Chapter

21

Blood Vessels and Circulation

Blood Pressure and Cardiovascular regulation Exercise

arteries arterioles capillaries venules veins 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

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.”

Controlling CO and bp Autoregulation of blood flow * Neural mechanisms * Hormonal mechanisms

CO = HR x SV neural mechanisms (reflex control of cardiovascular function)

Neural mechanisms Reflex control of cardiovascular function baroreceptors blood pressure chemoreceptors pH, [gases] negative feedback loops

Neural mechanisms Reflex control of cardiovascular function baroreceptors monitor degree of stretch in walls of expandable organs carotid sinuses aortic sinuses atrium

baroreceptors if blood pressure climbs reflex: decrease cardiac output lower HR (ACh SA) vasodilation lowers peripheral resistance reduce blood pressure

baroreceptors if blood pressure falls reflex: increase cardiac output NE on heart vasoconstriction NE inc. peri. resistance increase blood pressure

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 bp pressure on lungs sends pulmonary blood to atria 2. bp falls reduced venous return low CO reflexive vasoconstriction increase in heart rate

baroreceptors Valsalva maneuver 3. release pressure expansion of vessels (bp 6 ) ( 6 return, 5 aortic volume) 4. restore normal blood return up CO is up BP is up

graph of bp drop and HR increase during Valsalva

to here 4/2/07 Lec # 34

fig. 21-14

Neural mechanisms Reflex control of cardiovascular function baroreceptors chemoreceptors

Neural mechanisms chemoreceptors monitor pH (H + ) [CO 2 ] [O 2 ] of blood and CSF sensory neurons in: carotid body aortic bodies (med. oblong.)

Neural mechanisms chemoreceptors pH drops (H + 5 ) or 5 [CO 2 ] or 6 [O 2 ] reflex stimulation of cardio acceleratory centers (sym) stimulate vasomotor (vasoconstriction)

Neural mechanisms chemoreceptors pH drops (H + 5 ) or 5 [CO 2 ] or 6 [O 2 ] increase cardiac output peripheral vasoconstriction increase bp

Neural mechanisms chemoreceptors pH drops (H + 5 ) or 5 [CO 2 ] or 6 [O 2 ] receptors in medulla obl.

stimulate respiratory centers more O 2 and more venous return

Neural mechanisms chemoreceptors pH drops (H + 5 ) or 5 [CO 2 ] or 6 [O 2 ] increased bp and resp.

more O 2 to cells

fig. 21-15 here

CO = HR x SV NE, E ADH angiotensin II EPO natriuretic peptides all regulate blood volume

ADH Antidiuretic hormone made in hypothalamus released from posterior pituitary gland in response to 6 blood volume vasoconstriction ( 5 bp) H 2 O recovery in kidney

angiotensin II fall in bp renin release from kidney angiotensinogen (from liver) renin angiotensin I angiotensin II ACE

angiotensin II four functions: stimulates kidney to produce aldosterone stimulates secretion of ADH stimulates thirst stimulates CO and vasconstriction (bp)

EPO erythropoietin released from kidneys low bp low O 2 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 volume reduce blood pressure

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

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 hormones venous return filling time venous return preload contractility afterload SV = EDV-ESV CO = HR x SV

Exercise light slight sympathetic innervation slight increase in HR vasodilation get blood to tissues resistance drops more blood flows

Exercise light increase in venous return muscle pumps

fig. 21-6 muscle activity venous return

Exercise light increase in venous return muscle pumps increase respiratory pump cardiac output increases due to higher venous return

Exercise heavy more sympathetic stimulation vasocontriction to “non-essentials” (most internal organs except brain) blood lungs - heart skeletal muscle - heart -