted except
those to heart and brain
– Alter blood distribution to organs in response
to specific demands
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Short-term Mechanisms: Neural Controls
• Neural controls operate via reflex arcs
that involve
– Baroreceptors
– Cardiovascular center of medulla
– Vasomotor fibers to heart and vascular
smooth muscle
– Sometimes input from chemoreceptors and
higher brain centers
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The Cardiovascular Center
• Clusters of sympathetic neurons in medulla
oversee changes in CO and blood vessel
diameter
• Consists of cardiac centers and vasomotor
center
• Vasomotor center sends steady impulses via
sympathetic efferents to blood vessels
moderate constriction called vasomotor tone
• Receives inputs from baroreceptors,
chemoreceptors, and higher brain centers
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Short-term Mechanisms: Baroreceptor
Reflexes
• Baroreceptors located in
– Carotid sinuses
– Aortic arch
– Walls of large arteries of neck and thorax
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Short-term Mechanisms: Baroreceptor
Reflexes
• Increased blood pressure stimulates
baroreceptors to increase input to
vasomotor center
– Inhibits vasomotor and cardioacceleratory
centers, causing arteriolar dilation and
venodilation
– Stimulates cardioinhibitory center
– decreased blood pressure
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Short-term Mechanisms: Baroreceptor
Reflexes
• Decrease in blood pressure due to
– Arteriolar vasodilation
– Venodilation
– Decreased cardiac output
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Short-term Mechanisms: Baroreceptor
Reflexes
• If MAP low
– Reflex vasoconstriction increased CO
increased blood pressure
– Ex. Upon standing baroreceptors of carotid
sinus reflex protect blood to brain; in
systemic circuit as whole aortic reflex
maintains blood pressure
• Baroreceptors ineffective if altered blood
pressure sustained
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5
2
1
4a
3
2
1
5
4b
4b
3
4a
Baroreceptors
in carotid sinuses
and aortic arch
are stimulated.
Stimulus:
Blood pressure (arterial blood pressure rises above normal range).
CO and R return blood pressure to homeostatic range.
Sympathetic impulses to heart cause HR,
contractility, and CO.
Impulses from baroreceptors activate cardioacceleratory center (and inhibit cardioinhibitory center) and stimulate vasomotor center.
Baroreceptors in carotid sinuses and aortic arch are inhibited.
Stimulus:
Blood pressure (arterial blood pressure falls below normal range).
Vasomotor fibers stimulate vasoconstriction, causing R.
CO and Rreturn blood pressure to homeostatic range.
Sympathetic impulses to heartcause HR,
Impulses from baroreceptors stimulate cardioinhibitory center (and inhibit cardioacceleratory center) and inhibit vasomotor center.
Rate of vasomotor impulses allows vasodilation, causing R.
contractility, andCO.
Slide 1Figure 19.9 Baroreceptor reflexes that help maintain blood pressure homeostasis.
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Short-term Mechanisms: Chemoreceptor
Reflexes
• Chemoreceptors in aortic arch and large
arteries of neck detect increase in CO2, or
drop in pH or O2
• Cause increased blood pressure by
– Signaling cardioacceleratory center
increase CO
– Signaling vasomotor center increase
vasoconstriction
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Short-term Mechanisms: Influence of Higher
Brain Centers
• Reflexes in medulla
• Hypothalamus and cerebral cortex can
modify arterial pressure via relays to
medulla
• Hypothalamus increases blood pressure
during stress
• Hypothalamus mediates redistribution of
blood flow during exercise and changes in
body temperature
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Short-term Mechanisms: Hormonal Controls
• Short term regulation via changes in
peripheral resistance
• Long term regulation via changes in blood
volume
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Short-term Mechanisms: Hormonal Controls
• Cause increased blood pressure
– Epinephrine and norepinephrine from adrenal
gland increased CO and vasoconstriction
– Angiotensin II stimulates vasoconstriction
– High ADH levels cause vasoconstriction
• Cause lowered blood pressure
– Atrial natriuretic peptide causes decreased
blood volume by antagonizing aldosterone
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Direct renal mechanism Indirect renal mechanism (renin-angiotensin-aldosterone)
Arterial pressure Arterial pressure
Inhibits baroreceptors
Sympathetic nervous
system activity
Renin release
from kidneys
Angiotensinogen
Angiotensin I
Angiotensin II
Angiotensin converting
enzyme (ACE)
Urine formation
Filtration by kidneys
Blood volume
Adrenal cortex ADH release by
posterior pituitary
Secretes
Aldosterone
Sodium reabsorption
by kidneys
Water reabsorption
by kidneys Water intake
Blood volume
Mean arterial pressure
Vasoconstriction;
peripheral resistanceThirst via
hypothalamus
Mean arterial pressure
Initial stimulus
Physiological response
Result
Figure 19.10 Direct and indirect (hormonal) mechanisms for renal control of blood pressure.
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Long-term Mechanisms: Renal Regulation
• Baroreceptors quickly adapt to chronic
high or low BP so are ineffective
• Long-term mechanisms control BP by
altering blood volume via kidneys
• Kidneys regulate arterial blood pressure
1. Direct renal mechanism
2. Indirect renal (renin-angiotensin-aldosterone)
mechanism
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Direct Renal Mechanism
• Alters blood volume independently of
hormones
– Increased BP or blood volume causes
elimination of more urine, thus reducing BP
– Decreased BP or blood volume causes
kidneys to conserve water, and BP rises
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Indirect Mechanism
• The renin-angiotensin-aldosterone
mechanism
– Arterial blood pressure release of renin
– Renin catalyzes conversion of
angiotensinogen from liver to angiotensin I
– Angiotensin converting enzyme, especially
from lungs, converts angiotensin I to
angiotensin II
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Functions of Angiotensin II
• Increases blood volume
– Stimulates aldosterone secretion
– Causes ADH release
– Triggers hypothalamic thirst center
• Causes vasoconstriction directly
increasing blood pressure
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Direct renal mechanism Indirect renal mechanism (renin-angiotensin-aldosterone)
Arterial pressure Arterial pressure
Inhibits baroreceptors
Sympathetic nervous
system activity
Renin release
from kidneys
Angiotensinogen
Angiotensin I
Angiotensin II
Angiotensin converting
enzyme (ACE)
Urine formation
Filtration by kidneys
Blood volume
Adrenal cortex ADH release by
posterior pituitary
Secretes
Aldosterone
Sodium reabsorption
by kidneys
Water reabsorption
by kidneys Water intake
Blood volume
Mean arterial pressure
Vasoconstriction;
peripheral resistanceThirst via
hypothalamus
Mean arterial pressure
Initial stimulus
Physiological response
Result
Figure 19.10 Direct and indirect (hormonal) mechanisms for renal control of blood pressure.
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Figure 19.11 Factors that increase MAP.
Activity ofmuscularpump andrespiratory
pump
Release of ANP
Fluid loss fromhemorrhage,
excessivesweating
Crisis stressors:exercise, trauma,
bodytemperature
Vasomotor tone;bloodbornechemicals
(epinephrine,NE, ADH,
angiotensin II)
Dehydration,high hematocrit
Body size
Conservationof Na+ and
water by kidneys
Blood volumeBlood pressure
Blood pH
O2
CO2
Bloodvolume
Baroreceptors Chemoreceptors
Venousreturn
Activation of vasomotor and cardio-acceleratory centers in brain stem
Strokevolume
Heartrate
Diameter ofblood vessels
Bloodviscosity
Blood vessellength
Cardiac output Peripheral resistance
Mean arterial pressure (MAP)
Initial stimulus
Physiological response
Result
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Monitoring Circulatory Efficiency
• Vital signs: pulse and blood pressure,
along with respiratory rate and body
temperature
• Pulse: pressure wave caused by
expansion and recoil of arteries
• Radial pulse (taken at the wrist) routinely
used
• Pressure points where arteries close to
body surface
– Can be compressed to stop blood flow
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Figure 19.12 Body sites where the pulse is most easily palpated.
Superficial temporal artery
Facial artery
Common carotid artery
Brachial artery
Radial artery
Femoral artery
Popliteal artery
Posterior tibial
artery
Dorsalis pedis
artery
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Measuring Blood Pressure
• Systemic arterial BP
– Measured indirectly by auscultatory method
using a sphygmomanometer
– Pressure increased in cuff until it exceeds
systolic pressure in brachial artery
– Pressure released slowly and examiner
listens for sounds of Korotkoff with a
stethoscope
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Measuring Blood Pressure
• Systolic pressure, normally less than 120
mm Hg, is pressure when sounds first
occur as blood starts to spurt through
artery
• Diastolic pressure, normally less than 80
mm Hg, is pressure when sounds
disappear because artery no longer
constricted; blood flowing freely
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Variations in Blood Pressure
• Transient elevations occur during changes
in posture, physical exertion, emotional
upset, fever.
• Age, sex, weight, race, mood, and posture
may cause BP to vary
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Alterations in Blood Pressure
• Hypertension: high blood pressure
– Sustained elevated arterial pressure of 140/90
or higher
– Prehypertension if values elevated but not
yet in hypertension range
• May be transient adaptations during fever, physical
exertion, and emotional upset
• Often persistent in obese people
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Homeostatic Imbalance: Hypertension
• Prolonged hypertension major cause of
heart failure, vascular disease, renal
failure, and stroke
– Heart must work harder myocardium
enlarges, weakens, becomes flabby
– Also accelerates atherosclerosis
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Primary or Essential Hypertension
• 90% of hypertensive conditions
• No underlying cause identified
– Risk factors include heredity, diet, obesity,
age, diabetes mellitus, stress, and smoking
• No cure but can be controlled
– Restrict salt, fat, cholesterol intake
– Increase exercise, lose weight, stop smoking
– Antihypertensive drugs
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Homeostatic Imbalance: Hypertension
• Secondary hypertension less common
– Due to identifiable disorders including
obstructed renal arteries, kidney disease, and
endocrine disorders such as hyperthyroidism
and Cushing's syndrome
– Treatment focuses on correcting underlying
cause
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Alterations in Blood Pressure
• Hypotension: low blood pressure
– Blood pressure below 90/60 mm Hg
– Usually not a concern
• Only if leads to inadequate blood flow to tissues
– Often associated with long life and lack of
cardiovascular illness
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Homeostatic Imbalance: Hypotension
• Orthostatic hypotension: temporary low
BP and dizziness when suddenly rising
from sitting or reclining position
• Chronic hypotension: hint of poor
nutrition and warning sign for Addison's
disease or hypothyroidism
• Acute hypotension: important sign of
circulatory shock; threat for surgical
patients and those in ICU
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Circulatory Shock
• Hypovolemic shock: results from large-
scale blood loss
• Vascular shock: results from extreme
vasodilation and decreased peripheral
resistance
• Cardiogenic shock results when an
inefficient heart cannot sustain adequate
circulation
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Figure 19.18 Events and signs of hypovolemic shock.
Acute bleeding (or other events that reduce
blood volume) leads to:
1. Inadequate tissue perfusion
resulting in O2 and nutrients to cells
2. Anaerobic metabolism by cells, so lactic
acid accumulates
3. Movement of interstitial fluid into blood,
so tissues dehydrate
Initial stimulus
Physiological response
Signs and symptoms
Result
Chemoreceptors activated
(by in blood pH)Baroreceptor firing reduced
(by blood volume and pressure)
Hypothalamus activated
(by blood pressure)
Respiratory centers
activated
Cardioacceleratory and
vasomotor centers activated
Sympathetic nervous
system activated
ADH
releasedNeurons
depressed
by pH
Central
nervous system
depressed
Heart rateIntense vasoconstriction
(only heart and brain spared)
Renal blood flow
Renin released
Angiotensin II
produced in blood
Aldosterone
released
Kidneys retain
salt and waterWater
retention
Rate and
depth of
breathing
Tachycardia;
weak, thready
pulse
Skin becomes
cold, clammy,
and cyanotic
Urine output Thirst Restlessness
(early sign)
Coma
(late sign)
CO2 blown
off; blood
pH rises
Blood pressure maintained;
if fluid volume continues to
decrease, BP ultimately
drops. BP is a late sign.
Major effect Minor effect
Adrenal
cortex
Kidneys
Brain
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Figure 19.15 Intrinsic and extrinsic control of arteriolar smooth muscle in the systemic circulation.
Vasodilators
Metabolic Neuronal
Intrinsic mechanisms
(autoregulation) Vasoconstrictors
Extrinsic mechanisms
Myogenic
Metabolic
Neuronal
Hormonal
Sympathetic tone
• Neuronal or hormonal controls• Maintain mean arterial pressure (MAP)
• Redistribute blood during exerciseand thermoregulation
• Metabolic or myogenic controls• Distribute blood flow to individualorgans and tissues as needed
• Stretch
• Angiotensin II• Antidiuretic hormone• Epinephrine• Norepinephrine
• Endothelins
Hormonal
Sympathetic tone
• Atrial natriuretic
peptide
O2
CO2
H+
K+
• Prostaglandins• Adenosine • Nitric oxide
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Hydrostatic Pressures
• Capillary hydrostatic pressure (HPc)
(capillary blood pressure)
– Tends to force fluids through capillary walls
– Greater at arterial end (35 mm Hg) of bed
than at venule end (17 mm Hg)
• Interstitial fluid hydrostatic pressure
(HPif)
– Pressure that would push fluid into vessel
– Usually assumed to be zero because of
lymphatic vessels
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Colloid Osmotic Pressures
• Capillary colloid osmotic pressure
(oncotic pressure) (OPc)
– Created by nondiffusible plasma proteins,
which draw water toward themselves
– ~26 mm Hg
• Interstitial fluid osmotic pressure (OPif)
– Low (~1 mm Hg) due to low protein content
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Hydrostatic-osmotic Pressure Interactions:
Net Filtration Pressure (NFP)
• NFP—comprises all forces acting on
capillary bed
– NFP = (HPc + OPif) – (HPif + OPc)
• Net fluid flow out at arterial end
• Net fluid flow in at venous end
• More leaves than is returned
– Excess fluid returned to blood via lymphatic
system
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Capillary Exchange of Respiratory Gases
and Nutrients
• Diffusion down concentration gradients
– O2 and nutrients from blood to tissues
– CO2 and metabolic wastes from tissues to blood
• Lipid-soluble molecules diffuse directly through
endothelial membranes
• Water-soluble solutes pass through clefts and
fenestrations
• Larger molecules, such as proteins, are actively
transported in pinocytotic vesicles or caveolae
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Figure 19.21b Major arteries of the systemic circulation.
Arteries of the head and trunk
Internal carotid artery
External carotid artery
Common carotid arteries
Vertebral artery
Subclavian artery
Brachiocephalic trunk
Aortic arch
Ascending aorta
Coronary artery
Celiac trunk
Abdominal aorta
Superior mesenteric
artery
Renal artery
Gonadal artery
Inferior mesenteric artery
Common iliac artery
Internal iliac artery
Illustration, anterior view
Arteries that supply the upper limb
Subclavian artery
Axillary artery
Brachial artery
Radial artery
Ulnar artery
Deep palmar arch
Superficial palmar arch
Digital arteries
Arteries that supply the lower
limb
External iliac artery
Femoral artery
Popliteal artery
Anterior tibial artery
Posterior tibial artery
Arcuate artery
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Figure 19.22b Arteries of the head, neck, and brain.
• Maxillary artery
• Occipital artery
• Facial artery
• Lingual artery
• Superficial temporal artery
Branches of
the external
carotid artery
• Superior thyroid artery
Larynx
Thyroid gland(overlying trachea)
Clavicle (cut)
Brachiocephalic trunk
Internal thoracic artery
Ophthalmic artery
Basilar artery
Vertebral
artery
Internal
carotid artery
External
carotid artery
Common
carotid artery
Thyrocervical
trunk
Costocervical
trunk
Subclavian
artery
Axillary
artery
Arteries of the head and neck, right aspect
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Figure 19.22d Arteries of the head, neck, and brain.
Cerebral arterial
circle
(circle of Willis)
• Anterior
communicating
artery
• Posterior
communicating
artery
• Posterior
cerebral artery
Cerebellum
Basilar artery
Vertebral artery
Posterior
Major arteries serving the brain (inferior view, right side
of cerebellum and part of right temporal lobe removed)
Frontal lobe
Optic chiasma
Middle
cerebral
artery
Internal
carotid
artery
Mammillary
body
Temporal
lobe
Pons
Occipital lobe
Anterior
• Anterior
cerebral artery
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Figure 19.24b Arteries of the abdomen.
Liver (cut)
Inferior vena cava
Celiac trunk
Common hepatic artery
Hepatic artery proper
Gastroduodenal artery
Right gastric artery
Gallbladder
Pancreas(major portion liesposterior to stomach)
Duodenum
Abdominal aorta
Diaphragm
Esophagus
Left gastric artery
Stomach
Left gastroepiploicartery
Spleen
Right gastroepiploicartery
Superior mesentericartery
The celiac trunk and its major branches. The left half of the liver has been removed.
Splenic artery
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Figure 19.24c Arteries of the abdomen.
Hiatus (opening)for inferior vena cava
Hiatus (opening)for esophagus
Adrenal (suprarenal) gland
Celiac trunk
Kidney
Abdominal aorta
Lumbar arteries
Ureter
Median sacral artery
Diaphragm
Inferior phrenic artery
Middle suprarenal artery
Renal artery
Superior mesenteric artery
Gonadal (testicularor ovarian) artery
Inferior mesenteric artery
Common iliac artery
Major branches of the abdominal aorta.
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Figure 19.24d Arteries of the abdomen.
Celiac trunk
Superior mesentericartery
Branches of
the superior
mesenteric artery
• Middle colic artery
• Intestinal arteries
• Right colic artery
• Ileocolic artery
Ascending colon
Right common iliacartery
Ileum
Cecum
Appendix
Transverse colon
Aorta
Inferior mesenteric artery
Branches of
the inferior
mesenteric artery
• Left colic artery
• Sigmoidal arteries
• Superior rectalartery
Descending colon
Sigmoid colon
Rectum
Distribution of the superior and inferior mesenteric arteries.
The transverse colon has been pulled superiorly.
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Figure 19.25b Arteries of the right pelvis and lower limb.
Common iliac artery
Internal iliac artery
Superior gluteal artery
External iliac artery
Deep artery of thigh
Lateral circumflexfemoral artery
Medial circumflexfemoral artery
Obturator artery
Femoral artery
Adductor hiatus
Popliteal artery
Anterior tibial artery
Posterior tibial artery
Fibular artery
Dorsalis pedis artery
Arcuate artery
Dorsal metatarsalarteries
Anterior view
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Figure 19.25c Arteries of the right pelvis and lower limb.
Popliteal artery
Anterior tibial artery
Fibular artery
Dorsalis pedisartery (from topof foot)
Plantar arch
Posterior tibial artery
Lateral plantar artery
Medial plantar artery
Posterior view
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Figure 19.26b Major veins of the systemic circulation.
Veins of the head and trunk
Dural venous sinusesExternal jugular vein
Vertebral veinInternal jugular veinRight and leftbrachiocephalic veins
Superior vena cavaGreat cardiac vein
Hepatic veins
Splenic vein
Hepatic portal vein
Renal vein
Superior mesenteric veinInferior mesenteric vein
Inferior vena cava
Common iliac veinInternal iliac vein
Veins that drain
the upper limb
Subclavian veinAxillary vein
Cephalic veinBrachial veinBasilic vein
Median cubital veinUlnar veinRadial vein
Digital veins
Veins that drain
the lower limb
External iliac veinFemoral veinGreat saphenous veinPopliteal vein
Posterior tibial veinAnterior tibial vein
Small saphenous vein
Dorsal venous arch
Dorsal metatarsal veins
Illustration, anterior view. The vessels of the pulmonary circulation are not shown.
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Figure 19.27b Venous drainage of the head, neck, and brain.
Ophthalmic vein
Superficial temporal vein
Facial vein
Occipital vein
Posteriorauricular vein
Externaljugular vein
Vertebral vein
Internaljugular vein
Superior and middle thyroid veins
Brachiocephalicvein
Subclavian vein
Superiorvena cava
Veins of the head and neck, right superficial aspect
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Figure 19.27c Venous drainage of the head, neck, and brain.
Superior sagittal sinus
Falx cerebri
Inferior sagittal sinus
Straight sinus
Cavernous sinus
Transverse sinuses
Sigmoid sinus
Jugular foramen
Right internal jugular vein
Dural venous sinuses of the brain
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Figure 19.28b Veins of the thorax and right upper limb.
Brachiocephalic veins
Right subclavian vein
Axillary vein
Brachial vein
Cephalic vein
Basilic vein
Median cubitalvein
Median antebrachial vein
Cephalic vein
Radial vein
Basilic vein
Ulnar vein
Deep venous palmar arch
Superficial venous palmar arch
Digital veinsAnterior view
Internal jugular vein
External jugular vein
Left subclavian vein
Superior vena cava
Azygos veinAccessory hemiazygosvein
Hemiazygos vein
Posterior intercostals
Inferior vena cava
Ascending lumbar vein
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Figure 19.29a Veins of the abdomen.Inferior vena cava
Inferior phrenic veins
Hepatic veins
Hepatic portal vein
Superior mesenteric vein
Splenic vein
Inferiormesentericvein
L. ascending
lumbar vein
External iliac vein
Internal iliac veins
Common iliac veins
R. ascending
lumbar vein
Lumbar veins
Gonadal veins
Renal veins
Suprarenal veins
Hepatic
portal
system
Cystic vein
Schematic flowchart.
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Figure 19.29b Veins of the abdomen.
Hepatic veins
Inferior vena cava
Right suprarenalvein
Right gonadalvein
External iliacvein
Inferior phrenicvein
Left suprarenalvein
Renal veins
Left ascendinglumbar vein
Lumbar veins
Left gonadalvein
Common iliacvein
Internal iliacvein
Tributaries of the inferior vena cava.
Venous drainage of abdominal organs not drained by the hepatic portal vein.
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Figure 19.29c Veins of the abdomen.
Hepatic veins
Liver
Hepatic portal
vein
Small intestine
Rectum
Gastric veins
Spleen
Inferior vena cava
Splenic vein
Rightgastroepiploic vein
Inferiormesenteric vein
Superiormesenteric vein
Large intestine
The hepatic portal circulation.
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Figure 19.30b Veins of the right lower limb.
Common iliac veinInternal iliac veinExternal iliac vein
Inguinal ligament
Femoral vein
Great saphenousvein (superficial)
Popliteal vein
Smallsaphenous vein
Fibular vein
Anteriortibial vein
Dorsalispedis vein
Dorsalvenous arch
Dorsalmetatarsal veins
Anterior view