1. Chapter 14 Lecture Outline
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2. I. Cardiac Output

3. Introduction
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)
Average heart rate = 70 bpm
Average stroke volume = 70−80 ml/beat
Average cardiac output = 5,500 ml/minute

4. Regulation of Cardiac Rate
Spontaneous depolarization occurs at SA node when HCN channels open, allowing Na+ in.
Open due to hyperpolarization at the end of the preceding action potential
Sympathetic norepinephrine and adrenal epinephrine keep HCN channels open, increasing heart rate.
Parasympathetic acetylcholine opens K+ channels, slowing heart rate.
Controlled by cardiac center of medulla oblongata that is affected by higher brain centers

5. Regulation of Cardiac Rate, cont
Actual pace comes from the net affect of these antagonistic influences
Positive chronotropic effect – increases rate
Negative chronotropic effect – decreases rate

6. 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
1000
Time (msec)

7. Effects of ANS Activity on the Heart

8. Regulation of Stroke Volume
Regulated by three variables:
End diastolic volume (EDV): volume of blood in the ventricles at the end of diastole
Sometimes called preload
Stroke volume increases with increased EDV.
Total peripheral resistance: Frictional resistance in the arteries
Inversely related to stroke volume
Called afterload

9. Regulation of Stroke Volume, cont
Contractility: strength of ventricular contraction
Stroke volume increases with contractility.
Normally, about 60% of the EDV is ejected – ejection fraction

10. Frank-Starling Law of the Heart
Increased EDV results in increased contractility and thus increased stroke volume.
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Frank-Starling law
Increased contractility
caused by sympathetic
nerve stimulation
Stroke volume (ml)
Ventricular end-diastolic volume (ml)

11. Intrinsic Control of Contraction Strength
Due to myocardial stretch
Increased EDV stretches the myocardium, which increases contraction strength.
Due to increased myosin and actin overlap and increased sensitivity to Ca2+ in cardiac muscle cells

12. Intrinsic Control of Contraction Strength, cont
Adjustment for rise in peripheral resistance
Increased peripheral resistance will decrease stroke volume
More blood remains in the ventricles, so EDV increases
Ventricles are stretched more, so they contract more strongly

13. Frank-Starling Law of the Heart
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Resting sarcomere lengths A I I H
(d)
2.4 μm
(d)
Actin Z Z
Myosin
(c)
Tension (g)
Stretch
(c)
2.2 μm
(b)
(a)
(b)
2.0 μm
500
1000
msec
Time
(a)
1.5 μm

14. Extrinsic Control of Contractility
Contractility – strength of contraction at any given fiber length
Sympathetic norepinephrine and adrenal epinephrine (positive inotropic effect) can increase contractility by making more Ca2+ available to sarcomeres. Also increases heart rate.
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

15. Effect of muscle length & epinephrine on contractility
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100
Skeletal muscle
Cardiac muscle
with epinephrine
(inotropic effect) 80
Cardiac muscle
without epinephrine 60
Relative tension (%) 40 20 50 60 70 80 90
100
Length of muscle (as percent of optimum at 100%)

16. Regulation of Cardiac Output
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Total peripheral resistance
and mean arterial pressure
Cardiac output =
Cardiac rate X
Stroke volume
Contraction
strength
Sympathetic
nerves
End-
diastolic
volume
(EDV)
Parasympathetic
nerves
Stretch
Frank-
Starling

17. Venous Return
End diastolic volume is controlled by factors that affect venous return:
Total blood volume
Venous pressure (driving force for blood return)
Veins have high compliance - stretch more at a given pressure than arteries (veins have thinner walls).
Veins are capacitance vessels – 2/3 of the total blood volume is in veins
They hold more blood than arteries but maintain lower pressure.

18. 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%)
Capillaries
(4%–5%)
Large veins

19. Factors in Venous Return
Pressure difference between arteries and veins (about 10mm Hg)
Pressure difference in venous system - highest pressure in venules vs. lowest pressure in venae cavae into the right atrium (0mm Hg)
Sympathetic nerve activity to stimulate smooth muscle contraction and lower compliance
Skeletal muscle pumps
Pressure difference between abdominal and thoracic cavities (respiration)
Blood volume

20. 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
Skeletal
muscle
pump
Sympathetic
nerve stimulation

21. II. Blood Volume

22. Body Water Distribution
2/3 of our body water is found in the cells (intracellular).
Of the remaining, 80% exists in interstitial spaces and 20% is in the blood plasma (extracellular).
Osmotic forces control the movement of water between the interstitial spaces and the capillaries, affecting blood volume.
Urine formation and water intake (drinking) also play a role in blood volume.
Fluid is always circulating in a state of dynamic equilibrium

23. 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
Interstitial
fluid
volume
11–13 L
Blood
plasma
volume
3.0–3.5 L
Lungs
0.3–0.4 L
Cytoplasm
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

24. Tissue/Capillary Fluid Exchange
Net filtration pressure is the hydrostatic pressure of the blood in the capillaries minus the hydrostatic pressure of the fluid outside the capillaries
Hydrostatic pressure at arteriole end is 37 mmHg and at the venule end is 17 mmHg
Hydrostatic pressure of interstitial fluid is 1 mmHg
Net filtration pressure is 36 mmHg at arteriole end and 16 mmHg at venule end

25. Colloid osmotic pressure
Due to proteins dissolved in fluid
Blood plasma has higher colloid osmotic pressure than interstitial fluid. This difference is called oncotic pressure.
Oncotic pressure = 25 mmHg
This favors the movement of fluid into the capillaries.

26. Starling Forces
Combination of hydrostatic pressure and oncotic pressure that predicts movement of fluid across capillary membranes
Fluid movement is proportional to:
(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

27. Starling Forces, cont
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).
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

28. Distribution of fluid across walls of a capillary
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Tissue
fluid
Net filtration
Net absorption
Capillary
Blood
flow
Net
force out
Net
force out
Net
force in
Net
force in
Arteriole
Venule
Arterial end
of capillary
Venous end
of capillary
(Pc + πi) – (Pi + πp)
(Fluid out)
(Fluid in)
(37 + 0) – (1 + 25)
(17 + 0) – (1 + 25)
= 11 mmHg
= –9 mmHg
Net filtration
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

29. Edema Excessive accumulations of interstitial fluids
May be the result of:
High arterial blood pressure
Venous obstruction
Leakage of plasma proteins into interstitial space
Myxedema (excessive production of mucin in extracellular spaces caused by hypothyroidism)
Decreased plasma protein concentration
Obstruction of lymphatic drainage

30. Causes of Edema

31. Severe Edema of Elephantiasis

32. Regulation of Blood Volume by Kidneys
The formation of urine begins with filtration of fluid through capillaries in the kidneys called glomeruli.
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.
The amount of fluid reabsorbed is controlled by several hormones and the sympathetic nervous system in response to the body’s needs.

33. Role of the sympathetic nervous system
Increased blood volume in the atria stimulates stretch receptors that leads to increased sympathetic stimulation to the heart and decreased stimulation to the kidneys
Kidney arterioles dilate, increasing blood flow and increases urine production that will decrease blood volume

34. Antidiuretic Hormone (ADH or vasopressin)
Produced by the hypothalamus and released from the posterior pituitary when osmoreceptors detect increased plasma osmolality.
Plasma osmolarity can increase due to excessive salt intake or dehydration.
Increased plasma osmolarity also increases thirst.
ADH stimulates water reabsorption.

35. Antidiuretic Hormone, cont
Increased water intake and decreased urine formation increase blood volume.
Blood becomes dilute, and ADH is no longer released.
Stretch receptors in left atrium, carotid sinus, and aortic arch also inhibit ADH release.
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

36. Negative Feedback Control of Blood Volume by ADH
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Dehydration
( Blood volume)
Stimuli
Salt ingestion
Sensor
Blood osmolality
Integrating center
Effector
Osmoreceptors in
hypothalamus
Posterior
pituitary
Thirst
ADH
Water retention
by kidneys
Drinking
Negative feedback
responses
Blood volume
Blood osmolality

37. Regulation by Aldosterone
Secreted by adrenal cortex indirectly when blood volume and pressure are reduced
Stimulates reabsorption of salt and water in kidneys
Does not change blood osmolality since both salt and water are involved
Regulated by renin-angiotensin-aldosterone system

38. Renin-angiotensin-aldosterone system
When blood pressure is low, cells in the kidneys (juxtaglomerular apparatus) secrete the enzyme renin
Angiotensinogen is converted to angiotensin I by renin
Angiotensin I is converted to angiotensin II by ACE enzyme.

39. Renin-Angiotensin-Aldosterone System
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Blood pressure
Stimuli
Blood flow to kidneys
Juxtaglomerular
apparatus
in kidneys
Sensor
Integrating center
Effector
Renin
Angiotensinogen
Angiotensin I
ACE
Angiotensin II
Adrenal cortex
Vasoconstriction
of arterioles
Aldosterone
Salt and water
retention by kidneys
Negative feedback
responses
Blood volume
Blood pressure

40. Regulation by aldosterone, cont
Angiotensin II has many effects that result in a raise in blood pressure:
Vasoconstriction of small arteries and arterioles to increase peripheral resistance
Stimulates thirst center in hypothalamus
Stimulates production of aldosterone in adrenal cortex
Can also work the opposite direction to reduce blood pressure

41. Regulation by atrial natriuretic peptide
Produced by the atria of the heart when stretch is detected from high volume or increased venous return
Promotes salt and water excretion in urine in response to increased blood volume
Inhibits ADH secretion
Antagonist of aldosterone

42. increased blood volume
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
Antidiuretic
hormone (ADH)
Kidneys
H2O
reabsorption

43. III. Vascular Resistance to Blood Flow

44. Blood Flow to the Organs
Cardiac output is distributed unequally to different organs due to unequal resistance to blood flow through the organs.

45. Estimated Distribution of Cardiac Output at Rest

46. Physical Laws Describing Blood Flow
Blood flows from a region of higher pressure to a region of lower pressure.
The rate of blood flow is proportional to the differences in pressure.

47. Blood Flow is produced by a pressure difference
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Pressure = 0 mmHg RA LA RV LV
ΔP = 100 – 0 = 100 mmHg
Pressure = 120/80
(mean mmHg) = ~

48. Physical Laws describing Blood Flow, cont
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

49. Physical Laws Describing Blood Flow, cont
Resistance is measured as: Lη
resistance = r4
L = length of the vessel
η = viscosity of the blood
r = radius of the blood vessel

50. Poiseuille’s Law adds in physical constraints
ΔPr4(π)
blood flow =
ηL(8)
Vessel length (L) and blood viscosity (η) do not vary normally.
Mean arterial pressure and vessel radius (r) are therefore the most important factors in blood flow.
Vasoconstriction of arterioles provides the greatest resistance to blood flow and can redirect flow to/from particular organs

51. Relationship Between Blood Flow, Vessel Radius, and Resistance
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Radius = 1 mm
Resistance = R
Blood flow = F
Arterial
blood
Radius = 1 mm
Resistance = R
Blood flow = F
(a)
Radius = 2 mm
Resistance = 1/16 R
Blood flow = 16 F
Arterial
blood
Radius = 1/2 mm
Resistance = 16 R
Blood flow = 1/16 F
(b)

52. Pressure Differences in Different Parts of Systemic Circulation
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Small
arteries and
arterioles
Left
ventricle
Large
arteries
Large
veins
Capillaries
Venules
120
100 80
Pressure (mmHg) 60 40 20
Resistance
vessels
Exchange
vessels
Capacitance
vessels

53. Total Peripheral Resistance
The sum of all vascular resistance in systemic circulation
Blood flow to organs runs parallel to each other, so a change in resistance within one organ does not affect another.
Vasodilation in a large organ may decrease total peripheral resistance and mean arterial pressure.
Increased cardiac output and vasoconstriction elsewhere make up for this.

54. A Diagram of Systemic and Pulmonary Circulation
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Lungs
Vena
cava
Hepatic artery
Splenic artery
Liver
Hepatic
vein
Mesenteric artery
(from intestine)
Hepatic
portal vein
Kidney
Renal afferent
arterioles
Renal efferent
arterioles

55. Extrinsic Regulation of Blood Flow
Autonomic and endocrine control of blood flow
Sympathetic nerves
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).
Acetylcholine is released onto skeletal muscles, resulting in increased vasodilation to these tissues (cholinergic)

56. Sympathetic nerves, cont
Adrenal epinephrine stimulates beta-adrenergic receptors for vasodilation
During “flight or fight”, blood is diverted to skeletal muscles

57. Extrinsic Control of Vascular Resistance and Blood Flow

58. Extrinsic Regulation of Blood Flow, cont
Parasympathetic nerves (cholinergic)
Acetylcholine stimulates vasodilation.
Limited to digestive tract, external genitalia, and salivary glands
Less important in controlling total peripheral resistance due to limited influence

59. Paracrine Regulation of Blood Flow
Molecules produced by one tissue control another tissue within the same organ.
Example: The tunica interna produces signals to influence smooth muscle activity in the tunica media.
Smooth muscle relaxation influenced by bradykinin, nitric oxide, and prostaglandin I2 to produce vasodilation
Endothelin-1 stimulates smooth muscle contraction to produce vasoconstriction and raise total peripheral resistance.

60. Intrinsic Regulation of Blood Flow
Used by some organs (brain and kidneys) to promote constant blood flow when there is fluctuation of blood pressure; also called autoregulation.
Myogenic control mechanisms: Vascular smooth muscle responds to changes in arterial blood pressure.

61. Metabolic control mechanisms
Local vasodilation is controlled by changes in:
Decreased oxygen concentrations due to increased metabolism
Increased carbon dioxide concentrations
Decreased tissue pH (due to CO2, lactic oxide, etc.)
Release of K+ and paracrine signals

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

63. IV. Blood Flow to the Heart and Skeletal Muscles

64. Aerobic Requirements of the Heart
The coronary arteries supply blood to a massive number of capillaries (2,500–4,000 per cubic mm tissue).
Unlike most organs, blood flow is restricted during systole. Cardiac tissue therefore has myoglobin to store oxygen during diastole to be released in systole.
Cardiac tissue also has lots of mitochondria and respiratory enzymes, thus is metabolically very active.

65. Aerobic Requirements of the Heart, cont
Large amounts of ATPase are produced from the aerobic respiration of fatty acids, glucose, and lactate.
During exercise, the coronary arteries increase blood flow from 80 ml to 400 ml/ minute/100 g tissue.

66. Regulation of Coronary Blood Flow
Norepinephrine from sympathetic nerve fibers (alpha-adrenergic) stimulates vasoconstriction, raising vascular resistance at rest.
Adrenal epinephrine (beta-adrenergic) stimulates vasodilation and thus decreases vascular resistance during exercise.
Vasodilation is enhanced by intrinsic metabolic control mechanisms – increased CO2, K+, paracrine regulators

67. Exercise training
Increased density of coronary arterioles and capillaries
Increased production of NO to promote vasodilation
Decreased compression of coronary arteries during systole due to lower cardiac rate

68. Regulation of Blood Flow Through Skeletal Muscles
Arterioles have high vascular resistance at rest due to alpha-adrenergic sympathetic stimulation
Even at rest, skeletal muscles still receive 20−25% of the body’s blood supply.
Blood flow does decrease during contraction and can stop completely beyond 70% of maximum contraction.
Vasodilation is stimulated by both adrenal epinephrine and sympathetic acetylcholine.
Intrinsic metabolic controls enhance vasodilation during exercise

69. Changes in Skeletal Muscle Blood Flow Under Rest and Exercise

70. Circulatory Changes During Dynamic Exercise
Vascular resistance through skeletal and cardiac muscles decreases due to:
Increased cardiac output
Metabolic vasodilation
Diversion of blood away from viscera and skin
Blood flow to brain increases a small amount with moderate exercise and decreases a small amount during intense exercise.

71. Circulatory Changes During Dynamic Exercise, cont
Cardiac output can increase 5X due to increased cardiac rate.
Stroke volume can increase some due to increased venous return from skeletal muscle pumps and respiratory movements
Ejection fraction increases due to increased contractility

72. Endurance training
Lower resting cardiac rate due to greater inhibition of the SA node
Increase in stroke volume because of the increase in blood volume
Improved O2 delivery

73. Circulatory Changes During Exercise
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25 L/min
Cardiac output
= 25 L/min
100%
3%–5%
4%–5%
2%–4%
0.5%–1%
3%–4%
80%–85%
Heavy
exercise
~20 L/min
Heavy
exercise
Rest
~0.75 L/min
Rest
100%
20%–25%
4%–5%
20%
3%–5%
15%
4%–5%
15%–20%
5 L/min
Cardiac output
= 5 L/min

74. Cardiovascular Adaptations to Exercise
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Cardiac
output
Blood flow to
skeletal muscles
Cardiac
rate
Stroke
volume
Metabolic
vasodilation
in muscles
Sympathetic
vasoconstriction
in viscera
Sympathoadrenal
system
Improved
venous
return
Skeletal
muscle
activity
Deeper
breathing

75. Cardiovascular Changes During Exercise

76. V. Blood Flow to the Brain and Skin

77. Introduction
Cerebral flow primarily controlled by intrinsic mechanisms and is relatively constant; the brain can not tolerate much variation in blood flow.
Cutaneous flow primarily controlled by extrinsic mechanisms and shows the most variation; can handle low rates of blood flow

78. Cerebral Circulation Held constant at about 750 mL/min flow
Unless mean arterial pressure becomes very high, there is little sympathetic control of blood flow to the brain.
At high pressure, vasoconstriction occurs to protect small vessels from damage and stroke.

79. Myogenic Regulation
When blood pressure falls, cerebral vessels automatically dilate.
When blood pressure rises, cerebral vessels automatically constrict.
Decreased pH of cerebrospinal fluid (buildup of CO2) causes arteriole dilation.
Increased pH of cerebrospinal fluid (drop in CO2) causes constriction of vessels.

80. Metabolic Regulation
The most active regions of the brain must receive increased blood flow (hyperemia) due to arteriole sensitivity to metabolic changes.
Active neurons release K+, adenosine, NO, and other chemical that cause vasodilation
Astrocytes may play a role

81. Changing Patterns of Blood Flow in the Brain
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(a)
(b)
(c)
(d)
(all): © Niels A. Lassen, Copenhagen, Denmark

82. Cutaneous Blood Flow
The skin can tolerate the greatest fluctuations in blood flow.
The skin helps control body temperature in a changing environment by regulating blood flow = thermoregulation.
Increased blood flow to capillaries in the skin releases heat when body temperature increases.
Sweat is also produced to aid in heat loss.
Bradykinins in the sweat glands also stimulate vasodilation in the skin.

83. Cutaneous Blood Flow, cont
Vasoconstriction of arterioles keeps heat in the body when ambient temperatures are low.
This is aided by arteriovenous anastomoses, which shunt blood from arterioles directly to venules.
Cold temperatures activate sympathetic vasoconstriction.
This is tolerated due to decreased metabolic activity in the skin.

84. Cutaneous Blood Flow, cont
At average ambient temperatures, vascular resistance in the skin is high, and blood flow is low.
Sympathetic stimulation reduces blood flow further.
With continuous exercise, the need to regulate body temperature overrides this, and vasodilation occurs.

85. Sympathetic Stimulation, cont
May result in lowered total peripheral resistance if not for increased cardiac output
However, if a person exercises in very hot weather, he or she may experience extreme drops in blood pressure after reduced cardiac output.
This condition can be very dangerous.
Emotions can affect sympathetic activity and cause pallor or blushing

86. Circulation in the Skin
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Epidermis
Dermis
Capillary loop
Arteriovenous
anastomosis
Venule
Arteriole
Vein
Artery

87. VI. Blood Pressure

88. Blood Pressure
Affected by blood volume/stroke volume, total peripheral resistance, and cardiac rate
Increase in any of these will increase blood pressure.
Vasoconstriction of arterioles raises blood pressure upstream in the arteries.
Arterial blood = cardiac X total peripheral
pressure output resistance

89. Effect of Vasoconstriction on Blood Pressure
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Increased pressure
Decreased pressure
Constriction

90. Blood Pressure, cont
The blood pressure of blood vessels is related to the total cross-sectional area
Capillary blood pressure is low because of large total cross-sectional area.
Artery blood pressure is high because of small total cross-sectional area

91. Relationship between blood pressure and cross-sectional area of vessels
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5,000
4,000
3,000
Area (c2)
2,000
1,000
120
100 80
Pressure (mmHg) 60 40 20
Capillaries
Arterioles
Venules
Arteries
Veins
Aorta
Vena cava

92. Blood Pressure Regulation
Kidneys can control blood volume and thus stroke volume.
The sympathoadrenal system stimulates vasoconstriction of arterioles (raising total peripheral resistance) and increased cardiac output.

93. Baroreceptor Reflex
Activated by changes in blood pressure detected by baroreceptors (stretch receptors) in the aortic arch and carotid sinuses
Increased blood pressure stretches these receptors, increasing action potentials to the vasomotor and cardiac control centers in the medulla.
Most sensitive to drops in blood pressure
The vasomotor center controls vasodilation and constriction.
The cardiac center controls heart rate.

94. Effect of Blood Pressure on the Baroreceptor Response
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180
160
140
120
Action
potentials
Mean arterial pressure (mmHg)
100 80 60 40
Resting
potential
Time

95. Structures involved in the Baroreceptor Reflex
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Sensory neuron
Cerebrum
Sympathetic neuron
Carotid sinus
Parasympathetic neuron
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

96. Baroreceptor Reflex, cont
Fall in blood pressure = Increased sympathetic and decreased parasympathetic activity, resulting in increased heart rate and total peripheral resistance
Rise in BP has the opposite effects.
Good for quick beat-by-beat regulation like going from lying down to standing

97. Baroreceptor Reflex Going from laying to standing position Venous
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Going from laying
to standing position
Venous
return
End-diastolic
volume
Stroke
volume
Cardiac
output
Stimuli
Blood pressure
Sensor
Baroreceptors
Integrating center
Effector
Sensory neurons
Medulla oblongata
Sympathetic
Parasympathetic
Vasoconstriction
of arterioles
Cardiac
rate
Total peripheral
resistance
Cardiac
output
Negative feedback
response
Blood pressure

98. Atrial Stretch Reflexes
Activated by increased venous return to:
Stimulate reflex tachycardia
Inhibit ADH release; results in excretion of more urine
Stimulate secretion of atrial natriuretic peptide; results in excretion of more salts and water in urine

99. Blood Pressure Measurement
Measured in mmHg by an instrument called a sphygmomanometer.
A blood pressure cuff produces turbulent flow of blood in the brachial artery, which can be heard using a stethoscope; called sounds of Korotkoff.
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.

100. Blood Pressure Measurement, cont
The last Korotkoff sound is heard when the pressure in the cuff reaches diastolic pressure and a second reading can be taken.
The average blood pressure is 120/80.

101. Blood Flow & Korotkoff Sounds
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No sounds
First Korotkoff
sounds
Sounds at
every systole
Last Korotkoff
sounds
Cuff pressure = 140
Cuff pressure = 120
Cuff pressure = 100
Cuff pressure = 80
Systolic pressure
= 120 mmHg
Diastolic pressure
= 80 mmHg
Blood pressure = 120/80

102. Indirect, or Auscultatory, Method of Blood Pressure Measurement
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Cuff pressure
No flow
Turbulent flow
Laminar flow
120
mmHg
First
sound
Sound
Last
sound
Artery
silent
Artery
silent
Systole
Blood pressure
Diastole 80
mmHg

103. Five Phases of Blood Pressure Measurement
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Blood flows during
systole only
(turbulent flow)
systole and diastole
Blood flows during
(laminar flow)
No blood
flows
14 mmHg
20 mmHg
130
120
5 mmHg
110
5 mmHg
100 90 80 70 1 2 3 4 5
Silence
Snapping
sounds
Murmurs 60
Muffling
Silence
Thumping
Cuff pressure (mmHg)
Relative intensity of sounds

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

105. Mean Arterial Pressure
The average pressure in the arteries in one cardiac cycle is the mean arterial pressure.
This is significant because it is the difference between mean arterial pressure and venous pressure that drives the blood into the capillaries.
Calculated as:
diastolic pressure + 1/3 pulse pressure

106. VII. Hypertension, Shock, and Congestive Heart Failure

107. Hypertension Hypertension is high blood pressure.
Incidence increases with age
It can increase the risk of cardiac diseases, kidney diseases, and stroke.
Hypertension can be classified as “essential” or “secondary.”
Essential or primary hypertension is a result of complex and poorly understood processes
Secondary hypertension is a symptom of another disease, such as kidney disease.

108. Blood Pressure Classification in Adults

109. Possible Causes of Secondary Hypertension

110. Essential Hypertension
Most people fall in this category.
The cause is difficult to determine and may involve any of the following:
Increased salt intake coupled with decreased kidney filtering ability
Increased sympathetic nerve activity, increasing heart rate
Responses to paracrine regulators from the endothelium
Increased total peripheral resistance

111. Dangers of Hypertension
Vascular damage within organs, especially dangerous in the cerebral vessels and leading to stroke
Ventricular overload to eject blood due to abnormal hypertrophy, leading to arrhythmias and cardiac arrest
Contributes to the development of atherosclerosis

112. Treatments for Hypertension
Lifestyle modification: limit salt intake; limit smoking and drinking; lose weight; exercise
K+ (and possibly calcium) supplements
Diuretics to increase urine formation
Beta blockers to decrease cardiac rate
ACE inhibitors to block angiotensin II production

113. Mechanisms of Action of Selected Antihypertensive Drugs

114. Circulatory Shock
Occurs when there is inadequate blood flow to match oxygen usage in the tissues
Symptoms result from inadequate blood flow and how our circulatory system changes to compensate.
Sometimes shock leads to death.

115. Signs of Shock

116. Cardiovascular Reflexes to Compensate for Circulatory Shock

117. Hypovolemic Shock
Due to low blood volume from an injury, dehydration, or burns
Characterized by decreased cardiac output and blood pressure
Blood is diverted to the heart and brain at the expense of other organs.
Compensation includes baroreceptor reflex, which lowers blood pressure, raises heart rate, raises peripheral resistance, and produces cold, clammy skin and low urine output.

118. Septic Shock
Dangerously low blood pressure (hypotension) due to an infection (sepsis)
Bacterial toxins (endotoxins) induce NO production, causing widespread vasodilation.
Mortality rate is high (50−70%).

119. Other Causes of Circulatory Shock
Severe allergic reactions can cause anaphylactic shock due to production of histamine and resulting vasodilation.
Spinal cord injury or anesthesis can cause neurogenic shock due to loss of sympathetic stimulation.
Cardiac failure can cause cardiogenic shock due to significant myocardial loss.

120. Congestive Heart Failure
Occurs when cardiac output is not sufficient to maintain blood flow required by the body
Caused by myocardial infarction, congenital defects, hypertension, aortic valve stenosis, or disturbances in electrolyte levels (K+ and Ca2+)
Similar to hypovolemic shock in symptoms and response

121. Types of congestive heart failure
Left-side failure – raises left atrial pressure and produces pulmonary congestion and edema causing shortness of breath
Right-side failure – raises right atrial pressure and produces systemic congestion and edema