Blood Vessels

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Chapter 21
Blood Vessels and Circulation
2
Blood Pressure and Cardiovascular
regulation Exercise
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arteries arterioles capillaries venules vei
ns
carry blood away from heart thicker walls (smooth
muscle) branch and get narrower bifurcation
(tri-, rami-) smallest vessels in networks
(beds) exchange with ECF carry blood back to
heart thinner walls small v. join to form larger
veins anastomosis
4
blood circuit
fig. 21-8
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100 keys (pg. 725)
It is blood flow thats the goal, and total
peripheral blood flow is equal to cardiac output.
Blood pressure is needed to overcome friction
and elastic forces and sustain blood flow. If
blood pressure is too low, vessels collapse,
blood flow stops, and tissue die if blood
pressure is too high, vessel walls stiffen and
capillary beds may rupture.
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100 keys (pg. 732)
Cardiac output cannot increase indefinitely, and
blood flow to active versus inactive tissues must
be differentially controlled. This is
accomplished by a combination of autoregulation,
neural regulation and hormone release.
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Controlling CO and bp
Autoregulation of blood flow Neural
mechanisms Hormonal mechanisms


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CO HR x SV
neural mechanisms
(reflex control of cardiovascular function)
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Neural mechanisms
Reflex control of cardiovascular function
baroreceptors blood pressure chemoreceptors pH,
gases
negative feedback loops
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Neural mechanisms
Reflex control of cardiovascular function
baroreceptors
monitor degree of stretch in walls of expandable
organs
carotid sinuses aortic sinuses atrium
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baroreceptors
if blood pressure climbs
decrease cardiac output lower HR (ACh
SA) vasodilation lowers peripheral resistance
reflex
reduce blood pressure
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baroreceptors
if blood pressure falls
increase cardiac output NE on heart vasoconstrict
ion NE inc. peri. resistance
reflex
increase blood pressure
13
baroreceptors
atrial reflex
stretching the atrium (more blood returning)
will stimulate cardiac output (more blood
leaving)
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baroreceptors
Valsalva maneuver
exhale forcefully close glottis
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baroreceptors
Valsalva maneuver

• brief rise in bp
• pressure on lungs sends pulmonary blood to
  atria
• bp falls
• reduced venous return
• low CO
• reflexive vasoconstriction
• increase in heart rate

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baroreceptors
Valsalva maneuver

• release pressure
• expansion of vessels (bp6)
• (6return, 5aortic volume)
• 4. restore normal
• blood return up
• CO is up
• BP is up

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graph of bp drop and HR increase during
Valsalva
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to here 4/2/07 Lec 34
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fig. 21-14
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Neural mechanisms
Reflex control of cardiovascular function
baroreceptors chemoreceptors
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Neural mechanisms
chemoreceptors
monitor pH (H) CO2 O2 of blood and CSF
sensory neurons in carotid body aortic
bodies (med. oblong.)
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Neural mechanisms
chemoreceptors
pH drops (H5) or 5CO2 or 6O2
reflex stimulation of cardio- acceleratory
centers (sym)
stimulate vasomotor (vasoconstriction)
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Neural mechanisms
chemoreceptors
pH drops (H5) or 5CO2 or 6O2
increase cardiac output peripheral
vasoconstriction
increase bp
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Neural mechanisms
chemoreceptors
pH drops (H5) or 5CO2 or 6O2
receptors in medulla obl.
stimulate respiratory centers more O2
and more venous return
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Neural mechanisms
chemoreceptors
pH drops (H5) or 5CO2 or 6O2
increased bp and resp.
more O2 to cells
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fig. 21-15 here
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CO HR x SV
hormonal control
neural mechanisms
NE, E ADH angiotensin II EPO natriuretic peptides
all regulate blood volume
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ADH
Antidiuretic hormone
made in hypothalamus released from posterior
pituitary gland in response to 6 blood volume
vasoconstriction (5bp) H2O recovery in kidney
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angiotensin II
fall in bp renin release from kidney
angiotensinogen (from liver) angiotensin
I angiotensin II
renin
ACE
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angiotensin II
four functions
stimulates kidney to produce aldosterone stimula
tes secretion of ADH stimulates
thirst stimulates CO and vasconstriction
(bp)
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EPO
erythropoietin
released from kidneys low bp low O2 levels
stimulates bone marrow to make more RBCs
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natriuretic peptides
natrium sodium (Na)
atrial natriuretic peptide (ANP) brain
natriuretic peptide (BNP)
released in response to stretching
reduce blood volume reduce blood pressure
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natriuretic peptides
increase Na excretion at kidney increase volume
of urine produced reduce thirst block ADH, NE, E,
aldosterone release stimulate peripheral
vasodilation
reduce blood volume and blood pressure
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response to decrease in bp
fig 21-16a
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response - increase in bp
fig 21-16b
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100 keys (pg. 732)
Cardiac output cannot increase indefinitely, and
blood flow to active versus inactive tissues must
be differentially controlled. This is
accomplished by a combination of autoregulation,
neural regulation and hormone release.
37
fig. 20-23
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Summary
hormones venous return filling time venous
return preload contractility afterload
Heart rate EDV ESV SV EDV-ESV
CO HR x SV
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Exercise
light
slight sympathetic innervation slight increase
in HR vasodilation get blood to
tissues resistance drops more blood flows
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Exercise
light
increase in venous return muscle pumps
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muscle activity venous return
fig. 21-6
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Exercise
light
increase in venous return muscle pumps increase
respiratory pump cardiac output increases due
to higher venous return
43
Exercise
heavy
more sympathetic stimulation vasocontriction to
non-essentials (most internal organs except
brain) blood lungs
skeletal muscle
- heart -
- heart -