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Blood Vessels
Blood is carried in a closed system of vessels that begins and
ends at the heart
In adult, blood vessels stretch 60,000 miles!
The three major types of vessels are arteries, capillaries, and
veins
Arteries carry blood away from the heart (O2 rich, except
pulmonary)
Veins carry blood toward the heart (O2 poor, except
pulmonary)
They branch, diverge, fork
They join, merge, converge
Capillaries contact tissue cells and directly serve cellular needs
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Generalized Structure of Blood Vessels
Arteries and veins are composed of three tunics –
tunica interna, tunica media, and tunica externa
Lumen – central blood-containing space
surrounded by tunics
Capillaries are composed of endothelium with
sparse basal lamina
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Generalized Structure of Blood Vessels
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Figure 19.1b
Tunics
Tunica interna (tunica intima)
Endothelial layer that lines the lumen of all vessels
Continuation w/ the endocardial lining of the heart
Flat cells, slick surface
In vessels larger than 1 mm, a subendothelial connective
tissue basement membrane is present
Tunica media
Circularly arranged smooth muscle and elastic fiber layer,
regulated by sympathetic nervous system
Controls vasoconstriction/vasodilation of vessels
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Tunics
Tunica externa (tunica adventitia)
Collagen fibers that protect and reinforce vessels
Contains nerve fibers, lymphatic vessels, & elastin
fibers
Larger vessels contain vasa vasorum (capillary
network) that nourish more external tissues of the
blood vessel wall
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Blood Vessel Anatomy
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Table 19.1
Elastic (Conducting) Arteries
Thick-walled arteries near the heart; the aorta and
its major branches
Large lumen allow low-resistance conduction of
blood
Contain elastin in all three tunics
Inactive in vasoconstriction
Serve as pressure reservoirs expanding and
recoiling as blood is ejected from the heart
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Muscular (Distributing) Arteries and Arterioles
Muscular arteries – distal to elastic arteries; deliver
blood to body organs
Account for most of the named structures in lab
Have thickest tunica media (proportionally) of all
the vessels
Active in vasoconstriction
Arterioles – smallest arteries; lead to capillary beds
Control flow into capillary beds via vasodilation
and constriction
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Capillaries
Capillaries are the smallest blood vessels (microscopic)
Walls consisting of a thin tunica interna, one cell thick
Allow only a single RBC to pass at a time
Pericytes on the outer surface stabilize their walls
Tissues have a rich capillary supply
Tendons, ligaments are poorly vascularized
Cartilage, cornea, lens, and epithelia lack capillaries
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Vascular Components
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Figure 19.2a, b
Types of Capillaries
There are three structural types of capillaries:
Continuous
Fenestrated
Sinusoids
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Continuous Capillaries
Continuous capillaries are abundant in the skin and muscles
Endothelial cells provide an uninterrupted lining
Adjacent cells are connected with tight junctions
Intercellular clefts allow the passage of fluids & small
solutes
Brain capillaries do not have clefts (blood-brain barrier)
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Fenestrated Capillaries
Found wherever active capillary absorption or filtrate formation
occurs (e.g., small intestines, endocrine glands, and kidneys)
Characterized by:
An endothelium riddled with pores (fenestrations)
Greater permeability than other capillaries
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Sinusoids
Highly modified, leaky, fenestrated capillaries with large
lumens
Found in the liver, bone marrow, lymphoid tissue, and in some
endocrine organs
Allow large molecules (proteins and blood cells) to pass
between the blood and surrounding tissues
Blood flows sluggishly (e.g. in spleen) allowing for removal of
unwanted debris and immunogens
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Capillary Beds
A microcirculation moving from arterioles to
venules
Consist of two types of vessels:
Vascular shunts – metarteriole–thoroughfare
channel connecting an arteriole directly with a
postcapillary venule
True capillaries – the actual exchange vessels
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Blood Flow Through Capillary Beds
True capillaries: 10-100/bed
Branch from, then return to, the capillary bed
Precapillary sphincter
Cuff of smooth muscle that surrounds each true capillary at
the metarteriole and acts as a valve to regulate flow
Blood flow is regulated by vasomotor nerves and local
chemical conditions
True bed is open after meals, closed between meals
True bed is rerouted to skeletal muscles during physical
exercise
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Capillary Beds
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Figure 19.4a
Capillary Beds
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Figure 19.4b
Venous System: Venules
Venules are formed when capillary beds unite
Postcapillary venules – smallest venules,
composed of endothelium and a few pericytes
Allow fluids and WBCs to pass from the
bloodstream to tissues
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Venous System: Veins
Veins:
Formed when venules converge
Composed of three tunics, with a thin tunica media
and a thick tunica externa consisting of collagen
fibers and elastic networks
Accommodate a large blood volume
Capacitance vessels (blood reservoirs) that contain
65% of the blood supply
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Venous System: Veins
Veins have much lower blood pressure and thinner
walls than arteries
To return blood to the heart, veins have special
adaptations
Large-diameter lumens, which offer little
resistance to flow
Valves (resembling semilunar heart valves), which
prevent backflow of blood
Venous sinuses – specialized, flattened veins with
extremely thin walls (e.g., coronary sinus of the
heart and dural sinuses of the brain)
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Vascular Anastomoses
Merging blood vessels, more common in veins than
arteries
Arterial anastomoses provide alternate pathways (collateral
channels) for blood to reach a given body region
If one branch is blocked, the collateral channel can supply
the area with adequate blood supply
E.g. occur around joints, abdominal organs, brain, &
heart
E.g. poorly anastomized organs are retina, kidney,
spleen
Thoroughfare channels are examples of arteriovenous
anastomoses
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Physiology of Circulation: Blood Flow
Actual volume of blood flowing in a given period:
Is measured in ml per min.
Is equivalent to cardiac output (CO), considering
the entire vascular system
Is relatively constant when at rest
Varies widely through individual organs
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Blood Pressure (BP)
Force / unit area exerted on the wall of a blood
vessel by its contained blood
Expressed in millimeters of mercury (mm Hg)
Measured in reference to systemic arterial BP in
large arteries near the heart
The differences in BP within the vascular system
provide the driving force that keeps blood moving
from higher to lower pressure areas
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Resistance
Resistance – opposition to flow (friction)
Measure of the amount of friction blood encounters
Generally encountered in the systemic circulation away
from the heart
Referred to as peripheral resistance (PR)
The three sources of resistance are:
Blood viscosity
Total blood vessel length
Blood vessel diameter
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Resistance Factors: Viscosity and Vessel
Length
Resistance factors that remain relatively constant are:
Blood viscosity:
Internal resistance to flow that exist in all fluids
Increased viscosity increases resistance (molecules
ability to slide past one another)
Blood vessel length:
The longer the vessel, the greater the resistance
E.g. one extra pound of fat = 1 mile of small vessels
required to service it = more resistance
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Resistance Factors: Blood Vessel Diameter
Changes in vessel diameter are frequent and significantly
alter peripheral resistance
Fluid flows slowly
Fluid flows freely
The smaller the tube the greater the resistance
Resistance varies inversely with the fourth power of vessel
radius
For example, if the radius is doubled, the resistance is 1/16
as much
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Resistance Factors: Blood Vessel Diameter
Small-diameter arterioles are the major
determinants of peripheral resistance
Fatty plaques from atherosclerosis:
Cause turbulent blood flow
Dramatically increase resistance due to turbulence
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Blood Flow, Blood Pressure, and Resistance
Blood flow (F) is directly proportional to the difference in
blood pressure (∆P) between two points in the circulation
Blood flow is inversely proportional to resistance (R)
If ∆P increases, blood flow speeds up; if ∆P decreases,
blood flow declines
If R increases, blood flow decreases
R is more important than ∆P in influencing local blood
pressure
F = ∆P/R
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Systemic Blood Pressure
Any fluid driven by a pump thru a circuit of closed
channels operates under pressure
The fluid closest to the pump is under the greatest
pressure
The heart generates blood flow.
Pressure results when flow is opposed by
resistance…eg. Systemic Blood Pressure
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Systemic Blood Pressure
Systemic pressure:
Is highest in the aorta
Declines throughout the length of the pathway
Is 0 mm Hg in the right atrium
The steepest change in blood pressure occurs in the
arterioles which offer the greatest resistance to
blood flow
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Systemic Blood Pressure
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Figure 19.5
Arterial Blood Pressure
Arterial BP reflects two factors of the arteries close
to the heart
Their elasticity (how much they can be stretched)
The volume of blood forced into them at any given
time
Blood pressure in elastic arteries near the heart is
pulsatile (BP rises and falls)
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Arterial Blood Pressure
Systolic pressure – pressure exerted on arterial
walls during left ventricular contraction pushing
blood into the aorta (120 mm Hg)
Diastolic pressure – aortic SL valve closes
preventing backflow and the walls of the aorta
recoil resulting in pressure drop
lowest level of arterial pressure during a
ventricular cycle
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Arterial Blood Pressure
Pulse pressure – the difference between systolic and diastolic
pressure
Felt as a pulse during systole as arteries are expanded
Mean arterial pressure (MAP) – pressure that propels the blood
to the tissues
Because diastole is longer than systole…
MAP = diastolic pressure + 1/3 pulse pressure
E.g. systolic BP = 120 mm Hg
E.g. diastolic BP = 80 mm Hg
MAP = 93
MAP & pulse pressure decline w/ distance from the heart
At the arterioles blood flow is steady
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Capillary Blood Pressure
Capillary BP ranges from 40 (beginning) to 20
(end) mm Hg
Low capillary pressure is desirable because high
BP would rupture fragile, thin-walled capillaries
Low BP is sufficient to force filtrate out into
interstitial space and distribute nutrients, gases,
and hormones between blood and tissues
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Venous Blood Pressure
Venous BP is steady and changes little during the
cardiac cycle
The pressure gradient in the venous system is only
about 20 mm Hg (from venules to venae cavae) vs.
60 mm Hg from the aorta to the arterioles
A cut vein has even blood flow; a lacerated artery
flows in spurts
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Factors Aiding Venous Return
Venous BP alone is too low to promote adequate
blood return and is aided by the:
Respiratory “pump” – pressure changes created
during breathing suck blood toward the heart by
squeezing local veins
Muscular “pump” – contraction of skeletal muscles
surrounding deep veins “pump” blood toward the
heart with valves prevent backflow during venous
return
Smooth muscle contraction of the tunica media by
the SNS
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Factors Aiding Venous Return
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Figure 19.6
Maintaining Blood Pressure
Maintaining blood pressure requires:
Cooperation of the heart, blood vessels, and
kidneys
Supervision of the brain
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Maintaining Blood Pressure
The main factors influencing blood pressure are:
Cardiac output (CO)
Peripheral resistance (PR)
Blood volume
Blood pressure = CO x PR
Blood pressure varies directly with CO, PR, and
blood volume
Changes in one (CO, PR, BV) are compensated by
the others to maintain BP
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Cardiac Output (CO)
CO = stroke volume (ml/beat) x heart rate (beats/min)
Units are L/min
Cardiac output is determined by venous return and neural
and hormonal controls
Resting heart rate is controlled by the cardioinhibitory
center via the vagus nerves
Stroke volume is controlled by venous return (end diastolic
volume, or EDV)
Under stress, the cardioacceleratory center increases heart
rate and stroke volume
The end systolic volume (ESV) decreases and MAP
increases
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Cardiac Output (CO)
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Figure 19.7
Controls of Blood Pressure
Short-term controls:
Are mediated by the nervous system and
bloodborne chemicals
Counteract moment-to-moment fluctuations in
blood pressure by altering peripheral resistance
Long-term controls regulate blood volume
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Short-Term Mechanisms: Neural Controls
Neural controls of peripheral resistance:
Alter blood distribution in response to demands
Maintain MAP by altering blood vessel diameter
Neural controls operate via reflex arcs involving:
Baroreceptors & afferent fibers
Vasomotor centers of the medulla
Vasomotor fibers
Vascular smooth muscle
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Short-Term Mechanisms: Vasomotor Center
Vasomotor center – a cluster of sympathetic neurons in the
medulla that oversees changes in blood vessel diameter
Maintains blood vessel tone by innervating smooth muscles
of blood vessels, especially arterioles
Cardiovascular center – vasomotor center plus the cardiac
centers that integrate blood pressure control by altering
cardiac output and blood vessel diameter
Vasomotor fibers (T1-L2) innervate smooth muscle of the
arterioles
Vasomotor state is always in a state of moderate
constriction
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Short-Term Mechanisms: Vasomotor Activity
Sympathetic activity causes:
Vasoconstriction and a rise in BP if increased
BP to decline to basal levels if decreased
Vasomotor activity is modified by:
Baroreceptors (pressure-sensitive), chemoreceptors
(O2, CO2, and H+ sensitive), higher brain centers,
bloodborne chemicals, and hormones
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Short-Term Mechanisms: BaroreceptorInitiated Reflexes
When arterial blood pressure rises, it stretches
baroreceptos located in the carotid sinuses, aortic arch,
walls of most large arteries of the neck & thorax
Baroreceptors send impulses to the vasomotor center
inhibiting it resulting in vasodilation of arterioles and veins
and decreasing blood pressure
Venous dilation shifts blood to venous reservoirs causing a
decline in venous return and cardiac output
Baroreceptors stimulate parasympathetic activity and
inhibit the cardioacceletory center to decrease heart rate
and contractile force
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Short-Term Mechanisms: BaroreceptorInitiated Reflexes
Declining blood pressure stimulates the
cardioacceleratory center to:
Increase cardiac output and vasoconstriction
causing BP to rise
Peripheral resistance & cardiac output are
regulated together to minimize changes in BP
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Short-Term Mechanisms: Baroreceptor-Initiated
Reflexes
Baroreceptors respond to rapidly changing
conditions like when you change posture
They are ineffective against sustained pressure
changes, e.g. chronic hypertension, where they will
adapt and raise their set-point
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Impulse traveling along
afferent nerves from
baroreceptors:
Stimulate cardioinhibitory center
(and inhibit cardioacceleratory center)
Baroreceptors
in carotid
sinuses and
aortic arch
stimulated
Sympathetic
impulses to
heart
( HR and contractility)
CO
Inhibit
vasomotor center
R
Rate of vasomotor
impulses allows
vasodilation
( vessel diameter)
Arterial
blood pressure
rises above
normal range
Stimulus:
Rising blood
pressure
Im
ba
la
CO and R
return blood
pressure to
Homeostatic
range
nc
e
Homeostasis: Blood pressure in normal range
Im
CO and R
return blood
pressure to
homeostatic
range
Peripheral
resistance (R)
Cardiac
output
(CO)
ba
la
Stimulus:
Declining
blood pressure
nc
e
Impulses from
baroreceptors:
Stimulate cardioacceleratory center
(and inhibit cardioinhibitory center)
Sympathetic
impulses to heart
( HR and contractility)
Vasomotor
fibers
stimulate
vasoconstriction
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Arterial blood pressure
falls below normal range
Baroreceptors in
carotid sinuses
and aortic arch
inhibited
Stimulate
vasomotor
center
Figure 19.8
Short-Term Mechanisms: Chemical Controls
Blood pressure is regulated by chemoreceptor
reflexes sensitive to low oxygen and high carbon
dioxide levels
Prominent chemoreceptors are found in the carotid
and aortic bodies
Response is to increase cardiac output and
vasoconstriction
Increased BP speeds the return of blood to the
heart and lungs
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Influence of Higher Brain Centers
Reflexes that regulate BP are integrated in the
medulla
Higher brain centers (cortex and hypothalamus)
can modify BP via relays to medullary centers
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Chemicals that Increase Blood Pressure
Adrenal medulla hormones – norepinephrine and
epinephrine increase blood pressure
NE has a vasoconstrictive action
E increases cardiac output and causes
vasodilation in skeletal muscles
Nicotine causes vasoconstriction: stimulates
sympathetic neurons and the release of large
amounts of NE & E
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Chemicals that Increase Blood Pressure
Antidiuretic hormone (ADH, aka vasopressin)
produced by the hypothalamus
causes intense vasoconstriction in cases of extremely low
BP
stimulates the kidneys to conserve H2O
Angiotensin II
released when renal perfusion is inadequate
The kidney’s release of renin generates angiotensin II,
which causes vasoconstriction
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Chemicals that Decrease Blood Pressure
Atrial natriuretic peptide (ANP) – produced by the
atrium and causes blood volume and pressure to
decline along with general vasodilation
Nitric oxide (NO) – is a brief but potent
vasodilator
Inflammatory chemicals – histamine, prostacyclin,
and kinins are potent vasodilators
Alcohol – causes BP to drop by inhibiting
antidiuretic hormone (ADH)
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Long-Term Mechanisms: Renal Regulation
Long-term mechanisms control BP by altering
blood volume
Increased BP stimulates the kidneys to eliminate
water, thus reducing BP
Decreased BP stimulates the kidneys to increase
blood volume and BP
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Kidney Action and Blood Pressure
Kidneys act directly and indirectly to maintain
long-term blood pressure
Direct renal mechanism alters blood volume
Indirect renal mechanism involves the reninangiotensin mechanism
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Kidney Action and Blood Pressure: Direct Renal
Mechanism
Increase in BV causes an increase in BP
This stimulates the kidneys to release H2O which
lowers BV which in turn lowers BP
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Kidney Action and Blood Pressure: Indirect Renal
Mechanism
Declining BP causes the release of renin, which
triggers the release of angiotensin II
Angiotensin II is a potent vasoconstrictor that
stimulates aldosterone secretion
Aldosterone enhances renal reabsorption
resulting in increased BP and BP
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Kidney Action and Blood Pressure
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Figure 19.9
Monitoring Circulatory Efficiency
Efficiency of the circulation can be assessed by
taking pulse and blood pressure measurements
Vital signs – pulse and blood pressure, along with
respiratory rate and body temperature
Pulse – pressure wave caused by the expansion and
recoil of elastic arteries
Radial pulse (taken on the radial artery at the wrist)
is routinely used
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Palpated Pulse
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Figure 19.11
Measuring Blood Pressure
Systemic arterial BP is measured indirectly with
the auscultatory method
A sphygmomanometer is placed on the arm
superior to the elbow
Pressure is increased in the cuff until it is greater
than systolic pressure in the brachial artery
Pressure is released slowly and the examiner
listens with a stethoscope
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Measuring Blood Pressure
The first sound heard is recorded as the systolic
pressure
The pressure when sound disappears is recorded as
the diastolic pressure
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Alterations in Blood Pressure
Normal BP at rest: 110-140 mm Hg (systolic) &
70-80 mm Hg (diastolic)
Hypotension – low BP in which systolic pressure is
below 100 mm Hg
Hypertension – condition of sustained elevated
arterial pressure of 140/90 or higher
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Blood Flow Through Tissues
Blood flow, or tissue perfusion, is involved in:
Delivery of oxygen and nutrients to, and removal
of wastes from, tissue cells
Gas exchange in the lungs
Absorption of nutrients from the digestive tract
Urine formation by the kidneys
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Velocity of Blood Flow
Blood velocity:
Changes as it travels through the systemic
circulation
Is inversely proportional to the cross-sectional area
E.g. Fast in the aorta
Slow in capillaries
Fast again in the veins
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Velocity of Blood Flow
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Figure 19.13
Autoregulation: Local Regulation of Blood
Flow
Autoregulation – automatic adjustment of blood
flow to each tissue in proportion to its
requirements at any given point in time
Blood flow through an individual organ is
intrinsically controlled by modifying the diameter
of local arterioles feeding its capillaries
MAP remains constant, while local demands
regulate the amount of blood delivered to various
areas according to need
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Blood Flow: Skeletal Muscles
Capillary density & blood flow is greater in red
(slow oxidative) fibers than in white (fast
glycolytic) fibers
When muscles become active, blood flow to them
increases (hyperemia)
This autoregulation occurs in response to low O2
levels
SNS activity increases causing an increase in NE
which causes vasoconstriction of the vessels of
blood reservoirs to the skin and viscera diverting
blood away to the skeletal muscles
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Blood Flow: Brain
Blood flow to the brain is constant, as neurons are
intolerant of ischemia
Brain cannot store essential nutrients
Very precise autoregulatory system,
E.g. when you make a fist, blood supply
shifts to those neurons in the cerobral motor
cortex
Metabolic controls – brain tissue is extremely
sensitive to declines in pH, and increased carbon
dioxide causes marked vasodilation
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Blood Flow: Brain
Myogenic controls protect the brain from damaging
changes in blood pressure
Decreases in MAP cause cerebral vessels to dilate
to ensure adequate perfusion
Increases in MAP cause cerebral vessels to
constrict so smaller vessels do not rupture
MAP below 60mm Hg can cause syncope
(fainting)
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Blood Flow: Skin
Blood flow through the skin:
Supplies nutrients to cells in response to oxygen
need
Helps maintain body temperature
Provides a blood reservoir
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Blood Flow: Skin
Blood flow to venous plexuses below the skin
surface:
Varies from 50 ml/min (cold) to 2500 ml/min
(hot), depending on body temperature
Is controlled by sympathetic nervous system
reflexes initiated by temperature receptors and the
central nervous system
Does this via arteriole-venule shunts located at
fingertips, palms, toes, soles of feet, ears, nose, lips
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Temperature Regulation
As temperature rises (e.g., heat exposure, fever, vigorous
exercise):
Hypothalamic signals reduce vasomotor stimulation of the
skin vessels
Blood flushes into capillary beds
Heat radiates from the skin
Sweat also causes vasodilation via bradykinin in perspiration
Bradykinin stimulates the release of NO which increases
vasodilation
As temperature decreases, skin vessels constrict and blood is
shunted to deeper, more vital organs
Rosy cheeks: blood entrapment in superficial
capillary loops
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Blood Flow: Lungs (Think Reversal)
Blood flow in the pulmonary circulation is unusual
in that:
The pathway is short
Arteries/arterioles are more like veins/venules
(thin-walled, with large lumens)
Because of this they have a much lower arterial
pressure (24/8 mm Hg versus 120/80 mm Hg)
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Blood Flow: Lungs
The autoregulatory mechanism is exactly opposite
of that in most tissues
Low pulmonary oxygen levels cause
vasoconstriction; high levels promote
vasodilation
As lung air sacs fill w/ air, capillary beds dilate
to take it up
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Blood Flow: Heart
Small vessel coronary circulation is influenced by:
Aortic pressure
The pumping activity of the ventricles
During ventricular systole:
Coronary vessels compress
Myocardial blood flow ceases
Stored myoglobin supplies sufficient oxygen
During ventricular diastole, aortic pressure forces blood thru the
coronary circulation
During exercise, coronary blood vessels dilate in response to
elevated CO2 levels
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Capillary Exchange of Respiratory Gases and
Nutrients
Oxygen, carbon dioxide, nutrients, and metabolic
wastes diffuse between the blood and interstitial
fluid along concentration gradients
Oxygen and nutrients pass from the blood to
tissues
Carbon dioxide and metabolic wastes pass from
tissues to the blood
Water-soluble solutes pass through clefts and
fenestrations
Lipid-soluble molecules diffuse directly through
endothelial membranes
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Capillary Exchange of Respiratory Gases and
Nutrients
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Figure 19.15.1
Four Routes Across Capillaries
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Figure 19.15.2
Fluid Movement: Bulk Flow
Fluid is forced out of capillary beds thru clefts at
the arterial end, with most of it returning at the
venous end of the bed
This process determines relative fluid volume in
blood stream and extracellular space
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Capillary Exchange: Fluid Movements
Hydrostatic pressure is the force of a fluid pressed
against a wall
Direction and amount of fluid flow depends upon
the difference between:
Capillary hydrostatic pressure (HPc)
Capillary colloid osmotic pressure (OPc)
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Capillary Exchange: Fluid Movements
HPc – pressure of blood against the capillary walls:
Tends to force fluids through the capillary walls
(filtration) leaving behind cells and proteins
Is greater at the arterial end of a bed than at the
venule end
HPc is opposed by interstitial fluid hydrostatic
pressure (HPif)
Net pressure is the difference between HPc and
HPif
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Colloid Osmotic Pressure
The force opposing hydrostatic pressure (HPc)
OPc– created by nondiffusible plasma proteins,
which draw water toward themselves (osmosis)
E.g. serum albumin
OPc does not vary from one end of the capillary
bed to the other
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Net Filtration Pressure (NFP)
Hydrostatic-Osmotic Pressure interactions
determine if there is a net gain or loss of fluid from
the blood, calculated as the Net Filtration Pressure
(NFP)
NFP – all the forces acting on a capillary bed
Thus, fluid will leave the capillary bed if the NFP
is greater than the net OP and vice versa
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Net Filtration Pressure (NFP)
At the arterial end of a bed, hydrostatic forces
dominate (fluids flow out)
At the venous end of a bed, osmotic forces
dominate (fluids flow in)
More fluids enter the tissue beds than return to the
blood, and the excess fluid is returned to the blood
via the lymphatic system
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Net Filtration Pressure (NFP)
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Figure 19.16
Circulatory Shock
Circulatory shock – any condition in which blood
vessels are inadequately filled and blood cannot
circulate normally
E.g. hypovolemic shock: large scale blood loss
Blood volume decreases causing an increase in
heart rate resulting in a weak pulse
Vasoconstriction occurs enhancing venous
return
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Circulatory Shock
Vascular Shock:
Blood volume is normal, but circulation is poor as a result
of an abnormal expansion of the vascular bed caused by
extreme vasodilation
Results in rapid fall in blood pressure
Most common cause is anaphylactic shock
Body-wide vasodilation due to massive histamine
release
Neurogenic shock: failure of ANS regulation
Septic shock (septicemia): severe systemic bacterial
infection
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 19.17