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Chapter 14
Cardiac Output,
Blood Flow, and
Blood Pressure
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I. Cardiac Output
Introduction
1. Cardiac output – the volume of blood pumped
from each ventricle per minute:
CO
=
SV
x
HR
cardiac output = stroke volume X heart rate
(ml/minute)
(ml/beat)
(beats/min)
a. Average heart rate = 70 bpm
b. Average stroke volume = 70−80 ml/beat
c. Average cardiac output = 5,500 ml/minute
Regulation of Heart Rate
1. Spontaneous depolarization occurs at SA node
when HCN channels open, allowing Na+ in.
a. Open due to hyperpolarization at the end of the
preceding action potential
b. Sympathetic norepinephrine and adrenal
epinephrine keep HCN channels open,
increasing heart rate.
c. Parasympathetic acetylcholine opens K+
channels, slowing heart rate.
d. Controlled by cardiac center of medulla
oblongata that is affected by higher brain
centers
Regulation of Cardiac Rate
e. Actual pace comes from the net affect of these
antagonistic influences
1) Positive chronotropic effect – increases rate
2) Negative chronotropic effect – decreases rate
Effects of ANS on the SA Node
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= Pacemaker potential
Control
Threshold
–50mV
Sympathetic nerve effect
–50mV
Parasympathetic nerve effect
–50mV
250
500
750
Time (msec)
1000
Effects of ANS Activity on the Heart
Regulation of Stroke Volume
1. Regulated by three variables:
a. End diastolic volume (EDV): volume of blood
in the ventricles at the end of diastole
1) Sometimes called preload
2) Stroke volume increases with increased
EDV.
b. Total peripheral resistance: Frictional
resistance in the arteries
1) Inversely related to stroke volume
2) Called afterload
Regulation of Stroke Volume
c. Contractility: strength of ventricular
contraction
1) Stroke volume increases with contractility.

Ejection fraction (EF) – percentage of the EDV
that is ejected per cardiac cycle
Stroke volume = EDV – ESV
EF% = (SV / EDV) x 100

Normal ejection fraction is about 50-65%
Frank-Starling Law of the Heart
Intrinsic Control of Contraction Strength
1) Due to myocardial stretch
a) Increased EDV stretches the myocardium,
which increases contraction strength.
b) Due to increased myosin and actin overlap
and increased sensitivity to Ca2+ in cardiac
muscle cells
Intrinsic Control of Contraction Strength
2) Adjustment for rise in peripheral resistance
a) Increased peripheral resistance will decrease
stroke volume
b) More blood remains in the ventricles, so EDV
increases
c) Ventricles are stretched more, so they contract
more strongly
Frank-Starling Law of the Heart
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Resting sarcomere lengths
I
A
H
I
2.4 μm
(d)
(d)
Actin
Z
Z
Myosin
Stretch
Tension (g)
(c)
(b)
(c)
2.2 μm
(b)
2.0 μm
(a)
1.5 μm
(a)
0
500
1000
msec
Time
Extrinsic Control of Contractility
1) Contractility – strength of contraction at any given
fiber length
2) Sympathetic norepinephrine and adrenal
epinephrine (positive inotropic effect) can increase
contractility by making more Ca2+ available to
sarcomeres. Also increases heart rate.
3) Parasympathetic acetylcholine (negative
chronotropic effect) will decrease heart rate which
will increase EDV  increases contraction strength
 increases stroke volume, but not enough to
compensate for slower rate, so cardiac output
decreases
Effect of muscle length & epinephrine on
contractility
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100
Skeletal muscle
Cardiac muscle
with epinephrine
(inotropic effect)
Relative tension (%)
80
Cardiac muscle
without epinephrine
60
40
20
0
50
60
70
80
90
Length of muscle (as percent of optimum at 100%)
100
*Regulation of Cardiac Output
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Total peripheral resistance
and mean arterial pressure
Cardiac output
=
Heart rate
X
Stroke volume
Contraction
strength
Sympathetic
nerves
Parasympathetic
nerves
Stretch
Enddiastolic
volume
(EDV)
FrankStarling
Venous Return
1. End diastolic volume is controlled by factors that
affect venous return:
a. Total blood volume
b. Venous pressure (driving force for blood return)
2. Veins have high compliance – stretch more at a
given pressure than arteries (veins have thinner
walls).
3. Veins are capacitance vessels – 2/3 of the total
blood volume is in veins
4. They hold more blood than arteries but maintain
lower pressure.
Distribution of blood at rest
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Lungs
(10%–12%)
Heart
(8%–11%)
Small veins
and venules
Systemic arteries
(10%–12%)
Systemic veins
(60%–70%)
Large veins
Capillaries
(4%–5%)
Factors in Venous Return
a. Pressure difference between arteries and veins
(about 10mm Hg)
b. Pressure difference in venous system - highest
pressure in venules vs. lowest pressure in venae
cavae into the right atrium (0mm Hg)
c. Sympathetic nerve activity to stimulate smooth
muscle contraction and lower compliance
d. Skeletal muscle pumps
e. Pressure difference between abdominal and
thoracic cavities (respiration)
f. Blood volume
Factors in Venous Return
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End-diastolic volume
Venous return
Negative
intrathoracic
pressure
Blood volume
Venous pressure
Breathing
Urine
volume
Tissue-fluid
volume
Venoconstriction
Sympathetic
nerve stimulation
Skeletal
muscle
pump
II. Blood Volume
Body Water Distribution
1. 2/3 of our body water is found in the cells
(intracellular).
2. Of the remaining, 80% exists in interstitial spaces
and 20% is in the blood plasma (extracellular).
3. Osmotic forces control the movement of water
between the interstitial spaces and the capillaries,
affecting blood volume.
4. Urine formation and water intake (drinking) also
play a role in blood volume.
5. Fluid is always circulating in a state of dynamic
equilibrium
Body Water Distribution
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Intracellular
27–30 L
Extracellular
14–16.5 L
Water
excretion
per 24 hrs
Cell
membrane
Capillary wall
Kidneys
0.6–1.5 L
Cytoplasm
Interstitial
fluid
volume
11–13 L
Blood
plasma
volume
3.0–3.5 L
Lungs
0.3–0.4 L
Skin (sweat glands)
0.2–1.0 L
Water intake
per 24 hrs
(drink + food)
1.5–2.5 L H2O
GI tract
Feces
0.1–0.2 L H2O
Tissue/Capillary Fluid Exchange
1. Net filtration pressure is the hydrostatic pressure
of the blood in the capillaries minus the
hydrostatic pressure of the fluid outside the
capillaries
a. Hydrostatic pressure at arteriole end is 37
mmHg and at the venule end is 17 mmHg
b. Hydrostatic pressure of interstitial fluid is 1
mmHg
c. Net filtration pressure is 36 mmHg at
arteriole end and 16 mmHg at venule end
Colloid osmotic pressure
a. Due to proteins dissolved in fluid
b. Blood plasma has higher colloid osmotic pressure
than interstitial fluid. This difference is called
oncotic pressure.
1) Oncotic pressure = 25 mmHg
2) This favors the movement of fluid into the
capillaries.
Starling Forces
a. Combination of hydrostatic pressure and oncotic
pressure that predicts movement of fluid across
capillary membranes
b. Fluid movement is proportional to:
(pc + πi) - (pi + πp) or (BHP + IFOP) – (IFHP + BCOP)
fluid out
pc
πi
pi
πp
fluid in
fluid out
fluid in
= Hydrostatic pressure in capillary (BHP)
= Colloid osmotic pressure of interstitial fluid (IFOP)
= Hydrostatic pressure of interstitial fluid (IFHP)
= Colloid osmotic pressure of blood plasma (BCOP)
Starling Forces
c. Starling Forces predict the movement of fluid out
of the capillaries at the arteriole end (positive
value  filtration) and into the capillaries at the
venule end (negative value  reabsorption).
d. The return of fluids on the venous end is not
100%; 10% - 15% remains in the interstitial
spaces and will enter the lymphatic capillaries
and ultimately return to the venous system
Distribution of fluid across walls of a capillary
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Tissue
fluid
Capillary
Blood
flow
Arteriole
Net
force out
Net
force in
Arterial end
of capillary
Venul
e
Venous end
of capillary
(Pc + πi) – (Pi + πp)
(Fluid in)
(Fluid out)
(37 + 0) – (1 + 25)
= 11 mmHg
Net filtration
(17 + 0) – (1 + 25)
= –9 mmHg
Net absorption
Where Pc = hydrostatic pressure in the capillary
πi = colloid osmotic pressure of interstitial fluid
Pi = hydrostatic pressure of interstitial fluid
πp = colloid osmotic pressure of blood plasma
Edema
a. Excessive accumulations of interstitial fluids
b. May be the result of:
1) High arterial blood pressure
2) Venous obstruction
3) Leakage of plasma proteins into interstitial
space
4) Myxedema (excessive production of mucin in
extracellular spaces caused by hypothyroidism)
5) Decreased plasma protein concentration
6) Obstruction of lymphatic drainage
Causes of Edema
Severe Edema of Elephantiasis
Regulation of Blood Volume by Kidneys
1. The formation of urine begins with filtration of fluid
through capillaries in the kidneys called glomeruli.
a. 180 L of filtrate is moved across the glomeruli
per day, yet only about 1.5 L is actually
removed as urine. The rest is reabsorbed into
the blood.
b. The amount of fluid reabsorbed is controlled by
several hormones and the sympathetic nervous
system in response to the body’s needs.
Role of the sympathetic nervous system
a. Increased blood volume in the atria stimulates
stretch receptors that leads to increased
sympathetic stimulation to the heart and
decreased stimulation to the kidneys
b. Kidney arterioles dilate, increasing blood flow and
increases urine production that will decrease
blood volume
Antidiuretic Hormone (ADH or vasopressin)
a. Produced by the supraoptic nuclei of the
hypothalamus and released from the posterior
pituitary when osmoreceptors detect increased
plasma osmolality.
b. Plasma osmolarity can increase due to excessive
salt intake or dehydration.
c. Increased plasma osmolarity also increases thirst.
d. ADH stimulates water reabsorption from collecting
ducts of kidneys.
Antidiuretic Hormone
e. Increased water intake and decreased urine
formation increase blood volume.
f. Blood becomes dilute, and ADH is no longer
released.
g. Stretch receptors in left atrium, carotid sinus, and
aortic arch also inhibit ADH release.
h. Stretch receptors in the atria also stimulated the
release of atrial natriuretic peptide which
increases excretion of salt and water from kidneys
to reduce blood volume
Negative Feedback Control of Blood Volume by ADH
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Dehydration
( Blood volume)
Stimuli
Sensor
Integrating center
Effector
Salt ingestion
Blood osmolality
Osmoreceptors in
hypothalamus
Posterior
pituitary
Thirst
ADH
Water retention
by kidneys
Negative feedback
responses
Blood volume
Blood osmolality
Drinking
Regulation by Aldosterone
a. Secreted by adrenal cortex indirectly when blood
volume and pressure are reduced
1) Stimulates reabsorption of salt and water in
kidneys
2) Does not change blood osmolality since both
salt and water are involved
3) Regulated by renin-angiotensin-aldosterone
system
Renin-angiotensin-aldosterone system
1) When blood pressure is low, cells in the kidneys
(juxtaglomerular apparatus) secrete the enzyme
renin
a) Angiotensinogen is converted to angiotensin I
by renin
b) Angiotensin I is converted to angiotensin II by
ACE enzyme.
Renin-Angiotensin-Aldosterone System
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Blood pressure
Blood flow to kidneys
Stimuli
Sensor
Integrating center
Effector
Juxtaglomerular
apparatus
in kidneys
Renin
Angiotensinogen
Angiotensin I
ACE
Angiotensin II
Adrenal cortex
Aldosterone
Vasoconstriction
of arterioles
Salt and water
retention by kidneys
Negative feedback
responses
Blood volume
Blood pressure
Regulation by aldosterone
c. Angiotensin II has many effects that result in a
raise in blood pressure:
1) Vasoconstriction of small arteries and arterioles
to increase peripheral resistance
2) Stimulates thirst center in hypothalamus
3) Stimulates production of aldosterone in adrenal
cortex
d. Can also work the opposite direction to reduce
blood pressure
Regulation by atrial natriuretic peptide (ANP)
a. Produced by the atria of the heart when stretch
is detected from high volume or increased
venous return
b. Promotes salt and water excretion in urine in
response to increased blood volume
c. Inhibits ADH secretion
d. Antagonist of aldosterone
Negative feedback correction of increased
venous return
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Sensor
Water immersion
or
increased blood volume
Integrating center
Effector
Negative feedback
Venous return
Stretch of
left atrium
Blood volume
Vagus nerves
Brain
Urine volume
Atrial natriuretic
peptide (ANP)
Posterior pituitary
NaCl
and H2O
excretion
Kidneys
H2O
reabsorption
Antidiuretic
hormone (ADH)
III. Vascular Resistance to Blood
Flow
Blood Flow to the Organs
1. Cardiac output is distributed unequally to different
organs due to unequal resistance to blood flow
through the organs.
Estimated Distribution of Cardiac
Output at Rest
Physical Laws Describing Blood Flow
1. Blood flows from a region of higher pressure to a
region of lower pressure.
2. The rate of blood flow is proportional to the
differences in pressure.
Blood Flow is produced by a pressure difference
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Pressure = 0 mmHg
ΔP = 100 – 0
= 100 mmHg
RA
LA
RV
LV
Pressure = 120/80
(mean ~
= 100 mmHg)
Physical Laws describing Blood Flow
3. The rate of blood flow is also inversely
proportional to the frictional resistance to blood
flow within the vessels.
ΔP
blood flow =
resistance
ΔP = pressure difference between the two ends
of the tube
Physical Laws Describing Blood Flow
4. Resistance is measured as:
Lη
resistance =
r4
L = length of the vessel
η = viscosity of the blood
r = radius of the blood vessel
Poiseuille’s Law adds in physical constraints
ΔPr4(π)
blood flow =
ηL(8)
a. Vessel length (L) and blood viscosity (η) do not
vary normally.
b. Mean arterial pressure (ΔP) and vessel radius
(r) are therefore the most important factors in
blood flow.
c. Vasoconstriction of arterioles provides the
greatest resistance to blood flow and can
redirect flow to/from particular organs
Relationship Between Blood Flow, Vessel
Radius, and Resistance
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Radius = 1 mm
Resistance = R
Blood flow = F
(a)
Radius = 1 mm
Resistance = R
Blood flow = F
Radius = 2 mm
Resistance = 1/16 R
Blood flow = 16 F
(b)
Radius = 1/2 mm
Resistance = 16 R
Blood flow = 1/16 F
Arterial
blood
Arterial
blood
Pressure Differences in Different Parts of
Systemic Circulation
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Left
Large
ventricle arteries
Small
arteries and
arterioles Capillaries
Venules
Large
veins
120
Pressure (mmHg)
100
80
60
40
20
0
Resistance
vessels
Exchange
vessels
Capacitance
vessels
Total Peripheral Resistance
a. The sum of all vascular resistance in systemic
circulation
b. Blood flow to organs runs parallel to each other,
so a change in resistance within one organ does
not affect another.
c. Vasodilation in a large organ may decrease total
peripheral resistance and mean arterial pressure.
d. Increased cardiac output and vasoconstriction
elsewhere make up for this.
A Diagram of Systemic and Pulmonary Circulation
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Lungs
Vena
cava
Hepatic artery
Splenic artery
Liver
Hepatic
vein
Kidney
Hepatic
portal vein
Mesenteric artery
(from intestine)
Renal afferent
arterioles
Renal efferent
arterioles
Extrinsic Regulation of Blood Flow
1. Autonomic and endocrine control of blood flow
a. Sympathetic nerves
1) Increase in cardiac output and increase total
peripheral resistance through release of
norepinephrine onto smooth muscles of
arterioles in the viscera and skin to stimulate
vasoconstriction (alpha-adrenergic).
2) Acetylcholine is released onto skeletal
muscles, resulting in increased vasodilation
to these tissues (cholinergic)
Sympathetic nerves
3) Adrenal epinephrine stimulates beta-adrenergic
receptors for vasodilation
4) During “flight or fight”, blood is diverted to skeletal
muscles
Extrinsic Control of Vascular Resistance
and Blood Flow
Extrinsic Regulation of Blood Flow
b. Parasympathetic nerves (cholinergic)
1) Acetylcholine stimulates vasodilation.
2) Limited to digestive tract, external genitalia,
and salivary glands
3) Less important in controlling total peripheral
resistance due to limited influence
Paracrine Regulation of Blood Flow
1. Molecules produced by one tissue control another
tissue within the same organ.
a. Example: The tunica interna produces signals
to influence smooth muscle activity in the
tunica media.
2. Smooth muscle relaxation influenced by
bradykinin, nitric oxide, and prostaglandin I2 to
produce vasodilation
3. Endothelin-1 stimulates smooth muscle
contraction to produce vasoconstriction and raise
total peripheral resistance.
Intrinsic Regulation of Blood Flow
1. Used by some organs (brain and kidneys) to
promote constant blood flow when there is
fluctuation of blood pressure; also called
autoregulation.
2. Myogenic control mechanisms: Vascular
smooth muscle responds to changes in arterial
blood pressure.
Metabolic control mechanisms
a. Local vasodilation is controlled by changes in:
1) Decreased oxygen concentrations due to
increased metabolism
2) Increased carbon dioxide concentrations
3) Decreased tissue pH (due to CO2, lactic oxide,
etc.)
4) Release of K+ and paracrine signals
Intrinsic Regulation of Blood Flow
4. Reactive hyperemia – constriction causes buildup of metabolic wastes which will then cause
vasodilation (reddish skin)
5. Active hyperemia – increased blood flow during
increased metabolism (reddish skin)
IV. Blood Flow to the Heart and
Skeletal Muscles
Aerobic Requirements of the Heart
1. The coronary arteries supply blood to a
massive number of capillaries (2,500–4,000 per
cubic mm tissue).
a. Unlike most organs, blood flow is restricted
during systole. Cardiac tissue therefore has
myoglobin to store oxygen during diastole to
be released in systole.
b. Cardiac tissue also has lots of mitochondria
and respiratory enzymes, thus is
metabolically very active.
Aerobic Requirements of the Heart
c. Large amounts of ATPs are produced from the
aerobic respiration of fatty acids, glucose, and
lactate.
d. During exercise, the coronary arteries increase
blood flow from 80 ml to 400 ml/ minute/100 g
tissue.
 This is a 5x increase in blood demand!
Regulation of Coronary Blood Flow
a. Norepinephrine from sympathetic nerve fibers
(alpha-adrenergic) stimulates vasoconstriction,
raising vascular resistance at rest.
b. Adrenal epinephrine (beta-adrenergic) stimulates
vasodilation and thus decreases vascular
resistance during exercise.
c. Vasodilation is enhanced by intrinsic metabolic
control mechanisms – increased CO2, K+,
paracrine regulators
Exercise training
a. Increased density of coronary arterioles and
capillaries
b. Increased production of NO to promote
vasodilation
c. Decreased compression of coronary arteries
during systole due to lower cardiac rate
Regulation of Blood Flow Through Skeletal Muscles
1. Arterioles have high vascular resistance at rest
due to alpha-adrenergic sympathetic stimulation
a. Even at rest, skeletal muscles still receive
20−25% of the body’s blood supply.
2. Blood flow does decrease during contraction and
can stop completely beyond 70% of maximum
contraction.
3. Vasodilation is stimulated by both adrenal
epinephrine and sympathetic acetylcholine.
4. Intrinsic metabolic controls enhance vasodilation
during exercise
Changes in Skeletal Muscle Blood Flow
Under Rest and Exercise
Circulatory Changes During Dynamic Exercise
1. Vascular resistance through skeletal and cardiac
muscles decreases due to:
a. Increased cardiac output
b. Metabolic vasodilation
c. Diversion of blood away from viscera and
skin
2. Blood flow to brain increases a small amount with
moderate exercise and decreases a small amount
during intense exercise.
Circulatory Changes During Dynamic Exercise
3. Cardiac output can increase 5X due to increased
cardiac rate.
4. Stroke volume can increase some due to
increased venous return from skeletal muscle
pumps and respiratory movements
5. Ejection fraction increases due to increased
contractility
Endurance training
a. Lower resting cardiac rate due to greater inhibition
of the SA node
b. Increase in stroke volume because of the increase
in blood volume
c. Improved O2 delivery
Circulatory Changes During Exercise
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25 L/min
Cardiac output
= 25 L/min
Heavy
exercise
100%
3%–5%
4%–5%
2%–4%
0.5%–1%
3%–4%
80%–85%
~20 L/min
Heavy
exercise
Rest
~0.75 L/min
Rest
100%
5 L/min
20%–25%
4%–5%
20%
3%–5%
Cardiac output
= 5 L/min
15%
4%–5%
15%–20%
Cardiovascular Adaptations to Exercise
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Cardiac
output
Heart
rate
Blood flow to
skeletal muscles
Stroke
volume
Sympathoadrenal
system
Improved
venous
return
Deeper
breathing
Metabolic
vasodilation
in muscles
Skeletal
muscle
activity
Sympathetic
vasoconstriction
in viscera
Cardiovascular Changes During Exercise
V. Blood Flow to the Brain and Skin
Introduction
1. Cerebral flow primarily controlled by intrinsic
mechanisms and is relatively constant; the brain
can not tolerate much variation in blood flow.
2. Cutaneous flow primarily controlled by extrinsic
mechanisms and shows the most variation; can
handle low rates of blood flow
Cerebral Circulation
1. Held constant at about 750 mL/min flow
2. Unless mean arterial pressure becomes very high,
there is little sympathetic control of blood flow to
the brain.
a. At high pressure, vasoconstriction occurs to
protect small vessels from damage and stroke.
Myogenic Regulation
a. When blood pressure falls, cerebral vessels
automatically dilate.
b. When blood pressure rises, cerebral vessels
automatically constrict.
c. Decreased pH of cerebrospinal fluid (buildup of
CO2) causes arteriole dilation.
d. Increased pH of cerebrospinal fluid (drop in CO2)
causes constriction of vessels.
Metabolic Regulation
a. The most active regions of the brain must receive
increased blood flow (hyperemia) due to arteriole
sensitivity to metabolic changes.
b. Active neurons release K+, adenosine, NO, and
other chemical that cause vasodilation
c. Astrocytes play a role through the release of
PGE2
Changing Patterns of Blood Flow in the Brain
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(a)
(b)
(c)
(d)
(all): © Niels A. Lassen, Copenhagen, Denmark
Cutaneous Blood Flow
1. The skin can tolerate the greatest fluctuations in
blood flow.
2. The skin helps control body temperature in a
changing environment by regulating blood flow =
thermoregulation.
a. Increased blood flow to capillaries in the skin
releases heat when body temperature
increases.
b. Sweat is also produced to aid in heat loss.
c. Bradykinins in the sweat glands also stimulate
vasodilation in the skin.
Cutaneous Blood Flow
3. Vasoconstriction of arterioles keeps heat in the
body when ambient temperatures are low.
4. This is aided by arteriovenous anastomoses,
which shunt blood from arterioles directly to
venules.
a. Cold temperatures activate sympathetic
vasoconstriction.
b. This is tolerated due to decreased metabolic
activity in the skin.
Cutaneous Blood Flow
5. At average ambient temperatures, vascular
resistance in the skin is high, and blood flow
is low.
6. Sympathetic stimulation reduces blood flow
further.
a. With continuous exercise, the need to
regulate body temperature overrides
this, and vasodilation occurs.
Sympathetic Stimulation
b. May result in lowered total peripheral
resistance if not for increased cardiac
output
c. However, if a person exercises in very hot
weather, he or she may experience
extreme drops in blood pressure after
reduced cardiac output.
d. This condition can be very dangerous.
7. Emotions can affect sympathetic activity and
cause pallor or blushing
Circulation in the Skin
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Epidermis
Dermis
Capillary loop
Arteriovenous
anastomosis
Venule
Arteriole
Vein
Artery
VI. Blood Pressure
Blood Pressure



Systolic blood pressure (SBP) – highest
pressure in arteries during systole
Diastolic blood pressure (DBP) – lowest
pressure in arteries during diastole
Affected by blood volume, stroke volume, total
peripheral resistance, and heart rate
Effect of Vasoconstriction on Blood Pressure
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Increased
pressure
Decreased
pressure
Constriction
Blood Pressure

The blood pressure of blood vessels is related
to the total cross-sectional area
a. Capillary blood pressure is low because of
large total cross-sectional area.
b. Artery blood pressure is high because of
small total cross-sectional area
Relationship between blood pressure and crosssectional area of vessels
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5,000
Area (c2)
4,000
3,000
2,000
1,000
0
Pressure (mmHg)
120
100
80
60
40
20
0
Aorta
Capillaries
Arterioles Venules
Arteries
Veins
Vena cava
Pulse Pressure (PP)

“Taking the pulse” is a measure of heart rate.
• The difference between blood pressure at
systole and at diastole is the pulse pressure.
PP = SBP – DBP
•

If your blood pressure is 120/80, your pulse
pressure is 40 mmHg.
Pulse pressure is a reflection of stroke volume
Mean Arterial Pressure (MAP)
1. The average pressure in the arteries in one
cardiac cycle is the mean arterial pressure.
2. This is significant because it is the difference
between mean arterial pressure and venous
pressure that drives the blood into the capillaries.
3. Calculated as:
MAP = DBP + 1/3 (PP)
Blood Pressure Regulation
a. Kidneys can control blood volume and thus stroke
volume.
b. The sympathoadrenal system stimulates
vasoconstriction of arterioles (raising total
peripheral resistance) and increased cardiac
output.
Blood Pressure Measurement
1. Measured in mmHg by an instrument called a
sphygmomanometer.
2. A blood pressure cuff produces turbulent flow of
blood in the brachial artery, which can be heard
using a stethoscope; called sounds of Korotkoff.
3. The cuff is first inflated to beyond systolic blood
pressure to pinch off an artery. As pressure is
released, the first sound is heard at systole and a
reading can be taken.
Blood Pressure Measurement
4. The last Korotkoff sound is heard when the
pressure in the cuff reaches diastolic pressure and
a second reading can be taken.
5. The average blood pressure is 120/80.
Blood Flow & Korotkoff Sounds
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No sounds
Cuff pressure = 140
First Korotkoff
sounds
Cuff pressure = 120
Systolic pressure
= 120 mmHg
Sounds at
every systole
Cuff pressure = 100
Blood pressure = 120/80
Last Korotkoff
sounds
Cuff pressure = 80
Diastolic pressure
= 80 mmHg
Indirect, or Auscultatory, Method of
Blood Pressure Measurement
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Cuff pressure
No flow
120
mmHg
Artery
silent
Turbulent flow
First
sound
Sound
Laminar flow
Last
sound
Systole
Blood pressure
Diastole
80
mmHg
Artery
silent
Five Phases of Blood Pressure Measurement
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Blood flows during
systole and diastole
(laminar flow)
No blood
flows
Blood flows during
systole only
(turbulent flow)
14 mmHg
130
20 mmHg
5 mmHg
120
110
5 mmHg
100
90
80
2
3
4
5
Snapping
sounds
Murmurs
Muffling
Silence
Cuff pressure (mmHg)
1
Thumping
60
Silence
70
Relative intensity of sounds
Baroreceptor Reflex
1. Activated by changes in blood pressure detected
by baroreceptors (stretch receptors) in the aortic
arch and carotid sinuses
2. Increased blood pressure stretches these
receptors, impulse is carried by sensory fibers to
the vasomotor and cardiac control centers in the
medulla.
3. Most sensitive to drops in blood pressure
4. The vasomotor center controls vasodilation and
constriction.
5. The cardiac center controls heart rate.
Baroreceptor Reflex
6. Fall in blood pressure = Increased sympathetic
and decreased parasympathetic activity,
resulting in increased heart rate and total
peripheral resistance
7. Rise in BP has the opposite effects.
8. Good for quick beat-by-beat regulation like going
from lying down to standing
Structures involved in the Baroreceptor Reflex
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Sensory neuron
Sympathetic neuron
Parasympathetic neuron
Cerebrum
Carotid sinus
Common carotid artery
Sensory
fibers
Arch of aorta
Hypothalamus
Medulla
oblongata
Parasympathetic
vagus nerve
SA node
AV node
Spinal cord
Sympathetic
cardiac nerve
Sympathetic chain
Structures involved in the Baroreceptor Reflex
Baroreceptor Reflex
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Going from laying
to standing position
Venous
return
End-diastolic
volume
Stroke
volume
Cardiac
output
Stimuli
Blood pressure
Sensor
Integrating center
Baroreceptors
Effector
Sensory neurons
Medulla oblongata
Sympathetic
Parasympathetic
Vasoconstriction
of arterioles
Cardiac
rate
Total peripheral
resistance
Negative feedback
response
Cardiac
output
Blood pressure
Effect of Blood Pressure on the
Baroreceptor Response
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180
Mean arterial pressure (mmHg)
160
140
120
Action
potentials
100
80
60
Resting
potential
40
Time
Atrial Stretch Reflexes
1. Activated by increased venous return to:
a. Stimulate reflex tachycardia
b. Inhibit ADH release; results in excretion of
more urine
c. Stimulate secretion of atrial natriuretic peptide;
results in excretion of more salts and water in
urine
VII. Hypertension, Shock, and
Congestive Heart Failure
A.
Hypertension
1. Hypertension is high blood pressure.
a. Incidence increases with age
b. It can increase the risk of cardiac diseases,
kidney diseases, and stroke.
c. Hypertension can be classified as “essential” or
“secondary.”
1) Essential or primary hypertension is a result
of complex and poorly understood processes
2) Secondary hypertension is a symptom of
another disease, such as kidney disease.
Blood Pressure Classification in Adults
Possible Causes of Secondary Hypertension
B.
Essential Hypertension
1. Most people fall in this category.
2. The cause is difficult to determine and may
involve any of the following:
a. Increased salt intake coupled with decreased
kidney filtering ability
b. Increased sympathetic nerve activity,
increasing heart rate
c. Responses to paracrine regulators from the
endothelium
d. Increased total peripheral resistance
3.
Dangers of Hypertension
a. Vascular damage within organs, especially
dangerous in the cerebral vessels and leading to
stroke
b. Ventricular overload to eject blood due to
abnormal hypertrophy, leading to arrhythmias and
cardiac arrest
c. Contributes to the development of atherosclerosis
4.
Treatments for Hypertension
a. Lifestyle modification: limit salt intake; limit
smoking and drinking; lose weight; exercise
b. K+ (and possibly calcium) supplements
c. Diuretics to increase urine formation
d. Beta blockers to decrease cardiac rate
e. ACE inhibitors to block angiotensin II production
Mechanisms of Action of Selected
Antihypertensive Drugs
C.
Circulatory Shock
1. Occurs when there is inadequate blood flow to
match oxygen usage in the tissues
a. Symptoms result from inadequate blood flow
and how our circulatory system changes to
compensate.
b. Sometimes shock leads to death.
Signs of Shock
Cardiovascular Reflexes to Compensate for
Circulatory Shock
2.
Hypovolemic Shock
a. Due to low blood volume from an injury,
dehydration, or burns
b. Characterized by decreased cardiac output and
blood pressure
c. Blood is diverted to the heart and brain at the
expense of other organs.
d. Compensation includes baroreceptor reflex, which
lowers blood pressure, raises heart rate, raises
peripheral resistance, and produces cold, clammy
skin and low urine output.
3.
Septic Shock
a. Dangerously low blood pressure (hypotension)
due to an infection (sepsis)
b. Bacterial toxins (endotoxins) induce NO
production, causing widespread vasodilation.
c. Mortality rate is high (50−70%).
4.
Other Causes of Circulatory Shock
a. Severe allergic reactions can cause anaphylactic
shock due to production of histamine and resulting
vasodilation.
b. Spinal cord injury or anesthesis can cause
neurogenic shock due to loss of sympathetic
stimulation.
c. Cardiac failure can cause cardiogenic shock due
to significant myocardial loss.
D.
Congestive Heart Failure
1. Occurs when cardiac output is not sufficient to
maintain blood flow required by the body
a. Caused by myocardial infarction, congenital
defects, hypertension, aortic valve stenosis, or
disturbances in electrolyte levels (K+ and Ca2+)
b. Similar to hypovolemic shock in symptoms and
response
2.
Types of congestive heart failure
a. Left-side failure – raises left atrial pressure and
produces pulmonary congestion and edema
causing shortness of breath
b. Right-side failure – raises right atrial pressure and
produces systemic congestion and edema