Biol 215, Chapter 19 + 20 study guide
Biol 215, Chapter 19 + 20 study guide Biol 215
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Blood 19.1 Functions of Blood 1. Blood transports gases, nutrients, waste products, processed molecules, and regulatory molecules. 2. Blood is involved in the regulation of pH, osmosis, and body temperature. a. Bicarbonate buffer system. b. Maintenance of ion balance. c. Most body tissue pH is 7.357.45; body can typically function in range of 6.8 7.8 without irreversible damage. d. Acidemia: pH belpw 7.35 (acidic blood and tissues, increased H+ concentration). e. Alkalemia: pH above 7.45 (low H+ concentration). f. Most body heat is generated in the deep organs, especially the liver, brain, and heart, and in contraction of skeletal muscles. 3. Blood protects against disease and initiates tissue repair. a. White blood cells. b. Complement system. 4. Clot formation 19.2 Composition of Blood 1. Blood is a type of connective tissue that consists of plasma and formed elements. 2. Total blood volume in a male adult is 56 L and in female is 45 L. 19.3 Plasma 1. Liquid part of the blood a. Colloid: liquid containing suspended substances that don’t settle out of solution b. Colloidal osmotic pressure tends to pill fluid into the capillaries. 2. Plasma is mostly water (91%) and contains proteins, such as albumin (maintains osmotic pressure), globulins (function in transport and immunity), fibrinogen (involved in clot formation), and hormones and enzymes (involved in regulation). 3. Proteins: a. Albumins: viscosity, osmotic pressure, buffer, transports fatty acids, free bilirubin, thyroid hormones. i. 58% of plasma protein; maintains colloidal osmotic pressure. b. Globulins: transports lipids, carbohydrates, hormones, ions, antibodies, and complement. i. 38% of plasma proteins; carrier protein. c. Fibrinogen: blood clotting. i. 4% (coagulation). d. In conditions where plasma proteins are reduced, e.g. from being lost in the urine (proteinuria) or from malnutrition, there will be a reduction in colloidal osmotic pressure and an increase in filtration across the capillary, resulting in excess fluid buildup in the tissues (edema). 4. Serum: plasma without proteins. 5. Plasma contains ions, nutrients, waste products, and gases. a. Ions: involved in osmosis, membrane potentials, and acidbase balance. i. Ions are: sodium, potassium, calcium, magnesium, chloride, iron, phosphate, hydrogen, hydroxide, bicarbonate. b. Nutrients: glucose, amino acids, triacylglycerol, cholesterol, vitamins. c. Waste products: i. Urea, uric acid, creatinine, ammonia salts – breakdown products of protein metabolism ii. Bilirubin – breakdown product of RBCs iii. Lactic acid – end product of anaerobic respiration d. Gases: oxygen, carbon dioxide, and inert nitrogen. e. Regulatory substances: hormones, enzymes. 19.4 Formed Elements The formed elements are red blood cells (erythrocytes), white blood cells (leukocytes), and platelets (cell fragments). Production of Formed Elements 1. In the embryo and fetus, the formed elements are produced in a number of locations. 2. After birth, red bone marrow becomes the source of the formed elements. 3. In adults, red marrow is confined to ribs, sternum, vertebrae, pelvis, proximal femur, and proximal humerus. 4. All formed elements are derived from hemocytoblast, which gives rise to two intermediate stem cells: myeloid stem cells and lymphoid stem cells. Myeloid stem cells give rise to red blood cells, platelets, and most of the white blood cells. Lymphoid stem cells give rise to lymphocytes. 5. Hematopoiesis or hemopoiesis: process of blood cell production. 6. Stem cells: all formed elements derived from a single population. a. Proerythroblasts: develop into red blood cells. b. Myeloblasts: develop into basophils, neutrophils, and eosinophils. c. Lymphoblasts: develop into lymphocytes. d. Monoblasts: develop into monocytes. e. Megakaryoblasts: develop into platelets. Red Blood Cells 1. 95% of volume of formed elements. 2. Biconcave discs. a. Red blood cells are biconcave discs containing hemoglobin and carbonic anhydrase. 3. Transport oxygen and carbon dioxide. a. Oxygen from lungs to tissues: 98.5% attached to hemoglobin; 1.5% dissolved in plasma. b. Carbon dioxide from tissues to lungs: i. 7% dissolved in plasma. ii. 23% in combination with hemoglobin. iii. 70% transported as bicarbonate ions produced as a result of combination of H2O and CO2 because of enzyme carbonic anhydrase found within RBCs. c. A hemoglobin molecule consists of four heme and four globin molecules. The heme molecules transport oxygen, and the globin molecules transport carbon dioxide and nitric oxide. Iron is required for oxygen transport. d. Carbonic anhydrase is involved with the transport of carbon dioxide. e. Erythropoiesis is the production of red blood cells. i. Stem cells in red bone marrow eventually give rise to the late erythroblasts, which lose their nuclei and are released into the blood as reticulocytes. Loss of the endoplasmic reticulum by a reticulocyte produces a red blood cell. ii. In response to low blood oxygen, the kidneys produce erythropoietin, which stimulates erythropoiesis. iii. RBCs last 120 days in circulation (enucleated). iv. Stem cells (hemocytoblasts) → myeloid stem cell→ proerythroblasts → early erythroblasts → intermediate erythroblasts → late erythroblasts → reticulocytes. v. Production of single RBCs take about 4 days. vi. Intermediate erythroblasts continue to produce hemoglobin, then most of their ribosomes and other organelles degenerate. vii. 1/3 of cytoplasm in late erythroblasts is hemoglobin, so they are red. They lose nuclei to become immature RBCs (reticulocytes). viii. In ~2 days, ribosomes in reticulocytes degenerate and become mature RBCs. f. Erythropoietin (EPO). i. Hormone stimulates RBC production. ii. Produced by kidneys in response to low O l2 els. 4. Anucleate. 5. Contain hemoglobin. a. Types of hemoglobin: i. Embryonic ii. Fetal iii. Adult b. Hemoglobin from ruptured red blood cells is phagocytized by macrophages. The hemoglobin is broken down, and heme becomes bilirubin, which is secreted in bile. c. Hemoglobin is pigmented (hence red colour). i. Heme is a red pigmented molecule containing iron atom. d. It occupies 1/3 of the RBCs volume. e. Oxyhemoglobin: transporting oxygen. f. Deoxyhemoglobin: no oxygen. g. Carbaminohemoglobin: transporting carbon dioxide. h. Globin is a polypeptide. i. CO2 attaches to globin, not iron/heme. ii. Globulin molecules transport nitric oxide. NO brought from lungs to tissues, induces smooth muscles to relax, lowering BP. iii. Carbon monoxide (result of gas combustion) binds iron with high affinity, so O2 can’t bind. i. Hemoglobin breakdown: i. Hemoglobin is broken down by macrophages into heme and globin chains. ii. The globin chains of hemoglobin are broken down to individual amino acids. iii. The heme of hemoglobin releases the iron. iv. Blood transports iron in combination with transferrin to various tissues for storage or to the red bone marrow. v. Blood transports free bilirubin to the liver. vi. Coagulated bilirubin is excreted as part of the bile into the small intestine. vii. Some bilirubin derivatives contribute to the colour of feces. viii. Other bilirubin derivatives are reabsorbed from the intestine into the blood. 6. Red blood cell pathologies. a. Anemia: decrease in the amount of RBCs or hemoglobin in the blood. b. Hemolysis: abnormal breakdown of RBCs. i. RBCs rupture, release hemoglobin into plasma; hemoglobin denatures in new environment, becoming nonfunctional. ii. Grampositive bacteria, parasites. iii. Autoimmune disorders. iv. Genetic disorders. White Blood Cells 1. White blood cells protect the body against microorganisms and remove dead cells and debris. 2. Movements: a. Ameboid: pseudopods. b. Diapedesis: cells become thin, elongate and move either between or through endothelial cells of capillaries. c. Chemotaxis: attraction to and movement toward foreign materials or damaged cells. 3. Five types of white blood cells exist: a. Neutrophils are small, phagocytic cells. i. Stay in circulation 1012 hours. ii. Become motile, phagocytize bacteria, antigenantibody complexes and other foreign matter. iii. Secrete lysozyme. b. Eosinophils attack certain worm parasites and modulate inflammation. i. Defend against worm parasites. ii. Prevalent in allergic reactions. iii. Destroy inflammatory chemicals like histamine. c. Basophils release histamine and are involved with increasing the inflammatory response. i. Leave circulation and migrate through tissues. ii. Inflammatory response and allergic reactions. iii. Produce histamine and heparin. 1. Histamine: dilation of blood vessels. 2. Heparin: slows blood clotting. d. Lymphocytes are important in immunity, including the production of antibodies. i. Migrate to lymphatic tissues and proliferate. ii. Antibody production. iii. Immune function: Bcells, Tcells. e. Monocytes leave the blood, enter tissues, and become large, phagocytic cells called macrophages. i. Become macrophages and phagocytize bacteria, dead cells, and debris. ii. Stimulate responses in other cells. 4. Granulocytes: a. Cytoplasm contains large granules. b. Multilobed nuclei. c. Three distinctive types: neutrophils, eosinophils, basophils. 5. Agranulocytes: a. Cytoplasm contains small granules. b. Nuclei are not lobed. c. Two distinctive types: lymphocytes and monocytes. 6. WBC pathologies: a. Leukemia: cancer of red bone marrow. i. Cells usually immature or abnormal. ii. Lack of normal immune functions. Platelets 1. Platelets, or thrombocytes, are cell fragments pinched off from megakaryocytes in the red bone marrow. 2. Disc shaped cell fragment. 3. Form platelet plugs. a. Fill small holes. 4. Releases chemicals necessary for blood clotting. a. Seals larger wounds. 19.5 Hemostasis 1. Hemostasis, the cessation of bleeding, it is very important to the maintenance of homeostasis. Vascular Spasm 1. Vasoconstriction of damaged blood vessels reduces blood loss. a. It is immediate but temporary. Platelet Plug Formation 1. Platelets repair minor damage to blood vessels by forming platelet plugs: a. In platelet adhesion, platelets bind to collagen in damaged tissues. b. In the platelet release reaction, platelets release chemicals that activate additional platelets. i. ADP, thromboxane, and other chemicals released. ii. These bind receptors on surface of other platelets and activate them. iii. Positive feedback – activated platelets release chemicals and activate more platelets. c. Activated platelets change shape and express fibrinogen receptors. i. Fibrinogen is plasma protein. ii. Platelet aggregation – fibrinogen forms a bridge between fibrinogen receptors of different platelets, resulting in a platelet plug. 2. Platelets also release chemicals involved with coagulation. 3. Activated platelets also release coagulation factor V and phospholipid (platelet factor III) – important for coagulation. Coagulation 1. Coagulation is the formation of a blood clot. 2. Coagulation factors: a. Proteins found in plasma. b. Circulate in inactive state until tissues are injured. c. Damaged tissues and platelets produce chemicals that begin activation of the factors. 3. The first stage of coagulation occurs through the extrinsic or intrinsic pathway. Both pathways end with the production of activated factor X. a. The extrinsic pathway begins with the release of thromboplastin from damaged tissues. i. Stage 1: 1. Damaged tissues release thromboplastin (tissue factor III). 2. When Ca is present, forms complex with factor VII, activating factor X. 3. Prothrombinase is formed. ii. Stage 2: prothrombinase converts prothrombin into thrombin. iii. Stage 3: 1. Thrombin converts fibrinogen to fibrin. 2. Thrombin activates factor XIII, which stabilizes clot. b. The intrinsic pathway begins with the activation of factor XII and chemicals that are part of the blood. i. Stage 1: 1. In damaged blood vessels, factor XII comes in contact with exposed collagen, activating factor XII. 2. Stimulates factor XI, activated factor IX. 3. Activated factor IX joins with factor VIII, platelet phospholipids, and Ca to activate factor X. 4. Prothrombinase is formed. ii. Stages 2 and 3 progress to clot formation. 2+ 4. Activated factor X, factor V, phospholipids, and Ca form prothrombinase. 5. Prothrombinase converts prothrombin to thrombin. 6. Thrombin converts fibrinogen to fibrin. The insoluble fibrin forms the clot. 7. Thrombin also stimulates factor XII activation, which stabilizes clot. 8. Thrombin also activates many clotting proteins, creating a positivefeedback system (thrombin production stimulates more thrombin production). 9. Thrombin also stimulates platelet activation. Control of Clot Formation 1. Heparin and antithrombin inhibit thrombin activity. Therefore, fibrinogen is not yet converted to fibrin, and clot formation is inhibited. 2. Prostacyclin counteracts the effects of thrombin. 3. Anticoagulants: prevents coagulation factors from initiating clot formation. a. Antithrombin: i. Produced by the liver. ii. Slowly inactivates thrombin. b. Heparin: i. Produced by basophils and endothelial cells. ii. Increases effectiveness of antithrombin. c. Prostacyclin: i. Produced by endothelial cells. ii. Causes vasodilation and inhibits release of coagulating factors from platelets. 4. Uncontrolled clots: a. Thrombus: blood clot that forms in a vessel. b. Embolus: free floating clot in blood vessels. Clot Retraction and Dissolution 1. Clot retraction results from the contraction of platelets, which pull the edges of damaged tissue closer together. 2. Serum, which is plasma minus fibrinogen and some clotting factors, is squeezed out of the clot. 3. Factor XII, thrombin, tissue plasminogen activator, and urokinase activate plasmin, which dissolves fibrin (the clot). 4. Fibrinolysis: process of dissolving a blood clot. a. Inactive plasminogen is converted to the active enzyme plasmin. b. Plasmin breaks the fibrin molecules, and therefore the clot, into smaller pieces, which are washed away in the blood or phagocytized. 19.6 Blood Grouping 1. Blood groups are determined by antigens on the surface of red blood cells. 2. Antibodies can bind to red blood cells antigens, resulting in agglutination or hemolysis of red blood cells. 3. Transfusion: transfer of blood or blood components from one individual to another. 4. Infusion: introduction of fluid other than blood. 5. Determined by antigens (agglutinogens) on surface of RBCs. 6. Antibodies (agglutinins) can bind to RBC antigens, resulting in agglutination (clumping) or hemolysis (rupture) of RBCs. a. Antigen: toxin or other foreign substance that induces an immune response in the body. b. Antibodies are specific to certain antigens. ABO Blood Group 1. Type A blood has A antigens, type B blood has B antigens, type AB blood has A and B antigens, and type O blood has neither A nor B antigens. 2. Type A blood has antiB antibodies, type B blood has antiA antibodies, type AB blood has neither antiA nor antiB antibodies, and type O blood has both antiA and antiB antibodies. a. O is most common. b. A is next most common. c. B is not very common. d. AB is very uncommon. 3. Mismatching the ABO blood group results in a transfusion reaction. 4. Agglutination reaction: a. Type A blood of a donor antiB antibody in type A blood of recipient: no agglutination reaction. i. Type A blood donated to a type A recipient does not cause an agglutination reaction because the antiB antibodies in the recipient do not combine with the type A antigens on the red blood cells in the donated blood. b. Type A blood of donor antiA antibody in type B blood of recipient: agglutination. i. Type A blood donated to a type B recipient causes an agglutination reaction because the antiA antibodies in the recipient combine with the type A antigens on the red blood cells in the donated blood. Rh Blood Group 1. First studied in rhesus monkeys. 2. Rhpositive blood has the D antigen, whereas Rhnegative blood does not. 3. Antibodies against the D antigen are produced by an Rhnegative person when the person is exposed to Rhpositive blood. 4. The Rh blood group is responsible for hemolytic disease of the newborn. a. Rh positive fetus, Rh negative mother. b. Late in pregnancy, Rh antigens of fetus cross placenta. c. Mother creates antiRh antibodies (primary response). i. AntiRh antibodies do not develop unless person is exposed to opposite blood type (transfusion, motherfetus). d. Second Rh positive pregnancy might initiate secondary response and HDN. e. Mother can get an injection of RhoGAM. i. RhoGAM contains antibodies against Rh antigens. Antibodies attach to any fetal RBCs and they are destroyed. 19.6 Diagnostic Blood Tests Type and Crossmatch Blood typing determines the ABO and Rh blood groups of a blood sample. A crossmatch tests for agglutination reactions between donor and recipient blood. Complete Blood Count 1. A complete blood count consists of the following: a. Red blood count: number of RBCs per microliter of blood. b. Hemoglobin measurement: grams of hemoglobin per 100 mL of blood. c. Hematocrit measurement: percent volume of red blood cells. d. White blood count. 2. Differential white blood count: the percentage of each type of white blood cell. a. High neutrophil bacterial infection. b. High eosinophil/basophil allergic reaction. Clotting 1. Platelet count and prothrombin time measurement assess the blood’s ability to clot. a. Platelet count: 250,000 400,000/microliter. i. Thrombocytopenia: low platelet count. 1. Chronic bleeding in small vessels and capillaries. b. Prothrombin time measurement: measures how long it takes for blood to start clotting. Blood Chemistry 1. The composition of materials dissolved or suspended in plasma (e.g., glucose, urea, nitrogen, bilirubin, and cholesterol) can be used to assess the function and status of the body’s systems. Chapter 20 – The Heart 20.1 Functions of the Heart 1. The heart produces the force that causes blood to circulate. 2. Generate blood pressure. 3. Route blood: separates pulmonary and systemic circulations. 4. Ensuring oneway blood flow: valves. 5. Regulating blood supply. 6. Tissue metabolic needs change depending on rest, exercise, body position, etc.; blood supply must be regulated accordingly 20.2 Size, Shape, and Location of the Heart 1. The heart is approximately the size of a closed fist. 2. Shape: a. Apex: blunt rounded point of cone. b. Base: flat part at opposite end of cone. 3. The heart lies obliquely in the mediastinum, with its base directed posteriorly and slightly superiorly and its apex directed anteriorly, inferiorly, and to the left. a. Located in thoracic cavity in mediastinum. 4. The base is deep to the second intercostal space, and the apex extends to the fifth intercostal space. 5. Important clinically when using a stethoscope, performing an ECG, or performing CPR. 20.3 Anatomy of the Heart 1. The heart consists of two atria and two ventricles. Pericardium 1. The pericardium is a sac that surrounds the heart and consists of the fibrous pericardium and the serous pericardium. 2. Fibrous pericardium: a. Helps hold the heart in place. b. Tough fibrous outer layer. c. Prevents over distention. d. Acts as an anchor. 3. The serous pericardium reduces friction as the heart beats. It consists of the following parts: a. Parietal pericardium: lines the fibrous pericardium (outer layer). b. Visceral pericardium (epicardium): lines the exterior surface of the heart. c. The pericardial cavity lies between the parietal and visceral pericardia and is filled with pericardial fluid, which reduces friction as the heart beats. 4. Serous pericardium: a. Thin, transparent, inner layer. b. Simple squamous epithelium. 5. Pericardial effusion – excess fluid in pericardial sac. 6. Cardiac tamponade – enough pericardial effusion to adversely affect heart function. Heart Wall 1. The heart wall has three layers: a. The outer epicardium (visceral pericardium) provides protection against the friction of rubbing organs. i. Smooth outer surface of the heart. ii. Epicardium = visceral pericardium (epicardium when referring to it as part of heart; visceral pericardium when referring to it as part of serous membrane). b. The middle myocardium is responsible for contraction. i. Cardiac muscle cell. c. The inner endocardium reduces the friction resulting from blood passing through the heart. i. Smooth inner surface of heart chambers. 2. The inner surfaces of the atria are mainly smooth. The auricles have muscular ridges called pectinate muscles. a. Pectinate muscles: muscular ridges in auricles and right atrial wall. 3. The ventricles have ridges called trabeculae carneae. a. Trabeculae carneae: muscular ridges and columns on inside walls of ventricles. 4. Christae terminalis (terminal crest) – smooth ridge that separates pectinate muscle ridges from smooth muscle in the rest of the atrium. External Anatomy and Coronary Circulation 1. Each atrium gas a flap called an auricle. 2. The coronary sulcus separates the atria from the ventricles. The interventricular grooves separate the right and left ventricles. 3. The inferior and superior venae cavae and the coronary sinus enter the right atrium. The four pulmonary veins enter the left atrium. 4. The pulmonary trunk exits the right ventricle, and the aorta exits the left ventricle. 5. Coronary arteries branch off the aorta to supply the heart. Blood returns from the heart tissues to the right atrium through the coronary sinus and cardiac veins. 6. Blood enters the heart through: a. Superior and inferior vena cava – from body to right atrium. b. Coronary sinus – from exterior surface of heart to right atrium. c. Pulmonary veins – from lungs to left atrium. 7. Blood exits the heart through: a. Aorta – from left ventricle. b. Pulmonary trunk – from right ventricle. 8. Right coronary artery extends to posterior aspect of heart: a. Right marginal artery supplies lateral wall of right ventricle. b. Posterior interventricular artery supplies posterior and inferior aspects of the heart. 9. Left coronary artery branches: a. Anterior interventricular artery (left anterior descending artery, LAD, Widow Maker) supplies 4555% of left ventricle. b. Left marginal artery supplies lateral wall of left ventricle. c. Circumflex artery supplies posterolateral left ventricle. 10. Great cardiac vein drains left side of heart. 11. Small cardiac vein drains right margin of heart. 12. Coronary sinus: veins empty here then into the right atrium. 13. Number of small veins drain the rest of the heart. Heart Chambers and Valves 1. The interatrial septum separates the atria from each other, and the interventricular septum separates the ventricles. 2. The tricuspid valve separates the right atrium and ventricle. The bicuspid (mitral) valve separates the left atrium and ventricle. The chordae tendineae attach the papillary muscles to the atrioventricular valves. a. Atrioventricular valves: i. Attached to coneshaped papillary muscles by tendons (chordae tendineae). ii. Right has three cusps (tricuspid). iii. Left has two cusps (bicuspid/mitral). 3. The semilunar valves separate the aorta and pulmonary trunk from the ventricles. a. Semilunar valves: i. Pulmonary – right ventricle. ii. Aortic – left ventricle. 4. Atria: a. Right atrium: receives blood returning from the body. i. Openings: superior vena cava, inferior vena cava, coronary sinus. b. Left atrium: receives blood from the lungs. i. 4 pulmonary veins. c. Interatrial septum: wall between the atria. i. Fossa ovalis. 5. Ventricles: a. Atrioventricular canals: openings between atria and respective ventricles. b. Right ventricle opens to pulmonary trunk. c. Left ventricle opens to aorta. d. Interventricular septum is between the two. 20.4 Route of Blood Flow through the Heart 1. Blood from the body flows through the right atrium into the right ventricle and then to the lungs. 2. Blood returns from the lungs to the left atrium, enters the left ventricle, and is pumped back to the body. 20.5 Histology Heart Skeleton 1. Supports the openings of the heart. 2. Electrically insulates the atria from the ventricles. 3. Provides a point of attachment for heart muscle. 4. Plate of fibrous connective tissue between atria and ventricles. 5. Fibrous rings around valves to support. Cardiac Muscle 1. Cardiac muscle cells are branched and have 12 centrally located nucleus. Actin and myosin are organized to form sarcomeres. The sarcoplasmic reticulum and T tubules are not as organized as in skeletal muscle. a. Electrically, cardiac muscle of the atria and of the ventricles behaves as a single unit. 2. Cardiac muscle cells are joined by intercalated disks, which allow action potentials to move from one cell to the next. Thus, cardiac muscle cells function as a unit. a. Intercalated disks: specialized cell to cell contacts. i. Cell membranes interdigitate. ii. Desmosomes hold cells together. iii. Gap junctions allow action potentials to move from one cell to the next. 3. Cardiac muscle cells have a slow onset of contraction and a prolonged contraction time caused by the length of time required for Ca to move to and from the myofibrils. 4. Cardiac muscle is well supplied with blood vessels that support aerobic respiration. 5. Cardiac muscle aerobically uses glucose, fatty acids, and lactate to produce ATP for energy. Cardiac muscle does not develop a significant oxygen deficit. Conducting System 1. The SA node and the AV node are in the right atrium. 2. The AV node is connected to the bundle branches in the interventricular septum by the AV bundle. 3. The bundle branches give rise to Purkinje fibers, which supply the ventricles. 4. The SA node is made up of smalldiameter cardiac muscle cells that initiate action potentials, which spread across the atria and cause them to contract. 5. Action potentials are slowed in the AV node, allowing the atria to contract and blood to move into the ventricles. Then the action potentials travel through the AV bundles and bundle branches to the Purkinje fibers, causing the ventricles to contract, starting at the apex. The AV node is also made up of smalldiameter cardiac muscle fibers. 6. SA (sinoatrial) node: a. The pacemaker. b. Generates spontaneous action potentials. c. Action potentials pass to atrial muscle cells to the AV node. d. Medial to the opening of the superior vena cava. 7. AV (atrioventricular) node: a. Action potentials conducted more slowly here than in any other part of the system. b. Ensures ventricles receive signal to contract after atria have contracted. c. Medial to the right AV valve. 8. AV bundle: a. Passes through a hole in cardiac skeleton to reach interventricular septum. 9. Right and left bundle branches: a. Extend beneath endocardium to apices of right and left ventricles. 10. Purkinje fibers: a. Conduct action potential to ventricular muscle cells. 11. Because of the arrangement of conducting system in ventricles, first part of ventricular myocardium to contract is the apex, which then progress toward base of the heart. 20.6 Electrical Properties Action Potentials 1. After depolarization and partial repolarization, a plateau is reached, during which the membrane potential only slowly repolarizes. 2. The movement of Na through the voltagegated Na channels causes depolarization. + 2+ 3. During depolarization, voltagegated K channels close, and voltagegated Ca channels begin to open. 4. Early repolarization results from closure of the voltagegated Na channels and the + opening of some voltagegated K channels. 5. The plateau exists because voltagegated Ca channels remain open. 6. The rapid phase of repolarization results from closure of the voltagegated Ca channels + and the opening of many voltagegated K channels. 7. The entry of Ca into cardiac muscle cells causes Ca to be released from the sarcoplasmic reticulum to trigger contractions. 8. Membrane potential of a cell is electrical charge difference across the plasma membrane. a. Charge difference is a result of the cell’s regulation of ion movement into and out of the cell. b. Resting membrane potential – membrane potential when a cell is relaxed. c. When neurons or muscle cells are depolarized to their threshold level, action potentials result. Differenced Between Skeletal and Cardiac Muscle Physiology 1. Calciuminduced calcium release (CICR): a. Movement of Ca through plasma membrane and T tubules into sarcoplasm 2+ stimulates release of Ca from sarcoplasmic reticulum. 2. Cardiac: a. Action potentials conducted from cell to cell. b. Rate of action potential propagation is slow because of gap junctions and small diameter of fibers. c. Extracellular calcium required for contraction. 3. Skeletal: a. Action potential conducted along length of single fiber. b. Faster due to larger diameter fibers and great length. Autorhythmicity of Cardiac Muscle 1. Cardiac pacemaker muscle cells are autorhythmic because of the spontaneous development of a pacemaker potential. 2. The pacemaker potential results from the movement of Na and Ca into the pacemaker cells. 3. Ectopic foci are areas of the heart that regulate heart rate under abnormal conditions. Refractory Periods of Cardiac Muscle 1. Cardiac muscle has prolonged depolarization and thus a prolonged refractory period, which allows time for the cardiac muscle to relax before the next action potential causes a contraction. 2. Absolute: cardiac muscle cell completely insensitive to further stimulation. 3. Relative: cell exhibits reduced sensitivity to additional stimulation. 4. Long refractory period prevents tetanic contractions. a. Tetanic contraction is a sustained muscular contraction. Electrocardiogram 1. An ECG records only the electrical activities of the heart. a. Depolarization of the atria produces the P wave. i. Depolarization of atrial myocardium. ii. Onset of atrial contraction. b. Depolarization of the ventricles produces the QRS complex. c. Repolarization of the atria occurs during the QRS complex. i. Onset of ventricular contraction. d. Repolarization of the ventricles produces the T wave. i. Precedes ventricular relaxation. 2. PQ interval (PR interval): 0.16 sec; atria contracts and begins to relax, ventricles begin to contract. 3. QT interval: 0.36 sec; ventricles contract and begin to relax. 4. Based on the magnitude of the ECG waves and the time between waves, ECGs can be used to diagnose heart abnormalities. 20.7 Cardiac Cycle 1. The cardiac cycle involves repetitive contraction (systole) and relaxation (diastole) of the heart chambers. 2. Blood moves through the circulatory system from areas of higher pressure to areas of lower pressure. Contraction of the heart produces the pressure. 3. The cardiac cycle is divided into five periods: a. Active ventricular filling results when the atria contract and pump blood into the ventricles. b. Although the ventricles are contracting, during the period of isovolumetric contraction, ventricular volume does not change because all the heart valves are closed. c. During the period of ejection, the semilunar valves open, and blood is ejected from the heart. d. Although the heart is relaxing, during the period of isovolumetric relaxation, ventricular volume does not change because all the heart valves are closed. e. Passive ventricular filling results when blood flows from the higher pressure in the veins and atria to the lower pressure in the relaxed ventricles. Events Occurring During the Cardiac Cycle 1. Most ventricular filling occurs when blood flows from higher pressure in the veins and atria to the lower pressure in the relaxed ventricles. a. Passive ventricular filling: i. While the ventricles were in systole, the atria were filling with blood. ii. Atrial pressure rises above ventricular pressure and the AV valves open. iii. Blood flows into the relaxed ventricles, accounting for most of the ventricular filling (70%). b. Active ventricular filling: i. Depolarization of the SA node generates action potentials that spread over the atria (P wave) and the atria contract. This completes ventricular filling. ii. At rest, contraction of atria is not necessary for heart function. iii. During exercise, atrial contraction is necessary for function as the heart pumps 300400%. 2. Contraction of the atria completes ventricular filling. 3. Contraction of the ventricles closes the AV valves, opens the semilunar valves, and ejects blood from the heart. 4. The volume of blood in a ventricle just before it contracts is the enddiastolic volume. The volume of blood after contraction is the endsystolic volume. 5. Relaxation of the ventricles results in the closing of the semilunar valves, the opening of the AV valves, and the movement of blood into the ventricles. 6. Period of isovolumetric contraction: a. Begins at the completion of the QRS complex. b. Ventricles contract, but blood volume in ventricle does not change. c. 120130 mL of blood are in the ventricles, left from the last diastole when the atria emptied into the ventricles. This is referred to as the enddiastolic volume. 7. Period of ejection: a. Pressure in the ventricle has increased to the point where it is greater than the pressure in the pulmonary trunk/aorta. b. Blood is ejected from the ventricles. c. The pressures in the two ventricles are different: i. 120mm Hg in the left ventricle. ii. 25mm Hg in the right ventricle. d. After the first initial spurt, pressure starts to drop. e. At the end of the period of ejection, 5060 mL remain: endsystolic volume. 8. Period of isovolumetric relaxation: a. Completion of T wave results in ventricular repolarization and relaxation. b. Ventricular pressure falls very rapidly. c. Pulmonary trunk/aorta pressure is higher than ventricular pressure. d. Semilunar valves close, beginning ventricular diastole. Heart Sounds 1. Closure of the atrioventricular valves at the beginning of ventricular systole produces the first heart sound (LUBB). a. Systole is time between the first and second heart sounds. 2. Closure of the aortic and pulmonary semilunar valves at the beginning of ventricular diastole produces the second heart sound (DUPP). a. Diastole is time between second and next first. 3. Turbulent flow of blood into the ventricles can be heard in some people, producing a third heart sound. Aortic Pressure Curve 1. Contraction of the ventricles forces blood into the aorta, producing the peak systolic pressure. 2. Blood pressure in the aorta falls into the diastolic level as blood flows out of the aorta. a. Blood pressure measurement taken in the arm is a reflection of aortic pressures, not ventricular. b. Aorta fluctuates between systolic (120mm Hg) and diastolic (80mm Hg) for the average adult at rest. 3. Elastic recoil of the aorta maintains pressure in the aorta and produces the dicrotic notch and dicrotic wave. a. Dicrotic notch (incisura): when the aortic semilunar valve closes, pressure within the aorta increases slightly. 20.8 Mean Arterial Blood Pressure 1. Mean arterial pressure is the average blood pressure in the aorta. Adequate blood pressure is necessary to ensure delivery of blood to the tissues. 2. Mean arterial pressure is proportional to cardiac output (amount of blood pumped by the heart per minute) times peripheral resistance (total resistance to blood flow through blood vessels). a. MAP = CO x PR i. Cardiac output is equal to stroke volume times the heart rate. 1. CO = SV x HR a. Stroke volume, the amount of blood pumped by the heart per beat, is equal to enddiastolic volume minus end systolic volume. b. HR: heart rate. c. Cardiac reserve: difference between CO at rest and maximum CO. ii. PR is total resistance against which blood must be pumped. b. Venous return is the amount of blood returning to the heart. Increased venous return increases stroke volume by increasing enddiastolic volume. c. Increased force of contraction increases stroke volume by decreasing endsystolic volume. 3. Cardiac reserve is the difference between resting and exercising cardiac output. 20.9 Regulation of the Heart Intrinsic Regulation 1. Results from normal functional characteristics. 2. Venous return is the amount of blood that returns to the heart during each cardiac cycle. 3. The Starling law of the heart describes the relationship between preload and the stroke volume of the heart. An increased preload causes the cardiac muscle cells to contract with a greater force and produce a greater stroke volume. a. Preload: the amount of stretch of the ventricular walls. The greater the stretch, the greater the force of contraction. b. Afterload: pressure contracting ventricles must produce to overcome the pressure in the aorta and move blood into the aorta. Extrinsic Regulation 1. The cardioregulatory center in the medulla oblongata regulates parasympathetic and sympathetic nervous control of the heart. 2. Parasympathetic stimulation is supplied by the vagus nerve. a. Parasympathetic stimulation decreases heart rate. b. Postganglionic neurons secrete acetylcholine, which increases membrane permeability to K , producing hyperpolarization of the membrane. 3. Sympathetic stimulation is supplied by the cardiac nerves. a. Sympathetic stimulation increases heart rate and force of contraction (stroke volume). b. Postganglionic neurons secrete norepinephrine, which increases membrane + 2+ permeability to Na and Ca and produces depolarization of the membrane. c. Increased heart beat causes increased cardiac output. Increased force of contraction causes a lower endsystolic volume; heart empties to a greater extent. 4. Epinephrine and norepinephrine are released into the blood from the adrenal medulla as a result of sympathetic stimulation. a. The effects of epinephrine and norepinephrine on the heart are longlasting, compared with those of neural stimulation. b. Epinephrine and norepinephrine increase the rate and force of heart contraction. c. Occurs in response to increased physical activity, emotional excitement, stress. 20.10 The Heart and Homeostasis Effect of Blood Pressure 1. Baroreceptors monitor blood pressure. 2. In response to a decrease in blood pressure, the baroreceptor reflexes increase sympathetic stimulation and decrease parasympathetic stimulation of the heart, resulting in increased heart rate and force of contraction. Effect of pH, Carbon Dioxide, and Oxygen 1. Chemoreceptors monitor blood carbon dioxide, pH, and oxygen levels. 2. In response to increased carbon dioxide and decreased pH, medullary chemoreceptor reflexes increase sympathetic stimulation and decrease parasympathetic stimulation of the heart. 3. Carotid body chemoreceptor receptors stimulated by low oxygen levels result in decreased heart rate and vasoconstriction. 4. All regulatory mechanisms functioning together in response to low blood pH, high blood carbon dioxide, and low blood oxygen levels usually produce increased heart rate and vasoconstriction. Decreased oxygen levels stimulate an increase in heart rate indirectly by stimulating respiration, and the stretch of the lungs activates a reflex that increases sympathetic stimulation of the heart. Effect of Extracellular Ion Concentration + 1. An increase or a decrease i2+ xtracellular K decreases heart rate. 2. Increased extracellular Ca increases force of contraction of the heart and decreases heart rate. Decreased Ca levels produce the opposite effect. Effect of Body Temperature 1. Heart rate increases when body temperature increases, and it decreases when body temperature decreases. 20.11 Effects of Aging on the Heart 1. Aging results in gradual changes in heart function, which are minor under resting conditions but more significant during exercise. 2. Hypertrophy of the left ventricle is a common agerelated condition. 3. The maximum heart rate declines so that, by age 85, the cardiac output may be decreased by 3060%. 4. There is an increased tendency for valves to function abnormally and for arrhythmias to occur. 5. Because increased oxygen consumption is required to pump the same amount of blood, agerelated coronary artery disease is more severe. 6. Exercise improves the functional capacity of the heart at all ages.
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