Page 0: Page 1: LOG O  Chapter 13 Heart and Circulation Page 2: Functions of the Circulatory System Transportation:  Respiratory: • Transport 02 and C02.  Nutritive: • Carry absorbed digestion products to liver and to tissues.  Excretory: • Carry metabolic wastes to kidneys to be excreted. Page 3: Functions of the Circulatory System (continued) Regulation:  Hormonal: • Carry hormones to target tissues to produce their effects.  Temperature: • Divert blood to cool or warm the body.  Protection: • Blood clotting.  Immune: • Leukocytes, cytokines and complement act against pathogens. Page 4: Components of Circulatory System Cardiovascular System (CV):  Heart: • Pumping action creates pressure head needed to push blood through vessels.  Blood vessels: • Permits blood flow from heart to cells and back to the heart. – Arteries, arterioles, capillaries, venules, veins. Lymphatic System:  Lymphatic vessels transport interstitial fluid. • Lymph nodes cleanse lymph prior to return in venous blood. Page 5: Composition of Blood Plasma:  Straw-colored liquid. • Consists of H20 and dissolved solutes. – Ions, metabolites, hormones, antibodies. » Na+ is the major solute of the plasma. Plasma proteins:  Constitute 7-9% of plasma. • Albumin: – Accounts for 60-80% of plasma proteins. – Provides the colloid osmotic pressure needed to draw H20 from interstitial fluid to capillaries. » Maintains blood pressure. Page 6: Composition of the Blood Plasma proteins (continued):  Globulins: a globulin: – Transport lipids and fat soluble vitamins. (continued) b globulin: – Transport lipids and fat soluble vitamins. g globulin: – Antibodies that function in immunity. Fibrinogen:  Constitutes 4% of plasma proteins.  Important clotting factor. • Converted into fibrin during the clotting process. Page 7: Composition of the Blood Serum:  Fluid from clotted blood. • Does not contain fibrinogen. (continued) Plasma volume:  Number of regulatory mechanisms in the body maintain homeostasis of plasma volume. • Osmoreceptors. • ADH. • Renin-angiotensin-aldosterone system. Page 8: Erythrocytes Flattened biconcave discs. Provide increased surface area through which gas can diffuse. Lack nuclei and mitochondria.  Half-life ~ 120 days. Each RBC contains 280 million hemoglobin with 4 heme chains (contain iron). Removed from circulation by phagocytic cells in liver, spleen, and bone marrow. Page 9: Leukocytes Contain nuclei and mitochondria. Move in amoeboid fashion.  Can squeeze through capillary walls (diapedesis). Almost invisible, so named after their staining properties.  Granular leukocytes: • Help detoxify foreign substances. – Release heparin.  Agranular leukocytes: • Phagocytic. – Produce antibodies. Page 10: Platelets (thrombocytes) Smallest of formed elements.  Are fragments of megakaryocytes.  Lack nuclei. Capable of amoeboid movement. Important in blood clotting:  Constitute most of the mass of the clot.  Release serotonin to vasoconstrict and reduce blood flow to area. Secrete growth factors:  Maintain the integrity of blood vessel wall. Survive 5-9 days. Page 11: Blood Cells and Platelets Page 12: Hematopoiesis Undifferentiated cells gradually differentiate to become stem cells, that form blood cells. Occurs in myeloid tissue (bone marrow of long bones) and lymphoid tissue. 2 types of hematopoiesis:  Erythropoiesis: • Formation of RBCs.  Leukopoiesis: • Formation of WBCs. Page 13: Erythropoiesis  Active process.  2.5 million RBCs are produced every second.  Primary regulator is erythropoietin.     Binds to membrane receptors of cells that will become erythroblasts. Erythroblasts transform into normoblasts. Normoblasts lose their nuclei to become reticulocytes. Reticulocytes change into mature RBCs. • Stimulates cell division.  Old RBCs are destroyed in spleen and liver.  Iron recycled back to myeloid tissue to be reused in hemoglobin production.  Need iron, vitamin B12 and folic acid for synthesis. Page 14: Leukopoiesis  Cytokines stimulate different types and stages of WBC production.  Multipotent growth factor-1, interleukin1, and interleukin-3:  Stimulate development of different types of WBC cells.  Granulocyte-colony stimulating factor (GCSF):  Stimulates development of neutrophils.  Granulocyte-monocyte colony stimulating factor (GM-CSF):  Simulates development of monocytes and eosinophils. Page 15: RBC Antigens and Blood Typing Each person’s blood type determines which antigens are present on their RBC surface. Major group of antigens of RBCs is the ABO system: Type AB: Type A: Only A antigens present.  Both A and B antigens present.   Type B: Only B antigens present.   Type O: Neither A or B antigens present.  Page 16: RBC Antigens and Blood Typing Each person inherits 2 genes that control the production of ABO groups.  (continued) Type A:   Type AB:  May have inherited A gene from each parent. May have inherited A gene from one parent and O gene from the other.   Inherited the A gene from one parent and the B gene from the other parent. Type O: Inherited O gene from each parent.  Type B: May have inherited B gene from each parent. May have inherited B gene from one parent and O gene from the other parent.  Page 17: Transfusion Reactions  If blood types do not match, the recipient’s antibodies attach to donor’s RBCs and agglutinate.  Type O:  Universal donor: • Lack A and B antigens. • Recipient’s antibodies cannot agglutinate the donor’s RBCs. Insert fig. 13.6  Type AB:  Universal recipient: • Lack the anti-A and anti-B antibodies.  Cannot agglutinate donor’s RBCs. Page 18: Rh Factor  Another group of antigens found on RBCs.  Rh positive:  Has Rho(D) antigens.  Rh negative:  Does not have Rho(D) antigens.  Significant when Rh- mother gives birth to Rh+ baby.  At birth, mother may become exposed to Rh+ blood of fetus. • Mother at subsequent pregnancies may produce antibodies against the Rh factor.  Erythroblastosis fetalis:  Rh- mother produces antibodies, which cross placenta. • Hemolysis of Rh+ RBCs in the fetus. Page 19: Blood Clotting Function of platelets:  Platelets normally repelled away from endothelial lining by prostacyclin (prostaglandin). • Do not want to clot normal vessels. Damage to the endothelium wall:  Exposes subendothelial tissue to the blood. Page 20: Blood Clotting Platelet release reaction:  Endothelial cells secrete von Willebrand factor to cause platelets to adhere to collagen.  When platelets stick to collagen, they degranulate as platelet secretory granules: • Release ADP, serotonin and thromboxane A2. – Serotonin and thromboxane A2 stimulate vasoconstriction. – ADP and thromboxane A2 make other platelets “sticky.” » Platelets adhere to collagen. » Stimulates the platelet release reaction. (continued) • Produce platelet plug. – Strengthened by activation of plasma clotting factors. Page 21: Blood Clotting (continued) Platelet plug strengthened by fibrin. Clot reaction:  Contraction of the platelet mass forms a more compact plug.  Conversion of fibrinogen to fibrin occurs. Conversion of fibrinogen to fibrin:  Intrinsic Pathway: • Initiated by exposure of blood to a negatively charged surface (collagen). – This activates factor XII (protease), which activates other clotting factors. • Ca2+ and phospholipids convert prothrombin to thrombin. – Thrombin converts fibrinogen to fibrin. » Produces meshwork of insoluble fibrin polymers. Page 22: Blood Clotting (continued) Extrinsic pathway:  Thromboplastin is not a part of the blood, so called extrinsic pathway.  Damaged tissue releases thromboplastin. • Thromboplastin initiates a short cut to formation of fibrin. Page 23: Blood Clotting (continued) Page 24: Dissolution of Clots Activated factor XII converts an inactive molecule into the active form (kallikrein).  Kallikrein converts plasminogen to plasmin. Plasmin is an enzyme that digests the fibrin.  Clot dissolution occurs. Anticoagulants:  Heparin: • Activates antithrombin III.  Coumarin: • Inhibits cellular activation of vitamin K. Page 25: Acid-Base Balance in the Blood Blood pH is maintained within a narrow range by lungs and kidneys. Normal pH of blood is 7.35 to 7.45. Some H+ is derived from carbonic acid. H20 + C02 H2C03 H+ + HC03- Page 26: Acid-Base Balance in the Blood Types of acids in the body:  Volatile acids: • Can leave solution and enter the atmosphere as a gas. – Carbonic acid. (continued) H20 + C02 H2C03  Nonvolatile acids: H+ + HC03- • Acids that do not leave solution. – Byproducts of aerobic metabolism, during anaerobic metabolism and during starvation. – Sulfuric and phosphoric acid. Page 27: Buffer Systems Provide or remove H+ and stabilize the pH. Include weak acids that can donate H+ and weak bases that can absorb H+ . HC03- is the major buffer in the plasma. H+ + HC03- H2C03 Under normal conditions excessive H+ is eliminated in the urine. Page 28: Acid Base Disorders Respiratory acidosis:  Hypoventilation. • Accumulation of CO2. – pH decreases. Metabolic acidosis:  Gain of fixed acid or loss of HCO3-. • Plasma HCO3- decreases. – pH decreases. Respiratory alkalosis:  Hyperventilation. • Excessive loss of CO2. – pH increases. Metabolic alkalosis:  Loss of fixed acid or gain of HCO3-. • Plasma HCO3- increases. – pH increases. Page 29: pH Normal pH is obtained when the ratio of HCO3- to C02 is 20:1. Henderson-Hasselbalch equation: pH = 6.1 + log = [HCO3-] [0.03PC02] Page 30: Pulmonary and Systemic Circulations  Pulmonary circulation:  Path of blood from right ventricle through the lungs and back to the heart.  Systemic circulation:  Oxygen-rich blood pumped to all organ systems to supply nutrients.  Rate of blood flow through systemic circulation = flow rate through pulmonary Page 31: Atrioventricular and Semilunar Valves Atria and ventricles are separated into 2 functional units by a sheet of connective tissue by AV (atrioventricular) valves.  One way valves.  Allow blood to flow from atria into the ventricles. At the origin of the pulmonary artery and aorta are semilunar valves.  One way valves.  Open during ventricular contraction. Opening and closing of valves occur as a result of pressure differences. Page 32: Atrioventricular and Semilunar Valves Page 33: Cardiac Cycle Refers to the repeating pattern of contraction and relaxation of the heart.  Systole: • Phase of contraction.  Diastole: • Phase of relaxation.  End-diastolic volume (EDV): • Total volume of blood in the ventricles at the end of diastole.  Stroke volume (SV): • Amount of blood ejected from ventricles during systole.  End-systolic volume (ESV): • Amount of blood left in the ventricles at the end of Page 34: Cardiac Cycle  Step 1: Isovolumetric contraction: (continued)  QRS just occurred.  Contraction of the ventricle causes ventricular pressure to rise above atrial pressure. • AV valves close.  Ventricular pressure is less than aortic pressure. • Semilunar valves are closed. – Volume of blood in ventricle is EDV.  Step 2: Ejection:  Contraction of the ventricle causes ventricular pressure to rise above aortic pressure. • Semilunar valves open.  Ventricular pressure is greater than atrial pressure. • AV valves are closed. – Volume of blood ejected: SV. Page 35: Cardiac Cycle Step 3: T wave occurs:  Ventricular pressure drops below aortic pressure. (continued) Step 4: Isovolumetric relaxation:  Back pressure causes semilunar valves to close. • AV valves are still closed. – Volume of blood in the ventricle: ESV. Step 5: Rapid filling of ventricles:  Ventricular pressure decreases below atrial pressure. • AV valves open. – Rapid ventricular filling occurs. Page 36: Cardiac Cycle Step 6: Atrial systole:  P wave occurs.  Atrial contraction. • Push 10-30% more blood into the ventricle. (continued) Page 37: Heart Sounds  Closing of the AV and semilunar valves.  Lub (first sound):  Produced by closing of the AV valves during isovolumetric contraction.  Dub (second sound):  Produced by closing of the semilunar valves when pressure in the ventricles falls below pressure in the arteries. Page 38: Heart Murmurs  Abnormal heart sounds produced by abnormal patterns of blood flow in the heart.  Defective heart valves:  Valves become damaged by antibodies made in response to an infection, or congenital defects.  Mitral stenosis:  Mitral valve becomes thickened and calcified. • Impairs blood flow from left atrium to left ventricle. • Accumulation of blood in left ventricle may cause pulmonary HTN.  Incompetent valves:  Damage to papillary muscles. • Valves do not close properly. – Murmurs produced as blood regurgitates through valve flaps. Page 39: Heart Murmurs Septal defects:  Usually congenital. • Holes in septum between the left and right sides of the heart. • May occur either in interatrial or interventricular septum.  Blood passes from left to right. Page 40: Electrical Activity of the Heart  SA node:  Demonstrates automaticity: • Functions as the pacemaker.  Spontaneous depolarization (pacemaker potential): • Spontaneous diffusion caused by diffusion of Ca2+ through slow Ca2+ channels. – Cells do not maintain a stable RMP. Page 41: Pacemaker Action Potential Depolarization:  VG fast Ca2+ channels open. • Ca2+ diffuses inward.  Opening of VG Na+ channels may also contribute to the upshoot phase of the AP. Repolarization:  VG K+ channels open. • K+ diffuses outward. Ectopic pacemaker:  Pacemaker other than SA node: • If APs from SA node are prevented from reaching these areas, these cells will generate pacemaker potentials. Page 42: Myocardial Action Potentials Majority of myocardial cells have a RMP of –90 mV. SA node spreads APs to myocardial cells.  When myocardial cell reaches threshold, these cells depolarize. Rapid upshoot occurs:  VG Na+ channels open. • Inward diffusion of Na+. Plateau phase:  Rapid reversal in membrane polarity to –15 mV. • VG slow Ca2+ channels open. – Slow inward flow of Ca2+ balances outflow of K+. Page 43: Myocardial APs (continued)  Rapid repolarization:  VG K+ channels open.  Rapid outward diffusion of K+. Page 44: Conducting Tissues of the Heart APs spread through myocardial cells through gap junctions. Impulses cannot spread to ventricles directly because of fibrous tissue. Conduction pathway:     SA node. AV node. Bundle of His. Purkinje fibers. Stimulation of Purkinje fibers cause both ventricles to contract simultaneously. Page 45: Conducting Tissues of the Heart (continued) Page 46: Conduction of Impulse APs from SA node spread quickly at rate of 0.8 - 1.0 m/sec. Time delay occurs as impulses pass through AV node.  Slow conduction of 0.03 – 0.05 m/sec. Impulse conduction increases as spread to Purkinje fibers at a velocity of 5.0 m/sec.  Ventricular contraction begins 0.1–0.2 sec. after contraction of the atria. Page 47: Refractory Periods  Heart contracts as syncytium.  Contraction lasts almost 300 msec.  Refractory periods last almost as long as contraction.  Myocardial muscle cannot be stimulated to contract again until it has relaxed. Page 48: Excitation-Contraction Coupling in Heart Muscle Depolarization of myocardial cell stimulates opening of VG Ca2+ channels in sarcolema.  Ca2+ diffuses down gradient into cell. • Stimulates opening of Ca2+-release channels in SR.  Ca2+ binds to troponin and stimulates contraction (same mechanisms as in skeletal muscle). During repolarization Ca2+ actively transported out of the cell via a Na +Ca2+- exchanger. Page 49: Electrocardiogram (ECG/EKG) The body is a good conductor of electricity.  Tissue fluids have a high [ions] that move in response to potential differences. Electrocardiogram:  Measure of the electrical activity of the heart per unit time. • Potential differences generated by heart are conducted to body surface where they can be recorded on electrodes on the skin. Does NOT measure the flow of blood through the heart. Page 50: ECG Leads  Bipolar leads:  Record voltage between electrodes placed on wrists and legs.  Right leg is ground.  Unipolar leads:  Voltage is recorded between a single “exploratory electrode” placed on body and an electrode built into the electrocardiograph.  Placed on right arm, left arm, left leg, and chest. • Allow to view the changing pattern of electrical activity from different perspectives. Page 51: ECG P wave:  Atrial depolarization. QRS complex:  Ventricular depolarization.  Atrial repolarization. T wave:  Ventricular repolarization. Page 52: Correlation of ECG with Heart Sounds  First heart sound:  Produced immediately after QRS wave.  Rise of intraventricular pressure causes AV valves to close.  Second heart sound:  Produced after T wave begins.  Fall in intraventricular pressure causes semilunar valves to close. Page 53: Systemic Circulation Arteries. Arterioles. Capillaries. Venules. Veins. Role is to direct the flow of blood from the heart to the capillaries, and back to the heart. Page 54: Blood Vessels Walls composed of 3 “tunics:”  Tunica externa: • Outer layer comprised of connective tissue.  Tunica media: • Middle layer composed of smooth muscle.  Tunica interna: • Innermost simple squamous endothelium. • Basement membrane. • Layer of elastin. Page 55: Blood Vessels Elastic arteries: (continued)  Numerous layers of elastin fibers between smooth muscle. • Expand when the pressure of the blood rises. – Act as recoil system when ventricles relax. Muscular arteries:  Are less elastic and have a thicker layer of smooth muscle.  Diameter changes slightly as BP raises and falls. Arterioles:  Contain highest % smooth muscle. • Greatest pressure drop. – Greatest resistance to flow. Page 56: Blood Vessels Most of the blood volume is contained in the venous system.  Venules: • Formed when capillaries unite. – Very porous. (continued)  Veins: • Contain little smooth muscle or elastin. – Capacitance vessels (blood reservoirs). • Contain 1-way valves that ensure blood flow to the heart. Skeletal muscle pump and contraction of diaphragm:  Aid in venous blood return of blood to the heart. Page 57: Types of Capillaries  Capillaries:  Smallest blood vessels. • 1 endothelial cell thick. – Provide direct access to cells. » Permits exchange of nutrients and wastes.  Continuous: • Adjacent endothelial cells tightly joined together. – Intercellular channels that permit passage of molecules (other than proteins) between capillary blood and tissue fluid. » Muscle, lungs, and adipose tissue.  Fenestrated: • Wide intercellular pores. – Provides greater permeability. » Kidneys, endocrine glands, and intestines.  Discontinuous (sinusoidal): • Have large, leaky capillaries. – Liver, spleen, and bone marrow. Page 58: Atherosclerosis Most common form of arteriosclerosis (hardening of the arteries). Mechanism of plaque production:  Begins as a result of damage to endothelial cell wall. • HTN, smoking, high cholesterol, and diabetes.  Cytokines are secreted by endothelium; platelets, macrophages, and lymphocytes. • Attract more monocytes and lymphocytes. Page 59: Atherosclerosis  Monocytes become macrophages. • Engulf lipids and transform into foam cells. (continued)  Smooth muscle cells synthesize connective tissue proteins. • Smooth muscle cells migrate to tunica interna, and proliferate forming fibrous plaques. Page 60: Cholesterol and Plasma Lipoproteins High blood cholesterol associated with risk of atherosclerosis. Lipids are carried in the blood attached to protein carriers. Cholesterol is carried to the arteries by LDLs (low-density lipoproteins).  LDLs are produced in the liver. • LDLs are small protein-coated droplets of cholesterol, neutral fat, free fatty acids, and phospholipids. Page 61: Cholesterol and Plasma Lipoproteins (continued) Cells in various organs contain receptors for proteins in LDL.  LDL protein attaches to receptors. • The cell engulfs the LDL and utilizes cholesterol for different purposes. • LDL is oxidized and contributes to: – Endothelial cell injury. – Migration of monocytes and lymphocytes to tunica interna. – Conversion of monocytes to macrophages.  Excessive cholesterol is released from the cells. • Travel in the blood as HDLs (high-density lipoproteins), and removed by the liver. – Artery walls do not have receptors for HDL. Page 62: Ischemic Heart Disease  Ischemia:  Oxygen supply to tissue is deficient. • Most common cause is atherosclerosis of coronary arteries.  Increased [lactic acid] produced by anaerobic respiration.  Angina pectoris:  Substernal pain.  Myocardial infarction (MI):  Changes in T segment of ECG.  Increased CPK and LDH. Page 63: Arrhythmias Detected on ECG  Arrhythmias:  Abnormal heart rhythms.  Flutter:  Extremely rapid rates of excitation and contraction of atria or ventricles. • Atrial flutter degenerates into atrial fibrillation.  Fibrillation:  Contractions of different groups of myocardial cells at different times. • Coordination of pumping impossible. – Ventricular fibrillation is life-threatening. Page 64: Arrhythmias Detected on ECG  Bradycardia:  HR slower < 60 beats/min. (continued)  Tachycardia:  HR > 100 beats/min.  First–degree AV nodal block:  Rate of impulse conduction through AV node exceeds 0.2 sec. • P-R interval.  Second-degree AV nodal block:  AV node is damaged so that only 1 out of 2-4 atrial APs can pass to the ventricles. • P wave without QRS. Page 65: Arrhythmias Detected on ECG Third-degree (complete) AV nodal block:  None of the atrial waves can pass through the AV node.  Ventricles paced by ectopic pacemaker. (continued) Page 66: Lymphatic System 3 basic functions:  Transports interstitial (tissue) fluid back to the blood.  Transports absorbed fat from small intestine to the blood.  Helps provide immunological defenses against pathogens. Page 67: Lymphatic System  Lymphatic capillaries:  Closed-end tubules that form vast networks in intercellular spaces. (continued)  Lymph:  Fluid that enters the lymphatic capillaries. • Lymph carried from lymph capillaries, to lymph ducts, and then to lymph nodes.  Lymph nodes filter the lymph before returning it to the veins. Page 68: