Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Introduction to the Cardiovascular System A circulating transport system – A pump (the heart) – A conducting system (blood vessels) – A fluid medium (blood) Is specialized fluid of connective tissue Contains cells suspended in a fluid matrix © 2012 Pearson Education, Inc.

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Introduction to the Cardiovascular System To transport materials to and from cells – Oxygen and carbon dioxide – Nutrients – Hormones – Immune system components – Waste products © 2012 Pearson Education, Inc.

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings Physical Characteristics of Blood 38°C (100.4°F) is normal temperature High viscosity Slightly alkaline pH (7.35–7.45) Blood volume (liters) = 7% of body weight (kg) – Adult male: 5 to 6 liters – Adult female: 4 to 5 liters © 2012 Pearson Education, Inc.

Figure 19-1 The Composition of Whole Blood Plasma Proteins Other Solutes Water Platelets White Blood Cells Red Blood Cells Plasma Formed Elements 46–63% 37–54% 7% 1% 92% <.1% 99.9% p. 641

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc.

Figure The Origins and Differentiation of Formed Elements Blast Cells Progenitor Cells Lymphoid Stem Cells Myeloid Stem Cells Hemocytoblasts Red bone marrow Proerythroblast Erythroblast stages Ejection of nucleus Reticulocyte Erythrocyte Red Blood Cells (RBCs) Megakaryocyte Platelets Myelocytes Band Cells Agranulocytes Monoblast Promonocyte Monocyte Lymphoblast Prolymphocyte Lymphocyte Myeloblast BasophilEosinophil Neutrophil Granulocytes White Blood Cells (WBCs) p. 659

© 2012 Pearson Education, Inc. Figure 19-2a The Anatomy of Red Blood Cells Blood smear When viewed in a standard blood smear, RBCs appear as two-dimensional objects, because they are flattened against the surface of the slide. LM  477 p. 644

© 2012 Pearson Education, Inc. Figure 19-2b The Anatomy of Red Blood Cells Red blood cells The three-dimensional shape of RBCs SEM  1838 p. 644

© 2012 Pearson Education, Inc. Figure 19-2c The Anatomy of Red Blood Cells A sectional view of a mature RBC, showing the normal ranges for its dimensions 0.45–1.16 μm 2.31–2.85 μm 7.2–8.4 μm p. 644

© 2012 Pearson Education, Inc. Figure 19-2d The Anatomy of Red Blood Cells Sectioned capillaries Red blood cell (RBC) Rouleau (stacked RBCs) Nucleus of endothelial cell Blood vessels (viewed in longitudinal section) When traveling through relatively narrow capillaries, RBCs may stack like dinner plates. LM  1430 p. 644

© 2012 Pearson Education, Inc. Figure 19-3 The Structure of Hemoglobin Hemoglobin molecule Heme  chain 2  chain 2  chain 1  chain 1 p. 645

© 2012 Pearson Education, Inc. Figure 19-5 Recycling of Red Blood Cell Components Events Occurring in Macrophages Macrophages in liver, spleen, and bone marrow Heme Biliverdin Bilirubin Bilirubin bound to albumin in bloodstream Amino acids Liver Bilirubin Excreted in bile Urobilins, stercobilins Events Occurring in the LiverEvents Occurring in the Large Intestine Eliminated in feces Absorbed into the circulation Events Occurring in the Kidney Eliminated in urine Urobilins Kidney Hb Hemoglobin that is not phagocytized breaks down, and the alpha and beta chains are eliminated in urine. Fe 2+ Fe 2+ transported in circulation by transferrin 90% 10% Old and damaged RBCs Average life span of RBC is 120 days In the bloodstream, the rupture of RBCs is called hemolysis. New RBCs released into circulation RBC formation Events Occurring in the Red Bone Marrow p. 647

© 2012 Pearson Education, Inc. Figure White Blood Cells LM  1500 Neutrophil LM  1500 Eosinophil Basophil Monocyte Lymphocyte RBC p. 656

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings © 2012 Pearson Education, Inc. p. 659

© 2012 Pearson Education, Inc. Figure The Vascular, Platelet, and Coagulation Phases of Hemostasis and Clot Retraction (Step 1) Vascular Phase The vascular phase of hemostasis lasts for roughly 30 minutes after the injury occurs. The endothelial cells contract and release endothelins which stimulate smooth muscle contraction and endothelial division. The endothelial cells become “sticky” and adhere to platelets and each other. Knife blade Blood vessel injury Vascular spasm p. 662

© 2012 Pearson Education, Inc. Figure The Vascular, Platelet, and Coagulation Phases of Hemostasis and Clot Retraction (Step 2) Platelet Phase The platelet phase of hemostasis begins with the attachment of platelets to sticky endothelial surfaces, to the basement membrane, to exposed collagen fibers, and to each other. As they become activated, platelets release a variety of chemicals that promote aggregation, vascular spasm, clotting, and vessel repair. Release of chemicals (ADP, PDGF, Ca 2+, platelet factors) Plasma in vessel lumen Platelet adhesion to damaged vessel Platelet aggregation Endothelium Basement membrane Vessel wall Contracted smooth muscle cells Platelet plug may form Interstitial fluid Cut edge of vessel wall p. 662

© 2012 Pearson Education, Inc. Figure The Vascular, Platelet, and Coagulation Phases of Hemostasis and Clot Retraction (Step 3) Coagulation Phase Coagulation, or blood clotting, involves a complex sequence of steps leading to the conversion of circulating fibrinogen into the insoluble protein fibrin. As the fibrin network grows, blood cells and additional platelets are trapped in the fibrous tangle, forming a blood clot that seals off the damaged portion of the vessel. Prothrombin Prothrombinase Factor X Tissue factor complex Tissue factor (Factor III) Tissue damage Contracted smooth muscle cells Platelet factor (PF-3) Fibrinogen Fibrin Thrombin Clotting factor (VII) Common Pathway Extrinsic Pathway Ca 2+ Intrinsic Pathway Factor X activator complex Clotting factors (VIII, IX) Activated proenzymes (usually Factor XII) Blood clot containing trapped RBCs SEM  1200 Ca 2+ p. 663

© 2012 Pearson Education, Inc. Figure 19-7a Blood Types and Cross-Reactions Type A Type B Type A blood has RBCs with surface antigen A only. Type B blood has RBCs with surface antigen B only. Surface antigen A Surface antigen B If you have Type A blood, your plasma contains anti-B antibodies, which will attack Type B surface antigens. If you have Type B blood, your plasma contains anti-A antibodies, which will attack Type A surface antigens. p. 651

© 2012 Pearson Education, Inc. Figure 19-7a Blood Types and Cross-Reactions Type AB Type O Type AB blood has RBCs with both A and B surface antigens. Type O blood has RBCs lacking both A and B surface antigens. If you have Type AB blood, your plasma has neither anti-A nor anti-B antibodies. If you have Type O blood, your plasma contains both anti-A and anti-B antibodies. p. 651

© 2012 Pearson Education, Inc. Figure 19-7b Blood Types and Cross-Reactions In a cross-reaction, antibodies react with their target antigens causing agglutination and hemolysis of the affected RBCs. Surface antigens Opposing antibodies RBC Agglutination (clumping) Hemolysis p. 651

© 2012 Pearson Education, Inc. Figure 19-9 Hemolytic Disease of the Newborn Problems seldom develop during a first pregnancy, because very few fetal cells enter the maternal circulation then, and thus the mother’s immune system is not stimulated to produce anti-Rh antibodies. Fetal blood supply and tissue Maternal blood supply and tissue During First Pregnancy Placenta The most common form of hemolytic disease of the newborn develops after an Rh – woman has carried an Rh + fetus. Rh + fetus Rh – mother pp

© 2012 Pearson Education, Inc. Figure 19-9 Hemolytic Disease of the Newborn Exposure to fetal red blood cell antigens generally occurs during delivery, when bleeding takes place at the placenta and uterus. Such mixing of fetal and maternal blood can stimulate the mother’s immune system to produce anti-Rh antibodies, leading to sensitization. Hemorrhaging at Delivery Maternal blood supply and tissue Fetal blood supply and tissue Rh antigen on fetal red blood cells pp

© 2012 Pearson Education, Inc. Figure 19-9 Hemolytic Disease of the Newborn Roughly 20% of Rh – mothers who carried Rh + children become sensitized within 6 months of delivery. Because the anti-Rh antibodies are not produced in significant amounts until after delivery, a woman’s first infant is not affected. Maternal antibodies to Rh antigen Maternal blood supply and tissue Maternal Antibody Production pp

© 2012 Pearson Education, Inc. Figure 19-9 Hemolytic Disease of the Newborn In a subsequent pregnancy, the mother is sensitized to the Rh+ fetus. Therefore, the mother’s anti-Rh antibodies cross the placenta and attack the fetal red blood cells. During Second Pregnancy Fetal blood supply and tissue Maternal blood supply and tissue Maternal anti-Rh antibodies Rh + fetus Rh – mother Hemolysis of fetal RBCs pp

Copyright © 2009 Pearson Education, Inc., publishing as Pearson Benjamin Cummings