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Transcript of Copyright © 2008 Thomson Delmar Learning CHAPTER 5 The Anatomy and Physiology of the Circulatory...
Copyright © 2008 Thomson Delmar Learning
CHAPTER 5
The Anatomy and Physiology
of the Circulatory System
Copyright © 2008Thomson Delmar Learning
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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)Table 5-1
Cell Type Erythrocytes (Red Blood Cells, RBCs)
Description # of Cells/mm3 D & LS Function
Biconcave, 4-6 million D: 5-7 days Transport O2 & CO2 anucleate disc; DL: 100-120 salmon-colored; days diameter 7-8 microns
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)
Description # of Cells/mm3 D & LS Function
Nucleus multilobed; 3000-7000 D: 6-9 days Phagocytize inconspicuous; LS: 6 hours bacteria cytoplasmic; to a few diameter 10-14 days microns
Cell Type—Neutrophils
Table 5-1
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)
Cell Type—Eosinophils
Description # of Cells/mm3 D & LS Function
Nucleus multilobed; 100-400 D: 6-9 days Kills parasitic worms red cytoplasmic DL: 8-12 days destroy antigen- granules; antibody complexes; diameter 10-14 inactivate some microns inflammatory
chemical of allergy
Table 5-1
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)
Cell Type—Basophils
Table 5-1
Description # of Cells/mm3 D & LS Function
Nucleus lobed; 20-50 D: 3-7 days Release histamine large blue-purple DL: a few and other mediators cytoplasmic hours to a of inflammation; granules few days contains heparin,
an anticoagulant
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)
Cell Type—Lymphocytes
Table 5-1
Description # of Cells/mm3 D & LS Function
Nucleus spherical 1500-3000 D: days-wks Mount immune or indented; DL: hrs-yrs response by direct pale blue cell attack or via cytoplasm antibodies
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)
Cell Type—Monocytes
Table 5-1
Description # of Cells/mm3 D & LS Function
Nucleus U- or 100-700 D: 2-3 days Phagocytosis; kidney-shaped; DL: months develop into gray-blue macrophages cytoplasm; in tissues diameter 14-24 microns
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)
Cell Type—Platelets
Table 5-1
Description # of Cells/mm3 D & LS Function
Discoid cytoplasmic 250,000- D: 4-5 days Seals small tears fragments con- 500,000 DL: 5-10 in blood vessels; taining granules days instrumental in stain deep purple; blood clotting diameter 2-4 microns
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Centrifuged Blood-Filled Capillary Tube
Fig. 5-1. A centrifuged blood-filled capillary tube.
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Table 5-2
Normal Differential Count
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Chemical Composition of Plasma
Water Food Substance93% of plasma weight Amino acids
Glucose/carbohydratesProteins LipidsAlbumins Individual vitaminsGlobulinsFibrinogen Respiratory Gases
O2
Electrolytes CO2
Cations N2
Na+
K+ Individual Hormones Ca2+
Mg2+
Anions Waste Products Cl– Urea
PO43– Creatinine
SO42– Uric Acid
HCO3– Bilirubin
Table 5-3
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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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MAP = SBP + (2 x DBP)
3
= 120 + (2 x 80)
3
= 280
3
= 93 mm Hg
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:
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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
↑ RESISTANCE ↓ RESISTANCE
(VASCULAR (VASCULAR
CONSTRICTION) DILATION)
ACTIVE MECHANISMS
Pharmacologic Stimulations
Epinephrine X
Norepinephrine X
Dobutamine X
Dopamine X
Phenylephrine
Oxygen X
Isoproterenol X
Aminophylline X
Calcium-channel blocking agents X
Table 5-4.
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Effects of Active and Passive Mechanisms on Vascular Resistance
↑ RESISTANCE ↓ RESISTANCE
(VASCULAR (VASCULAR
CONSTRICTION) DILATION)
ACTIVE MECHANISMS
Pathologic Conditions
Vessel blockage/obstruction X
Vessel wall disease X
Vessel destruction X
Vessel compression X
Table 5-4.
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Effects of Active and Passive Mechanisms on Vascular Resistance
↑ RESISTANCE ↓ RESISTANCE
(VASCULAR (VASCULAR
CONSTRICTION) DILATION)
PASSIVE MECHANISMS
Pathologic Conditions
↑ Pulmonary arterial pressure X
↑ Left atrial pressure X
↑ Lung volume (extreme) X
↓ Lung volume X
↑ Blood volume X
↑ Blood viscosity X
Table 5-4.
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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?