biol 121 chp 21: the cardiovascular system - blood vessels and hemodynamics
DESCRIPTION
This is a lecture presentation for my BIOL 121 Anatomy and Physiology I students on Chapter 21: The Cardiovascular System: Blood Vessels and Hemodynamics (Principles of Anatomy and Physiology, 14th Ed. by Tortora and Derrickson). Rob Swatski, Associate Professor of Biology, Harrisburg Area Community College - York Campus, York, PA. Email: [email protected] Please visit my website for more anatomy and biology learning resources: http://robswatski.virb.com/TRANSCRIPT
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Rob Swatski Associate Professor of Biology
HACC – York Campus
Chapter 21
The Cardiovascular System: Blood Vessels & Hemodynamics
Textbook images - Copyright © 2014 John Wiley & Sons, Inc. All rights reserved.
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Blood Vessels Structure & FuncHon
Arteries & Arterioles
Veins & Venules Capillaries
Hemodynamics
Circula4on Regula4on
Types of Blood Vessels
Arteries: transport blood away from
heart
Arterioles: transport blood to capillaries
Capillaries: gas & solute exchange
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Types of Blood Vessels
Venules: drain blood
from capillaries into larger veins
Veins: return blood to the heart
Vaso Vasorum: transport blood to 4ssues of BV
wall
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Anastomosis
End artery
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Layers of the Artery
Wall
Tunica externa
Tunica media
Tunica interna
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Layers of the Artery Wall
Tunica externa
Elas4c & collagen fibers
Tunica media
Circular smooth muscle
External elasHc lamina
Tunica interna
Internal elasHc
lamina & basement membrane
Endothelium (simple
squamous epithelium)
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Transverse SecHon Through an Artery
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FuncHonal ProperHes of Arteries
ElasHcity (elas4c lamina)
ContracHlity (smooth muscle)
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SympatheHc Nervous System
RegulaHon
VasoconstricHon (Vasospasm)
VasodilaHon (NO, K+, H+)
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ElasHc Arteries
= ConducHng arteries
Largest diameter & thicker elas4c lamina (elas4c
lamellae)
Less smooth muscle
Pressure reservoir
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Muscular Arteries
= DistribuHng arteries
Medium diameter & thinner elas4c
lamina
More smooth muscle & thicker
walls
Stronger vasoconstric4on
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Arterioles
Very small diameter & less smooth muscle
Deliver blood to capillaries
Regulate blood flow
Adjust arterial blood pressure
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Metarterioles
Regulate blood flow into capillaries
Precapillary sphincters
Thoroughfare channel
VasomoHon: fills bed 5-‐10x/min
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Blood Flow Into Capillary Bed
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Blood Flow Into Thoroughfare Channel
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Capillaries Connect arterioles
to venules Capillary bed MicrocirculaHon Gas, nutrient, & waste exchange
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ConHnuous Capillaries
Endothelium with “leaky” 4ght junc4ons
Intercellular cleQs
In skeletal & smooth muscle, lungs, connec4ve
4ssue
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Fenestrated Capillaries
Endothelium with many fenestraHons
(pores)
Intercellular cleds
In kidneys, small intes4ne, glands, choroid plexuses
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Glomerulus
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Sinusoids
Endothelium with incomplete basement membrane
Very large fenestra4ons & intercellular cleds
In liver, bone marrow, spleen, pituitary gland
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Venules Drain capillary beds
Thin walls & less smooth muscle
Blood reservoir
Postcapillary venules: very porous endothelium
Microcircula4on, emigra4on of WBCs
Lead to muscular venules
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Veins
Have same 3 layers as arteries
Thinner walls with valves
Lifle smooth muscle & no elas4c
lamina
Thicker tunica externa
Adapt to changes in volume & pressure
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Venous (Vascular) Sinuses
Very thin walls
No smooth muscle
Surrounded by dense CT for support
Superior sagifal sinus, coronary sinus
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Other Differences
Between Veins and Arteries
Veins are more abundant
Veins can be found in double sets called anastomoHc veins
Many superficial veins in SubQ layer
Deep veins
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Varicose Veins Dilated, twisted superficial veins caused by leaky
valves
Congenital or due to physical
stress
Blood pools-‐up in veins
Higher pressure forces fluids into
ECF
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Varicose Veins
In legs, esophagus, anal
canal (hemorrhoids)
Why is it uncommon for deeper veins to
become varicose?
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Anastomoses
2 or more BVs supplying same
region
Angiogenesis
Collateral circulaHon
(alternate routes)
Ex: circle of Willis, coronary circulaHon
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Blood DistribuHon
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Capillary Exchange
Transfer of chemicals b/w
blood & inters44al fluid
Through diffusion, transcytosis, and
bulk flow
Across endothelium,
through cleds & fenestra4ons
O2, CO2, glu, AA, hormones, solutes
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Blood-‐Brain Barrier (BBB) No diffusion of water-‐soluble
solutes
Con4nuous capillaries with 4ght junc4ons
No cleds or fenestra4ons
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Transcytosis
Moves substances through
endothelium
Uses vesicular transport
(endocytosis & exocytosis)
Transports larger, lipid-‐insoluble molecules (proteins)
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Bulk Flow
Moves large amounts of substances in same direc4on
Faster transport rates (high to low pressure)
Regulates blood & inters44al fluid volumes
FiltraHon & ReabsorpHon
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FiltraHon
Moves substances out of blood and into inters88al
fluid
Blood HydrostaHc Pressure (BHP)
IntersHHal Fluid OsmoHc
Pressure (IFOP)
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ReabsorpHon
Moves substances from inters44al fluid into capillaries
Blood Colloid OsmoHc Pressure (BCOP)
IntersHHal Fluid
HydrostaHc Pressure (IFHP)
Net filtration pressure (NFP)
Blood plasma
Blood flow from arteriole into capillary
Lymphatic fluid (lymph) returns to Lymphatic
capillary Key: BHP = Blood hydrostatic pressure IFHP = Interstitial fluid hydrostatic pressure BCOP = Blood colloid osmotic pressure IFOP = Interstitial fluid osmotic pressure NFP = Net filtration pressure
Blood flow from capillary into venule
BHP = 16 mmHg
BCOP = 26 mmHg
IFHP = 0 mmHg
Interstitial fluid IFOP =
1 mmHg
BCOP = 26 mmHg
BHP = 35 mmHg
Tissue cell
N F P
Net filtration at arterial end of capillaries (20 liters per day)
(BHP + IFOP)
Pressures promoting filtration
Net reabsorption at venous end of capillaries (17 liters per day)
(BCOP + IFHP)
Pressures promoting reabsorption
Arterial end Venous end
NFP = (35 + 1) – (26 + 0) = 10 mmHg
NFP = (16 + 1) – (26 + 0) = –9 mmHg
Net filtration Net reabsorption
N F P
= –
Result
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Net FiltraHon Pressure (NFP) Net outward pressure = 10 mmHg at arterial end
Net inward pressure = 9 mm Hg at venous end
85% of filtered fluid returns to capillaries via lympha4cs (3L/
day)
Volume Reabsorbed
Volume Filtered
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Starling’s Law of the Capillaries
Edema
Due to excess filtraHon
High blood pressure
(hypertension)
High capillary permeability (leaks plasma proteins)
Due to poor reabsorpHon
Low plasma proteins (lowers
BCOP)
Slow protein synthesis or loss due to liver or renal problems
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Blood Pressure (BP)
Cardiac Output (CO) Volume
Viscosity Velocity Resistance
ElasHcity Venous Return
Factors AffecHng Hemodynamics
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Resistance
Opposi4on to blood flow due to
fric8on
Highest in arterioles,
capillaries, & venules
Vascular resistance: varies with diameter, viscosity, length
Systemic Resistance: total
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Blood Pressure (BP)
Due to ventricular systole (120 mmHg in
aorta)
BP increases as CO increases
BP decreases away from led ventricle
35 mmHg @ capillaries
0 mmHg @ right atrium
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Venous Return Volume of blood flow returning to heart from veins
Skeletal muscle pump: muscle contrac4on &
valves
Respiratory pump: moves blood into
right atrium
Lower thoracic pressure à Higher
abdominal pressure during
inhala4on
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Velocity of Blood Flow
Inversely related to BV cross-‐sec4onal
area
Flow is slowest where cross-‐
sec4onal area is highest
Velocity decreases from: aorta à arteries à capillaries
Velocity increases from: veins à right atrium
3-‐5 cm2
40 cm/sec
4500-‐6000 cm2
0.1 cm/sec
14 cm2
15 cm/sec
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Factors that Increase Blood Pressure
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Control of BP and Blood
Flow Cardiovascular
Center: in medulla oblongata of brainstem
Sympathe4c & parasympathe4c
control
Regulates HR, contrac4lity, & BV
diameter
Vasomotor nerves: adjust BV diameter
vasodilator center
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vasomotor tone
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Neural RegulaHon
of BP Baroreceptors: in major arteries
CaroHd sinus reflex: maintains
brain BP
AorHc reflex: maintains general
systemic BP
If BP decreases: HR, contrac4lity, & vasoconstric4on
increase
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Syncope (FainHng)
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Syncope A sudden loss of consciousness due to cerebral ischemia (fainHng)
Vasodepressor syncope
Sudden emo4onal distress
SituaHonal syncope
Pressure stress of coughing, defeca4on, urina4on
Drug-‐induced syncope
Diure4cs, an4-‐hypertensives, vasodilators, tranquilizers
OrthostaHc hypotension
BP decrease upon standing
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Chemoreceptor Reflexes
CaroHd bodies & AorHc bodies
Detect changes in blood O2, CO2, H+
Hypoxia, hypercapnia, acidosis
S4mulate CV center: increases
vasoconstric4on & respiratory rate
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Hormonal RegulaHon of
BP
Renin-‐Angiotensin-‐Aldosterone system (RAA)
Ac4vated by drop in BP or reduced blood flow to kidney
Kidneys à Renin
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Renin
Angiotensin (vasoconstricHon)
Aldosterone (H2O & salt
reabsorpHon)
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Hormonal RegulaHon of BP, cont.
Epinephrine & Norepinephrine
Increases HR & contrac4lity à
raises BP
ADH (AnHdiureHc Hormone) [aka vasopressin]
Triggers vasoconstric4on à raises BP
Promotes reabsorp4on of H2O into blood à
increases blood volume & decreases urine output
ANP (Atrial NatriureHc PepHde)
Triggers vasodila4on à lowers BP
Increases loss of Na+ and H2O in urine à lowers blood volume
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Pulse Alterna4ng
expansion & recoil of elas4c arteries ader every le< ventricle systole
ResHng pulse rate: avg 70-‐80 bpm
Tachycardia: >100 bpm
Bradycardia: <50 bpm
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Measurement of BP
Sphygmomanometer (BP cuff)
Korotkoff sounds: provide info about systemic resistance
Systolic BP: ventricular
contrac4on (120 mmHg)
Diastolic BP: ventricular relaxa4on
(80 mmHg)
Pulse pressure: difference b/w
systolic & diastolic BP (= 40 mmHg)
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Shock Poor CO: cannot deliver enough O2
& nutrients
Cell membrane dysfunc4on & abnormal metabolism
Cell death due to: poor perfusion,
switch to anaerobic
respira4on, & lac4c acid build-‐up
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Weak, but rapid, res4ng pulse (tachycardia)
Clammy, cool, pale skin (vasoconstric8on)
Altered mental state (cerebral ischemia)
Hypotension Low cardiac output (CO) Swea4ng (sympathe8c s8mula8on)
Thirst (loss of ECF) Acidosis (lac8c acid build-‐up)
Decreased urine forma4on
(vasoconstric8on, increased aldosterone &
ADH)
Signs & Symptoms of Shock
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Types of Shock
Hypovolemic
Decreased blood or body fluid volume
Hemorrhage, poor fluid intake, excessive
swea4ng, vomi4ng, diarrhea
Cardiogenic
Poor heart func4on
MI, ischemia, valve disorders, high preload/aderload, arrhythmias,
poor contrac4lity
ObstrucHve
Blockage of blood flow
Pulmonary embolism
Vascular
Inappropriate vasodila4on
Anaphylac4c, sep4c, or neurogenic shock
Hypovolemic shock
CONTROLLED CONDITION Blood volume and blood
pressure
RECEPTORS
CONTROL CENTER CONTROL CENTER CONTROL CENTER
Liver and lungs Hypothalamus and posterior pituitary
Cardiovascular center in medulla oblongata
EFFECTORS
Adrenal cortex
Kidneys Blood vessels
Heart
Increased blood volume
Increased systemic vascular resistance Increased blood
pressure
Return to homeostasis when responses bring blood volume and blood pressure back to normal
Increased sympathetic stimulation and hormones from adrenal medulla
ADH in blood Angiotensin II in blood
Increased secretion of renin
Decreased rate of nerve impulses
Inputs
Outputs
Disrupts homeostasis by moderately decreasing
Baroreceptors in kidneys (juxtaglomerular cells)
Baroreceptors in arch of aorta and carotid sinus
ADH
EFFECTOR
RESPONSE RESPONSE RESPONSE
Kidneys conserve salt and water
Blood vessels constrict
Heart rate and contractility increase
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Decreased elas4city of aorta
Smaller size of cardiac muscle fibers
Decreased CO, but maximum HR Increased systolic BP
Increased total cholesterol & LDL; decreased HDL
Increased risk of conges4ve heart
failure, coronary artery disease,
atherosclerosis
Aging & the Cardiovascular System
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Hypertension
Chronically high BP (systolic > 140 mmHg; diastolic > 90 mmHg)
Primary hypertension: most common (no
iden4fiable underlying cause)
Secondary hypertension (has iden4fiable cause)
Damages BVs, heart, brain, & kidneys before onset of no4ceable
symptoms
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Lose weight Reduce alcohol Increase exercise
Reduce salt Eat healthy diet to maintain K+, Ca+2,
and Mg+2 Don’t smoke
Manage stress
Meds: diure4cs, beta-‐blockers,
vasodilators, Ca+2 channel blockers
Treatment of Hypertension
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