CHAPTER 5
The Anatomy and Physiology
of the Circulatory System
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The Circulatory System
• Blood
• Heart
• Vascular System
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THE BLOOD
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Formed Elements of Blood
Table 5-1
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Cell Type Erythrocytes (Red Blood Cells, RBCs)
)
Description
# of Cells/mm3 D & LS
Biconcave,
4-6 million
anucleate disc;
salmon-colored;
diameter 7-8 microns
D: 5-7 days
DL: 100-120
days
Table 5-1
Function
Transport O2 & CO2
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Cell Type—Neutrophils
)
Description
# of Cells/mm3 D & LS
Function
Nucleus multilobed;
inconspicuous;
cytoplasmic;
diameter 10-14
microns
3000-7000
Phagocytize
bacteria
D: 6-9 days
LS: 6 hours
to a few
days
Table 5-1
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Cell Type—Eosinophils
)
Description
# of Cells/mm3 D & LS
Nucleus multilobed; 100-400
red cytoplasmic
granules;
diameter 10-14
microns
Table 5-1
Function
D: 6-9 days
Kills parasitic worms
DL: 8-12 days destroy antigenantibody complexes;
inactivate some
inflammatory
chemical of allergy
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Cell Type—Basophils
)
Description
# of Cells/mm3 D & LS
Function
Nucleus lobed;
large blue-purple
cytoplasmic
granules
20-50
Release histamine
and other mediators
of inflammation;
contains heparin,
an anticoagulant
D: 3-7 days
DL: a few
hours to a
few days
Table 5-1
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Cell Type—Lymphocytes
)
Description
# of Cells/mm3 D & LS
Function
Nucleus spherical
or indented;
pale blue
cytoplasm
1500-3000
Mount immune
response by direct
cell attack or via
antibodies
D: days-wks
DL: hrs-yrs
Table 5-1
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Cell Type—Monocytes
Table 5-1
)
Description
# of Cells/mm3
D & LS
Function
Nucleus U- or
kidney-shaped;
gray-blue
cytoplasm;
diameter 14-24
microns
100-700
D: 2-3 days
DL: months
Phagocytosis;
develop into
macrophages
in tissues
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Cell Type—Platelets
Table 5-1
)
Description
# of Cells/mm3
D & LS
Function
Discoid cytoplasmic
fragments containing granules
stain deep purple;
diameter 2-4
microns
250,000500,000
D: 4-5 days
DL: 5-10
days
Seals small tears
in blood vessels;
instrumental in
blood clotting
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Centrifuged Blood-Filled Capillary Tube
Fig. 5-1. A centrifuged bloodfilled capillary tube.
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Normal Differential Count
Table 5-2
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Chemical Composition of Plasma
Water
93% of plasma weight
Proteins
Albumins
Globulins
Fibrinogen
Electrolytes
Cations
Na+
K+
Ca2+
Mg2+
Anions
Cl–
PO43–
SO42–
HCO3–
Food Substance
Amino acids
Glucose/carbohydrates
Lipids
Individual vitamins
Table 5-3
Respiratory Gases
O2
CO2
N2
Individual Hormones
Waste Products
Urea
Creatinine
Uric Acid
Bilirubin
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THE HEART
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The Heart
Fig. 5-2. (A) anterior view of
the heart. (B) posterior view
of the heart.
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Anterior View of Heart
Fig. 5-2. (A) Anterior view of
the heart.
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Posterior View of Heart
Fig. 5-2. (B) posterior view of
the heart.
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Relationship of Heart to Other Body Parts
Fig. 5-3. (A) the relationship
of the heart to the sternum,
ribs, and diaphragm. (B)
Cross-sectional view showing
the relationship of the heart to
the thorax. (C) Relationship
of the heart to the lungs great
vessels.
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Layers of the Pericardium and Heart Wall
Fig. 5-4. The layers of the
pericardium and the heart
wall.
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Cardiac Muscle Bundles
Fig. 5-5. View of the spiral
and circular arrangement of
the cardiac muscle bundles.
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Coronary Circulation
Fig. 5-6. Coronary circulation.
(A) Arterial vessels.
(B) Venous vessels.
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BLOOD FLOW
THROUGH
THE HEART
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Chambers and Valves of the Heart
Fig. 5-7. Internal chambers
and valves of the heart.
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THE PULMONARY
AND SYSTEMIC
VASCULAR SYSTEM
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Pulmonary and Systemic Circulation
Fig. 5-8. Pulmonary and
systemic circulation.
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Neural Control and the Vascular System
Fig. 5-9. Neural control
of the vascular system.
Sympathetic neural fibers
to the arterioles are
especially abundant.
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Components of the Pulmonary Blood Vessels
Fig. 1-29. Components of the
pulmonary blood vessels.
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THE BARORECEPTOR
REFLEX
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Location of the Arterial Baroreceptors
Fig. 5-10. Location of the
arterial baroreceptors.
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Arterial Blood Pressure
• When arterial blood pressure decreases,
the baroreceptor reflex causes the
following to increase:
–
–
–
–
Heart Rate
Myocardial Force of Contraction
Arterial Constriction
Venous Constriction
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The Net Result
• Increased cardiac output
• Increase in total peripheral resistance
• Return of blood pressure to normal
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PRESSURES IN THE
PULMONARY AND
SYSTEMIC VASCULAR
SYSTEMS
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Types of Pressures Used to Study Blood Flow
• Intravascular
• Transmural
• Driving
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Intravascular Pressure
• The actual blood pressure in the lumen of
any vessel at any point, relative to the
barometric pressure
• Also known as “intraluminal pressure”
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Transmural Pressure
• The difference between intravascular
pressure of a vessel and pressure
surrounding the vessel
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Transmural Pressure
• Transmural pressure is positive when
the pressure inside the vessel exceeds
pressure outside the vessel, and
• Negative when the pressure inside
the vessel is less than the pressure
surrounding the vessel
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Driving Pressure
• The pressure difference between the
pressure at one point in a vessel and the
pressure at any other point downstream
in the vessel
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Blood Pressures
Fig. 5-11. Types of blood
pressures used to study
blood flow.
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THE CARDIAC CYCLE
AND ITS EFFECT ON
BLOOD PRESSURE
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Sequence of Cardiac Contraction
Fig. 5-12. Sequence of
cardiac contraction. (A)
ventricular diastole and atrial
systole. (B) ventricular
systole and atrial diastole.
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Systemic Circulation
Fig. 5-13. Summary of
diastolic and systolic
pressures in various
segments of the circulatory
system. Red vessels:
oxygenated blood. Blue
vessels: deoxygenated blood.
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Mean Arterial Blood Pressure (MAP)
• MAP can be estimated by measuring the
systolic blood pressure (SBP) and the
diastolic blood pressure (DBP) and using
the following formula:
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Mean Arterial Blood Pressure (MAP)
• For example, the mean arterial blood
pressure of the systemic system, which
has a SBP of 120 mm Hg and a DBP
of 80 mm Hg, would be calculated
as follows:
MAP = SBP + (2 x DBP)
3
= 120 + (2 x 80)
3
= 280
3
= 93 mm Hg
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Mean Intraluminal Blood Pressure
Fig. 5-14. Mean intraluminal
blood pressure at various
points in the pulmonary and
systemic vascular systems.
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Major Arterial Pulse Sites
Fig. 5-15. Major sites where
an arterial pulse can be
detected.
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The Blood Volume and Its Effect on Blood Pressure
• Stroke Volume
• Cardiac Output
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Cardiac Output
• Cardiac output (CO) is calculated by
multiplying the stroke volume (SV)
by the heart rate (HR)
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Example
• If the stroke volume is 70 mL, and
the heart rate is 72 bpm, the cardiac
output is:
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Cardiac Output and Blood Pressure
• Cardiac output directly influences blood
pressure. Thus,
– When either SV or HR increase, blood
pressure increases
– When either SV or HR decrease, blood
pressure decreases
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Distribution of Pulmonary Blood Flow
• Gravity
• Cardiac output
• Pulmonary vascular resistance
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GRAVITY
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Distribution of Pulmonary Blood Flow
Fig. 5-16. Distribution of
pulmonary blood flow. In
the upright lung, blood flow
steadily increases from the
apex to the base.
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Distribution of Pulmonary Blood Flow
Fig. 5-17. Blood flow
normally moves into the
gravity-dependent areas of
the lungs. Erect (A), supine
(B), lateral (C), upside-down
(D).
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Distribution of Pulmonary Blood Flow
Fig. 5-18. Relationship
between gravity, alveolar
pressure, pulmonary arterial
pressure, and pulmonary
venous pressure in different
zones.
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Determinants of Cardiac Output
• Ventricular Preload
• Ventricular Afterload
• Myocardial Contractility
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Ventricular Preload
• Ventricular preload
– Degree to which the myocardial fiber is
stretched prior to contraction (end-diastole)
• Within limits, the more myocardial fiber
is stretched during diastole (preload),
the more strongly it will contract
during systole
– Thus, the greater myocardial contractility
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Ventricular Preload Reflected In . . .
• Ventricular end-diastolic pressure (VEDP)
– which, in essence, reflects the . . .
• Ventricular end-diastolic volume (VEDV)
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Ventricular Preload
• As the VEDV increases or decreases . . .
the VEDP . . . and, therefore, the cardiac
output . . . increases or decreases,
respectively.
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Frank-Starling Curve
Fig. 5-19. Frank-Starling
curve.
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Appendix V—Cardiopulmonary Profile
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Ventricular Afterload
• Ventricular afterload is defined as the
force against which the ventricles must
work to pump blood
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Ventricular Afterload Directly Influenced By:
• Volume and viscosity of blood ejected
• Peripheral vascular resistance
• Total cross-sectional areas of the
vascular space into which blood
is ejected
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Ventricular Afterload
• Arterial systolic blood pressure best
reflects the ventricular afterload
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Ventricular Afterload
• Blood pressure (BP) is a function of
cardiac output (CO) times the systemic
vascular resistance (SVR)
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Myocardial Contractility
• Regarded as the force generated by the
myocardium when the ventricular muscle
fibers shorten
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Myocardial Contractility
• In general, when the contractility of the
heart increases or decreases
– Cardiac output increases or decreases
respectively
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Myocardial Contractility
• Positive inotropism
– Increase in myocardial contractility
• Negative inotropism
– Decrease in myocardial contractility
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Vascular Resistance
• Circulatory resistance is approximated by
dividing the mean arterial pressure (MAP)
by the cardiac output (CO)
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Vascular Resistance
• In general, when the vascular resistance
increases:
– Blood pressure increases
– In turn increases ventricular afterload
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ACTIVE AND PASSIVE
MECHANISMS
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ACTIVE MECHANISMS
AFFECTING VASCULAR
RESISTANCE
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Active Mechanisms—Vascular Constriction (↑ Resistance)
• Abnormal Blood Gases
– ↓ PO2
(Hypoxia)
– ↑ PCO2 (Hypercapnia)
– ↓ pH
(Acidemia)
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Active Mechanisms—Vascular Constriction (↑ Resistance)
• Pharmacologic Stimulation
– Epinephrine
– Norepinephrine
– Dobutamine
– Dopamine
– Phenylephrine
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Active Mechanisms—Vascular Dilation (↑ Resistance)
• Pharmacologic Stimulation
– Oxygen
– Isoproterenol
– Aminophylline
– Calcium-channel blocking
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Active Mechanisms—Vascular Dilation (↑ Resistance)
• Pathologic Conditions
– Vessel blockage/obstruction
– Vessel wall disease
– Vessel destruction
– Vessel compression
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PASSIVE MECHANISMS
AFFECTING VASCULAR
RESISTANCE
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Passive Mechanisms—Vascular Dilation (↑ Resistance)
• ↑ Pulmonary arterial pressure
• ↑ Left atrial pressure
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Pulmonary Arterial Pressure
Fig. 5-20. Increased mean
pulmonary arterial pressure
decreases pulmonary
vascular resistance.
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Pulmonary Vascular Resistance
Fig. 5-21. Schematic drawing
of the mechanisms that may
be activated to decrease
pulmonary vascular
resistance when the mean
pulmonary artery pressure
increases.
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Passive Mechanisms—Vascular Constriction (↑ Resistance)
• ↑ Lung volume (extreme)
• ↓ Lung volume
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Pulmonary Vessels During Inspiration
Fig. 5-22. Schematic
illustration of pulmonary
vessels during inspiration.
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Pulmonary Vascular Resistance
Fig. 5-23. Schematic drawing
of the extra-alveolar “corner
vessels” found at the junction
of the alveolar septa.
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Pulmonary Vascular Resistance
Fig. 5-24. PVR is lowest
near the FRC and increases
at both high and low lung
volumes.
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Passive Mechanisms—Vascular Dilation (↑ Resistance)
• ↑ Blood volume
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Passive Mechanisms—Vascular Constriction (↑ Resistance)
• ↑ Blood viscosity
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Effects of Active and Passive Mechanisms on
Vascular Resistance
Table 5-4.
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Effects of Active and Passive Mechanisms on
Vascular Resistance
Table 5-4.
↑ RESISTANCE
(VASCULAR
CONSTRICTION)
ACTIVE MECHANISMS
Pharmacologic Stimulations
Epinephrine
Norepinephrine
Dobutamine
Dopamine
Phenylephrine
Oxygen
Isoproterenol
Aminophylline
Calcium-channel blocking agents
↓ RESISTANCE
(VASCULAR
DILATION)
X
X
X
X
X
X
X
X
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Effects of Active and Passive Mechanisms on
Vascular Resistance
Table 5-4.
↑ RESISTANCE
(VASCULAR
CONSTRICTION)
ACTIVE MECHANISMS
Pathologic Conditions
Vessel blockage/obstruction
Vessel wall disease
Vessel destruction
Vessel compression
↓ RESISTANCE
(VASCULAR
DILATION)
X
X
X
X
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Effects of Active and Passive Mechanisms on
Vascular Resistance
Table 5-4.
↑ RESISTANCE
(VASCULAR
CONSTRICTION)
PASSIVE MECHANISMS
Pathologic Conditions
↑ Pulmonary arterial pressure
↑ Left atrial pressure
↑ Lung volume (extreme)
↓ Lung volume
↑ Blood volume
↑ Blood viscosity
↓ RESISTANCE
(VASCULAR
DILATION)
X
X
X
X
X
X
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Clinical Application 1 Discussion
• How did this case illustrate …
– Activation of the baroreceptor reflex?
– Hypovolemia and how it relates to preload?
– Negative transmural pressure?
– Effects of gravity on blood flow?
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Clinical Application 2 Discussion
• How did this case illustrate …
– Ventricular afterload?
– Ventricular contractility?
– Ventricular preload?
– Transmural pressure?
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