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Ch. 20: Blood Vessels and Circulation
I. General Vessel Anatomy
(A) Circulatory Routes: Heart-> arteries -> arterioles-> capillaries ->
venules-> veins-> heart. Deviations:
-1- portal systems – capillary to capillary. Between the hypothalamus and
anterior pituitary, between intestines and liver (hepatic portal).
-2- anastomoses – merging of vessels. Arteriovenous (shunts); arterial
(collateral routes); venous (alternative drainage routes).
(B) Vessel Walls
-1- tunica externa/ advetitia: loose CT, contains vasa vasorum.
-2- tunica media: usually thickest. Smooth muscle, collagen. Vasoconstriction
vs. vasodilation.
-3- tunica interna/ intima: endothelium- simple squamous ET.
(C) Arteries and Metarterioles relatively thick muscular walls
-1- conducting (elastic) arteries: largest.
-2- distributing (muscular) arteries
-3- resistance (small) arteries: don’t have names. Smallest ones are arterioles:
constrict and dilate.
-4- metarterioles: link arterioles to capillaries, separated by pre-capillary
sphincter.
(D) Capillaries – exchange vessels. Walls only with endothelium and
basement membranes.
-1- capillary beds – metarteriole becomes a thoroughfare channel in middle. Fill
when pre-capillary sphincter open. ~75% closed at any given time.
-2- types:
a. continuous = most.
b. fenestrated: holes in endothelium. In kidneys, choroid plexus.
Sinusoids = irregular spaces, not vessels. In liver, marrow, spleen.
(E) Veins – receive tributaries. Venules exchange some fluid. Venous
sinuses with no smooth muscle, e.g. coronary sinus. Very low BP. Thin walls,
less muscle and elastic tissue. Valves prevent backflow. Varicose veins,
hemorrhoids in anal canal- distended due to pressure.
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II. Blood Pressure, Resistance and Flow
Perfusion = flow/ volume/ time. ml/ min/ g. Hemodynamics: physical
properties of blood flow. Based on pressure and resistance. Flow is related to
the difference in pressure divided by resistance.
(A) Blood Pressure – ranges between systolic and diastolic. Normal ~
120/ 75 mmHg. The difference between the two is pulse pressure, indicates
stress on small arteries, as does MAP = mean arterial pressure (closer to
diastolic than the average).
Greater than 140/ 90 = hypertension. Creates risk for aneurysm. Rises
with age. Hypotension – too low.
(B) Resistance – peripheral (in blood vessels). Dependent upon:
-1- blood viscosity.
-2- vessel length.
-3- vessel radius. Affected by vasomotion (dilation and constriction). A very
powerful effect.
(C) Regulation of BP and Flow
-1- local control = autoregulation. Hypoxia, increasing CO2, H+, lactic acid,
lead to vasodilation. Platelets release vasoactive chemicals. Ischemia leads to
reactive hyperemia. Long-term hypoxia -> angiogenesis.
-2- neural control: vasomotor center of medulla. Sympathetic responsevasodilation in skeletal and cardiac muscle. Coordinates baroreflexes and
chemoreflexes (pH, O2, CO2). Receptors in aorta and carotid arteries.
Medullary ischemic reflex responds to decreased brain perfusion.
-3- hormonal control:
a. angiotensin II: causes vasoconstriction. Created by ACE (angiotensinconverting enzyme). ACE inhibitors treat hypertension.
b. aldosterone: increases Na+ retention.
c. ANP: decreases Na+ retention.
d. ADH (vasopressin): increases water retention. May cause
vasoconstriction.
e. epinephrine and norepinephrine: cause vasoconstriction.
(D) Vasomotion & Routing of Blood Flow
Vasoconstriction in one area directs blood to other areas.
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III. Capillary Exchange
Through endothelial intercellular clefts, fenestrations (when present), endothelial
cell cytoplasm.
(A) Diffusion – most important. Glucose, O2, CO2, wastes.
(B) Transcytosis – via pinocytosis, then exocytosis. Fatty acids, albumin,
come hormones (insulin).
(C) Filtration & Reabsorption – filtration from arterial capillaries;
reabsorption into venous capillaries. Opposite forces= hydrostatic pressure
and COP (colloid osmotic pressure).
(D) Edema – fluid retention, caused by:
-1- increased capillary filtration: due to increased BP or permeability.
-2- decreased caplllary reabsorption: due to low blood albumin.
-3- obstructed lymphatic drainage.
IV. Venous Return & Circulatory Shock
(A) Mechanisms of Venous Return
-1- pressure gradient, based on pressure generated by heart.
-2- gravity – works for upper body.
-3- skeletal muscle pump.
-4- thoracic (respiratory) pump.
-5- cardiac suction – when atria expand during ventricular systole.
(B) Venous Return and Physical Activity
Enhanced by increased CO2 and BP. Lack of exercise leads to venous pooling.
Can cause syncope (dizziness).
(C) Circulatory Shock
-1- cardiogenic shock, due to diminished pumping (MI).
-2- low venous return (LVR) shock.
a. hypovolumic most common, blood loss or dehydration.
b. obstructed venous return – due to tumor, aneurysm.
c. venous pooling (vascular) shock. May be neurogenic, loss of
vasomotor tone.
Septic shock from bacterial toxins; anaphylactic shock from severe allergies.
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responses: compensated lead to recovery;
decompensated lead to positive feedback and death.
V. Special Circulatory Routes
(A) Brain: very little fluctuation in cerebral perfusion. Local control
important, mostly via pH. Brief cerebral ischemia = TIAs. When infarction
(tissue death) = CVA = stroke.
(B) Skeletal Muscle: perfusion highly variable. Contraction compresses
blood vessels.
(C) Lungs: pulmonary circulation with lower pressure. Slows blood down
for gas exchange, makes capillaries more absorptive. When pulmonary pressure
increases, edema in lungs.
VI. Blood Vessel Anatomy
Study from Figures 20.20: Arteries; 20.32: Veins.
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