CHAPTER 5 The Anatomy and Physiology of the Circulatory System
The Circulatory System Blood Heart Vascular System
THE BLOOD
Formed Elements of Blood Table 5-1
Cell Type Erythrocytes (Red Blood Cells, RBCs) ) Table 5-1 Description # of Cells/mm 3 D & LS Function Biconcave, 4-6 million D: 5-7 days Transport O 2 & CO 2 anucleate disc; DL: 100-120 salmon-colored; days diameter 7-8 microns
Cell Type Neutrophils ) Table 5-1 Description # of Cells/mm 3 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 Eosinophils ) Table 5-1 Description # of Cells/mm 3 D & LS Function Nucleus multilobed; 100-400 D: 6-9 days Kills parasitic worms red cytoplasmic DL: 8-12 days destroy antigengranules; antibody complexes; diameter 10-14 inactivate some microns inflammatory chemical of allergy
Cell Type Basophils ) Table 5-1 Description # of Cells/mm 3 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
Cell Type Lymphocytes ) Table 5-1 Description # of Cells/mm 3 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
Cell Type Monocytes ) Table 5-1 Description # of Cells/mm 3 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
Cell Type Platelets ) Table 5-1 Description # of Cells/mm 3 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
Centrifuged Blood-Filled Capillary Tube Fig. 5-1. A centrifuged bloodfilled capillary tube.
Normal Differential Count Table 5-2
Chemical Composition of Plasma Water Food Substance 93% of plasma weight Amino acids Glucose/carbohydrates Proteins Lipids Albumins Individual vitamins Globulins Fibrinogen Respiratory Gases O 2 Table 5-3 Electrolytes CO 2 Cations N 2 Na + K + Ca 2+ Mg 2+ Anions Cl PO 3 4 SO 2 4 HCO 3 Individual Hormones Waste Products Urea Creatinine Uric Acid Bilirubin
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:
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) = 280 3 3 = 93 mm Hg
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
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.
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).
Distribution of Pulmonary Blood Flow 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
Ventricular Afterload Arterial systolic blood pressure best reflects the ventricular afterload
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
Myocardial Contractility In general, when the contractility of the heart increases or decreases Cardiac output increases or decreases respectively
Myocardial Contractility 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 PO 2 (Hypoxia) PCO 2 (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.
Pulmonary Vascular Resistance Fig. 5-23. Schematic drawing of the extra-alveolar corner vessels found at the junction of the alveolar septa.
Pulmonary Vascular Resistance 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.
Effects of Active and Passive Mechanisms on Vascular Resistance Table 5-4. RESISTANCE RESISTANCE (VASCULAR (VASCULAR CONSTRICTION) DILATION) ACTIVE MECHANISMS Pharmacologic Stimulations Epinephrine Norepinephrine Dobutamine Dopamine Phenylephrine Oxygen Isoproterenol Aminophylline Calcium-channel blocking agents X X X X X X X X
Effects of Active and Passive Mechanisms on Vascular Resistance Table 5-4. RESISTANCE RESISTANCE (VASCULAR (VASCULAR CONSTRICTION) DILATION) ACTIVE MECHANISMS Pathologic Conditions Vessel blockage/obstruction Vessel wall disease Vessel destruction Vessel compression X X X X
Effects of Active and Passive Mechanisms on Vascular Resistance Table 5-4. RESISTANCE RESISTANCE (VASCULAR (VASCULAR CONSTRICTION) DILATION) PASSIVE MECHANISMS Pathologic Conditions Pulmonary arterial pressure Left atrial pressure Lung volume (extreme) Lung volume Blood volume Blood viscosity X X X X X X
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?