Transcript blood vessels - Cloudfront.net

THE CARDIOVASCULAR
SYSTEM: BLOOD VESSELS
BLOOD VESSEL
STRUCTURE
AND
FUNCTION
BLOOD VESSELS
• Three major types:
– Arteries: blood away from the
heart
– Capillaries: exchange
between blood and tissues
– Veins: blood toward the heart
• Heart—arteries—arterioles—
capillaries—venules—
veins—Heart
• Altogether, the blood vessels
in the adult human stretch for
about 100,000 km (60,000
miles) through the internal
body landscape
BLOOD VASCULAR SYSTEM
and
LYMPHATIC SYSTEM
STRUCTURE
OF
BLOOD VESSEL WALLS
• The walls of all blood
vessels except the smallest
consist of three layers:
– Tunica interna (intima): lining
of slick simple squamous
epithelium that reduces friction
between the vessel walls and
blood
– Tunica media: mostly
circularly arranged smooth
muscle cells and sheets of
elastin that controls
vasoconstriction and
vasodilation of the vessel
– Tunica externa (adventitia):
contains woven collagen fibers
that protects, reinforces, and
anchors the vessel to
surrounding structures
GENERALIZED STRUCTURE
of
ARTERIES, VEINS, and CAPILLARIES
ARTERIAL SYSTEM
Elastic (Conducting) Arteries
•
Elastic, or conducting, arteries contain
large amounts of elastin, which enables
these vessels to withstand and smooth
out pressure fluctuations due to heart
action
– Thick-walled arteries near the heart
– The abundant elastin enables these
arteries to withstand and smooth out
large pressure fluctuations by
expanding when the heart forces blood
into them, and then recoiling to propel
blood onward into the circulation when
the heart relaxes
– Arteriosclerosis: blood vessels
become hard and less elastic
• Increases blood pressure
• Without the pressuresmoothing effect of the elastic
arteries, the walls of arteries
throughout the body experience
higher pressure
– Battered by high pressure,
the arteries eventually
weaken and may balloon
out or even burst
ARTERIAL SYSTEM
Muscular (Distributing) Arteries
• Distally the elastic arteries
give way to the muscular, or
distributing, arteries
• Muscular, or distributing,
arteries deliver blood to
specific body organs, and
have the greatest proportion of
tunica media of all vessels,
making them more active
vasoconstriction
• Their tunica media contains
relatively more smooth
muscle and less elastic
tissue than do elastic
arteries
– More active in
vasoconstriction and
less distensible
ARTERIAL SYSTEM
Arterioles
• Arterioles are the
smallest arteries and
regulate blood flow into
capillary beds through
vasoconstriction and
vasodilation
• Lead into capillary
beds:
– When constricted, the local
capillaries (tissues) served
are largely by-passed
– When dilated, blood flow
into the local capillaries
(tissues) increases
dramatically
Capillaries
• Capillaries are the smallest vessels (microscopic) and allow for
exchange of substances between the blood and interstitial fluid
– Thin walls consist of just a thin tunica
• In some cases, one endothelial cell forms the entire circumference of the
capillary wall
• Along the outer surface of the capillaries are spider-shaped pericytes,
smooth muscle-like cells that stabilize the capillary wall
• Diameter just large enough for red blood cells to slip through in
single file
• Most tissues have a rich capillary supply
– Exceptions:
• Tendons and ligaments are poorly vascularized
• Cartilage and epithelia lack capillaries
– Receive nutrients from blood vessels in nearby connective tissues
• Cornea and lens of eye: avascular
– Receive nutrients from aqueous humor
TYPES of CAPILLARIES
(a)Continuous Capillary
•
•
•
•
Most common and allow passage of
fluids and small solutes
Abundant in the skin and muscles
They are continuous in the sense that
their endothelial cells provide an
uninterrupted lining, adjacent cells
being joined laterally by tight junctions
– These junctions are usually
incomplete and leave gaps of
unjoined membrane called
intercellular clefts, which are just
large enough to allow limited
passage of fluids and small
solutes (exception in the brain)
Endothelial cell cytoplasm contains
numerous pinocytotic vesicles
believed to ferry fluids across the
capillary wall
(a)Continuous Capillary
• Brain capillaries are
unique:
– Tight junctions are
complete and extend
around the entire
perimeter of the
endothelial cells,
constituting the
structural basis of the
blood-brain barrier
CAPILLARY
(b)Fenestrated Capillary
• Endothelial cells are
riddled with oval pores
(fenestrations)
• More permeable to
fluids and solutes than
continuous capillaries
• Found wherever active
capillary absorption or
filtrate formation
occurs:
– Small intestine
– Endocrine glands
– kidneys
CAPILLARY
(c)Sinusoidal Capillary
•
•
•
•
•
•
Highly modified, leaky
capillaries that allow large
molecules to pass between the
blood and surrounding tissues
Found only in the liver, bone
marrow, lymphoid tissues, and
some endocrine organs
Irregularly shaped lumens
Usually fenestrated
Endothelial lining has fewer tight
junctions
Larger intercellular clefts than
ordinary capillaries
– Allow large molecules and even
blood cells to pass between the
blood and surrounding tissues
(c)Sinusoidal Capillary
• In the liver, the endothelium of
the sinusoids is
discontinuous and large
macrophages called Kupffer
cells, which remove and
destroy any contained
bacteria, form part of the lining
• In the spleen, phagocytes
located just outside the
sinusoids stick cytoplasmic
extensions through the
intercellular clefts into the
sinusoidal lumen to get at their
“prey”
CAPILLARY
Capillary Beds
•
•
Interwoven microcirculatory
networks
Consists of two types of vessels:
–
1. A vascular shunt (metarteriolethoroughfare channel)
•
–
•
Short vessel that directly connects the
arteriole and venule at opposite ends of
the bed
2. True capillaries, which function as
the exchange vessels
The terminal arteriole feeding the
bed leads into a metarteriole (a
vessel structurally intermediate
between an arteriole and a capillary),
which is continuous with the
thoroughfare channel (intermediate
between a capillary and a venule)
–
The thoroughfare channel, in turn, joins
the postcapillary venule that drains
the bed
Capillary Beds
True Capillaries
• Number from 10 to
100 per capillary bed,
depending on the
organ or tissues
served
• Usually branch off the
metarteriole (proximal
end of the shunt) and
return to the
thoroughfare channel
(distal end)
Capillary Beds
True Capillary
• A cuff of smooth muscle,
called a precapillary
sphincter, surrounds the
root of each true capillary at
the metarteriole and acts as
a valve to regulate blood
flow into the capillary
– Open during digestion in
gastrointestinal organs when
you are relaxing
– Closed in the gastrointestinal
organs during exercising
(open in the muscle)
• Cramps when vigorous
exercise after a meal
GENERALIZED STRUCTURE
of
ARTERIES, VEINS, and CAPILLARIES
CAPILLARY BED
Venous System
• Blood is carried from the capillary beds
toward the heart by veins
Venules
•
•
•
Venules are formed where
capillaries converge
The smallest venules, the
postcapillary venules, consist
entirely of endothelium around
which a few pericytes congregate
They are extremely porous
(more like capillaries than veins
in this way), and allow fluid and
white blood cells to move easily
between the blood and tissues
– A sign of inflammation is
adhesion of WBC to the
postcapillary venule
endothelium, followed by their
migration through the wall into
the inflamed tissue
Venules/Veins
• Venules join to form
veins, which are
relatively thin-walled
vessels with large
lumens containing
about 65% of the total
blood volume
Veins
• Walls are thinner and their
lumens larger than those of
corresponding arteries
• Large lumens and thin walls
• Three distinct layers:
– Tunica externa
• Thickest layer
• Collagen and elastic networks
– Tunica media
• Relatively little smooth
muscle and elastin
• thin
– Tunica interna
• Forms venous valves
Veins
• Blood pressure low
• Venous valves:
– Resemble semilunar
valves of heart
– Abundant in veins of
the limbs, where the
upward flow of blood
is opposed by
gravity
– Absent in the ventral
body cavity
GENERALIZED STRUCTURE
of
ARTERIES, VEINS, and CAPILLARIES
HOMEOSTATIC IMBALANCE
• Varicose veins:
– Veins that have become dilated because of
incompetent valves
• Blood pools in the lower limbs, and with time,
the valves weaken and the venous walls
stretch and become floppy
• Elevated venous pressure:
– Straining to deliver a baby or have a bowel movement
» Hemorrhoids
VASCULAR ANASTOMOSES
• Most organs receive blood from more than
one arterial branch, and arteries supplying
the same territory often merge, forming
arterial anastomoses
– Provide alternate pathways (collateral channels), for
blood to reach a given body region
• If one branch is cut or blocked by a clot, the collateral
channel can supply the area with adequate blood supply
• Venous anastomoses:
– Interconnect much more freely than arteries
• Example: skin on the dorsum of your hand
– Occlusion of a vein rarely blocks blood flow or leads
to tissue death
PHYSIOLOGY
OF
CIRCULATION
Circulatory Dynamics
• To sustain life, blood must be kept
circulating (blood flow, blood pressure, and
resistance)
–
–
–
–
–
–
–
Heart: pump
Aorta: pressure reservoir
Arteries: conduits
Arterioles: resistance vessels
Capillaries: exchange sites
Venules: exchange sites and conduits
Veins: conduits and blood reservoirs
BLOOD FLOW
• Blood flow is the volume of blood
flowing through a vessel, organ, or the
entire circulation in a given period, and
may be expressed as ml/min
• Under resting conditions it is relatively
constant
• At any given moment, it may vary
BLOOD PRESSURE
• Blood pressure (BP) is the force per unit area
exerted by the blood against a vessel wall, and
is expressed in millimeters of mercury (mm Hg)
– For example: a blood pressure of 120 mm Hg is equal
to the pressure exerted by a column of mercury 120
mm high
• Usually measure systemic arterial blood
• It is the pressure gradient—the difference in
blood pressure within the vascular system—that
provides the driving force that keeps blood
moving—always from an area of higher pressure
to an area of lower pressure—through the body
RESISTANCE
• Opposition to flow
• Measure of the amount of friction blood
encounters as it passes through the vessels
• Measure of the friction between blood and the
vessel wall, and arises from three sources: blood
viscosity, blood vessel length, and blood vessel
diameter
• Because most friction is encountered in the
peripheral (systemic) circulation, well away from
the heart, we generally use the term peripheral
resistance
RESISTANCE
BLOOD VISCOSITY
• Internal resistance to flow that exists in all fluids and
is related to the thickness or “stickiness” of a fluid
• The greater the viscosity, the less easily molecules slide
pass one another and the more difficult it is to get and
keep the fluid moving
• More viscous than water (formed elements and plasma
proteins): hence flows more slowly
• Polycythemia: excessive RBC count
– Increase viscosity
• Anemia: low RBC count
– Resistance declines
RESISTANCE
VESSEL LENGTH
• Longer the vessel—the greater the
resistance
– An extra pound or two of fat requires that
miles of small vessels be added to service the
extra tissue
• Increases the peripheral resistance
RESISTANCE
VESSEL DIAMETER
•
Because blood viscosity and vessel length are normally unchanging, the
influence of these factors can be considered constant in healthy people
– Changes in blood vessel diameter are frequent and significantly alter peripheral
resistance
•
•
•
Fluid close to the wall of a vessel is slowed by friction as it passes
along the wall, whereas fluid in the center of the vessel flows more
freely and faster
The smaller the vessel, the greater the friction, because relatively
more of the fluid contacts the vessel wall where its movement is
impeded
Resistance varies inversely with the fourth power of the vessel radius (1/2
the diameter)
– Example:
• If the radius of a vessel is doubled, the resistance drops to 1/16 of its original value
– R4 = 2x2x2x2=16 and 1/r4 = 1/16
•
Thus, the large arteries close to the heart, which do not change dramatically
in diameter, contribute little to peripheral resistance, and the small-diameter
arterioles, which can enlarge or constrict in response to neural and chemical
controls, are the major determinants of peripheral resistance
RESISTANCE
VESSEL DIAMETER
• When blood encounters either an
abrupt change in the vessel size or
rough or protruding areas of the vessel
wall (fatty plaques of atherosclerosis),
the smooth laminar blood flow is
replaced by turbulent flow, that is,
irregular fluid motion where blood from
the different laminae mixes
– Turbulence dramatically increases resistance
Relationship Between Flow, Pressure,
and Resistance
– If blood pressure increases, blood flow increases; if
peripheral resistance increases, blood flow decreases
• Blood flow (F) is directly proportional to the difference in blood
pressure (∆P) between two points in the circulation, that is, the
blood pressure, or hydrostatic pressure, gradient
– When ∆P increases, blood flow speeds up
– When ∆P decreases, blood flow declines
• Blood flow is inversely proportional to the peripheral resistance (R)
in the systemic circulation
– If R increases, blood flow decreases
– If R decreases, blood flow increases
• F = ∆P/R
– Peripheral resistance is the most important factor
influencing local blood flow, because vasoconstriction or
vasodilation can dramatically alter local blood flow, while
systemic blood pressure remains unchanged
SYSTEMIC BLOOD PRESSURE
•
•
•
•
Blood flows through the blood
vessels along a pressure
gradient, always moving from
higher-to lower-pressure areas
The pumping action of the heart
generates blood flow
Pressure results when blood
flow is opposed by resistance
Systemic blood pressure is
highest in the aorta, and declines
throughout the pathway until it
reaches 0 mm Hg in the right
atrium
– The steepest drop in blood
pressure occurs in the
arterioles, which offer the
greatest resistance to blood
flow
ARTERIAL BLOOD PRESSURE
•
Arterial blood pressure reflects how
much the arteries close to the heart
can be stretched (compliance, or
distensibility), and the volume forced
into them at a given time
–
When the left ventricle contracts, blood
is forced into the aorta, producing a
peak in pressure called systolic
pressure (120 mm Hg)
•
–
Blood moves forward into the arterial
bed because the pressure in the aorta is
higher than the pressure in the more
distal vessels
Diastolic pressure occurs when blood
is prevented from flowing back into the
ventricles by the closed semilunar
valve, and the aorta recoils (70-80 mm
Hg)
•
Elastic arteries are pressure
reservoirs that operate as auxiliary
pumps to keep blood circulating
throughout the period of diastole,
when the heart is relaxing
ARTERIAL BLOOD PRESSURE
– The difference between diastolic and systolic
pressure is called the pulse pressure
• It is felt as a throbbing pulsation in an artery (a pulse)
during systole, as the elastic arteries are expanded by
the blood being forced into them by ventricular
contraction
– Increased stroke volume and faster blood injection from the
heart cause temporary increases in the pulse pressure
– Pulse pressure increased by arteriosclerosis (thickening of
the walls of the arterioles, with loss of elasticity and
contractility) because the elastic arteries become less stretchy
» Atherosclerosis: the most common form of
arteriosclerosis, marked by cholesterol-lipid-calcium
deposits in the walls of arteries
ARTHEROSCLEROSIS PLAQUE
ARTERIAL BLOOD PRESSURE
•
•
Because aortic pressure fluctuates up and down with each heartbeat, the
important pressure to consider is the mean arterial pressure
The mean arterial pressure (MAP) represents the pressure that propels
blood to the tissues
– Because diastole usually lasts longer than systole the MAP is roughly equal to
the diastolic pressure plus 1/3 of the pulse pressure (systolic pressure-diastolic
pressure)
• MAP = diastolic pressure + pulse pressure/3
• Thus a person with a systolic blood pressure of 120 mm Hg and a diastolic pressure of
80 mm Hg:
– MAP = 80 mm Hg + 40 mm Hg/3 = 93 mm hg
» ***remember you are adding factions
•
MAP and pulse pressure both decline with increasing distance from the
heart
– The MAOP loses ground to the never-ending friction between the blood and the
vessel walls, and the pulse pressure is gradually phased out in the less elastic
muscular arteries (elastic rebound of the vessels ceases to occur)
– At the end of the arterial tree, blood flow is steady and the pulse pressure has
disappeared
BLOOD PRESSURE
CAPILLARY BLOOD PRESSURE
• By the time blood
reaches the capillaries,
blood pressure has
dropped to
approximately 40 mm
Hg and by the end of
the capillary bed is only
20 mm Hg or less
– Which protects the
capillaries from rupture, but
is still adequate to ensure
exchange between blood
and tissues
BLOOD PRESSURE
VENOUS BLOOD PRESSURE
• Unlike arterial pressure, which pulsates with each
contraction of the left ventricle, venous blood
pressure is steady and changes very little during the
cardiac cycle
• The pressure gradient in the veins, from venules to the
termini of the venae cavae, is only about 20 mm Hg (that
from the aorta to the ends of the arterioles is about 60
mm Hg)
– If a vein is cut, the blood flows evenly from the wound; a
lacerated artery produces rapid spurts of blood
• Very low pressure reflects the cumulative effects of
peripheral resistance, which dissipates most of the
energy of blood pressure (as heat) during each circuit
VENOUS BLOOD PRESSURE
•
•
Too low to promote adequate
venous return
Two functional adaptations are
important to venous return
–
1. Respiratory “pump”:
•
Pressure changes occurring in the
ventral body cavity during breathing
create the respiratory pump that moves
blood up toward the heart
–
–
Inhale, abdominal pressure increases,
squeezing the local veins and forcing
blood toward the heart
» At the same time, the pressure
in the chest decreases, allowing
thoracic veins to expand and
speeding blood entry into the
right atrium
2. Muscular “pump”: Skeletal muscle
activity is the most important pumping
mechanism
•
As the skeletal muscles surrounding the
deep veins contract and relax, they
“milk” blood toward the heart, and once
blood passes each successive valve, it
cannot flow back
OPERATION OF MUSCLE PUMP
for
VENOUS BLOOD FLOW
MAINTAINING BLOOD
PRESSURE
• Maintaining a steady flow of blood from
the heart to the toes is vital for proper
organ function:
– Making sure a person jumping out of bed in
the morning does not keel over from
inadequate blood flow to the brain requires
the finely tuned cooperation of the heart,
blood vessels, and kidneys—all supervised by
the brain
MAINTAINING BLOOD
PRESSURE
•
Blood pressure varies directly with
changes in blood volume and cardiac
output, which are determined primarily
by venous return and neural and
hormonal controls:
– BP = Force/area
– F = ∆P/R
– CO = ∆P/R
– ∆P = CO x R
– Blood pressure varies directly with CO,
R, and blood volume
• In theory, a change (increase or
decrease) in any of these
variables causes a corresponding
change in blood pressure
• HOWEVER, what really happens
in the body is that changes in one
variable that threaten blood
pressure homeostasis are quickly
compensated for by changes in
the other variable
Major Factors Enhancing Cardiac Output
Summary of Factors causing an increase
in
Mean Systemic Arterial Blood Pressure
Neural Controls of Blood Pressure
• Short-term neural controls of peripheral resistance
(blood pressure), mediated by the nervous system and
blood borne chemicals, alter blood distribution to meet
specific tissue demands, and maintain adequate MAP by
altering blood vessel diameter
• Neural controls of peripheral resistance are directed
at two main goals:
– 1. Altering blood distribution to respond to specific
demands of various organs
• Example: during exercise blood is shunted temporarily from the
digestive organs to the skeletal muscles
– 2. Maintaining adequate MAP by altering blood vessel
diameter
Neural Controls of Blood Pressure
Role of Vasomotor Center
•
The vasomotor center is a cluster of sympathetic neurons in the
medulla that controls changes in the diameter of blood vessels
– Integrates blood pressure control by altering cardiac output and blood vessel
diameter
– Nerves innervate smooth muscles of blood vessels, mainly arterioles which are
almost always in a state of moderate constriction (vasomotor tone)
• Most vasomotor fibers release norepinephrine, which is a potent vasoconstrictor
• Rise in blood pressure
– Decreased sympathetic activity allows the vascular muscle to relax causing
blood pressure to decline
– In skeletal muscle, vasomotor fibers release acetylcholine causing vasodilation
•
Modified by inputs from:
– 1. Baroreceptors (pressure-sensitive mechanoreceptors that respond to changes
in arterial pressure and stretch)
– 2. Chemoreceptors (receptors that respond to changes in blood levels of oxygen,
carbon dioxide, and H+)
– 3. Higher brain centers
– 4. Hormones
– 5. Bloodborne chemicals
Neural Controls of Blood Pressure
Baroreceptor-Initiated Reflexes
•
•
When arterial blood pressure
rises, it stretches
baroreceptors, neural receptors
located in the:
– Carotid sinuses (carotid
arteries: blood supply to the
brain)
– Aortic arch (brain, neck, upper
limbs)
– Walls of nearly every large
artery of the neck and thorax
When stretched baroreceptors
send impulses to the vasomotor
center, inhibiting its activity and
promoting vasodilation of
arterioles and veins
– Decline in blood pressure
Baroreceptor Reflexes that help to maintain
Blood Pressure
Neural Controls of Blood Pressure
Baroreceptor-Initiated Reflexes
• While dilation of the arterioles substantially
reduces peripheral resistance, venodilation
shifts blood to the venous reservoirs, causing a
decline in both venous return and cardiac output
• Stimulates parasympathetic activity and
inhibits the cardioacceleratory center,
reducing heart rate and contractile force
– A decline in MAP initiates reflex vasoconstriction and
increases cardiac output, causing blood pressure to
rise
– Thus, peripheral resistance and cardiac output are
regulated in tandem so that changes in blood
pressure are minimized
Neural Controls of Blood Pressure
Baroreceptor-Initiated Reflexes
• The function of rapidly responding
baroreceptors is to protect the circulation
against short-term (acute) changes in
blood pressure, such as those occurring
when you change your posture
– Example: blood pressure falls (head) when
one stands up after reclining
Neural Controls of Blood Pressure
Chemoreceptor-Initiated Reflexes
• When the oxygen content or pH of the blood drops
sharply or the carbon dioxide levels rise,
chemoreceptors in the aortic arch and large arteries
of the neck transmit impulses to the
cardioacceleratory center, which then increases
cardiac output, and to the vasomotor center, which
causes reflex vasoconstriction
– The rise in blood pressure that follows speeds the return of blood
to the heart and lungs
• The most prominent chemoreceptors are the carotid and
aortic bodies located close by the baroreceptors in the
carotid sinus and aortic arch
• More important in regulating respiratory rate than
blood pressure
Neural Controls of Blood Pressure
Influence of Higher Brain Centers
• The cerebral cortex and hypothalamus
can modify arterial pressure by
signaling the medullary centers
– Example: fight-or-flight response
Controls of Blood Pressure
Short-Term Mechanisms
Chemical Controls
• Chemical controls influence blood pressure by acting on
vascular smooth muscle or the vasomotor center
– Adrenal medulla hormones:
• Norepinephrine and epinephrine promote an increase in cardiac output and
generalized vasoconstriction (except in skeletal and cardiac muscle, where it
generally causes vasodilation)
– Both hormones enhance the sympathetic fight-or-flight response
– Nicotine mimics these hormones causing intense vasoconstriction
– Atrial natriuretic peptide (ANP):
• Hormone produced by the atria of the heart
• Causes blood volume and blood pressure to decline
• Acts as a vasodilator and an antagonist to aldosterone (hormone produced
by the adrenal cortex which stimulates the kidneys to increase sodium
reabsorption)
– Prods the kidney to excrete more sodium and water from the body causing blood
volume to drop
• Causes a generalized vasodilation and reduces cerebrospinal fluid formation
in the brain
Controls of Blood Pressure
Short-Term Mechanisms
Chemical Controls
• Antidiuretic hormone (ADH):
– Hormone produced by the hypothalamus and
stimulates vasoconstriction and water conservation by
the kidneys, resulting in an increase in blood volume
• Angiotensin II:
– When renal nutrient (blood) supply is inadequate, the
kidneys release renin, an enzyme
– Release of renin causes the generation of angiotensin
II which:
• Acts as a vasoconstrictor promoting a rapid rise in systemic
blood pressure
• Promotes the release of aldosterone and antidiuretic
hormone which act in long-term regulation of blood pressure
by enhancing blood volume
Controls of Blood Pressure
Short-Term Mechanisms
Chemical Controls
•
Endothelium (lining of blood vessels) is the source of several
chemicals that:
– Promote vasoconstriction, and are released in response to low blood flow
• Example:
– Endothelin: most potent vasoconstrictor known by enhancing calcium entry into vascular
smooth muscle
– Nitric oxide (NO):
• Produced in response to high blood flow or other signaling molecules, and promotes
systemic and localized vasodilation
•
Inflammatory chemicals, such as histamine, prostacyclin, and kinins, are
potent vasodilators
– They also promote fluid loss from the bloodstream by increasing capillary
permeability
•
Alcohol inhibits antidiuretic hormone (ADH) release by the Hypothalamus
– Depresses the vasomotor center
– Results in vasodilation especially in the skin (flushed appearance)
– Drop in blood pressure
MAINTAINING BLOOD PRESSURE
Long-Term Mechanisms
• The long-term controls of blood pressure, mediated by renal
mechanisms, counteract fluctuations in blood pressure not by
altering peripheral resistance (as in short-term controls) but
rather by altering blood volume
• Renal mechanisms usually maintain blood volume close to 5L
(varies with age, body size, and sex)
– Increased in blood volume is followed by an increase in blood
pressure
• Example: excessive salt intake
• The dynamic system will eventually stimulate the kidneys to eliminate water,
which reduces blood volume and consequently blood pressure
– Decrease in blood volume is followed by a decrease in blood
pressure
• Example: dehydration during exercise
• The dynamic system responds to falling blood volume triggering renal
mechanisms that increase blood volume and blood pressure
– Blood pressure can be stabilized or maintained within normal
limits only when blood volume is stable
MAINTAINING BLOOD PRESSURE
Long-Term Mechanisms
• The kidneys act both directly and
indirectly to regulate pressure and
provide the major long-term mechanism of
blood pressure control
MAINTAINING BLOOD PRESSURE
Long-Term Mechanisms
– The direct renal mechanism
counteracts an increase in
blood pressure by altering
blood volume, which
increases the rate of kidney
filtration (as blood volume
goes, so goes the arterial
blood pressure)
• When either blood volume or
blood pressure rises, kidney
filtration is speeded up
(increase urination)
– Blood volume and blood
pressure falls
• When blood pressure or
blood volume is low, water is
conserved and returned to
the bloodstream, and blood
pressure rises
Slowly Acting Renal Hormonal Mechanisms
for
Blood Pressure Control
Summary of Factors causing an increase
in
Mean Systemic Arterial Blood Pressure
MAINTAINING BLOOD PRESSURE
Long-Term Mechanisms
•
The indirect renal mechanism is the
renin-angiotensin mechanism
–
–
When arterial blood pressure
declines, the kidneys release the
enzyme renin into the blood
Renin triggers a series of reactions
that produce angiotensin II (potent
vasoconstrictor)
•
•
–
Increases systemic blood pressure
Increases the rate of blood delivery
to the kidneys and the rate of renal
perfusion (passing of fluid through
tissues)
Also stimulates the adrenal cortex to
secrete aldosterone, a hormone that
enhances renal reabsorption of sodium,
and prods the posterior pituitary to
release ADH (antidiuretic hormone),
which promotes more water
reabsorption:
•
•
Sodium moves into the bloodstream,
water follows
Both blood volume and blood
pressure rise
Slowly Acting Renal Hormonal Mechanisms
for
Blood Pressure Control
Monitoring Circulatory Efficiency
• Efficiency can be assessed by taking pulse
and blood pressure measurements
• Accomplished by measuring pulse and blood
pressure; these values together with respiratory
rate and body temperature are called vital signs
– Vital signs:
•
•
•
•
Pulse
Blood pressure
Respiratory rate
Body temperature
Monitoring Circulatory Efficiency
Pulse
•
•
The alternating expansion and
recoil of elastic arteries during each
cardiac cycle create a pressure
wave—a pulse—that is transmitted
through the arterial tree
You can feel a pulse in any artery that
lies close to the body surface by
compressing the artery against firm
tissue, and this provides an easy way
to count heart rate
– Radial pulse: radial artery in wrist
• Routinely used to take a
pulse measurement since it
so accessible (DO NOT use
thumb)
– There are other clinically
important arterial pulse points:
• These same points are
compressed to stop blood
flow into distal tissues during
hemorrhage
• Called pressure points
Body sites where Pulse is most easily palpated
Monitoring Circulatory Efficiency
Blood Pressure
• Systemic blood pressure is measured indirectly in the brachial
artery of the arm by using the ascultatory method
– Which relies on the use of a blood pressure cuff (sphygmomanometer)
to alternately stop and reopen blood flow into the brachial artery of the
arm
• Inflated to a point that exceeds systolic pressure
– Blood flow is stopped and the brachial pulse cannot be heard
• Cuff pressure is gradually reduced
• Examiner listens (auscultates) with a stethoscope for sounds in the brachial
artery
– First soft tapping sounds heard (the first point at which a small amount of blood
is spurting through the constricted artery) is systolic pressure
• Cuff pressure is reduced further
– Sounds become louder and more distinct (sounds of Korotkoff)
• When the artery is no longer constricted and blood flows freely, the
sounds can no longer be heard
– Pressure at which the sounds disappear is the diastolic pressure
Monitoring Circulatory Efficiency
Blood Pressure
• Normal adult at rest:
– Systolic pressure: between 110 and 140 mm Hg
– Diastolic pressure: between 75 and 80 mm Hg
• Cycles over a 24-hour period:
– Waning and waxing according to the amount of retinoic acid
(vitamin A derivative) in blood
– Blood vessels like certain brain cells contain “clock” proteins
that regulates circadian rhythms in response to retinoic acid
(used in treatment of cystic acne)
• Varies with age, sex, weight, race, mood, physical
activity, posture, and socioeconomic status
• What is normal for you may not be normal for someone
else
Alterations in Blood Pressure
• Hypotension:
– Low blood pressure
– Systolic pressure below 100 mm Hg
– In many cases simply reflects individual
variations and is no cause for concern
• Low blood pressure is often associated with long
life and an old age free of illness
HOMEOSTATIC IMBALANCE
HYPOTENSION
•
Orthostatic hypotension:
– Elderly
– Temporary low blood pressure and dizziness when they rise suddenly from a
reclining or sitting position
• Aging sympathetic nervous system does not respond as quickly
• Blood pools briefly in the lower limbs, reducing blood pressure and delivery to the brain
• Making postural changes slowly to give the nervous system time to adjust usually
prevents this problem
•
Chronic hypotension:
–
–
–
–
–
–
•
Poor nutrition
Often anemic and inadequate levels of blood proteins
Blood viscosity low
Warning of Addison’s disease (inadequate adrenal cortex function)
Hypothyroidism
Severe tissue wasting
Acute hypotension:
– One of the most important signs of circulatory shock
• Threat to patients undergoing surgery and those in intensive care units
Alterations in Blood Pressure
• Hypertension:
– High blood pressure
– Transient: short-lived
• Elevations in systolic pressure occur as normal
adaptations during fever, physical exertion, and
emotional upset
– Persistent: long-lived
• Common in obese people because the total length
of their blood vessels is relatively greater than in
thinner individuals
HOMEOSTATIC IMBALANCE
HYPERTENSION
•
Chronic: long duration:
– Common and dangerous disease that warns of increased peripheral resistance
– Estimated 30% of people over 50 years
– Silent killer
• Usually asymptomatic for the first 10 to 20 years
• Slowly but surely strains the heart and damages the arteries
• Major cause of heart failure, vascular disease, renal failure, and stroke
– Heart is forced to pump against greater resistance, it must work harder, and in
time the myocardium enlarges
• Finally strained beyond its capacity to respond, the heart weakens and its walls become
flabby
– Ravages blood vessels
• Small tears in the endothelium
• Accelerates the progress of atherosclerosis
– Vessels become increasing blocked
– Elevated arterial pressure of 140/90 or higher
• Higher the pressure, the greater the risk for serious cardiovascular problems
• Elevated diastolic pressures are more significant medically, because they always
indicate progressive occlusion (closure) and/or hardening of the arterial tree
HOMEOSTATIC IMBALANCE
Primary (Essential) Hypertension
• No underlying cause has been identified
• Following factors are believed to be involved
– Diet:
• High sodium, saturated fat, cholesterol intake
• Deficiencies in certain metal ions: K+, Ca2+, Mg2+
– Obesity
– Age:
• Clinical signs of the disease usually appear after age 40
– Race:
• Varies in different populations
– Higher in Africans
– Heredity
– Stress
– Smoking:
• Nicotine enhances the sympathetic nervous system’s vasoconstrictor effects
HOMEOSTATIC IMBALANCE
Primary (Essential) Hypertension
• Cannot be cured
– Must adjust life style
– Drugs:
• Antihypertensive
–
–
–
–
Diuretics
Beta-blockers
Calcium channel blockers
Angiotensin-converting enzyme (ACE) inhibitors
» Suppresses the renin-angiotensin mechanism
HOMEOSTATIC IMBALANCE
Secondary Hypertension
•
•
•
•
•
Accounts for 10% of cases
Due to identifiable disorders
Excessive renin secretion by the kidneys
Arteriosclerosis
Endocrine disorders
– Hyperthyroidism
– Cushing’s disease
• Excessive production of adrenocorticotropic (ACTH) hormone from
the anterior pituitary
• Influences the activity of the adrenal cortex
– High sugar
– Loss in muscle and bone protein
– Edema: water and salt retention
• Treatment is directed toward the cause
BLOOD FLOW THROUGH BODY
TISSUE: TISSUE PERFUSION
•
•
•
Tissue perfusion is involved in
delivery:
– Of oxygen and nutrients to tissue
cells
– Removal of wastes from tissue
cells
– Gas exchange in the lungs
– Absorption of nutrients from the
digestive tracts
– Urine formation in the kidneys
Rate of blood flow to each tissue
and organ is almost exactly the
right amount to provide for proper
function—no more, no less
During exercise, nearly all of the
increased cardiac output flushes
into the skeletal muscles and blood
flow to the kidneys and digestive
organs is reduced
Distribution of blood flow to selected body
organs at rest and during strenuous exercise
Velocity of Blood Flow
•
Velocity or speed of blood flow
changes as it passes through the
systemic circulation; it is fastest in the
aorta, and declines in velocity as
vessel diameter decreases
–
•
Fastest in the aorta and other large
arteries, slowest in the capillaries, and
then picks up speed again in the veins
Inversely related to the crosssectional area of the blood vessels
to be filled
–
Blood flows fastest where the total
cross-sectional area is least
•
•
As the arterial system branches, the
total cross-sectional area of the
vascular bed increases, and the velocity
of blood flow declines proportionately
Slow capillary flow is beneficial
because it allows adequate time for
exchange between the blood and
tissue cells
Relationship between blood flow velocity and total
cross-sectional area in various blood vessels of
the systemic circulation
BLOOD FLOW THROUGH BODY TISSUE: TISSUE
PERFUSION
Autoregulation: Local Regulation of Blood Flow
•
Autoregulation is the automatic adjustment of blood flow to each tissue in
proportion to its needs, and is controlled intrinsically by modifying the diameter
of local arterioles feeding the capillaries
– Metabolic controls of autoregulation are most strongly stimulated by a shortage
of oxygen at the tissues
• Vasodilation of the arterioles serving the capillary beds of the “needy” tissue
• Temporary increase of blood flow to the area
– Myogenic control involves the localized response of vascular smooth muscle to
passive stretch (increased intravascular pressure) with increase tone (resistance
of muscle to passive stretch)
• Resist the stretch and causes vasoconstriction
– Long-term autoregulation develops over weeks or months, and involves an
increase in the size of existing blood vessels and an increase in the number of
vessels in a specific area, a process called angiogenesis
• Example:
– Common in the heart when a coronary vessel is partially occluded
– Occurs throughout the body in people who live in high-altitude areas,
where the air contains less oxygen
BLOOD FLOW in SPECIFIC AREAS
• Blood Flow in Special Areas:
– Blood flow to skeletal muscles varies with level of
activity and fiber type
• When muscles become active, blood flow increases
(hyperemia) in direct proportion to their greater metabolic
activity (active or exercise hyperemia)
• Capillary density and blood flow is greater in red (slow
oxidative) fibers than in white (fast glycolytic) fibers
– Muscular autoregulation occurs almost entirely in
response to decreased oxygen concentrations
BLOOD FLOW in SPECIFIC AREAS
• Brain:
– Cerebral blood flow is tightly regulated to meet neuronal needs,
since neurons cannot tolerate periods of ischemia
– Most metabolically active organ in the body, it is the least able to
store essential nutrients
– Sensitive to declining pH, and increased blood carbon dioxide
levels causing marked vasodilation
• Skin:
–
–
–
–
Blood supplies nutrients to the cells
Aids in body temperature regulation
Provides a blood reservoir
Local autoregulatory events control oxygen and nutrient delivery
to the cells
– Neural mechanisms control the body temperature regulation
functions
BLOOD FLOW in SPECIFIC AREAS
– Lungs:
• Autoregulatory controls of blood flow to the lungs are the opposite of what
happens in most tissues
– Low pulmonary oxygen (air sacs) causes vasoconstriction, while higher oxygen
(air sacs) causes vasodilation
– Heart:
• Movement of blood through the coronary circulation (vessels of the heart) is
influenced by aortic pressure and the pumping of the ventricles
– When the ventricles contract and compress the coronary vessels, blood flows
through the myocardium stops
– As the heart relaxes, the high aortic pressure forces blood through the coronary
circulation
– Abnormally rapid heartbeat seriously reduces the ability of the myocardium to
receive adequate oxygen and nutrients during diastole
• Any event that decreases the oxygen content of the blood causes release of
a vasodilator that adjust the oxygen supply
– Increasing the blood flow is the only way to make sufficient additional oxygen
available to a more vigorously working heart
Blood Flow Through Capillaries and
Capillary Dynamics
• Blood flow through capillary networks
is slow and intermittent
– This phenomenon, called vasomotion, the
slow, intermittent flow of blood through the
capillaries, reflects the action of the
precapillary sphincters (opening and closing)
in response to local autoregulatory controls
Capillary Exchange of Respiratory
Gases and Nutrients
• Capillary exchange of
nutrients, gases, and
metabolic wastes occurs
between the blood and
interstitial space through
diffusion
– Movement always occurs
along a concentration
gradient—one substance
moving from an area of
its higher concentration
to an area of its lower
concentration
Capillary Exchange of Respiratory
Gases and Nutrients
•
•
•
•
•
Direct diffusion: oxygen, carbon
dioxide, nutrients, metabolic waste
Intercellular clefts and
sometimes fenestrations: small
water-soluble solutes, such as
amino acids and sugars
Direct diffusion through the
lipid bilayer of the endothelial
cell plasma membrane: lipidsoluble molecules, such as
respiratory gases
Caveoli: translocate some larger
molecules, such as small proteins
Pinocytotic vesicles: imbibe
solute-containing fluid
Capillary Transport Mechanisms
Blood Flow Through Capillaries and
Capillary Dynamics
• Fluid Movements:
– While nutrient and gas exchanges are
occurring across the capillary walls by
diffusion, bulk fluid flows are also going on
• Fluid is forced out of the capillaries through the
clefts at the arterial end of the bed, but most of it
returns to the bloodstream at the venous end
– Direction and amount of fluid that flows across
the capillary walls reflect the balance between
two dynamic and opposing forces—
hydrostatic and colloid osmotic pressures
Blood Flow Through Capillaries and Capillary Dynamics
Hydrostatic Pressures
• Hydrostatic pressure (HP) is the force exerted by a
fluid against a membrane
– Capillaries: hydrostatic pressure is the same as capillary blood
pressure (pressure exerted by blood on the capillary wall)
• Capillary hydrostatic pressure (HPc) tends to force fluids through the
capillary walls
– Higher at the arterial (35 mm Hg)
– Lower at the venous end (17 mm Hg)
• In theory, blood pressure—which forces fluid out of
the capillaries—is opposed by the interstitial fluid
hydrostatic pressure (HPif) acting outside the
capillaries and pushing fluid in
Blood Flow Through Capillaries and Capillary Dynamics
Hydrostatic Pressures
•
Net hydrostatic pressure acting
on the capillaries at any point is
the difference between HPc and
HPif
– There is usually very little fluid in
the interstitial space, because any
fluid there is constantly withdrawn
by the lymphatic vessels
– HPif may vary from slightly
negative to slightly positive,
traditionally it is assumed to be
zero
•
The net effective hydrostatic
pressures at the arterial and
venous ends of the capillary bed
are essentially equal to HPc (in
other words, to blood pressure) at
those locations
Forces responsible for fluid flows at Capillaries
Blood Flow Through Capillaries and Capillary Dynamics
Colloid Osmotic Pressures
• Colloid osmotic pressure (OP):
– Force opposing hydrostatic pressure
• Force created by the presence in a fluid of large
nondiffusible molecules, such as plasma proteins,
that are prevented from moving through the
capillary membrane
– Such molecules draw water toward themselves
– These molecules encourage osmosis whenever the
water concentration in their vicinity is lower than it is on
the opposite side of the capillary membrane
Blood Flow Through Capillaries and Capillary Dynamics
Colloid Osmotic Pressures
•
The abundant plasma proteins
in capillary blood (primarily
albumin molecules) develop a
capillary colloid osmotic
pressure (OPc), also called
oncotic pressure (26 mm Hg)
– Because interstitial fluid contains
few proteins, its colloid osmotic
pressure (OPif) is lower—from 0.1
to 5 mm Hg
• A value of 1 mm Hg is used
•
•
Unlike HP, OP does not vary from
one end of the capillary bed to the
other
Net osmotic pressure that pulls
fluid back into the capillary blood
is:
– OPc – OPif = 26 mm Hg – 1 mm
Hg = 25 mm Hg
Forces responsible for fluid flows at Capillaries
Hydrostatic-Osmotic Pressure Interactions
• To determine whether there is a net
gain or net loss of fluid from the blood,
you have to calculate the net filtration
pressure (NFP)
– Fluids will leave the capillaries if net HP
exceeds net OP, but fluids will enter the
capillaries if net OP exceeds net HP
Hydrostatic-Osmotic Pressure Interactions
• Hydrostatic forces
dominate at the
arterial end:
– NFP = (HPc – HPif) –
(OPc – OPif)
–
–
(35 – 0) - (26
1)
(35 – 25) = 10 mm
Hg
– A pressure of 10 mm
Hg (net excess of
HP) is forcing fluid
out of the capillary
Hydrostatic-Osmotic Pressure Interactions
• Osmotic forces
dominates at the
venous end:
– NFP = (HPc – HPif) – (OPc
– OPif)
– (17 - 0)
- (26 - 1)
– (17 – 25) = -8 mm Hg
– The negative pressure
value indicates that the
NFP (due to net excess of
OP) is driving fluid into
the capillary bed
Hydrostatic-Osmotic Pressure Interactions
• Thus, net fluid flow is
out of the circulation at
the arterial ends of
capillary beds and into
the circulation at the
venous ends
• The fluid that does not
return to the blood enters
the lymph system which
eventually returns this
fluid to the blood
Forces responsible for fluid flows at Capillaries
Circulatory Shock
Hypovolemic Shock
•
Any condition in which blood
vessels are inadequately filled and
blood cannot circulate normally
–
•
Inadequate blood flow to meet tissue
needs
Hypovolemic shock results from a
large-scale loss of blood:
–
–
–
–
–
Acute hemorrhage
Severe vomiting
Severe diarrhea
Extensive burns
Characterized by:
•
•
•
•
•
Drop in blood volume
Weak pulse
Intense vasoconstriction (shifting of
blood from various reservoirs)
An elevated heart rate trying to correct
problem
Drop in blood pressure
Events and signs of compensated
(nonprogressive) hypovolemic shock
Circulatory Shock
Vascular Shock
• Blood volume is normal and constant
• Poor circulation as a result of an abnormal
expansion of the vascular bed caused by extreme
vasodilation
– Huge drop in peripheral resistance followed by rapidly falling
blood pressure
– Loss of vasomotor muscle tone
• Most common causes:
– Anaphylactic shock: systemic allergic reaction in which bodywide
vasodilation is triggered by the massive release of histamine
– Neurogenic shock: failure of autonomic nervous system
regulation
– Septic shock: septicemia
• Severe systemic bacterial infection
• Bacterial toxins are notorious vasodilators
Circulatory Shock
Transient/Cardiogenic
• Transient vascular shock is due to prolonged
exposure to heat, such as while sunbathing,
resulting in vasodilation of cutaneous blood vessels
– If you stand up abruptly, blood pools because of gravity into the
dilated blood vessels of the lower limbs
– Blood pressure falls
– Dizziness: signal that the brain is not receiving enough oxygen
• Cardiogenic shock: pump failure
– Occurs when the heart is too inefficient to sustain normal blood
flow, and is usually related to myocardial damage, such as
repeated myocardial infarcts
CIRCULATORY PATHWAYS:
BLOOD VESSELS OF THE BODY
• Two distinct pathways
travel to and from the
heart:
• Pulmonary circulation:
– Runs from the heart to the
lungs and back to the heart
• Systemic circulation:
– Runs to all parts of the
body before returning to
the heart
CIRCULATORY PATHWAYS
PULMONARY CIRCULATION
SYSTEMIC CIRCULATION
Differences Between Arteries and Veins
• There is one terminal
systemic artery:
– Aorta
• But two terminal
systemic veins:
– Superior and inferior
vena cava
PULMONARY CIRCULATION
SYSTEMIC CIRCULATION
Differences Between Arteries and Veins
• Arteries run deep
and are well
protected
• Veins are both deep
and superficial:
– Deep, which run
parallel to the arteries
• In most cases
– Superficial, which run
just beneath the skin
MAJOR ARTERIES OF THE
SYSTEMIC CIRCULATION
THE VENAE CAVAE AND THE MAJOR
VEINS OF THE SYSTEMIC CIRCULATION
Differences Between Arteries and Veins
• Arterial pathways tend to be clear, but there
are often many interconnections in venous
pathways, making them difficult to follow
• There are at least two areas where venous
drainage does not parallel the arterial supply:
– The dural sinuses draining the brain
– The hepatic portal system draining from the digestive
organs to the liver before entering the main systemic
circulation
Aorta and Major Arteries
of the
Systemic Circulation
• Four paired arteries
supply the head and
neck:
– Common carotid
arteries
– Three branches of the
subclavian artery
• Vertebral arteries
• Thyrocervical trunks
• Costocervical trunks
ARTERIES OF THE HEAD, NECK, AND BRAIN
THE AORTA AND MAJOR ARTERIES OF THE
SYSTEMIC CIRCULATION
Aorta and Major Arteries
of the
Systemic Circulation
ARTERIES OF THE HEAD AND NECK
ARTERIES OF THE BRAIN
Aorta and Major Arteries
of the
Systemic Circulation
• The upper limbs are
supplied entirely by
arteries arising from
the subclavian
arteries
MAJOR ARTERIES OF THE
SYSTEMIC CIRCULATION
THE AORTA AND MAJOR ARTERIES OF THE
SYSTEMIC CIRCULATION
ARTERIES OF THE UPPER LIMBS AND THORAX
ARTERIES OF THE RIGHT
UPPER AND THORAX
Aorta and Major Arteries
of the
Systemic Circulation
• The arterial supply
to the abdomen
arises from the
aorta
THE AORTA AND MAJOR ARTERIES OF THE
SYSTEMIC CIRCULATION
MAJOR ARTERIES OF THE
SYSTEMIC CIRCULATION
ARTERIES OF THE ABDOMEN
ARTERIES OF THE ABDOMEN
ARTERIES OF THE ABDOMEN
ARTERIES OF THE ABDOMEN
Aorta and Major Arteries
of the
Systemic Circulation
• The internal iliac
arteries serve mostly
the pelvic region
• The external iliacs
supply blood to the
lower limb and
abdominal wall
THE AORTA AND MAJOR ARTERIES OF THE
SYSTEMIC CIRCULATION
MAJOR ARTERIES OF THE
SYSTEMIC CIRCULATION
ARTERIES OF THE ABDOMEN
ARTERIES OF THE ABDOMEN
ARTERIES OF THE ABDOMEN
ARTERIES OF THE PELVIS AND
LOWER LIMBS
ARTERIES OF THE PELVIS AND
LOWER LIMBS
Venae Cavae and the Major Veins
of the
Systemic Circulation
• The venae cavae are
the major tributaries
of the venous
circulation
THE VENAE CAVAE AND THE MAJOR VEINS OF
THE SYSTEMIC CIRCULATION
THE VENAE CAVAE AND THE MAJOR
VEINS OF THE SYSTEMIC CIRCULATION
Venae Cavae and the Major Veins
of the
Systemic Circulation
• Blood drained from the
head and neck is
collected by three pairs
of veins:
– External jugular veins:
• Empty into the
subclavians
– Internal jugular veins:
• Drains into the
Brachiocephalic veins
– Vertebral veins:
• Drains into the
Brachiocephalic veins
VEINS OF THE HEAD AND NECK
VEINS OF THE HEAD AND NECK
Venae Cavae and the Major Veins
of the
Systemic Circulation
• The deep veins of
the upper limbs
follow the paths of
the common arteries
VEINS OF THE UPPER LIMBS
AND THORAX
THE VENAE CAVAE AND THE MAJOR
VEINS OF THE SYSTEMIC CIRCULATION
VEINS OF THE UPPER LIMBS
AND THORAX
Venae Cavae and the Major Veins
of the
Systemic Circulation
• Blood draining from
the abdominopelvic
viscera and
abdominal walls is
returned to the heart
by the inferior vena
cava
VEINS OF THE ABDOMEN
THE VENAE CAVAE AND THE MAJOR
VEINS OF THE SYSTEMIC CIRCULATION
VEINS OF THE ABDOMEN
VEINS OF THE ABDOMEN
Venae Cavae and the Major Veins
of the
Systemic Circulation
• Most deep veins of
the lower limb have
the same names as
the arteries they
accompany
Deep Veins and Arteries
Deep Veins and Arteries
VEINS OF THE PELVIS AND
LOWER LIMB
VEINS OF THE PELVIS AND
LOWER LIMB
DEVELOPMENTAL ASPECTS
OF
THE BLOOD VESSELS
•
•
•
•
•
•
•
The vascular endothelium is formed by mesodermal cells that collect
throughout the embryo in blood islands, which give rise to extensions that
form rudimentary vascular tubes
By the fourth week of development, the rudimentary heart and vessels are
circulating blood
Fetal vascular modifications include shunts to bypass fetal lungs (the
foramen ovale and ductus arteriosus), the ductus venosus that bypasses
the liver, and the umbilical arteries and veins, which carry blood to and from
the placenta
At birth, the fetal shunts and bypasses close and become occluded
Congenital vascular problems are rare, but the incidence of vascular
diseases increases with age, leading to varicose veins, tingling in fingers
and toes, and muscle cramping
Atherosclerosis begins in youth, but rarely causes problems until old age
Blood pressure changes with age: the arterial pressure of infants is about
90/55, but rises steadily during childhood to an average 120/80, and finally
increases to 150/90 on old age