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© Annie Leibovitz/Contact Press Images
Chapter 19
The
Cardiovascular
System:
Blood Vessels
MDufilho 1/20/2016 1
Review of Study Guide
• OYO – Blood Vessel Anatomy p. 699-706
• Physiology of Circulation p. 706
• Maintaining Systemic Blood Pressure p. 708
– Short-Term Mechanisms
• Neural Controls
• Hormonal Controls
– Long-Term Mechanisms
• Renal Regulation
• OYO IP CD: Autoregulation and Capillary Dynamics
• OYO – Homeostatic imbalances p. 716
• OYO – Circulatory Shock p. 717 and handout
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Part 2 Physiology of Circulation
Definition of Terms
• Blood flow: volume of blood flowing through vessel, organ,
or entire circulation in given period
– Measured in ml/min, it is equivalent to cardiac output
(CO) for entire vascular system
• Blood pressure (BP): force per unit area exerted on wall of
blood vessel by blood
– Expressed in mm Hg
– Measured as systemic arterial BP in large arteries near
heart
– Pressure gradient provides driving force that keeps blood
moving from higher- to lower-pressure areas
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Definition of Terms (cont.)
• Resistance (peripheral resistance): opposition
to flow
– Measurement of amount of friction blood
encounters with vessel walls, generally in
peripheral (systemic) circulation
– Three important sources of resistance
• Blood viscosity
• Total blood vessel length
• Blood vessel diameter
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Relationship between Flow, Pressure, and
Resistance
• Blood flow (F) is directly proportional to blood
pressure gradient (P)
– If P increases, blood flow speeds up
• Blood flow is inversely proportional to peripheral
resistance (R)
– If R increases, blood flow decreases, so
F = P/R
• R is more important in influencing local blood
flow because it is easily changed by altering
blood vessel diameter
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Figure 19.6 Blood pressure in various blood vessels of the systemic circulation.
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Systolic pressure
Mean pressure
Diastolic pressure
0
20
40
60
80
100
120
Blo
od
p
re
ssure (m
m H
g)
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Arterial Blood Pressure
• Determined by two factors:
1. Elasticity (compliance or distensibility) of
arteries close to heart
2. Volume of blood forced into them at any time
• Blood pressure near heart is pulsatile
– Rises and falls with each heartbeat
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Arterial Blood Pressure (cont.)
• Systolic pressure:
• Diastolic pressure:
• Pulse pressure:
• Pulse:
• Mean Arterial Pressure (MAP)
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Arterial Blood Pressure (cont.)
• MAP is calculated by adding diastolic pressure +
1/3 pulse pressure
– Example: BP = 120/80; Pulse Pressure =
120 − 80 = 40; so MAP = 80 + (1/3)40 = 80 +
13 = 93 mm Hg
• Pulse pressure and MAP both decline with
increasing distance from heart
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19.8 Regulation of Blood Pressure
• Maintaining blood pressure requires cooperation
of heart, blood vessels, and kidneys
– All supervised by brain
• Three main factors regulating blood pressure
– Cardiac output (CO)
– Peripheral resistance (PR)
– Blood volume
• Blood pressure varies directly with CO, PR, and
blood volume
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19.8 Regulation of Blood Pressure
• Remember:
F = P/R
and that F = CO, so substituting gives
CO = P/R
and rearranging,
P = CO R
• Shows that blood pressure (MAP) is directly
proportional to CO and PR
– Changes in one variable are quickly
compensated for by changes in other variables
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19.8 Regulation of Blood Pressure
• Recall that CO = SV HR, so if MAP = CO R,
then
MAP = SV HR R
• Anything that increases SV, HR, or R will also
increase MAP
– SV is effected by venous return (EDV)
– HR is maintained by medullary centers
– R is effected mostly by vessel diameter
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19.8 Regulation of Blood Pressure
• Factors can be affected by:
– Short-term regulation: neural controls
– Short-term regulation: hormonal controls
– Long-term regulation: renal controls
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Figure 19.9 Major factors
determining MAP.
MDufilho
Peripheral resistance
Diameter of blood vessels
Blood viscosity
Heart rate
Stroke volume
Blood vessel length
Cardiac output
Mean arterial pressure (MAP)
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Short-Term Regulation: Neural Controls
• Two main neural mechanisms control peripheral resistance
1. MAP is maintained by altering blood vessel diameter,
which alters resistance
• Example: If blood volume drops, all vessels constrict
(except those to heart and brain)
2. Can alter blood distribution to organs in response to
specific demands
• Neural controls operate via reflex arcs that involve:
– Cardiovascular center of medulla
– Baroreceptors
– Chemoreceptors
– Higher brain centers
• Goals?
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Short-Term Regulation: Neural Controls
(cont.)
• Baroreceptor reflexes
– Located in carotid sinuses, aortic arch, and walls
of large arteries of neck and thorax
– If MAP is high:
• Increased blood pressure stimulates baroreceptors to
increase input to vasomotor center
• Inhibits vasomotor and cardioacceleratory centers
• Stimulates cardioinhibitory center
• Results in decreased blood pressure
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Short-Term Regulation: Neural Controls
(cont.)
• Baroreceptor reflexes (cont.)
– If MAP is low:
• Reflex vasoconstriction is initiated that increases CO
and blood pressure
• Example: when a person stands, BP falls and triggers:
– Carotid sinus reflex: baroreceptors that monitor BP to
ensure enough blood to brain
– Aortic reflex maintains BP in systemic circuit
• Baroreceptors are ineffective if altered blood pressure
is sustained
– Become adapted to hypertension, so not triggered by
elevated BP levels
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Figure 19.10 Baroreceptor reflexes that help maintain blood pressure homeostasis.
MDufilho
Baroreceptors
in carotid sinuses and aortic arch
are stimulated.
Rate of
vasomotor impulses allows vasodilation,
causing R. CO and R
return blood pressure to
homeostatic range.
Sympathetic
impulses to heart cause HR,
contractility, and
CO.
Impulses from baroreceptors
stimulate cardioinhibitory center (and inhibit cardioacceleratory
center) and inhibit vasomotor center.
Stimulus:
Blood pressure (arterial blood
pressure rises
above normal range).
CO and R
return blood pressure to
homeostatic
range.
Vasomotor
fibers stimulate vasoconstriction,
causing R.
Stimulus:
Blood pressure (arterial blood
pressure falls below
normal range).
Baroreceptors
in carotid sinuses and aortic arch
are inhibited Sympathetic
impulses to heart Cause HR,
contractility, and
CO.
Impulses from baroreceptors
activate cardioacceleratory center (and inhibit cardioinhibitory center)
and stimulate vasomotor center.
Homeostasis: Blood pressure in normal range
2
3
4b
5
4a
1
5 4b
1
2
3
4a
Slide 6
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Short-Term Regulation: Neural Controls
(cont.) • Chemoreceptor reflexes
– Aortic arch and large arteries of neck detect increase in CO2, or drop
in pH or O2
– Cause increased blood pressure by:
• Signaling cardioacceleratory center to increase CO
• Signaling vasomotor center to increase vasoconstriction
• Influence of higher brain centers
– Reflexes that regulate BP are found in medulla
– Hypothalamus and cerebral cortex can modify arterial pressure via
relays to medulla
– Hypothalamus increases blood pressure during stress
– Hypothalamus mediates redistribution of blood flow during exercise
and changes in body temperature
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Short-Term Mechanisms: Hormonal Controls
• Hormones regulate BP in short term via
changes in peripheral resistance or long term
via changes in blood volume
• Adrenal medulla hormones
– Epinephrine and norepinephrine from adrenal
gland increase CO and vasoconstriction
• Angiotensin II stimulates vasoconstriction
• ADH: high levels can cause vasoconstriction
• Atrial natriuretic peptide decreases BP by
antagonizing aldosterone, causing decreased
blood volume
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Long-Term Mechanisms: Renal Regulation
• Baroreceptors quickly adapt to chronic high or
low BP so are ineffective for long-term
regulation
• Long-term mechanisms control BP by altering
blood volume via kidneys
• Kidneys regulate arterial blood pressure by:
1. Direct renal mechanism
2. Indirect renal mechanism (renin-angiotensin-
aldosterone)
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Long-Term Mechanisms: Renal Regulation
(cont.)
• Direct renal mechanism
– Alters blood volume independently of hormones
• Increased BP or blood volume causes elimination of
more urine, thus reducing BP
• Decreased BP or blood volume causes kidneys to
conserve water, and BP rises
– ADH
– Alcohol
MDufilho 1/20/2016 22
Long-Term Mechanisms: Renal Regulation
(cont.)
• Indirect mechanism – The renin-angiotensin-aldosterone mechanism
• Decreased arterial blood pressure causes release of renin from
kidneys
• Renin enters blood and catalyzes conversion of angiotensinogen
from liver to angiotensin I
• Angiotensin-converting enzyme, especially from lungs, converts
angiotensin I to angiotensin II
– Angiotensin II acts in four ways to stabilize arterial BP and ECF:
• Stimulates aldosterone secretion
• Causes ADH release from posterior pituitary
• Triggers hypothalamic thirst center to drink more water
• Acts as a potent vasoconstrictor, directly increasing blood
pressure
MDufilho
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Figure 19.11 Direct and indirect (hormonal) mechanisms for renal control of blood pressure.
MDufilho
Arterial pressure
Blood volume
Aldosterone
Mean arterial pressure
Blood volume
Mean arterial pressure
Filtration by kidneys
Urine formation
Arterial pressure
Inhibits baroreceptors
Sympathetic nervous system activity
Water intake Water reabsorption
by kidneys
Sodium reabsorption
by kidneys
ADH release by
posterior pituitary
Vasoconstriction;
peripheral resistance Thirst via
hypothalamus Adrenal cortex
Angiotensin II
Angiotensin converting
enzyme (ACE)
Secretes
Initial stimulus
Physiological response
Result
Direct renal mechanism
Angiotensin I
Angiotensinogen
Renin release from kidneys
Indirect renal mechanism (renin-angiotensin-aldosterone)
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Clinical Applications
• ACE Inhibitors
• Nitroglycerin
• What if ?????? Worksheet.
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Summary of Blood Pressure Regulation
• Goal of blood pressure regulation is to keep
blood pressure high enough to provide
adequate tissue perfusion, but not so high that
blood vessels are damaged
– Example: If BP to brain is too low, perfusion is
inadequate, and person loses consciousness
– If BP to brain is too high, person could have
stroke
MDufilho 1/20/2016 26
Figure 19.12 Factors that increase MAP.
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Activity of muscular pump and respiratory
pump
Fluid loss from hemorrhage,
excessive sweating
Crisis stressors: exercise, trauma,
body temperature
Baroreceptors
Release of ANP P
Vasomotor tone; bloodborne chemicals
(epinephrine, NE, ADH,
angiotensin II)
Dehydration, high hematocrit
Body size
Conservation of Na+ and
water by kidneys
Blood volume Blood pressure
Blood pH O2
CO2
Chemoreceptors Blood volume
Venous return
Activation of vasomotor and cardio- acceleratory centers in brain stem
Stroke volume
Heart rate
Diameter of blood vessels
Blood viscosity
Blood vessel length
Peripheral resistance Cardiac output
Mean arterial pressure (MAP)
Initial stimulus
Physiological response
Result
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19.9 Control of Blood Flow
• Tissue perfusion: blood flow through body
tissues; involved in:
1. Delivery of O2 and nutrients to, and removal of
wastes from, tissue cells
2. Gas exchange (lungs)
3. Absorption of nutrients (digestive tract)
4. Urine formation (kidneys)
• Rate of flow is precisely right amount to provide
proper function to that tissue or organ
MDufilho 1/20/2016 28
19.9 Control of Blood Flow
• Rate of blood flow is controlled by extrinsic and intrinsic
factors
– Extrinsic control: sympathetic nervous system and
hormones control blood flow through whole body
• Act on arteriolar smooth muscle to reduce flow to
regions that need it the least
– Intrinsic control: Autoregulation (local) control of
blood flow: blood flow is adjusted locally to meet specific
tissue’s requirements
• Local arterioles that feed capillaries can undergo
modification of their diameters
• Organs regulate own blood flow by varying resistance
of own arterioles
MDufilho 1/20/2016 29
Figure 19.13 Distribution of blood flow at rest and during strenuous exercise.
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Brain
Heart
Skeletal muscles
Skin
Kidneys
Abdomen
Other
750
250
1200
500
1100
1400
600
750
750
12,500
600
600
400
1900
Total blood flow during strenuous exercise 17,500 ml/min
Total blood flow at rest 5800 ml/min
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Autoregulation: Intrinsic (Local)
Regulation of Blood Flow
• Autoregulation: local (intrinsic) conditions that
regulate blood flow to that area
– Reactive hyperemia: increased blood flow to an
area due to intrinsic factors
• Two types of intrinsic mechanisms both
determine final autoregulatory response
– Metabolic controls
– Myogenic controls
MDufilho 1/20/2016 31
Autoregulation: Intrinsic (Local)
Regulation of Blood Flow (cont.)
• Metabolic controls
– Increase in tissue metabolic activities results in:
• Declining levels of O2
• Increasing levels of metabolic products (H+, K+,
adenosine, and prostaglandins)
– Effects of change in levels of local chemicals
• Cause direct relaxation of arterioles and relaxation of
precapillary sphincters
• Cause release of nitric oxide (NO), a powerful
vasodilator, by endothelial cells
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Autoregulation: Intrinsic (Local)
Regulation of Blood Flow (cont.)
• Metabolic controls (cont.)
• Endothelins, also released from endothelium, are
potent vasoconstrictors
• NO and endothelins are usually balanced unless
blood flow is inadequate, in which case NO wins
control, causing vasodilation
– Inflammatory chemicals can also cause
vasodilation
MDufilho 1/20/2016 33
Autoregulation: Intrinsic (Local)
Regulation of Blood Flow (cont.)
• Myogenic controls
– Myogenic responses: local vascular smooth
muscle responds to changes in MAP to keep
perfusion constant to avoid damage to tissue
• Passive stretch: increased MAP stretches vessel wall
more than normal
– Smooth muscle responds by constricting, causing
decreased blood flow to tissue
• Reduced stretch: decreased MAP causes less stretch
than normal
– Smooth muscle responds by dilating, causing increased
blood flow to tissue
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Autoregulation: Intrinsic (Local)
Regulation of Blood Flow (cont.)
• Long-term autoregulation
– Occurs when short-term autoregulation cannot
meet tissue nutrient requirements
• Long-term autoregulation may take weeks or months
to increase blood supply
– Number of vessels to region increases
(angiogenesis), and existing vessels enlarge
– Common in heart when coronary vessel
occluded, or throughout body in people in
high-altitude areas
MDufilho 1/20/2016 35
Figure 19.14 Intrinsic and extrinsic control of arteriolar smooth muscle in the systemic circulation.
MDufilho
Intrinsic controls
(autoregulation)
• Metabolic or myogenic controls
• Distribute blood flow to individual
organs and tissues as needed
Vasoconstrictors
Myogenic
• Stretch
Metabolic
• Endothelins
Sympathetic tone
Neural
Ho r monal
• Angiotensin II
• Antidiuretic hormone
• Epinephrine
• Norepinephrine
Extrinsic controls
• Neural or hormonal controls
• Maintain mean arterial pressure
(MAP)
• Redistribute blood during exercise
and thermoregulation
Metabolic
• Prostaglandins
• Adenosine
• Nitric oxide
O2
CO2
H+
K+
Neural
Hormonal
• Atrial natriuretic
peptide
Sympathetic tone
Vasodilators
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Figure 19.16 Blood flow velocity and total cross-sectional area of vessels.
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50
40
30
20
10
0
5000
Relative cross- sectional area of different vessels of the vascular bed
4000
3000
2000
1000
0
Total area
(cm2) of the
vascular
bed
Velocity of
blood flow
(cm/s)
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Vasomotion
• Vasomotion: intermittent flow of blood through
capillaries
– Due to on/off opening and closing of precapillary
sphincters
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Figure 19.17-1 Capillary transport mechanisms.
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Red blood cell in lumen
Endothelial cell
Intercellular cleft
Fenestration (pore)
Endothelial cell nucleus
Tight junction
Basement membrane
Pinocytotic vesicles
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Figure 19.17-2 Capillary transport mechanisms.
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Basement membrane
Endothelial fenestration (pore)
Intercellular cleft
Pinocytotic vesicles
Caveolae
Transport via vesicles or caveolae (large substances)
Movement through fenestrations (water-soluble substances)
Movement through intercellular clefts (water-soluble substances)
Diffusion through membrane (lipid-soluble substances)
Lumen
3
2
1
4
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Focus Figure 19.1 Bulk fluid flow across capillary walls causes continuous mixing of fluid between the plasma and the interstitial fluid
compartments, and maintains the interstitial environment.
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Piston
Venule
Arteriole
Lymphatic
capillary
Solute
molecules
(proteins) Boundary Boundary
Hydrostatic pressure (HP)
The big picture
Each day, 20 L of fluid filters from capillaries at their
arteriolar end and flows through the interstitial
space. Most (17 L) is reabsorbed at the venous end.
Recall from Chapter 3 (p. 71) that two kinds
of pressure drive fluid movement:
17 L of fluid per
day is reabsorbed
into the capillaries
at the venous end.
Fluid moves
through the
interstitial space.
For all capillary
beds, 20 L of fluid
is filtered out per
day—almost 7
times the total
plasma volume! Osmotic pressure (OP)
• Due to fluid pressing against a
boundary (e.g., capillary wall)
• HP “pushes” fluid across the
boundary
• In blood vessels, is due to
blood pressure
• Due to nondiffusible solutes
that cannot cross the boundary
• OP “pulls” fluid across the
boundary
• In blood vessels, is due to
plasma proteins
“Pushes” “Sucks”
About 3 L per
day of fluid
(and any leaked
proteins) are
removed by the
lymphatic
system (see
Chapter 20).
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Focus Figure 19.1-3 Bulk fluid flow across capillary walls causes continuous mixing of fluid between the plasma and the interstitial fluid
compartments, and maintains the interstitial environment.
MDufilho
HPif = 0 mm Hg
NFP = 10 mm Hg
HPc = 35 mm Hg
OPif = 1 mm Hg
OPc = 26 mm Hg
Osmotic pressure (OPif) in interstitial fluid “pulls” fluid out of capillary.
Hydrostatic pressure (HPif) in interstitial fluid “pushes” fluid into capillary.
Hydrostatic pressure in capillary (HPc) “pushes” fluid out of capillary.
Osmotic pressure in capillary (OPc) “pulls” fluid into capillary.
Boundary
(capillary wall)
Interstitial fluid Capillary lumen
How do the pressures drive fluid flow across a capillary?
Net filtration occurs at the arteriolar end of a capillary.
Let’s use what we know about pressures
to determine the net filtration pressure
(NFP) at any point. (NFP is the pressure
driving fluid out of the capillary.) To do
this we calculate the outward pressures
(HPc and OPif) minus the inward
pressures (HPif and OPc). So,
As a result, fluid moves from the
capillary into the interstitial space.
NFP = (HPc + OPif) (HPif + OPc)
= (35 + 1) (0 + 26)
= 10 mm Hg (net outward pressure)
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Focus Figure 19.1-4 Bulk fluid flow across capillary walls causes continuous mixing of fluid between the plasma and the interstitial fluid
compartments, and maintains the interstitial environment.
MDufilho
NFP= 8 mm Hg
HPif = 0 mm Hg
HPc = 17 mm Hg
OPc = 26 mm Hg
OPif = 1 mm Hg
Net reabsorption occurs at the venous end of a capillary.
Hydrostatic pressure in capillary “pushes” fluid out of capillary. The pressure has dropped because of resistance encountered along the capillaries.
Osmotic pressure in capillary “pulls” fluid into capillary.
Boundary (capillary wall)
Interstitial fluid
Hydrostatic pressure in interstitial fluid “pushes” fluid into capillary.
Osmotic pressure in interstitial fluid “pulls” fluid out of capillary.
Again, we calculate the NFP:
NFP = (HPc + OPif) (HPif + OPc)
= (17 + 1) (0 + 26)
= 8 mm Hg (net inward pressure)
Notice that the NFP at the venous end is a negative number. This means that reabsorption, not filtration, is occurring and so fluid moves from the
interstitial space into the capillary.
Capillary lumen
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Circulatory Shock OYO from handout
• Any condition in which
– Blood vessels inadequately filled
– Blood cannot circulate normally
• Results in inadequate blood flow to meet tissue
needs
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