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Chapter 13 - PowerPoint PPT Presentation


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Chapter 13. Heart and Circulation. 13-1. Chapter 13 Outline Overview Blood Pulmonary & Systemic Circulations Heart Valves Cardiac Cycle Electrical Activity of the Heart Structure of Blood Vessels Heart Disease Lymphatic System . 13-2. Overview . 13-3.

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Chapter 13


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    1. Chapter 13 Heart and Circulation 13-1

    2. Chapter 13 Outline • Overview • Blood • Pulmonary & Systemic Circulations • Heart Valves • Cardiac Cycle • Electrical Activity of the Heart • Structure of Blood Vessels • Heart Disease • Lymphatic System 13-2

    3. Overview 13-3

    4. Functions of Circulatory System • Include transportation of respiratory gases, delivery of nutrients & hormones, & waste removal • Include roles in temperature regulation, clotting, & immune function 13-4

    5. Components of Circulatory System • Include cardiovascular & lymphaticsystems • Heart pumps blood thru cardiovascular system • Blood vessels carry blood from heart to cells & back • Includes arteries, arterioles, capillaries, venules, veins • Lymphatic system picks up excess fluid filtered out in capillary beds & returns it to veins • Its lymph nodes are part of immune system 13-5

    6. Blood 13-6

    7. Composition of Blood • Consists of formed elements (cells) suspended & carried in plasma (fluid part) • Total blood volume is about 5L • Plasma is straw-colored liquid consisting of H20 & dissolved solutes • Includes ions, metabolites, hormones, antibodies 13-7

    8. Plasma Proteins • Constitute 7-9% of plasma • Three types of plasma proteins: albumins, globulins, & fibrinogen • Albumin accounts for 60-80% • Creates colloid osmotic pressure that draws H20 from interstitial fluid into capillaries to maintain blood volume & pressure • Globulins carry lipids • Gamma globulins are antibodies • Fibrinogen serves as clotting factor • Converted to fibrin • Serum is fluid left when blood clots 13-8

    9. Formed Elements Fig 13.3 • Are erythrocytes (RBCs) & leukocytes (WBCs) • RBCs are flattened biconcave discs • Shape provides increased surface area for diffusion • Lack nuclei & mitochondria • Each RBC contains 280 million hemoglobins 13-9

    10. Leukocytes • Have nucleus, mitochondria, & amoeboid ability • Can squeeze through capillary walls (diapedesis) • Granular leukocytes help detoxify foreign substances & release heparin • Include eosinophils, basophils, & neutrophils Fig 13.3 13-10

    11. Leukocytes continued • Agranular leukocytes are phagocytic & produce antibodies • Include lymphocytes & monocytes Fig 13.3 13-11

    12. Platelets (thrombocytes) • Are smallest of formed elements, lack nucleus • Are fragments of megakaryocytes; amoeboid • Constitute most of mass of blood clots • Release serotonin to vasoconstrict & reduce blood flow to clot area • Secrete growth factors to maintain integrity of blood vessel wall • Survive 5-9 days Fig 13.3 13-12

    13. Hematopoiesis • Is formation of blood cells from stem cells in marrow (myeloid tissue) & lymphoid tissue • Erythropoiesis is formation of RBCs • Stimulated by erythropoietin (EPO) from kidney • Leukopoiesis is formation of WBCs • Stimulated by variety of cytokines • = autocrine regulators secreted by immune system 13-13

    14. Erythropoiesis • 2.5 million RBCs are produced/sec • Lifespan of 120 days • Old RBCs removed from blood by phagocytic cells in liver, spleen, & bone marrow • Iron recycled back into hemoglobin production Fig 13.4 13-14

    15. RBC Antigens & Blood Typing • Antigens present on RBC surface specify blood type • Major antigen group is ABOsystem • Type A blood has only A antigens • Type B has only B antigens • Type AB has both A & B antigens • Type O has neither A or B antigens 13-15

    16. Transfusion Reactions • People with Type A blood make antibodies to Type B RBCs, but not to Type A • Type B blood has antibodies to Type A RBCs but not to Type B • Type AB blood doesn’t have antibodies to A or B • Type O has antibodies to both Type A & B • If different blood types are mixed, antibodies will cause mixture to agglutinate Fig 13.5 13-16

    17. Transfusion Reactions continued • If blood types don't match, recipient’s antibodies agglutinate donor’s RBCs • Type O is “universal donor” because lacks A & B antigens • Recipient’s antibodies won’t agglutinate donor’s Type O RBCs • Type AB is “universal recipient” because doesn’t make anti-A or anti-B antibodies • Won’t agglutinate donor’s RBCs • Insert fig. 13.6 Fig 13.6 13-17

    18. Rh Factor • Is another type of antigen found on RBCs • Rh+ has Rho(D) antigens; Rh- does not • Can cause problems when Rh- mother has Rh+ babies • At birth, mother may be exposed to Rh+ blood of fetus • In later pregnancies mom may produce Rh antibodies • In Erythroblastosis fetalis, this happens & antibodies cross placenta causing hemolysis of fetal RBCs 13-18

    19. Hemostasis • Is cessation of bleeding • Promoted by reactions initiated by vessel injury: • Vasoconstriction restricts blood flow to area • Platelet plug forms • Plug & surroundings are infiltrated by web of fibrin, forming clot 13-19

    20. Role of Platelets • Platelets don't stick to intact endothelium because of presence of prostacyclin (PGI2--a prostaglandin) & NO • Keep clots from forming & are vasodilators Fig 13.7a 13-20

    21. Role of Platelets • Damage to endothelium allows platelets to bind to exposed collagen • von Willebrand factor increases bond by binding to both collagen & platelets • Platelets stick to collagen & release ADP, serotonin, & thromboxane A2 • = platelet release reaction Fig 13.7b 13-21

    22. Role of Platelets continued • Serotonin & thromboxane A2 stimulate vasoconstriction, reducing blood flow to wound • ADP & thromboxane A2 cause other platelets to become sticky & attach & undergo platelet release reaction • This continues until platelet plug is formed Fig 13.7c 13-22

    23. Role of Fibrin • Platelet plug becomes infiltrated by meshwork of fibrin • Clot now contains platelets, fibrin & trapped RBCs • Platelet plug undergoes plug contraction to form more compact plug 13-23

    24. Conversion of Fibrinogen to Fibrin • Can occur via 2 pathways: • Intrinsic pathway clots damaged vessels & blood left in test tube • Initiated by exposure of blood to negatively charged surface of glass or blood vessel collagen • This activates factor XII (a protease) which initiates a series of clotting factors • Ca2+ & phospholipids convert prothrombin to thrombin • Thrombin converts fibrinogen to fibrin which polymerizes to form a mesh • Damage outside blood vessels releases tissuethromboplastin that triggers a clotting shortcut (= extrinsic pathway) 13-24

    25. Fig 13.9 13-25

    26. Dissolution of Clots • When damage is repaired, activated factor XII causes activation of kallikrein • Kallikrein converts plasminogen to plasmin • Plasmin digests fibrin, dissolving clot 13-26

    27. Anticoagulants • Clotting can be prevented by Ca+2 chelators (e.g. sodium citrate or EDTA) • or heparin which activates antithrombin III (blocks thrombin) • Coumarin blocks clotting by inhibiting activation of Vit K • Vit K works indirectly by reducing Ca+2 availability 13-27

    28. Pulmonary & Systemic Circulations 13-28

    29. Structure of Heart • Heart has 4 chambers • 2 atria receive blood from venous system • 2 ventricles pump blood to arteries • 2 sides of heart are 2 pumps separated by muscular septum Fig 13.10 13-29

    30. Structure of Heart continued • Between atria & ventricles is layer of dense connective tissue called fibrous skeleton • Which structurally & functionally separates the two • Myocardial cells of atria attach to top of fibrous skeleton & form 1 unit (or myocardium) • Cells from ventricles attach to bottom & form another unit • Fibrous skeleton also forms rings, the annuli fibrosi, to hold heart valves 13-30

    31. Pulmonary & Systemic Circulations • Blood coming from tissues enters superior & inferior vena cavae which empties into right atrium, then goes to right ventricle which pumps it through pulmonary arteries to lungs Fig 13.10 13-31

    32. Pulmonary & Systemic Circulations continued • Oygenated blood from lungs passes thru pulmonary veins to left atrium, then to left ventricle which pumps it through aorta to body Fig 13.10 13-32

    33. Pulmonary & Systemic Circulations continued • Pulmonary circulation is path of blood from right ventricle through lungs & back to heart • Systemic circulation is path of blood from left ventricle to body & back to heart • Rate of flow through systemic circulation = flow rate thru pulmonary circuit Fig 13.10 13-33

    34. Pulmonary & Systemic Circulations continued • Resistance in systemic circuit > pulmonary • Amount of work done by left ventricle pumping to systemic is 5-7X greater • Causing left ventricle to be more muscular (3-4X thicker) Fig 13.11 13-34

    35. Heart Valves 13-35

    36. Atrioventricular Valves • Blood flows from atria into ventricles thru 1-way atrioventricular (AV) valves • Between right atrium & ventricular is tricuspid valve • Between left atrium & ventricular is bicuspid or mitral valve Fig 13.11 13-36

    37. Atrioventricular Valves continued • Opening & closing of valves results from pressure differences • High pressure of ventricular contraction is prevented from everting AV valves by contraction of papillary muscles which are connected to AVs by chorda tendinea 13-37

    38. Semilunar Valves • During ventricular contraction blood is pumped through aortic & pulmonary semilunar valves • Close during relaxation Fig 13.11 13-38

    39. Cardiac Cycle 13-39

    40. Cardiac Cycle • Is repeating pattern of contraction & relaxation of heart • Systole refers to contraction phase • Diastole refers to relaxation phase • Both atria contract simultaneously; ventricles follow 0.1-0.2 sec later 13-40

    41. Cardiac Cycle • End-diastolic volume is volume of blood in ventricles at end of diastole • Stroke volume is amount of blood ejected from ventricles during systole • End-systolic volume is amount of blood left in ventricles at end of systole 13-41

    42. Cardiac Cycle continued • As ventricles begin contraction, pressure rises closing AV valves • Called isovolumetric contraction because all valves are closed • When pressure in ventricles exceeds that in aorta, semilunar valves open & ejection begins • As pressure in ventricle falls below that in aorta, back pressure closes semilunars • All valves are closed & ventricles undergo isovolumetricrelaxation • When pressure in ventricles falls below atria, AVs open & ventricles fill • Atrial systole sends its blood into ventricles 13-42

    43. Fig 13.14 13-43

    44. Heart Sounds • Closing of AV & semilunar valves produces sounds that can be heard thru stethoscope • Lub (1st sound) produced by closing of AV valves • Dup (2nd sound) produced by closing of semilunars 13-44

    45. Heart Murmurs • Are abnormal sounds produced by abnormal patterns of blood flow in heart • Many caused by defective heart valves • Can be of congenital origin • In rheumatic fever, damage can be from antibodies made in response to strep infection 13-45

    46. Heart Murmurs continued • In mitral stenosis, mitral valve becomes thickened & calcified, impairing blood flow from left atrium to left ventricle • Accumulation of blood in left ventricle can cause pulmonary hypertension • Valves are incompetent when don't close properly • Can be from damage to papillary muscles 13-46

    47. Heart Murmurs continued • Mumurs caused by septal defects are usually congenital • Due to holes in septum between left & right sides of heart • Pressure causes blood to pass from left to right Fig 13.16 13-47

    48. Electrical Activity of Heart 13-48

    49. Electrical Activity of Heart • Myocardial cells are short, branched, & interconnected by gap junctions • Entire muscle that forms a chamber is called a myocardium or functional syncitium • Because APs originating in any cell are transmitted to all others • Chambers separated by nonconductive tissue 13-49

    50. SA Node Pacemaker • In normal heart, SA node functions as pacemaker • Depolarizes spontaneously to threshold (= pacemaker potential) Fig 13.20 13-50