3.Cardiac Output, Blood Flow, and Blood Pressure {UoK}.pptx

©McGraw-Hill Education
CARDIAC OUTPUT
&
BLOOD FLOW
PRESENTED
BY
N. G. AKUNGA B. PHARM, MSc

© 2019 McGraw-Hill Education
2
I. Cardiac Output

3
A. Introduction to Cardiac Output
1. Cardiac output – the volume of blood
pumped each minute by each ventricle:
cardiac output = stroke volume X heart rate
(ml/minute) (ml/beat) (beats/min)
a. Average heart rate = 70 bpm
b. Average stroke volume = 70 to 80 ml/beat
c. Average cardiac output = 5,500 ml/minute

4
B. Regulation of Cardiac 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

5
Regulation of Cardiac Rate (2)
e. Actual pace comes from the net affect of these
antagonistic influences
1) Positive chronotropic effect – increases rate
2) Negative chronotropic effect – decreases rate
Actions of the heart are classified into four types:
1. Chronotropic action - heart rate
2. Inotropic action – Force of contraction
3. Dromotropic action – Rate of conduction of APs
4. Bathmotropic action – Excitability of cardiac muscle

6
Effects of ANS on the SA Node

7
Effects of ANS Activity on the Heart
Effects of Autonomic Nerve Activity on the Heart
Region Affected Sympathetic Nerve Effects Parasympathetic Nerve
Effects
SA node Increased rate of diastolic
depolarization; increased
cardiac rate
Decreased rate of diastolic
depolarization; decreased
cardiac rate
AV node Increased conduction rate Decreased conduction rate
Atrial muscle Increased strength of
contraction
No significant effect
Ventricular
muscle
Increased strength of
contraction
No significant effect

8
C. Regulation of Stroke Volume (1)
1. Regulated by three variables: EDV,TPR &
HEART CONTRACTILITY
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) Called afterload
2) Inversely related to stroke volume

9
Regulation of Stroke Volume (2)
c. Contractility: strength of ventricular
contraction
1) Stroke volume increases with increased
contractility.
2. Normally, about 60% of the EDV is ejected –
This is known as the ejection fraction
3. EF = (EDV – ESV)/EDV
4. EF = APPROX. 60-65%

10
3. Frank-Starling
Law of the
Heart
a. Increased
EDV results
in increased
contractility
and thus
increased
stroke
volume.

11
b. 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

12
Intrinsic Control of Contraction Strength,
Continued
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

13
Frank-Starling Law of the Heart

14
c. 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.

15
Extrinsic Control of Contractility, Continued
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

16
Effect of Muscle Length and Epinephrine
on Contractility

17
Regulation of Cardiac Output
MAP = 1/3(SBP) + 2/3(DBP)

18
D. 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.

19
Distribution of Blood at Rest

20
Venous Return (2)
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 versus lowest pressure in
venae cavae into the right atrium (0mm Hg)

21
Venous Return (3)
Factors affecting Venous Return, Continued
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 (RAAS)

22
Factors in Venous Return

23
II.Blood Volume

24
A. Body Water Distribution (1)
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

25
Body Water Distribution (2)

26
B. 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

27
Tissue/Capillary Fluid Exchange (2)
2. Colloid osmotic pressure
a. Due to proteins dissolved in fluid
b. Blood plasma has higher colloid osmotic
pressure than interstitial fluid.
c. This difference is called oncotic pressure
1) Oncotic pressure = 25 mmHg
2) This favors the movement of fluid into the
capillaries.

28
3. Starling Forces
a. Combination of hydrostatic pressure and oncotic
pressure that predicts movement of fluid across
capillary membranes
b. Fluid movement is proportional to:
NFP = (pc + πi) - (pi + πp)
fluid out fluid in
pc = Hydrostatic pressure in capillary
πi = Colloid osmotic pressure of interstitial fluid
pi = Hydrostatic pressure of interstitial fluid
πp = Colloid osmotic pressure of blood plasma
NFP= Net filtration pressure

29
Starling Forces, Continued
c. Starling Forces predict the movement of fluid
out of the capillaries at the arteriole end
(positive value) and into the capillaries at the
venule end (negative value).
d. The return of fluids on the venous end is not
100%; 10% to 15% remains in the interstitial
spaces and will enter the lymphatic capillaries and
ultimately return to the venous system

30
Distribution of Fluid Across Walls of a
Capillary

31
4. 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

32
Edema, Continued
4) Myxedema (excessive production of mucin in
extracellular spaces caused by hypothyroidism)
5) Decreased plasma protein concentration
(plasma)
6) Obstruction of lymphatic drainage

33
EDEMA
Causes of Edema
Cause Comments
Increased blood pressure
or venous obstruction
Increases capillary filtration pressure so that more interstitial fluid
is formed at the arteriolar ends of capillaries.
Increased tissue protein
concentration
Decreases osmosis of water into the venular ends of capillaries.
Usually a localized tissue edema due to leakage of blood plasma
proteins through capillaries during inflammation and allergic
reactions. Myxedema due to hypothyroidism is also in this
category.
Decreased plasma protein
concentration
Decreases osmosis of water into the venular ends of capillaries.
May be caused by liver disease (which can be associated with
insufficient plasma protein production), kidney disease (due to
leakage of plasma protein into urine), or protein malnutrition.
Obstruction of lymphatic
vessels
Infections by filaria roundworms (nematodes) transmitted by a
certain species of mosquito
block lymphatic drainage, causing edema and tremendous
swelling of the affected areas.

34
1. Filariasis
1. Filariasis is a tropical disease in which
bloodsucking insects such as mosquitos spread a
parasitic nematode worm( Wuchereria bancrofti &
Brugia malayi ).
2. In elephantiasis, species of these worms take up
residence in the lymphatic system, where their
larvae block the lymphatic drainage.
3. This disease is found in about 72 tropical
countries, where over a billion people live and
are threatened by infection.
4. There is effective drug therapy available against the
filariasis parasite.

35
Severe Edema of Elephantiasis
© John Greim/Science Source

36
C. Regulation of Blood Volume by Kidneys
(1)
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.

37
Regulation of Blood Volume by Kidneys
(2)
2. 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

38
Regulation of Blood Volume by Kidneys
(3)
3. Antidiuretic Hormone (ADH or vasopressin)
a. Produced by 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.

39
Regulation of Blood Volume by Kidneys (4)
Antidiuretic Hormone, Continued
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

40
Negative Feedback Control of Blood
Volume by ADH

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4. 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 (RAS)

42
Regulation by Aldosterone, Continued
b. 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
angiotensin converting enzyme (ACE).

43
Renin-Angiotensin-Aldosterone System

44
Regulation by Aldosterone, Continued
c. Angiotensin II has many effects that result in a
rise 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. ACE inhibitors and Angiotensin receptor
blockers (antagonists) can reduce blood
pressure and used to treat hypertension.

45
5. 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. Physiological antagonist of aldosterone

46
Negative Feedback Correction
of Increased Venous Return

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Fluid Loss During Exercise
1. Prolonged exercise can cause the loss of water and
electrolytes due to sweating.
2. Effects of this include :lowered blood volume,
lowered cardiac output and blood flow, reduced
ability of the body to dissipate heat.
3. Drinking appropriate amounts of water can alleviate
this, but electrolytes—primarily Na+, K+ and Cl- that
are also lost in sweat must be replenished.
4. Sports drinks containing electrolytes and a mixture
of different sugars can improve physical
performance when exercise lasts 60 minutes or
longer.

48
III.Vascular
Resistance to
Blood Flow

49
A. Characteristics of Protein
1. Cardiac output is distributed unequally to
different organs due to unequal
resistance to blood flow through the
organs.

50
Estimated Distribution of Cardiac
Output at Rest
Estimated Distribution of the Cardiac Output at Rest
Organs Blood Flow
Milliliters
per Minute
Percent
Total
Gastrointestinal tract
and liver
1,400 24
Kidneys 1,100 19
Brain 750 13
Heart 250 4
Skeletal muscles 1,200 21
Skin 500 9
Other organs 600 10
Total organs 5,800 100
Source: Wade, O. L., and J. M. Bishop, Cardiac Output and Regional Blood Flow. Blackwell Science, Ltd., 1962.

51
B. Physical Laws Describing Blood Flow (1)
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.

52
Blood Flow is Produced by a Pressure
Difference

53
Physical Laws Describing Blood Flow (2)
3. The rate of blood flow is also inversely
proportional to the frictional resistance to
blood flow within the vessels.
blood flow =
ΔP
resistance
ΔP = pressure difference between the two
ends of the tube

54
4. Resistance is measured as:
resistance =
L
r4
L = length of the vessel
η = viscosity of the blood
r = radius of the blood vessel

55
5. 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 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

56
Relationship Between Blood Flow, Vessel
Radius, and Resistance

57
Pressure Differences in Different
Parts of Systemic Circulation

58
6. 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.

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A Diagram of Systemic and Pulmonary
Circulation

60
C. Extrinsic Regulation of Blood Flow (1)
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)

61
Extrinsic Regulation of Blood Flow (2)
Sympathetic Nerves, Continued
3) Adrenal epinephrine stimulates beta-
adrenergic receptors for vasodilation
4) During “flight or fight”, blood is diverted to
skeletal muscles

62
Extrinsic Control of Vascular Resistance
and Blood Flow
Extrinsic Control of Vascular Resistance and Blood Flow
Extrinsic Agent Effect Comments
Sympathetic nerves
Alpha-adrenergic Vasoconstriction
Vasoconstriction is the dominant effect of sympathetic nerve stimulation on the vascular system,
and it occurs throughout the body.
Beta-adrenergic Vasodilation
There is some activity in arterioles in skeletal muscles and in coronary vessels, but effects are
masked by dominant alpha-receptor-mediated constriction.
Cholinergic Vasodilation
Effects are localized to arterioles in skeletal muscles and are produced only during defense
(fight-or-flight) reactions.
Parasympathetic nerves Vasodilation
Effects are restricted primarily to the gastrointestinal tract, external genitalia, and salivary glands
and have little effect on total peripheral resistance.
Angiotensin II Vasoconstriction
A powerful vasoconstrictor produced as a result of secretion of renin from the kidneys; it may
function to help maintain adequate filtration pressure in the kidneys when systemic blood flow
and pressure are reduced.
ADH (vasopressin) Vasoconstriction
Although the effects of this hormone on vascular resistance and blood pressure in anesthetized
animals are well documented, the importance of these effects in conscious humans is
controversial.
Histamine Vasodilation Histamine promotes localized vasodilation during inflammation and allergic reactions.
Bradykinins Vasodilation
Bradykinins are polypeptides secreted by sweat glands and by the endothelium of blood vessels;
they promote local vasodilation.
Prostaglandins
Vasodilation or
vasoconstriction
Prostaglandins are cyclic fatty acids that can be produced by most tissues, including blood
vessel walls. Prostaglandin I2 is a vasodilator, whereas thromboxane A2 is a vasoconstrictor.
The physiological significance of these effects is presently controversial.

63
Extrinsic Regulation of Blood Flow (3)
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

64
D. 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.

65
E. Paracrine Regulation of Blood Flow (1)
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.

66
Intrinsic Regulation of Blood Flow (2)
3. 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 acid, etc.)
4) Release of K+ and paracrine signals (nitric oxide
etc.)

67
Intrinsic Regulation of Blood Flow (3)
4. Reactive hyperemia – constriction causes
build-up of metabolic wastes which will then
cause vasodilation (reddish skin)
5. Active hyperemia – increased blood flow
during increased metabolism (reddish skin)

68
IV.Blood Flow to the
Heart
and Skeletal Muscles

69
A. Aerobic Requirements of the Heart
(1)
1. The coronary arteries supply blood to a
massive number of capillaries (2,500 to
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.

70
Aerobic Requirements of the Heart
(2)
c. Large amounts of ATPase 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.

71
(3)
2. 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

72
Angiography
1. An angiogram is an X-ray picture with a contrast dye. An
angiogram of the coronary arteries might reveal narrowing
caused by atherosclerotic plaques, a thrombus, or a spasm. A
coronary angiogram is the standard method for assessing coronary
artery disease.
2. Coronary angioplasty is the technique of inserting a catheter
with a balloon into the occluded site of a coronary artery and
then inflating the balloon to push the artery open. Stents are
often inserted to support the opened section of the coronary
artery.
3. Coronary artery bypass grafting (CABG) surgery is the most
common open-heart surgery, involving the grafting of a vessel
taken from the patient onto the aorta so that it bypasses the
narrowed coronary artery.

73
Angiogram and Coronary Artery
Bypass
© Zephyr/Science Source

74
(4)
3. Exercise training (results)
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

75
B. 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 to 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

76
Changes in Skeletal Muscle Blood
Flow Under Rest and Exercise
Changes in Skeletal Muscle Blood Flow Under Conditions
of Rest and Exercise
Condition
Blood Flow
(ml/min)
Mechanism
Rest 1,000
High adrenergic sympathetic stimulation of vascular alpha receptors, causing
vasoconstriction
Beginning exercise
Increased
Dilation of arterioles in skeletal muscles due to cholinergic sympathetic nerve
activity and stimulation of beta-adrenergic receptors by the hormone epinephrine
Heavy exercise 20,000
Fall in alpha-adrenergic activity
Increased cholinergic sympathetic activity
Increased metabolic rate of exercising muscles, producing intrinsic vasodilation

77
C. Circulatory Changes During
Dynamic Exercise (1)
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.

78
Circulatory Changes During Dynamic
Exercise (2)
3. Cardiac output can increase 5X due to
increased cardiac rate.
4. Stroke volume can increase due to
increased venous return from skeletal
muscle pumps and respiratory
movements
5. Ejection fraction increases due to
increased contractility

79
Circulatory Changes During Dynamic
Exercise (3)
1. 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

80
Circulatory Changes During
Exercise

81
Cardiovascular Adaptations to
Exercise

82
Cardiovascular Changes During
Exercise
Cardiovascular Changes During Moderate Exercise
Variable Change Mechanisms
Cardiac output Increased Increased cardiac rate and stroke volume
Cardiac rate Increased Increased sympathetic nerve activity; decreased activity of the vagus nerve
Stroke volume Increased
Increased myocardial contractility due to stimulation by sympathoadrenal system;
decreased total peripheral resistance
Total peripheral resistance Decreased
Vasodilation of arterioles in skeletal muscles (and in skin when thermoregulatory
adjustments are needed)
Arterial blood pressure Increased
Increased systolic and pulse pressure due primarily to increased cardiac output; diastolic
pressure rises less due to decreased total peripheral resistance
End-diastolic volume Unchanged
Decreased filling time at high cardiac rates is compensated for by increased venous
pressure, increased activity of the skeletal muscle pump, and decreased intrathoracic
pressure aiding the venous return
Blood flow to heart and
muscles
Increased
Increased muscle metabolism produces intrinsic vasodilation; aided by increased cardiac
output and increased vascular resistance in visceral organs
Blood flow to visceral organs Decreased Vasoconstriction in digestive tract, liver, and kidneys due to sympathetic nerve stimulation
Blood flow to skin Increased
Metabolic heat produced by exercising muscles produces reflex (involving hypothalamus)
that reduces sympathetic constriction of arteriovenous shunts and arterioles
Blood flow to brain Unchanged*
Autoregulation of cerebral vessels, which maintains constant cerebral blood flow despite
increased arterial blood pressure
*There can be slight changes in cerebral blood flow (see text), but the extent of these changes is buffered by autoregulation due to myogenic
control mechanisms.

83
V. Blood Flow to the
Brain and Skin

84
A. Introduction
1. Cerebral flow is 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

85
B. Cerebral Circulation (1)
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.

86
Cerebral Circulation (2)
3. 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.

87
Cerebral Circulation (3)
4. 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 may play a role

88
Changing Patterns of Blood Flow in
the Brain
© Kul Bhatia/Science Source

89
C. 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.

90
Cutaneous Blood Flow (2)
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.

91
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.

92
Sympathetic Stimulation, Continued
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

93
Circulation in the Skin

94
VI. Blood Pressure

95
A. Blood Pressure (1)
1. Affected by blood volume/stroke volume,
total peripheral resistance, and cardiac rate
a. Increase in any of these will increase blood pressure.
b. Vasoconstriction of arterioles raises blood pressure
upstream in the arteries.
c. Arterial blood = cardiac X total peripheral
pressure output resistance
Cardiac
Rate
Stroke
Volume
Vasoconstriction

96
Effect of Vasoconstriction on Blood
Pressure

97
Blood Pressure (2)
2. 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

98
Relationship Between Blood Pressure
and Cross-Sectional Area of Vessels

99
Blood Pressure (3)
3. 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 (Afterload).

100
B. Baroreceptor Reflex (1)
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, increasing action potentials 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.

101
Effect of Blood Pressure on the
Baroreceptor Response

102
Structures Involved in the Baroreceptor
Reflex

103
Baroreceptor Reflex (2)
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

104
Baroreceptor Reflex (3)

105
C. 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

106
D. Blood Pressure Measurement (1)
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.

107
Blood Pressure Measurement (2)
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.

108
Blood Flow and Korotkoff Sounds

109
Indirect, or Auscultatory, Method of
Blood Pressure Measurement

110
Five Phases of Blood Pressure
Measurement

111
E. Pulse Pressure
1. “Taking the pulse” is a measure of heart rate.
2. What the health professional feels is increased blood
pressure in that artery at systole.
a. The difference between blood pressure at systole and
at diastole is the pulse pressure.
b. If your blood pressure is 120/80, your pulse pressure
is 40 mmHg.
3. Pulse pressure is a reflection of stroke volume

112
F. Mean Arterial Pressure
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:
diastolic pressure + 1/3 pulse pressure

113
VII. Hypertension,
Shock, and
Congestive Heart
Failure

114
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.

115
Blood Pressure Classification in
Adults
Blood Pressure Classification in Adults
Blood Pressure
Classification
Systolic Blood
Pressure
Diastolic Blood
Pressure
Drug Therapy
Normal Under 120 mmHg and Under 80 mmHg No drug therapy
Prehypertension 120–139 mmHg or 80–89 mmHg Lifestyle modification;* no antihypertensive drug indicated
Stage 1 Hypertension 140–159 mmHg or 90–99 mmHg Lifestyle modification; antihypertensive drugs
Stage 2 Hypertension 160 mmHg or greater or 100 mmHg or greater Lifestyle modification; antihypertensive drugs
*Lifestyle modifications include weight reduction; reduction in dietary fat and increased consumption of
vegetables and fruit; reduction in dietary sodium (salt); engaging in regular aerobic exercise, such as brisk
walking for at least 30 minutes a day, most days of the week; and moderation of alcohol consumption.
Source: The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure: The JNC 7 Report, Journal of the American Medical Association; 289 (2003): 2560–2572, pp. 160;
The Eighth Joint National Committee Guidelines (2014) Recommended: (1) Focusing more on diastolic than systolic
pressure for people under the age of 60; (2) Setting a more conservative goal for people over 60—150/90 for otherwise
healthy people and 140/90 for those with diabetes or chronic kidney disease.

116
Possible Causes of Secondary
Hypertension
Possible Causes of Secondary Hypertension
System Involved Examples Mechanisms
Kidneys
Kidney disease
Renal artery disease
Decreased urine formation
Secretion of vasoactive chemicals
Endocrine
Excess catecholamines (tumor of
adrenal medulla)
Excess aldosterone (Conn’s
syndrome)
Increased cardiac output and total peripheral resistance
Excess salt and water retention by the kidneys
Nervous
Increased intracranial pressure
Damage to vasomotor center
Activation of sympathoadrenal system
Activation of sympathoadrenal system
Cardiovascular
Complete heart block; patent ductus
arteriosus
Arteriosclerosis of aorta; coarctation of
aorta
Increased stroke volume
Decreased distensibility of aorta

117
B. Essential Hypertension (1)
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

118
Essential Hypertension (2)
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

119
Essential Hypertension (3)
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
f. Angiotensin II receptor blockers (ARBs) inhibit
actions of angiotensin II

120
Mechanisms of Action of Selected
Antihypertensive Drugs
Mechanisms of Action of Selected Antihypertensive Drugs
Category of Drugs Examples Mechanisms
Diuretics Thiazide; furosemide
Increase volume of urine excreted, thus lowering blood
volume
Sympathoadrenal
system inhibitors
Clonidine; alpha-methyldopa
Act to decrease sympathoadrenal stimulation by bonding
to α2-adrenergic receptors in the brain
Guanethidine; reserpine Deplete norepinephrine from sympathetic nerve endings
Atenolol
Blocks beta-adrenergic receptors, decreasing cardiac
output and/or renin secretion
Phentolamine
Blocks alpha-adrenergic receptors, decreasing
sympathetic vasoconstrictio
Direct vasodilators
Hydralazine; minoxidil sodium
nitroprusside
Cause vasodilation by acting directly on vascular smooth
muscle
Calcium channel
blockers
Verapamil; diltiazem
Inhibit diffusion of Ca2+ into vascular smooth muscle cells,
causing vasodilation and reduced peripheral resistance
Angiotensin-
converting enzyme
(ACE) inhibitors
Captopril; enalapril Inhibit the conversion of angiotensin I into angiotensin II
Angiotensin II–
receptor blockers
Losartan Blocks the binding of angiotensin II to its receptor

121
1. Preeclampsia (1)
1. Formerly called toxemia of pregnancy, occurs in up
to 8% of women worldwide who are pregnant beyond
their twentieth week.
2. It is characterized by the new onset of hypertension,
but differs from gestational hypertension by evidence
of damage to organs such as the liver and kidneys.
3. Thrombocytopenia and proteinuria may be
present. This lowers the plasma protein
concentration and oncotic pressure, producing
edema and swelling of the feet, legs, or hands.

122
Preeclampsia (2)
4. The causes of preeclampsia are not well
understood, but it is believed to stem from
dysfunction of the placenta, and the risk of
preeclampsia is increased by obesity.
5. If preeclampsia becomes severe, the
hypertension can cause seizures and
stroke. The only cure for preeclampsia is
delivery of the baby.

123
C. Circulatory Shock (1)
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.

124
Signs of Shock
Signs of Shock
Early Sign Late Sign
Blood pressure Decreased pulse pressure Decreased systolic pressure
Increased diastolic pressure
Urine Decreased Na+ concentration Decreased volume
Increased osmolality
Blood pH
Increased pH (alkalosis) due to
hyperventilation
Decreased pH (acidosis) due to
metabolic acids
Effects of poor
tissue perfusion
Slight restlessness; occasionally warm, dry
skin
Cold, clammy skin; “cloudy” senses
Source: Principles and Techniques of Critical Care, Vol. 1, R. F. Wilson, ed. Philadelphia, PA: F. A. Davis Company, 1977.

125
Cardiovascular Reflexes to Compensate
for Circulatory Shock
Cardiovascular Reflexes That Help to Compensate for
Circulatory Shock
Organ(s) Compensatory Mechanisms and Effects
Heart
Sympathoadrenal stimulation produces increased cardiac rate and increased
stroke volume due to a positive inotropic effect on myocardial contractility
Digestive tract and skin
Decreased blood flow due to vasoconstriction as a result of sympathetic nerve
stimulation (alpha-adrenergic effect)
Kidneys
Decreased urine production as a result of sympathetic-nerve-induced constriction
of renal arterioles; increased salt and water retention due to increased plasma
levels of aldosterone and antidiuretic hormone (ADH)

126
Circulatory Shock (2)
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.

127
Circulatory Shock (3)
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 to 70%).

128
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.

129
D. Congestive Heart Failure (1)
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

130
Congestive Heart Failure (2)
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

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