Copyright © 2008 Thomson Delmar Learning CHAPTER 5 The Anatomy and Physiology of the Circulatory System

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


THE BLOOD


Formed Elements of Blood

Table 5-1


)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


)


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


)

Cell Type—Eosinophils


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


)

Cell Type—Basophils

Table 5-1


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


)

Cell Type—Lymphocytes

Table 5-1


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


)

Cell Type—Monocytes

Table 5-1


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


)

Cell Type—Platelets

Table 5-1


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


Centrifuged Blood-Filled Capillary Tube

Fig. 5-1. A centrifuged blood-filled capillary tube.


Table 5-2

Normal Differential Count


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


THE HEART


The Heart

Fig. 5-2. (A) anterior view of the heart. (B) posterior view of the heart.


Anterior View of Heart

Fig. 5-2. (A) Anterior view of the heart.


Posterior View of Heart

Fig. 5-2. (B) posterior view of the heart.


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.


Layers of the Pericardium and Heart Wall

Fig. 5-4. The layers of the pericardium and the heart wall.


Cardiac Muscle Bundles

Fig. 5-5. View of the spiral and circular arrangement of the cardiac muscle bundles.


Coronary Circulation

Fig. 5-6. Coronary circulation. (A) Arterial vessels. (B) Venous vessels.


BLOOD FLOW THROUGH THE HEART


Chambers and Valves of the Heart

Fig. 5-7. Internal chambers and valves of the heart.


THE PULMONARY AND SYSTEMIC

VASCULAR SYSTEM


Pulmonary and Systemic Circulation

Fig. 5-8. Pulmonary and systemic circulation.


Neural Control and the Vascular System

Fig. 5-9. Neural control of the vascular system. Sympathetic neural fibers to the arterioles are especially abundant.


Components of the Pulmonary Blood Vessels

Fig. 1-29. Components of the pulmonary blood vessels.


THE BARORECEPTOR REFLEX


Location of the Arterial Baroreceptors

Fig. 5-10. Location of the arterial baroreceptors.


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


The Net Result

• Increased cardiac output• Increase in total peripheral resistance• Return of blood pressure to normal


PRESSURES IN THE PULMONARY AND

SYSTEMIC VASCULAR SYSTEMS


Types of Pressures Used to Study Blood Flow

• Intravascular • Transmural • Driving


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”


Transmural Pressure

• The difference between intravascular pressure of a vessel and pressure surrounding the vessel


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


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


Blood Pressures

Fig. 5-11. Types of blood pressures used to study blood flow.


THE CARDIAC CYCLE AND ITS EFFECT ON BLOOD PRESSURE


Sequence of Cardiac Contraction

Fig. 5-12. Sequence of cardiac contraction. (A) ventricular diastole and atrial systole. (B) ventricular systole and atrial diastole.


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.


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:


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:


Mean Intraluminal Blood Pressure

Fig. 5-14. Mean intraluminal blood pressure at various points in the pulmonary and systemic vascular systems.


Major Arterial Pulse Sites

Fig. 5-15. Major sites where an arterial pulse can be detected.


The Blood Volume and Its Effect on Blood Pressure

• Stroke Volume• Cardiac Output


Cardiac Output

• Cardiac output (CO) is calculated by multiplying the stroke volume (SV) by the heart rate (HR)


Example

• If the stroke volume is 70 mL, and the heart rate is 72 bpm, the cardiac output is:


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


Distribution of Pulmonary Blood Flow

• Gravity• Cardiac output• Pulmonary vascular resistance


GRAVITY



Fig. 5-16. Distribution of pulmonary blood flow. In the upright lung, blood flow steadily increases from the apex to the base.



Fig. 5-17. Blood flow normally moves into the gravity-dependent areas of the lungs. Erect (A), supine (B), lateral (C), upside-down (D).



Fig. 5-18. Relationship between gravity, alveolar pressure, pulmonary arterial pressure, and pulmonary venous pressure in different zones.


Determinants of Cardiac Output

• Ventricular Preload• Ventricular Afterload• Myocardial Contractility


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


Ventricular Preload Reflected In . . .

• Ventricular end-diastolic pressure (VEDP)– which, in essence, reflects the . . .

• Ventricular end-diastolic volume (VEDV)


Ventricular Preload

• As the VEDV increases or decreases . . . the VEDP . . . and, therefore, the cardiac output . . . increases or decreases, respectively.


Frank-Starling Curve

Fig. 5-19. Frank-Starling curve.


Appendix V—Cardiopulmonary Profile


Ventricular Afterload

• Ventricular afterload is defined as the force against which the ventricles must work to pump blood


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



• Arterial systolic blood pressure best reflects the ventricular afterload



• Blood pressure (BP) is a function of cardiac output (CO) times the systemic vascular resistance (SVR)


Myocardial Contractility

• Regarded as the force generated by the myocardium when the ventricular muscle fibers shorten



• In general, when the contractility of the heart increases or decreases

– Cardiac output increases or decreases respectively



• Positive inotropism – Increase in myocardial contractility

• Negative inotropism – Decrease in myocardial contractility


Vascular Resistance

• Circulatory resistance is approximated by dividing the mean arterial pressure (MAP) by the cardiac output (CO)


Vascular Resistance

• In general, when the vascular resistance increases:

– Blood pressure increases– In turn increases ventricular afterload


ACTIVE AND PASSIVE MECHANISMS


ACTIVE MECHANISMS AFFECTING VASCULAR

RESISTANCE


Active Mechanisms—Vascular Constriction (↑ Resistance)

• Abnormal Blood Gases– ↓ PO2 (Hypoxia)

– ↑ PCO2 (Hypercapnia)

– ↓ pH (Acidemia)


Active Mechanisms—Vascular Constriction (↑ Resistance)

• Pharmacologic Stimulation– Epinephrine– Norepinephrine– Dobutamine– Dopamine– Phenylephrine


Active Mechanisms—Vascular Dilation (↑ Resistance)

• Pharmacologic Stimulation– Oxygen– Isoproterenol– Aminophylline– Calcium-channel blocking


Active Mechanisms—Vascular Dilation (↑ Resistance)

• Pathologic Conditions– Vessel blockage/obstruction– Vessel wall disease– Vessel destruction– Vessel compression


PASSIVE MECHANISMS AFFECTING VASCULAR

RESISTANCE


Passive Mechanisms—Vascular Dilation (↑ Resistance)

• ↑ Pulmonary arterial pressure• ↑ Left atrial pressure


Pulmonary Arterial Pressure

Fig. 5-20. Increased mean pulmonary arterial pressure decreases pulmonary vascular resistance.


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.


Passive Mechanisms—Vascular Constriction (↑ Resistance)

• ↑ Lung volume (extreme)• ↓ Lung volume


Pulmonary Vessels During Inspiration

Fig. 5-22. Schematic illustration of pulmonary vessels during inspiration.



Fig. 5-23. Schematic drawing of the extra-alveolar “corner vessels” found at the junction of the alveolar septa.



Fig. 5-24. PVR is lowest near the FRC and increases at both high and low lung volumes.


Passive Mechanisms—Vascular Dilation (↑ Resistance)

• ↑ Blood volume


Passive Mechanisms—Vascular Constriction (↑ Resistance)

• ↑ Blood viscosity


Effects of Active and Passive Mechanisms on Vascular Resistance

Table 5-4.



↑ 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.




(VASCULAR (VASCULAR


ACTIVE MECHANISMS

Pathologic Conditions

Vessel blockage/obstruction X

Vessel wall disease X

Vessel destruction X

Vessel compression X

Table 5-4.




(VASCULAR (VASCULAR


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.


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?


Clinical Application 2 Discussion

• How did this case illustrate …– Ventricular afterload?– Ventricular contractility?– Ventricular preload?– Transmural pressure?

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Copyright © 2008 Thomson Delmar Learning CHAPTER 5 The Anatomy and Physiology of the Circulatory System