Blood, Blood Vessels
& Circulation
21-1
Cardiovascular System
Blood vessels: Types
A. Arteries
-carry oxygenated blood (most of the time)
away from the heart
-thicker than veins
-three layers: inner endothelium
middle smooth muscle
outer connective tissue
-arteriole = small artery
C. Capillaries
-site of gas exchange with tissues
-connect arterioles and venules
-network of microscopic vessels
(one cell thick) = capillary bed
-site of exchange: gases, nutrients,
wastes
-can be closed off when not needed
B. Veins
-carry deoxygenated blood (most of
the time) – toward the heart
-same three layers as arteries
(less SM and connective tissue)
-thinner and more expansive than
arteries
-contain valves - to help the flow
of blood back to heart
-small vein = venule
21-2
21-3
• Tunica interna (intima)
– simple squamous epithelium known as
endothelium
– basement membrane
– internal elastic lamina
Arteries
• Tunica media
– circular smooth muscle & elastic fibers
– smooth muscle is innervated by
sympathetic nervous system
– decrease in stimulation or presence of
certain chemicals causes vasodilation
• increases diameter of vessel
• nitric oxide, K+, H+ and lactic acid
cause vasodilation
– increase in stimulation causes muscle
contraction or vasoconstriction
• decreases diameter of vessel
• Tunica externa
– elastic & collagen fibers
21-4
Blood Distribution
– Arterial circuit
21-5
Blood flow & Pressure gradients
•
blood flow is fastest in the arteries
– slows within arterioles
– slowest rate in capillaries - allows for
exchange
– blood flow becomes faster when vessels merge to form veins
•
flow rate through a vessel is proportional to the pressure
gradient and inversely proportional to the vascular resistance
(diameter)
– F = ΔP/R
• F = flow rate
• ΔP = pressure gradient
• R = resistance
•
ΔP is the pressure gradient = difference in P between the
beginning and end of a vessel
– this is what determines flow rate – NOT the absolute pressure!
– resistance changes as the radius changes
• R increases as r decreases – F will decrease (if P stays the same)
• R decreases as r increases – F will increase (if P stays the same)
– this relationship applies to non-viscous fluids
21-6
Blood flow & Pressure
gradients
•
frictional losses (resistance) causes a drop
in P as the blood travels through a section
of vessel
– caused by friction between the moving
fluid and the stationary wall
– if pressure gradient is unchanged – then
increasing R will inhibit blood flow and
decrease F
– R depends on three factors
• 1. blood viscosity (η) - # of circulating
RBCs
• 2. vessel length (L)
• 3. vessel radius (r) – major determinant of
R
–
R = 1/r4
21-7
Pouiseuille’s Law (Snooty French Guy Law)
-true description of how blood flow through
our vessels – description of viscous fluids
Flow rate = η ΔP r4
8 ηL
-changing the viscosity (η) of the blood does
NOT change the F value (go ahead try it!)
-but changing the L value does
-this is because thick, viscous blood “sticks”
to the blood vessel wall
-so the longer the vessel – the more sticking
and the slower the blood flows
21-8
Blood Pressure
•
Pressure exerted by blood on walls of a
vessel
–
–
–
•
depends on the volume of blood within the vessel and the
distensibility of the vessel
caused by contraction of the ventricles
highest in aorta
• difference between systole and diastole – pulse pressure
the volume of blood entering an artery is not the same as the
volume leaving it
–
–
–
during ventricular systole – the SV leaving the artery is 1/3 of
that entering the artery
the artery will distend with increasing volumes
during diastole – the recoil of the vessel drives the exit of the blood
•
•
mean arterial pressure – average pressure driving blood
forward into the tissues throughout the cardiac cycle
–
–
•
BUT no blood enters the vessel
at resting heart rate – about 2/3 of the cardiac cycle is spent in
diastole
MAP = diastolic pressure + 1/3 (systolic pressure – diastolic
pressure)
MAP falls steadily in
systemic circulation with distance from left ventricle
–
–
35 mm Hg entering the capillaries
0 mm Hg entering the right atrium
21-9
• mean arterial pressure – average pressure driving blood
forward into the tissues throughout the cardiac cycle
– at resting heart rate – about 2/3 of the cardiac cycle is spent in
diastole
– MAP = diastolic pressure + 1/3 (systolic – diastolic pressure)
– MAP is what is regulated by homeostatic mechanisms
• MAP falls steadily in
systemic circulation with distance from left ventricle
– 35 mm Hg entering the capillaries
– 0 mm Hg entering the right atrium
• our bodies need to control MAP – to keep it in a narrow
range
– we do this a few ways
• 1. elastic arteries help decrease pressure in them by distending
• 2. muscular arteries can vasodilate and decrease pressure in them by
increasing diameter
• 3. we can also decrease the SV of the heart
21-10
– F = ΔP/R applies to the entire circulatory
system in addition to a single vessel
– F = cardiac output
– ΔP = MAP (mean arterial pressure)
– R = total peripheral resistance
• total resistance offered by all systemic peripheral
vessels
• influenced by sympathetic nervous activity
– rearrange the equation - ΔP = F X R
– OR MAP = CO X total peripheral resistance
21-11
•
•
•
•
•
•
•
1 – CO and total peripheral
resistance
2 – CO depends on heart rate and
SV
3 & 4– heart rate depends on
balance between the parasymp
and symp divisions of the ANS
5 – SV increases in response to
symp activation (extrinsic
control)
6 – SV also increases with
increasing venous return
(instrinsic control)
7- 10 – venous return is increased
by symp induced vasoconstriction
(7), skeletal muscle pump (8),
respiratory pump (9) and cardiac
suction (10)
11 – 13 – venous return is also
influenced by how much blood
returns to the heart (11), actual
blood volume (balance between
passive bulk-flow fluid exchange
between plasma and ECF (12),
water and salt balance (13) and
hormonal control (14)
21-12
• 15 & 16 – MAP is also
determined by radius of the vessel
(15) and the number of RBCs
(16)
• 17 - 20– arteriole radius can be
controlled by metabolic factors
which control blood need (17) which leads to vasodilation (18)
ALSO by sympathetic activity
(19) which can cause
vasocontriction (20) OR
hormonally (20)
21-13
Arterioles
• major resistance vessels in the vascular tree
• radius is small enough to offer resistance to flow
• high arteriolar resistance causes a marked
drop in the MAP as blood flows through these
vessels
– MAP arteriole entrance = 93 mm Hg
– MAP arteriole exit = 37 mm Hg
• resistance also converts the pulsatile nature of
systolic-diastolic pressure to nonpulsatile
pressure within the capillaries
• radius of the arteriole can be adjusted to
– 1. variably distribute cardiac output among the organs
– 2. help regulate arterial blood pressure
21-14
Arterioles and Arteriolar
resistance
• vasoconstriction and vasodilation
– presence of a thick layer of smooth
muscle
– sensitive to many systemic, local factors
+ neurogenic stimulation
• vascular tone
– arterioles normally exhibit a state of
slight constriction = vascular tone
– helps establish a baseline of arteriolar
resistance
– tonic activity makes it possible to either
vasoconstrict or vasodilate
– two facets are responsible
• 1. myogenic activity of smooth muscle
layer
– smooth muscle layer is responsive to
neural or hormonal influences – selfinduced contractile activity
• 2. continuous release of NE by
sympathetic fibers of the ANS
21-15
Arteriolar diameter
• Intrinsic Factors/Local changes – at the tissue, organ
specific
– local chemical factors
• metabolic factors
• vasoactive mediators
– histamine
– local physical factors
• hot/cold
• passive stretch of arteriole
• shear stress within arteriole
• Extrinsic factors
– sympathetic nervous system
– hormones
21-16
Chemical influences and arteriole
radius = local metabolic changes
•
•
•
most important local chemical influences on arteriolar smooth muscle are local changes in
metabolism within that organ
local metabolic changes can affect the diameter of an arteriole without neural influence
active hyperemia = local arteriolar vasodilation that increases blood flow into an organ
– arterioles are found within an organ and can be directly affected by that organ’s metabolic needs
•
local metabolic factors
–
–
–
–
decreased/increased oxygen = vasodilation/vasoconstriction
increase carbon dioxide = vasodilation
increased carbonic acid= vasodilation
increased K+ - repeated APs that outpace the Na/K pump’s ability to correct ionic changes =
vasodilation
– increased osmolarity – concentration of solutes accumulates in actively metabolic cells =
vasodilation
– prostaglandin release = vasodilation
•
relative concentration of these factors can determine the state of arteriolar muscle tone
21-17
Vasoactive Mediators
• these local chemical changes do not act
directly on smooth muscle but act on the
endothelial cells
• ECs – simple squamous epithelia cells
– found lining the inside of the arteriole and
capillary
• ECs then release chemical factors called
vasoactive mediators
– e.g. endothelin = vasoconstriction
– e.g. nitric oxide = vasodilation by relaxing
arteriolar smooth muscle
• inhibits entrance of calcium into the smooth
muscle which inhibits the opening of the foot
proteins on the sarcoplasmic reticulum
• ECs have multiple roles
21-18
Histamine
•
•
•
•
NOT released by metabolic changes
NOT produce by endothelial cells
released upon pathology
released by connective tissue cells within the organ or by
circulating white blood cells (mast cells, basophils)
• usually released in response to organ damage
• causes vasodilation to increase blood flow and speed healing
21-19
Local Physical factors
• application of heat or cold
– heat causes localized arteriolar vasodilation
• increases blood flow
– cold – counteracts histamine-induced swelling by inducing vasoconstriction
• shear stress
– blood flowing over the endothelial lining creates friction = shear stress
– increase in shear stress can cause increased release of NO – promotes
vasodilation
– increased blood flow now reduces shear stress
• myogenic response to stretch
– increased MAP drives more blood into the arteriole which pushes out against the
vessel wall = passive stretch
• leads to vasoconstriction to reduce this blood volume
– arteriolar smooth muscle responds to passive stretch by increasing its tone
through vasoconstriction
– this increased tone acts to resist the passive stretch
– done by the release of vasoactive mediators from the EC (e.g. endothelin)
– arterial occlusion can block blood flow and reduce this stretch
• arterioles will dilate in response=reactive hyperemia
21-20
Extrinsic control of arteriolar diameter
• includes both neural and hormonal control
• sympathetic division innervates arteriolar smooth muscle everywhere
except the brain
• NO parasympathetic innervation of arteriolar smooth muscle!
(exception – ciltoris and penis)
• sympathetic activity contributes to arteriolar vascular tone
• increased sympathetic activity induces vasodilation of arterioles in
heart and skeletal muscle– drops arteriolar resistance and changes
MAP
• main area of the brain to adjust sympathetic output = cardiovascular
control center
• other brain regions involved – hypothalamus
• Hormones: ADH, angiotensin II, epinephrine, norepinephrine
21-21
HORMONAL CONTROL OF ARTERIOLAR
DIAMETER:
• angiotensin II – converted from angiotensin I by the
enzyme ACE (produced in the lungs)
– regulates body’s salt balance
– causes the release of aldosterone from the adrenal cortex
– increased salt reabsorption
– powerful vasoconstrictor
• vasopressin (ADH) – released from the posterior pituitary
in response to changes in water volume
– drop in water content, release of vasopressin, decreased
urine volume, increased water retention
– also construction of peripheral vessels =
vasoconstrictor
– plays a role in reducing hemorrhage
21-22
-Epinephrine and Norepinephrine can be
released from the adrenal medulla
(sympathetic activity) or NE can be released
from neurons (sympathetic)
-Ep and NE can cause vasoconstriction or
vasodilation!!! depends on receptor and its
location
-NE binds to a1-adrenergic receptors on ALL
arteriolar smooth muscle to increase
vasoconstriction
-Epi binds to b2-adrenergic receptors on
arteriolar smooth muscle in heart and muscles to
cause vasodilation
-cerebral arterioles do NOT have a1adrenergic receptors !!!
-influenced entirely by local physical and
chemical changes (intrinsic changes)
-during the “flight or fight” response - Epi is
more abundant and has more affinity for the
b2-adrenergic receptors which are expressed
in large amounts on arteriolar smooth muscle in
skeletal and cardiac muscle – so overall effect
is vasodilation to heart and skeletal muscles
21-23
21-24
Evaluating Circulation
• Pulse is a pressure wave
– alternate expansion & recoil of elastic artery after each systole
of the left ventricle
– pulse rate is normally between 70-80 beats/min
• tachycardia is rate over 100 beats/min/bradycardia under 60
• Measuring blood pressure with sphygmomanometer
– Korotkoff sounds are heard while taking pressure
– systolic blood pressure from ventricular contraction
– diastolic blood pressure during ventricular contraction
• provides information about systemic vascular resistance
– pulse pressure is difference between systolic & diastolic
– normal ratio is 3:2:1 -- systolic/diastolic/pulse pressure
21-25
Measuring Blood pressure
21-26
• the sympathetic nervous system essentially
maintains an appropriate driving pressure to
each organ (i.e. MAP) but the organ itself
controls the amount of blood that actually enters
it.
• sympathetic control over arteriolar vascular tone
constricts most vessels to ensure adequate MAP
throughout the systemic circuit
• BUT the organ can override the sympathetic control
using local control mechanisms
– analogy = water pressure in pipes
21-27
– analogy – pipe carrying water
• water pressure remains constant
• differences in the amount of water
entering the beaker depends on which
valves are open and to what extent these
valves are open
• no water flows when the valve is closed
• more water flows when the valve is wide
open (low resistance) versus when a
valve is partially open (high resistance)
• so the sympathetic NS maintains the
“water pressure” (i.e. the MAP), but
each organ can control the amount of
blood that enters them
• when increased blood flows into one
organ the others must compensate by
changing their arteriolar diameter
• SO THAT MAP IS MAINTAINED
WITHIN AN APPROPRIATE
RANGE
21-28
Regulation of BP
• regulation of mean arterial pressure by the body done mainly through
arteriolar diameter
• Blood pressure = MAP within a small length of blood vessel
• our body uses BP to immediately determine heart rate and contraction
strength
• BP is measured constantly by baroreceptors
– changes in pressure within blood vessels
– initiates either short-term or long-term reflexes
– two major BRs: carotid sinus & aortic arch baroreceptors (mechanoreceptors)
• as the BP within the vessels increase –increases the rate of firing of the afferent
neurons within these BRs
• decreasing pressure decreases the rate of firing
• role of cardiovascular center in the medulla
– help regulate heart rate & stroke volume
– integrating center for information sent by the carotid and aortic BRs
– divided into two centers: vasomotor & cardiac centers (made up of
cardioacceleratory, cardioinhibitory divisions)
– alters the ratio between sympathetic and parasympathetic activity to the heart and
BVs
– Vasomotor center = specific neurons regulate blood vessel diameter sympathetic vasomotor nerves
– Cardiac center = signals sent out through vagus & cardiac accelerator nerves changes heart rate
21-29
• Higher brain centers such as cerebral cortex, limbic system
(emotions) & hypothalamus
– anticipation of competition
– increase in body temperature
• Hypothalamus
– osmoreceptors control salt and water balance and therefore long-term
regulation of BP
– cerebral cortex-hypothalamus preprograming – fight or flight responses,
sexual orgasm, blushing
– control over cutaneous arterioles for temperature regulation takes
control over the cardiovascular center’s control over these vessels for
regulation BP
• therefore BP can fall dramatically as arteries dilate to allow cooling
• Proprioceptors
– input during physical activity
• Chemoreceptors
–
–
–
–
monitor concentration of chemicals in the blood (O2, CO2 and H+ions)
also located in the carotid and aortic arteries
increase respiratory activity to bring in more O2 or blow off more CO2
also increase BP by sneding excitatory impulses to the cardiovascular
center
21-30
Role of the ANS in Blood pressure
21-31
•
Capillaries
•
•
Microscopic vessels that connect
arterioles to venules
Found near every cell in the body but
more extensive in highly active tissue
(muscles, liver, kidneys & brain)
– entire capillary bed fills with blood
when tissue is active
– lacking in epithelia, cornea and lens
of eye & cartilage
•
•
Function is exchange of nutrients &
wastes between blood and tissue fluid
Structure is single layer of simple
squamous epithelium and its
basement membrane
Continuous capillaries
– skeletal & smooth,
connective tissue and
lungs
•
Fenestrated capillaries
– plasma membranes have
many holes
– kidneys, small intestine,
choroid plexuses, ciliary
process & endocrine
glands
•
Sinusoids
– very large fenestrations
– incomplete basement
membrane
– liver, bone marrow,
spleen, anterior
pituitary, & parathyroid
gland
21-32
•
•
•
•
•
•
•
capillaries are not open under resting conditions in most tissues
prevents the flow of blood through the capillary bed
capillaries branch from a metarteriole or directly from an arteriole
metarteriole acts like a thoroughfare connecting a larger arteriole and a venule
these MAs are surrounded by spiralling smooth muscle cells – form a
precapillary sphincter
the sphincters are not innervated by the nervous system by still possess a high
degree of myogenic tone to contract in response to chemical factors released
by the tissue
the more metabolically active the tissue, the greater the number of capillaries
– e.g. muscle
– only 10% of the capillaries are open in resting muscle
– as the muscle increases its activity – local chemical factors change and the
precapillary sphincters open to allow more blood flow
21-33
•
•
•
•
ECs fit together like a jigsaw puzzle with considerable gaps in between the
cells = pores
sizes vary from capillary to capillary
brain capillaries have EC cells held together by tight junctions – no pores
most tissue capillaries allow the passage of small water-soluble substances like
but glucose, small amino acids and peptides and ions
– prevents the passage of larger proteins like plasma proteins
•
this transport may actually be regulated by the capillary itself
– ECs may secrete substances that “tighten” up their junctions
– histamine increases the gaps by inducing a contractile response in the EC and
widening the gaps (actin-myosin interaction in the cytoskeleton)
•
in the liver, the capillary walls have larger pores to allow the passage of
proteins
– liver synthesizes the plasma proteins which must be allowed to pass into the
circulatory system
21-34
Interstitial Fluid or ECF
• passive intermediary between blood and cells – not a direct exchange
between the blood and the ICF of cells
– only 20% of the ECF circulates as plasma
– the remaining 80% is interstitial fluid
– exchange between the inside of the cell and the interstitial fluid (across the
plasma membrane) is passive or active – depending on the cell and the
solute being moved
– BUT exchange between the interstitial fluid and the capillary wall is
primarily PASSIVE
– because the gaps in a capillary wall are quite large, the interstitial fluid
and the composition of the blood are essentially the same
– two ways to exchange materials between the blood and interstitial fluid
• 1. diffusion
• 2. bulk-transport
21-35
Capillary Exchange
• Movement of materials in & out of a capillary
– diffusion (most important method)
• substances move down concentration gradient
• all plasma solutes except large proteins pass freely across
– through lipid bilayer, fenestrations or intercellular clefts
– blood brain barrier does not allow diffusion of water-soluble materials
(nonfenestrated epithelium with tight junctions)
– transcytosis (vesicular transport)
• passage of material across endothelium in tiny vesicles by endocytosis and
exocytosis
– large, lipid-insoluble molecules such as insulin or maternal antibodies passing
through placental circulation to fetus
– bulk flow
•
•
•
•
•
movement of large amount of dissolved or suspended material in same direction
move in response to pressure - from area of high pressure to area of low
faster rate of movement than diffusion or osmosis
regulates relative volumes of blood & interstitial fluid
comprised of: filtration (movement of material into interstitial fluid) + reabsorption
21-36
(movement from interstitial fluid into capillaries)
Diffusion
• diffusion is promoted by several factors:
– 1. short distance of travel
• 1. thinness of the capillary wall – 1 um in thickness
(simple squamous epithelium + basement membrane)
• 2. narrowness of the capillary – thinner than the RBC so
the cells must pass through one at a time
• 3. proximity to cells – every cell is approximately
0.01cm from a capillary
– 2. total surface area – 10 to 40 billion capillaries
• produces a tremendous surface area for exchange =
600m2
– 3. velocity of blood through the capillary
• Slowest blood velocity is found in the capillaries
• velocity is inversely proportional to the total crosssectional area of all the capillaries
• slow velocity of flow allows for sufficient exchange
time
• analogy – river – lake – river
– flow rate (volume of water) flowing past any point along
the river equals that of the lake
– BUT the speed of the water flowing is slower in the
lake
21-37
•
•
•
•
•
•
•
most capillary walls solutes cross via diffusion
so the chemical concentration of arterial blood is carefully regulated to promote the diffusion of
specific solutes in a specific direction
the lungs add oxygen and remove carbon dioxide from the blood, the digestive organs supply
glucose
the cells use this oxygen and glucose and replace them with waste products
the job of the blood is to continuously replace these waste products with fresh O2 and glucose
because O2 and glucose pass easily through the walls of the capillary – their movement is
dependent upon their specific concentration gradient
as cells use more O2, this creates a larger concentration gradient between the cell and the blood –
greater movement of O2
21-38
21-39
Bulk-flow
• a volume of protein-free plasma filters out of the capillary and mixes
with the surrounding interstitial fluid and then is reabsorbed = bulk flow
• the various components are moved in bulk in contrast to the movement
of individual components as seen in diffusion
• when blood pressure inside the capillary exceeds that of the osmotic
pressure of the blood – fluid is pushed out through the pores in the
capillary wall = ultrafiltration
• with the fluid comes the movement of multiple other components
• when inward driving osmotic pressure exceeds the outward blood
pressure– net inward movement of fluid and fluid components =
reabsorption
• ultrafiltration and reabsorption are collectively known as bulk flow
• does NOT play a role in the exchange of individual solutes
• does play a role in regulating the distribution of ECF between the
circulating plasma and interstitial fluid
• this is the way we establish the composition of our interstitial fluid
21-40
Bulk Flow
• (Pc + πIF) – (πP + PIF) = outward
pressure – inward pressure
• major factors are Pc and πP
21-41
•
factors affecting bulk flow
– 1. Pc = capillary blood pressure
• fluid or hydrostatic pressure exerted on the inside of the capillary wall by blood
• tends to force fluid OUT of the capillaries into the interstitial fluid
• in general the blood pressure at the arteriolar end of a capillary = 37 mm Hg due to frictional
losses in the upstream arterioles - declines to 17 mm Hg at the venous end of a capillary
– 2. πP = plasma osmotic pressure (oncotic pressure)
• osmotic pressure encourages inward movement of fluid into the capillary
• 25 mm Hg – doesn’t change
– 3. PIF = interstitial fluid hydrostatic pressure
• fluid pressure exerted on the outside of the capillary wall by interstitial fluid
• tends to force fluid into the capillaries and into the blood plasma
– 4. πIF = interstitial fluid-colloid osmotic pressure (πIF is close to zero)
• does not normally contribute significantly to bulk flow
• Caused by the osmotic pressure of proteins in the IF - promotes the osmotic movement of
water out of the blood and into the fluid
• but during pathologic conditions – i.e. release of histamine which widens the capillary pores
– increased leakage of plasma proteins into the interstitial fluid and πIF can increase
21-42
Net exchange of fluid across capillaries
•
•
•
•
•
•
•
•
•
Net exchange pressure = (Pc + πIF) – (πP + PIF) = outward pressure – inward pressure
two pressures forcing fluid out of the plasma are capillary blood pressure and
interstitial fluid-osmotic pressure
two pressures forcing fluid into the plasma are plasma-osmotic pressure and interstitial
fluid hydrostatic pressure
the imbalance between the forces produces a net exchange of fluid at a given point along
the capillary wall
as the blood enters the capillary – outward forces exceed that of inward and fluid is
forced out into the interstitial fluid (no protein movement!) – ultrafiltration forces
result
at the venular end the inward pressure now exceeds the outward pressure and
reabsorption will take place
as the blood moves through the capillary – pressure drops
so the amount of fluid moving out of the blood drops as the blood travels through the
capillary region and progressively increasing amounts of fluid re-enter the blood as the
blood reaches the venular end of the capillary
BUT these pressure values are controversial
21-43
Lymph
• even under normal circumstances –
more fluid is filtered from the
blood plasma into the interstitial
fluid than is reabsorbed back into
the blood plasma
• excess fluid = lymph
• this excess fluid is directed into a
series of vessels that are similar in
structure and composition to veins
– lymphatic vessels
• one-way system of vessels that
leads back to the circulatory system
via the right lymphatic duct and the
thoracic duct
21-44
Veins
• Proportionally thinner walls than same
diameter artery
– tunica media less muscle – little inherent
myogenic tone
– lack external elastic lamina
– tunica externa has more collagen than
elastic fibers
– strong and stretchy but possess poor elastic
recoil
• Still adaptable to variations
in volume & pressure
• Valves are thin folds of
tunica interna designed to prevent
backflow
• Venous sinus has no muscle at all
– coronary sinus or dural venous sinuses
21-45
Blood Distribution
•
60% of blood volume at rest is in systemic veins
and venules
– function as blood reservoir
– often called capacitance vessels
– venous capacity = volume of blood the veins can
accomodate
– body at rest – much of the blood bypasses the
closed capillary beds and enters the venous return
circuit – this increases the blood volume in the
veins
•
15% of blood volume in arteries & arterioles
21-46
Veins & Venules
• veins & venules have little tone and resistance
• the arteriole communicates chemically with the
venule to ensure that inflow and outflow
surrounding the capillary region matches
• venous return is enhanced by many extrinsic
factors
– venous return = volume of blood entering the atria
from the veins (pulmonary and systemic)
– much of the driving force on the blood (blood
pressure) has been lost as it enters the veins
– BP averages on 17 mm Hg in the veins
– but because the pressure of the blood entering the
right atrium in o mm Hg – there is still a small
driving force that helps to return the blood through
the veins
– clinical note – if atrial pressure becomes
pathologically elevated (e.g. leaky AV valves) –
this pressure differential can be lost, reducing the
venous return
21-47
1. sympathetic activity – venous smooth muscle has an
abundant nervous innervation by the sympathetic
nervous division
- can produce a small amount of constriction in the veins increasing venous BP
and increasing the forces driving blood back to the heart
- this contraction also decreases the amount of blood that can be held in the
veins (decreases venous capacity) by decreasing the diameter of the vein itself
- so less blood remains in the veins but is returned faster to the heart
2. skeletal muscle activity – contraction of skeletal
muscles can push on the vein walls, decreasing their
size and decreasing their capacity
3. venous valves – venous vasoconstriction and skeletal
muscle contraction also drive blood away from the
heart
-evolved extensions off the endothelium – valves
-these valves can shut off sections of veins to prevent back-flow towards the feet
when standing
•
4. respiratory activity– pressure in the chest is 5 mm
Hg less than atmospheric
–
–
blood flowing through the thoracic cavity on the way back to the heart is exposed
to subatmospheric conditions
this creates a pressure differential between the pressure in the limb veins and those
in the thoracic region veins – drives more blood from the limbs = respiratory pump
21-48
Veins and gravity
- gravity – when lying down, forces of gravity are equally
applied to all veins
-when standing, vessels below the heart become more subject to
gravitational forces
-so the veins increase their volume to counteract the increased
volume
-this reduces the amount of blood returning to the heart –
decreases CO
-also increases the pressure in the capillaries – forces more fluid
out into the tissues from the blood
-compensatory mechanisms – fall in MAP triggers the
sympathetic NS to induce venous constriction to drive some
of the pooled blood up toward the heart + skeletal muscle
tone will increase to help propel blood to the heart
21-49
21-50