Download Chapter 21: Blood Vessels and Circulation

Chapter 21: Blood Vessels and
Circulation
BIO 211 Lecture
Instructor: Dr. Gollwitzer
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• Today in class we will discuss:
– The relationship between blood flow and
• Cardiac output
• Pressure and resistance
– Pressure differences in various vessels in the CVS
– Blood pressure , mean arterial pressure, and pulse
– The basis for systolic pressure and diastolic pressure
– Total peripheral resistance and its major components
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Cardiovascular Physiology
• Goal of cardiovascular physiology
– To maintain adequate blood flow through peripheral
tissues and organs
• Cardiovascular system (CVS) continuously
adjusted to maintain homeostasis
• Contracting ventricle must produce enough
tension to force open the semilunar valve and
eject blood
• Determined by interplay between pressure and
resistance in cardiovascular network
• If no resistance to blood flow, heart would not
have to generate pressure to force blood through
pulmonary and systemic circuits
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Cardiovascular Physiology
Figure 21-8
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Cardiovascular Physiology
• Cardiac output (CO)
– Normally = blood flow
– When CO goes up, blood flow through the capillary beds goes up;
and vice versa
• Blood (arterial) pressure (BP)
– Responsible for maintaining blood flow within capillaries
• Peripheral resistance controls:
– Blood flow
– Capillary pressure
• Drives exchange via diffusion and osmosis between blood and
interstitial fluid
• Venous pressure
– Due to venoconstriction
– Aided by valves, skeletal muscle contraction
• Venous return
– Brings blood back to heart
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Cardiovascular Pressures
• General concepts
– Liquids, including blood, cannot be compressed
– Force exerted against an enclosed liquid (blood
in CVS) generates hydrostatic pressure
– If pressure gradient exists, hydrostatic pressure
will push liquid from an area of higher pressure
to an area of lower pressure
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Cardiovascular Pressures
• Pressure gradient of systemic circuit =
circulatory pressure (approx 100 mm Hg)
– Difference between pressure at base of ascending
aorta (100 mm Hg) and entrance to R atrium (2
mm Hg)
• This pressure needed to force blood through
arterioles (resistance vessels) and into
peripheral capillaries
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Cardiovascular Pressures
• 3 components
– Blood pressure (BP)
• = force exerted against vessel walls by blood in vessels in systemic
arterial system
• Ranges from 100 at heart to 35 mm Hg at start of capillary
network
• Capillary blood flow is directly proportional to BP
– Capillary hydrostatic pressure
• = Pressure in capillary beds
• Declines from 35 to 18 mm Hg along length of capillary
– Venous pressure
• = Pressure in venous system
• Pressure gradient from venules to R atrium approx. 18 mm Hg
(ranges from 18 to 2 mm Hg)
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Figure 20–1
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Pressures in the Systemic Circuit
Figure 21-10
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Arterial Blood Pressure
• Important because it maintains blood flow
through capillary beds
• Must be high enough to overcome
peripheral resistance
• Not stable
– Rises during ventricular systole and falls
during ventricular diastole
– Systolic pressure (SP) = peak arterial pressure
during ventricular systole
– Diastolic pressure (DP) = minimum arterial
pressure during diastole
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Arterial Blood Pressure
• Measure with sphygmomanometer
– Compress brachial artery
– Place stethoscope over artery, distal to compress
– Inflate cuff until pressure is great enough to collapse
artery and blood flow stops, pulse is eliminated
– Let air out slowly
• When pressure is less than SP = blood enters, pulse appears
• When pressure is less than DP = pulse disappears and flow is
continuous
– Record by separating systolic and diastolic pressures
by a slash mark (e.g., 120/80)
– Normal = 120/80
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Arterial Blood Pressure
• Pulse
– = Rhythmic pressure oscillation that accompanies each
heart beat
– Common site: inner wrist (radial artery pressed against
radius)
• Pulse pressure (PP)
– = Difference between systolic and diastolic pressure
(i.e., SP-DP)
• Mean arterial pressure (MAP)
– = Diastolic pressure + (pulse pressure/3), e.g.,
– If SP = 120, DP = 80
• MAP = 80 + ((120-80)/3) = 80 + 13 = 93 mm Hg
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Resistance
• Any force that opposes movement of fluid
– Resistance of CVS
• Due to friction between blood and vessel walls
• Opposes movement of blood
• The greater the resistance, the slower the
movement of blood
• For circulation to occur, pressure gradient must
be great enough to overcome total peripheral
resistance = resistance of the entire CVS
(mostly arterial resistance b/c venous resistance so low)
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Peripheral Resistance
• = Resistance of the arterial system
• For blood to flow into peripheral capillaries the
pressure gradient must be great enough to
overcome peripheral resistance
• 3 sources of peripheral resistance
– Vascular resistance (resistance of blood vessels)
– Viscosity
– Turbulence
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Peripheral Resistance:
Vascular Resistance
•
•
•
•
= Resistance of blood vessels
Largest component of peripheral resistance
Due to friction between blood and vessel wall
Depends on:
– Vessel length
– Vessel diameter
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Peripheral Resistance:
Vascular Resistance
• Vessel length
– Resistance directly proportional to length, i.e., pulmonary vs. systemic circuit
– Constant in adults
• Vessel diameter
– Much greater effect on resistance
– Effects of friction occur in zone close to vessel wall
• In large diameter vessel, blood near center does not encounter resistance
• In small diameter vessel, nearly all blood is slowed by friction with walls
– Increases exponentially as vessel diameter decreases
• ½ diameter = 16 X resistance
– Mechanisms that alter diameter of arterioles provide control over peripheral
resistance and blood flow
• Vessel diameter varies by vasodilation (bigger) and vasoconstriction (smaller)
– Most resistance occurs in arterioles (smallest diameter) = resistance vessels
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Figure 21-10 a, c
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Peripheral Resistance: Viscosity
• = Resistance to flow caused by interactions
among molecules in a liquid
• Low viscosity liquids (water) flow at low
pressure
• Blood is 4X as viscous as water due to
presence of plasma proteins and blood cells
• Viscosity remains stable except in anemia,
polycythemia (elevated hematocrit) and other
disorders that affect hematocrit
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Peripheral Resistance: Turbulence
• = Swirling action disturbs smooth flow of blood
• Created by:
– High flow rates
• Between atria and ventricles
• Between ventricles and trunks
• In aorta
– Irregular surfaces, e.g.,
• Scar tissue
• Atherosclerotic plaques
– Sudden changes in vessel diameter, e.g.,
• Vasoconstriction
• Slows flow and increases resistance
• Does not develop in small vessels except when
damaged
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Figure 21-10 b, c
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Figure 21-10 b, d
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Vascular Pathology
• Arteriosclerosis
– = Thickening and toughening of arterial walls;
hardening of the arteries
– Complications account for half of all deaths in US
– CAD (coronary artery disease) = arteriosclerosis
of coronary vessels
– Stroke = result of arteriosclerosis of arteries
supplying brain
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Vascular Pathology
• Arteriosclerosis (Cont.)
– 2 Forms of arteriosclerosis
• Focal calcification
– = Gradual degeneration of smooth muscle in tunica media and
deposition of Ca2+ salts
– Typically involves arteries of limbs and genitals
– Rapid and severe calcification may occur as complication of
diabetes mellitus
• Atherosclerosis
– Aka: Fatty degeneration
– = Damage to endothelial lining and formation of lipid deposits
(plaque) in tunica media
– Most common form of arteriosclerosis
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Vascular Pathology
• Arteriosclerosis (Cont.)
– Factors involved in development
• Lipid levels; high cholesterol
– High lipids in blood for an extended period of time
– Monocytes begin removing them and become filled with lipid
droplets (foam cells)
– Attach to endothelial walls, release growth factors that stimulate
smooth muscle to divide near the tunica interna, thickening the
vessel wall, decreasing diameter
– Other monocytes migrate resulting in a fatty mass of tissue (plaque)
that projects into lumen
– Because cells swollen with lipids, gaps appear in endothelial lining
– Platelets appear to repair, clot forms which further restricts blood
flow
• High blood pressure, smoking, diabetes mellitus, obesity, stress,
chronic bacterial infection, chronic inflammation
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Vascular Pathology
• Hypertension
– = Abnormally high BP (>140/90)
– Increases workload on heart, L ventricle gradually
enlarges, more muscle mass
– Greater O2 demand, coronary circulation can’t
keep pace, eventually coronary ischemia
(inadequate blood supply)
– Increases stress on walls of blood vessels,
accelerates development of arteriosclerosis and
aneurysms
• Hypotension
– Abnormally low BP (SP < 90 mm Hg)
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• Today in class we will discuss:
– The importance of maintaining adequate blood flow
through the capillaries and the mechanisms involved
in capillary exchange
– Venous return and its role in moving blood
– How autoregulatory, neural, and hormonal
mechanisms compensate for a reduction in blood
flow and blood pressure
– How the cardiovascular system responds to
hemorrhage
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Capillary Exchange
• As blood flows through peripheral tissues,
BP forces water and solutes out of plasma,
across capillary walls
• Most of water is reabsorbed by capillaries
• A portion (approx. 3.6 L) enters the
lymphatic system and eventually re-enters
bloodstream
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Blood-lymph Cycle
• = Continuous movement of water out of the
capillaries, through peripheral walls, to lymphatics,
then back to bloodstream
• Has 4 important functions
– Ensures plasma and interstitial fluid are in constant
communication
– Accelerates distribution of nutrients, hormones, dissolved
gases through tissues
– Transports insoluble lipids and tissue proteins that can’t
cross capillary walls
– Flushes bacterial toxins and chemicals into immune
system tissues
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Capillary Exchange
• 3 processes involved in moving materials
across capillary walls
– Filtration
– Diffusion
– Reabsorption
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Forces Across Capillary Walls
Figure 21-13
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Capillary Exchange
• Filtration
– Driving force is hydrostatic pressure
• Forces water out of a solution from high to low
pressure area (35 mm Hg in capillaries vs. 25 mm Hg in
tissues)
– When water is forced out of capillary walls, small
solute particles travel with the water
– Larger molecules and protein stay in bloodstream
– Because BP drops from 35 to 18 mm Hg in
capillaries, filtration occurs mostly at the arterial
end
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Capillary Exchange
• Diffusion
– = Movement of ions or molecules from high to
low concentration
– Does not involve pressure effects
– Primary route for capillary exchange
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Capillary Exchange
• Capillary diffusion occurs by 5 routes
– Between endothelial cells, e.g., water, ions, small organic
compounds (glucose, amino acids, urea)
– Through channels in cell membrane, e.g., water, Na+, K+,
Ca2+, Cl- ions
– At fenestrated capillaries, e.g., above and large watersoluble compounds otherwise unable to leave
bloodstream
• Found in hypothalamus, kidneys, endocrine organs, intestinal
tract
– Through endothelial cell membranes, e.g., lipids (FAs,
steroids), lipid-soluble materials including gases (O2 and
CO2
– In sinusoids, e.g., where plasma proteins are produced
and enter bloodstream in liver
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Capillary Exchange
• Reabsorption
– Result of osmosis = diffusion of water across membrane
toward higher solute concentration, e.g, blood + plasma
proteins
– From arterial to venous ends of capillaries, rates of
filtration and reabsorption change at about 25 mm Hg
• Filtration higher at beginning and reabsorption higher at end
– Of the 24 L of fluid that moves out of capillaries every day,
85% is reabsorbed
– Remainder enters lymphatic vessels and eventually
venous system
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Capillary Exchange
• Summary
– Hydrostatic pressure
• Forces water and solutes out of capillaries
• Into interstitial fluid
• At arterial end of capillary
– Osmotic pressure
• Pulls water and solutes into capillaries
• Out of interstitial fluid
• At venous end of capillary
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Edema
• = Abnormal accumulation of interstitial
fluid (ECF)
– Filtration out > reabsorption in
– Results from a disturbance between
hydrostatic and osmotic forces at capillary level
– Causes
• Damage to capillary, increase BP from heart
problems, blockage of lymphatic vessels, kidney
failure
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Venous Pressure and Venous
Return
• BP very low at venules (18 mm Hg), but
they provide very little resistance
• As blood approaches heart
– Veins become larger
– Resistance drops even more
– Velocity of blood increases
• When individual stands, venous blood
entering IVC must overcome gravity
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Venous Pressure and Venous
Return
• 2 factors help venous blood overcome gravity
– Muscular compression
• Muscular contraction near vein push blood toward heart
because of 1-way valves
• Is why standing still for long time results in little blood flow to
the brain and person faints
– Respiratory pump
• When inhale:
–
–
–
–
Thoracic cavity expands
Pressure in pleural cavities drops
Pulls air into lungs
Also pulls blood into IVC and R atrium from smaller veins in
abdominal cavity
• When exhale:
– Pressure in pleural cavities rises
– Pushes blood into R atrium
– Important during heavy exercise
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Cardiovascular Regulation
• 3 Regulatory mechanisms control
cardiovascular function, i.e, CO and BP
– Autoregulation
• Local factors at tissue level cause immediate, localized
adjustments
– Neural mechanisms
• Respond quickly to changes at specific sitesflex control
– Endocrine mechanisms
• Direct long-term changes
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Cardiovascular Responses
Figure 21-13, 8th edition
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Cardiovascular Regulation:
Autoregulation
• Local factors change pattern of blood flow in capillary bed in
response to chemical changes in interstitial fluid
• Affect precapillary sphincters
– Local vasodilators – dilate sphincters
• Accelerate blood flow through tissues brings O2, other nutrients to restore
homeostasis
• e.g., low O2 or high CO2, lactic or other acid, NO, high K+ or H+, histamine,
high temperatures
– Local vasoconstrictors – constrict sphincters
– e.g., compounds produced by platelets and damaged tissues
(antihemorrhage prostaglandins and thromboxanes from platelets and
WBCs)
• Cause immediate, localized hemostatic adjustments
• If this fails, then neural and endocrine factors activated
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Cardiovascular Regulation:
Neural Mechanisms
• Reflexes regulated through negative feedback
loop
• 2 types of reflex control
– Baroreceptor reflexes
– Chemoreceptor reflexes
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Cardiovascular Regulation
• Special cardiovascular receptors monitor conditions
– Baroreceptors
• Monitor and respond to stretch in blood vessels and atrium
– Chemoreceptors
• Monitor composition of arterial blood and CSF
• Respond to changes in CO2, O2, or pH in blood
• Found near carotid sinus (carotid bodies) and aortic arch (aortic
bodies)
• Receptors trigger neural reflex arcs to neurons in
cardiovascular centers in medulla oblongata
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Cardiovascular Regulation:
Neural Mechanisms
• Baroreceptor reflexes
– Stretch receptors respond to changes in BP
– Found in vessel walls and heart (carotid sinuses, R atrium,
aortic sinuses)
– Controlled by ANS
– When BP increases, CV centers
• Dec HR
• Cause peripheral vasodilation  dec BP
– When BP decreases, CV centers
• Inc HR and stroke volume
• Cause peripheral vasoconstriction  inc BP
– Maintains normal/adequate arterial pressure
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Baroreceptor Reflexes
Figure 21-14, 8th edition
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Cardiovascular Regulation:
Neural Mechanisms
• Chemoreceptor reflexes
– Receptors respond to changes in O2, CO2 levels and
pH in blood and CSF
– Found in aortic bodies, carotid bodies, and medulla
oblongata
– Lead to increased HR and BP by sympathetic
activation or decreased by parasympathetic
activation
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Chemoreceptor Reflexes
Figure 21–15
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Cardiovascular Regulation:
Endocrine Mechanisms
• Short-term regulation
– Of cardiac output and peripheral vasoconstriction
(resistance)
– With E and NE
• Long-term regulation
– Of BP and/or volume
– With:
•
•
•
•
ADH – increases BP and volume
Angiotensin II – increases BP and volume
Erythropoietin – increases volume
Atrial natriuretic peptide (ANP) - decreases volume
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Cardiovascular Regulation:
Endocrine Mechanisms
• ADH
– Released from post pit in response to:
• Low blood volume
• High plasma Na+
• Angiotensin II
– Immediate result is vasoconstriction that increases
BP
– Stimulates conservation of water at kidneys which
prevents further drop in blood volume
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Cardiovascular Regulation:
Endocrine Mechanisms
• Angiotensin II
– Responds to decreased renal BP
– Stimulates production of
• Aldosterone from adrenal cortex which causes Na (and
water) retention and K loss at kidneys
• ADH production which causes water retention
– Stimulates thirst
– Increases CO
– Stimulates vasoconstriction
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Cardiovascular Regulation:
Endocrine Mechanisms
• Erythropoietin
– Released at kidneys
– Responds to low BP or O2
– Stimulates RBC production and maturation which
increases blood volume and improves O2 carrying
capacity
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Cardiovascular Regulation:
Endocrine Mechanisms
• Atrial natriuretic peptide (ANP)
– Natural diuretic produced by cardiac muscle cells in
R atrium
– Respond to excessive stretch during diastole
– Reduces stress on heart
• Decreases blood volume and BP by increasing Na loss at
kidneys, promoting water loss, decreasing thirst
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Hormonal Regulation
Figure 21-16
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Circulatory Shock
• Acute circulatory crisis marked by:
– Low BP (hypotension)
– Inadequate peripheral blood flow
• Severe, potentially fatal symptoms develop as vital
tissues become starved for O2 and nutrients
• Causes:
–
–
–
–
Blood fluid loss (hemorrhage, dehydration, severe burns)
Extensive peripheral vasodilation
Heart damage
External pressure on heart
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Circulatory Shock
• Symptoms
– Hypotension (SP < 90 mm Hg)
– Pale, cool (due to vasoconstriction), moist
(clammy) skin (sweat glands activated)
– Confusion, disorientation (due to dec. BP in
brain)
– Increased heart rate; rapid, weak pulse
– Cessation of urination (due to reduced blood
flow to kidneys)
– Dec. blood pH (acidosis) (due to lactic acid
formed by O2 starved tissues)
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Circulatory Shock
• When BP declines more than 35%:
– Normal homeostatic mechanisms can no
longer handle:
• Sustained vasoconstriction
• Mobilization of venous return
– BP remains low  damage to myocardium 
decreased CO  decreased BP  decreased
flow to brain
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Circulatory Shock
• When MAP < 50 mm Hg
– Carotid sinus baroreceptors  massive activation of
vasomotor centers in brain stem  maximal
vasoconstriction (central ischemic response)
• Goal: preserve circulation to brain at expense of other tissues
– May progress to irreversible shock
• In absence of treatment, CV damage becomes irreversible
• Conditions in heart, liver, kidneys, CNS deteriorate to point at which
death will occur, even with medical treatment
• Results in widespread peripheral vasodilation and immediate, fatal
decline in BP (circulatory collapse) due to capillary collapse  cell
death
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Circulatory Shock
• Treatment
– Prevent further fluid losses
– Transfuse whole blood, plasma expanders, or
blood substitutes
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Age-related Changes
• Linked to arteriosclerosis
• Sudden pressure increase in (more inelastic)
artery walls may cause aneurysm 
– Stroke
– Myocardial infarction
– Massive hemorrhage
• Ca2+ salts deposit on vessel walls 
– Stroke
– Myocardial infarction
• Thrombi form at atherosclerotic plaques
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