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Chapter 21
Blood Vesselsand
Circulation
Blood Pressure andCardiovascular regulation
Exercise
arteries
arterioles
capillaries
venules
veins
carry blood away from heartthicker walls (smooth muscle)branch and get narrower
bifurcation (tri-, rami-)
smallest vesselsin networks (beds)exchange with ECF
carry blood back to heartthinner wallssmall v. join to form larger veins
anastomosis
fig. 21-8
blood circuit
100 keys (pg. 725)
“It is blood flow that’s 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.”
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.”
Autoregulation of blood flow
Neural mechanisms
Hormonal mechanisms
Controlling CO and bp
*
*
CO = HR x SV
(reflex control of cardiovascular function)
neural mechanisms
Neural mechanisms
baroreceptorsblood pressure
chemoreceptorspH, [gases]
Reflex control of cardiovascular function
negative feedback loops
Neural mechanisms
baroreceptors
Reflex control of cardiovascular function
monitor degree of stretch in walls of expandable organs
carotid sinusesaortic sinusesatrium
baroreceptors
if blood pressure climbs
decrease cardiac outputlower HR (ACh SA)
vasodilationlowers peripheral resistance
reduce blood pressure
reflex:
baroreceptors
if blood pressure falls
increase cardiac outputNE on heart
vasoconstrictionNE inc. peri. resistance
increase blood pressure
reflex:
baroreceptors
atrial reflex
stretching the atrium(more blood returning)
will stimulate cardiac output(more blood leaving)
baroreceptors
Valsalva maneuver
exhale forcefully
close glottis
baroreceptors
Valsalva maneuver
1. brief rise in bppressure on lungs sends pulmonary blood to atria
2. bp fallsreduced venous returnlow COreflexive vasoconstrictionincrease in heart rate
baroreceptors
Valsalva maneuver
3. release pressureexpansion of vessels (bp)
(return, aortic volume)
4. restore normalblood return upCO is upBP is up
graph ofbp drop and HR increase
during Valsalva
to here 4/2/07Lec # 34
fig. 21-14
Neural mechanisms
baroreceptors
chemoreceptors
Reflex control of cardiovascular function
Neural mechanisms
chemoreceptors
monitor pH (H+)[CO2][O2]
of blood and CSF
sensory neurons in: carotid bodyaortic bodies(med. oblong.)
Neural mechanisms
chemoreceptors
pH drops (H+)or [CO2]or [O2]
reflex stimulation of cardio-acceleratory centers (sym)
stimulate vasomotor(vasoconstriction)
Neural mechanisms
chemoreceptors
pH drops (H+)or [CO2]or [O2]
increase cardiac outputperipheral vasoconstriction
increase bp
Neural mechanisms
chemoreceptors
pH drops (H+)or [CO2]or [O2]
receptors in medulla obl.
stimulate respiratory centers
more O2and more venous return
Neural mechanisms
chemoreceptors
pH drops (H+)or [CO2]or [O2]
increased bp and resp.
more O2 to cells
fig. 21-15 here
CO = HR x SV
neural mechanismshormonal control
NE, E
ADHangiotensin IIEPOnatriuretic peptides
all regulateblood volume
ADH
Antidiuretic hormone
made in hypothalamusreleased from posterior pituitary glandin response to blood volume
vasoconstriction (bp)H2O recovery in kidney
angiotensin II
fall in bprenin release from kidney
angiotensinogen (from liver)
angiotensin I
angiotensin II
renin
ACE
angiotensin II
four functions:
stimulates kidney toproduce aldosterone
stimulates secretion of ADH
stimulates thirst
stimulates CO and vasconstriction
(bp)
EPO
erythropoietin
released from kidneys
low bp
low O2 levels
stimulates bone marrow to make more RBC’s
natriuretic peptides
natrium = sodium (Na)
atrial natriuretic peptide (ANP)brain natriuretic peptide (BNP)
released in response to stretching
reduce blood volumereduce blood pressure
natriuretic peptides
increase Na+ excretion at kidneyincrease volume of urine producedreduce thirstblock ADH, NE, E, aldosterone releasestimulate peripheral vasodilation
reduce blood volume and blood pressure
fig 21-16a
response to decrease in bp
fig 21-16b
response - increase in bp
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.”
fig. 20-23
Summary
Heart rate
EDV
ESV
SV = EDV-ESV
hormonesvenous return
filling timevenous return
preloadcontractilityafterload
CO = HR x SV
Exercise
light
slight sympathetic innervationslight increase in HR
vasodilationget blood to tissuesresistance dropsmore blood flows
Exercise
light
increase in venous returnmuscle pumps
fig. 21-6
muscle activityvenous return
Exercise
light
increase in venous returnmuscle pumpsincrease respiratory pump
cardiac output increasesdue to higher venous return
skeletalmuscle
Exercise
heavy
more sympathetic stimulation
vasocontriction to “non-essentials”(most internal organs except brain)
bloodlungs - heart - - heart -