Download Physiology of Circulation

Chapter 21
The Cardiovascular system: physiology of circulation
blood vessel structure and function
physiology of circulation:
blood flow, blood pressure, and resistance
blood flow
the amount of blood flowing through an organ, tissue or blood vessel in a given
time (normally ml/min)
perfusion is the rate of blood flow per given mass of tissue
(normally ml/min/gram)
I use these interchangeably
blood flow/perfusion determines the speed of nutrient delivery and
waste removal
this is very important so they are carefully regulated
the blood flow through the entire systemic circulation is 5L/ml or
the cardiac output of the left ventricle
of this cardiac output each tissue gets a small but ever
changing (regulated) percentage of CO that increases
with need
What determines blood flow
two factors that determine blood flow
1) blood pressure differences
2) resistance (R)
flow = P1-P2/R
blood pressure (BP) liquids like blood cannot be compressed. A force exerted
against a liquid generates a hydrostatic pressure (HP) that is
conducted in all directions
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in a blood vessel this force will push blood against the
blood vessel walls and push blood down the vessel towards
an area of lower pressure
differences in blood pressure (∆P) between different areas
of the circulation provide the driving force for blood
flow in the circulation
the greater the ∆P the greater the flow
in the systemic circuit the pressure gradient (∆P) is the
pressure difference between the base of the aorta and the
entrance of the right atrium (95mmHg – 5-2mmHg) or about
90mmHg
flow = ∆P /R
thus increases in blood pressure increase flow
characterization of blood pressure through the circulatory system
1) arterial pressure (typically called blood pressure):
is not a steady pressure it is pulsatile
peak pressure is the systolic pressure
occurs during ventricular systole
lowest pressure is the diastolic pressure
occurs during ventricular diastole
normally written 120/75
pulse pressure
systolic - diastolic pressure
120-75=45
is felt as the pulse with our finger
is a measurement of the stress exerted on the wall of the arteries
by the pressure surges generated by the heart
remember the farther from the heart the lower the systolic and
diastolic pressures
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mean arterial pressure (MAP)
is used to convert the pulsatile pressure of the blood into a
single pressure value
MAP is used to determine the ∆P
is the average pressure during an entire cardiac cycle
heart spends more time in diastole then systole so is
not the sum of the two divided by two
MAP = diastolic pressure + (pulse pressure/3)
for 120/75
MAP = 75 + (120-75)/3 = 90mmHg
MAP at aorta = 90-95mmHg
MAP at just before capillaries =
35mmHg
2) capillary blood pressure
pressure is not pulsatile due to elastic recoil
pressure at the start of the capillaries is 35mm Hg
by the end of cap bed it is 18 mm Hg
low pressure is important
1. capillaries are fragile
2. capillaries are permeable -- high pressures
would force out too much filtrate
capillaries are very numerous so have largest cross section
thus rate of blood flow is very low
helps with exchange
3) venous blood pressure
pressure is not pulsatile but steady and changes very
little during the cardiac cycle
entering small venules 18mmHg
right atrium is 2-5 mmHg
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as blood travels toward heart veins converge so cross sec. area drops
resistance remains low and velocity of flow increases
systemic circulatory pressure gradient = the pressure difference
between the aorta and the entrance of the right atrium
this is the ∆P for the systemic circulation
MAP of aorta = 90-95 mmHg
Blood pressure of right atrium = 2-5 mmHg
systemic circulatory pressure gradient (∆P) averages 90 mmHg
this is mainly need to force blood through the arterioles
which are the source of most resistance
resistance
any force that opposes movement
the amount of friction blood encounters as it passes
through the vessels
greater the resistance the slower the flow of blood
remember F = ∆P/R
thus increases in resistance decreases flow and an increase in pressure
is required to maintain flow
peripheral resistance (PR)
is the resistance that the blood encounters in the vessels
as it travels through the circulatory system
the resistance of the arterial system is the site
of most peripheral resistance (mostly the
arterioles)
(venous resistance is very low so not
important)
greater the PR the higher the pressure must be
to maintain flow
F = ∆P/R
sources of resistance
blood flow (F) = π∆P r4/8ηl (Poiseuille’s law)
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η = viscosity
l = length
r = radius
1. blood viscosity = η
thickness or stickiness of blood
greater the viscosity the greater the resistance
thus lower the flow
blood is 5X thicker then water mainly
due to erythrocytes and albumin
changed by living at altitude,
polycythemia, anemia, dehydration,
liver disease, ect.
2. vessel length
longer the vessel length the greater the
cumulative friction between blood and the wall
so the greater the resistance
change in vessel length occurs slowly so not
changed minute to minute
added fat adds resistance
3. blood vessel radius = r
the smaller the radius the greater the friction so
more resistance
radius is the only one that is not fairly constant
and is changed moment to moment to adjust
blood flow blood and pressure
vasoconstriction
narrowing
stimulating the
contraction of smooth
muscle of the vessels
vasodilation
widening
relaxing the smooth
muscle of the vessels
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resistance varies inversely with the fourth
power of the vessels radius
R ∝ 1/r4 thus F ∝ r4
double the radius the resistance is
1/16 and flow is 16 times more
thus small changes in resistances equals
big changes in flow
small arterioles with the lowest total
cross sectional area account for most of
the peripheral resistance
the resistance of a maximally
constricted arteriole is 80 times
the maximally dilated arteriole
4. turbulence (pathological)
normally blood flow is laminar
smoothly flowing in layers
fastest in the middle
irregular surfaces upset the smooth flow of
blood and create eddies and swirls
this turbulence increases resistance and
lowers flow rates
abnormal turbulence occurs with damaged
heart valves and damaged blood vessels
(atherosclerosis)
abnormal turbulence causes a sound called a
bruit in vessels and a murmur in the heart
Cardiovascular Regulation (regulation of blood flow)
The main purpose of the cardiovascular system is ensure that tissues are provided with
the appropriate amounts of oxygen and nutrients
If demand is not met cellular function drops and tissues begin to die
To meet tissue demands blood flow is carefully regulated
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Tissue blood flow is regulated by three factors
1. cardiac output- covered in the previous chapter but done forget it now
2. peripheral resistance
3. blood pressure
all three are closely interrelated
The goal or cardiovascular regulation is to ensure that changes in blood flow occur
1. at an appropriate time
2. in the right area
3. without drastically changing blood pressure flow to vital organs
all three conditions must be met simultaneously
Blood flow is regulated by controlling blood pressure and peripheral
resistance
Remember blood flow ∝ ∆P/R
blood pressure = (cardiac output) X (peripheral resistance)
Resistance ∝ 1/r4 ηl
mechanisms involved in regulation of cardiovascular function
1. local control or autoregulation
work by controlling peripheral resistance in response to
chemical changes at the tissues
2. neural mechanisms
ANS
work by controlling both peripheral resistance and
cardiac output in response to changes in autonomic
activity, blood gases and arterial pressure
3. endocrine factors
work by controlling both peripheral resistance and
cardiac output
1. autoregulation of blood flow within tissues
while cardiac output remains stable the peripheral resistance within a
tissue is adjusted to control local blood flow
work by changing peripheral resistance
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important in short-term regulation
local vasodilators
produced by tissues that have inadequate blood flow
1. decreased tissue oxygen
2. increases CO2 levels
3. rising K
4. H levels (lactic acid)
5. nitric oxide (NO)
6. heat
Work by relaxing the smooth muscle of the precapillary
sphincters
produced due to high pressure
local vasoconstrictors
1. endothelin
2. prostaglandins
3. thromboxanes
Released from platelets, WBC, and endothelial
cells following injury
Work by triggering constriction of precapillary
sphincters
High concentrations will affect arterioles
further reducing flow to the tissue
2. Neural mechanisms (ANS) controlling flow
operates to control cardiac output and regulate peripheral
resistance (thus blood pressure) to maintain adequate blood flow to
vital tissues and organs
important in short-term regulation
cardiovascular centers
medulla oblongata contains a complex cardiovascular centers
has a cardiac and a vasomotor center
can act independently
cardiac center
regulates cardiac output thus regulates blood
pressure
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change pressure= change flow
blood flow ∝ ∆P/R
vasomotor center
regulates peripheral resistance thus regulates
blood flow
controls sympathetic activity to the arterioles
and blood vessels in general
have two populations of neurons :
both populations are part or the sympathetic
nervous system
1. vasoconstriction center
largest group of vasomotor neurons that
decrease blood flow
sympathetic fibers that
release norepinephrine
that cause constriction of
smooth muscle in the vessels of
the skin urinary, reproductive
and the GI tract
2. vasorelaxation center
small group of neurons that cause
vasorelaxation thus stimulates flow
sympathetic fibers that
release Ach that relax vessels
of the skeletal muscle heart and
brain
When sympathetic nervous system is activated the
vasomotor center is activated
constriction is greater then relaxation so initially
blood pressure increases somewhat
later on local autoregulation my result in
a drop in return or even a drop in BP
reflex control of vasomotor center
1. baroreceptor reflex
located in the aortic arch and carotid art.
Also have a similar medullary ischemic receptors
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located in the hypothalamus and medulla
Important for short term changes like adjustments in
posture
A drop in blood pressure as two effects
1. stimulation of cardioacceleratory center and
thus increase heart rate thus increases CO =
rise in pressure
2. stimulation of vasoconstriction center and
thus increase in blood pressure
By increasing CO and peripheral resistance
blood pressure goes up
Active tissues can know get higher flow
through autoregulation
An increase in blood pressure as two effects
1. inhibition of cardioacceleratory center and if
severe, stimulation of cardioinhibitroy center
resulting in a drop of CO = drop in
pressure
2. inhibitition of vasoconstriction center and
stimulation of vasorelaxation center = drop
in pressure
2. chemoreceptor reflexes
involve receptors located aortic arch subclavian art and
carotid art. that monitors the blood
Also have a receptor in medulla oblongata the
monitors CSF
All are sensitive to CO2, acid and O2
mostly CO2 and acid
Major role is adjusting respiration
High CO2 and acid and low O2 has two effects
1. stimulates the cardioacceleratory center
while inhibiting the cardioinhibitory center
= increase CO = increase in ? P =
increase in flow
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So more blood returns to the
lungs
2. stimulates vasoconstriction center to increase
blood pressure
increases blood flow to lungs
low CO2 and acid and high O2 has opposite effects
3. hormones
endocrine system provides both long-term and short-term regulation
of blood flow
F = ? P/R
long-term is the result of regulating of blood volume which has
an effect on blood pressure
blood pressure = (cardiac output) X (peripheral
resistance)
remember that CO = (HR) X (stroke volume)
increase in blood volume increases venous
return which increases stroke volume thus
increasing CO
short-term regulation is the result of regulating peripheral
resistance and cardiac output which has an effect on blood
pressure
epinephrine and norepinephrine
from adrenal medulla
effects
1. binds to α receptors and triggers vasoconstriction in
most vessels thus increases blood pressure (? P)
the vessels that not constricted receive more
flow
active tissue receive more flow due to
autoregulation
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also increases cardiac output
thus increases blood pressure (? P)
2. binds to β receptors in the vessels of the heart, brian
and muscle and triggers relaxation
both effects are short-term
antidiuretic hormone
released from the posterior pituitary when
1. blood volume drops
2. when osmotic concentration of the plasma
increases
3. in response to circulation angiotension II
effects
immediately effect
stimulates peripheral vasoconstriction
increases blood pressure (? P)
long-term effect
stimulates the kidneys to conserve water by
reabsorption from the urine
increasing water in blood increases blood
volume thus increases pressure
angiotensin II
produced in response to falling renal blood pressure
cascade
1. low pressure stimulates release of renin
2. renin convert circulation angiotensinogen to
angiotensin I
3. in lungs angiotensin converting enzyme (ACE)
converts AI to AII
short-term effects of AII
1. powerful vasoconstriction
increase blood pressure
2. positive inotropic effects on heart
increase contractility increase CO
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long-term effects
1. stimulates the release of ADH
vasoconstriction (short-term)
water retention
increase blood volume
increase pressure
2. stimulates the release of aldosterone from adrenal
cortex
aldosterone stimulates sodium reabsorption
from kidney
water will follow
increase blood volume
increase pressure
3. stimulates thirst
intake water
increase blood volume
increase pressure
Erythropoietin
release from kidneys if blood pressure drops or low O2
long-term effects
increase RBC
elevating blood volume
increase pressure
atrial natriuretic peptide
released form right atrium when stretch is high
works to lower pressure
long-term effects
1. increase sodium loss from kidneys
water will follow
lower blood volume
lower pressure
2. reduces thirst
3. blocks release of ADH
4. stimulates peripheral vasodilation
blood flow through capillaries and capillary dynamics
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the movement of materials across the typical capillary wall is mediated by three
mechanisms
1. diffusion
2. transcytosis
3. filtration and reabsorption
diffusion
must have a concentration gradient for diffusions and must be permeable
clefts and fenestrations make most substances permeable
lipid-soluble substances pass through plasma membrane
can move small amounts short distances
not adequate for all movement of nutrients
movement of oxygen, carbon dioxide and most nutrients and metabolic
wastes between blood and interstitial fluid is by diffusions
constant uptake of nutrients by cells keeps the gradient in
place
small water-soluble solutes like amino acids and sugars pass
through capillary clefts or fenestrations if present
lipid-soluble substances pass through cell membrane of endothelial
cells
transcytosis
movement by pinocytosis of a droplet of fluid from one side of the plasma
membrane to the opposite side
can occur in ether directions
is minor mechanism
used to move large molecules like fatty acids albumin and some
hormones
filtration and reabsorption
allows the movement of a large amount of fluid and substances dissolved in the
fluid
fluid leaves the arterial end and reenters the venous end
filtration and reabsorption is determined by the balance of hydrostatic
pressure and colloid osmotic pressure at the capillary
1) hydrostatic pressure is the pressure the fluid is under
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2) osmotic pressure
deals with movement of water
works to hold water in the vessel
occurs as the result of osmosis
water tends to diffuse across the membrane towards the
solution containing the higher concentration of solute
the force of water movement towards the solution with the
higher concentration of solute is called osmotic pressure
in the capillary the only thing that can not cross the membrane
(endothelial cells) are proteins
so call it blood colloid osmotic pressure (BCOP)
Arteriole side
hydrostatic pressure at the arteriole side
1) capillary blood pressure = 30 mmHg outward
2) interstitial hydrostatic pressure = -3 so also outward
-3 means there is a slight suction)
so have 33 mmHg of outward pressure pushing fluid
out of cap.
Colloid osmotic pressure at arteriole side
1) Blood COP
= 28 inward
2) interstitial hydrostatic pressure COP = 8 outward (very little
protein
here)
so have 20 mmHg of inward pressure holding fluid in
cap.
Net filtration at the arteriole side is the difference between the
outward and inward pressures
33out - 20in = 13 mmHg out of cap.
Venous side
hydrostatic pressure at the venous side
1) capillary blood pressure = 10 mmHg outward
2) interstitial hydrostatic pressure= -3 outward (suction)
so have 13 mmHg pushing fluid out of cap.
Colloid osmotic pressure at venous side (same as arterial end)
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1) Blood COP
= 28 inward
2) interstitial fluid COP = 8 outward (very little protein
here)
so have 20 mmHg of inward pressure holding fluid in
cap.
Net reabsorption at the venous side is the difference between the
inward and outward pressures
20in - 13out = 7 mmHg inward into the cap.
Because more pressure into the capillary we will see
reabsorption of fluid
Final tally
we have 13mmHg pushing fluid out of arterial end
and 7 mmHg pushing fluid into venous end
there is not a balance of outward and inward pressures over the
capillary bed so not all fluid is returned to the cap
13mmHg outward vs 7mmHg inward = 6mmHg is left
This translates into 3.6L/day
This volume enters the lymph vessels and returns to heart
this leak would empty almost the entire blood in 24
hours
if volume of fluid lost at the capillary is larger then lymph
vessels can remove
edema or fluid retention occurs
a rise in interstitial hydrostatic pressure
caps the amount of edema
factors aiding in venous return
pressure is normally too low to promote adequate venous return
espicially if standing
1. respiratory pump
pressure changes occurring in the ventral body cavity
during breathing create a pumping action that sucks
blood upward toward the heart
inhale = lower pressure in chest allowing thoracic
veins to expand and pulls blood toward heart
speeding blood entry into the right atrium
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exhale = increase pressure in abdomen pushing
blood from the vessels into the atrium
Valsalva’s maneuver
2. muscular pump
skeletal muscle activity “milk” blood toward the heart
valves keep it in one direction
3. cardiac suction
during ventricular systole the chordae tendineae pull the valves
downward expanding the atrial space creating a slight suction
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