Chapter 13&14 lecture-1

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Chapter 13&14 lecture-1

  1. 1. Chapters 13 & 14Blood, Heart, andCirculationLecture PowerPointCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
  2. 2. Overview13-3
  3. 3. Circulatory System Components• Cardiovascular system– Heart: four-chambered pump– Blood vessels: arteries, arterioles, capillaries,venules, and veins• Lymphatic system– Lymphatic vessels, lymphoid tissues,lymphatic organs (spleen, thymus, tonsils,lymph nodes)
  4. 4. Circulatory System Functions• Transportation– Respiratory gases, nutrients, and wastes• Regulation– Hormonal and temperature• Protection– Clotting and immune
  5. 5. I. Composition of the Blood
  6. 6. Composition of the Blood1. Plasma: fluid part of blood– Plasma proteins– Serum
  7. 7. Composition of the Blood1. Plasma: fluid part of blood•Nutrients and metabolites– Glucose, amino acids, fatty acids etc•Hormones– Insulin, glucagon, sex hormones etc.•Ions– Na+(major ion; maintains osmotic pressure)– K+, Ca++, Cl-, Mg++etc•Bicarbonate; important buffer•Respiratory gasses– O2, CO2•Waste products– Urea, food additives etc.
  8. 8. Composition of the BloodPlasma: fluid part of blood (Continued)• Proteins constitute 7-9% of plasma• Three types of plasma proteins: albumins, globulins, &fibrinogen– Albumin accounts for 60-80% (Major protein)• Creates colloid osmotic pressure that draws H20 frominterstitial fluid into capillaries to maintain blood volume &pressure– Globulins• Alpha and beta globulins transport lipid soluble molecules• Gamma globulins are antibodies (fight infection)– Fibrinogen• a soluble protein that functions in clotting• Converted to fibrin; an insoluble protein polymer• Serum is fluid left when blood clots (plasma minus fibrinogen)
  9. 9. Composition of the Blood2. Formed ElementsGranulocytesNeutrophilsEosinophilsBasophilsAgranulocytesLymphocytesMonocytes
  10. 10. Composition of the Blood2. Erythrocytes– Carry oxygen– Lack nuclei andmitochondria– Have a 120-day lifespan– Contain hemoglobinand transferrin
  11. 11. Composition of the Blood
  12. 12. Composition of the Blood• 3. Leukocytes• Have nucleus, mitochondria, & amoeboid ability• Can squeeze through capillary walls (diapedesis)– Granular leukocytes help detoxify foreignsubstances & release heparin• Include eosinophils, basophils, & neutrophils13-10
  13. 13. Composition of the Blood• 3. Leukocytes (Contd)• Agranular leukocytesare phagocytic &produce antibodies• Include lymphocytes& monocytes13-11
  14. 14. Composition of the Blood4. Platelets (thrombocytes)- Smallest formed element– Lack nuclei- Very short-lived (5−9 days)- Clot blood- Need fibrinogen
  15. 15. Formed Elements in the Blood
  16. 16. Hematopoiesis• Is formation of blood cells from stem cells inbone marrow (myeloid tissue) & lymphoidtissue• 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 system13-13
  17. 17. Erythropoiesis• 2.5 million RBCsare produced/sec• Lifespan of 120days• Old RBCs removedfrom blood byphagocytic cells inliver, spleen, &bone marrow– Iron recycledback intohemoglobinproduction 13-14
  18. 18. Blood Clotting• Hemostasis: cessation of bleeding when ablood vessel is damaged• Damage exposes collagen fibers to blood,producing:1. Vasoconstriction2. Formation of platelet plug3. Formation of fibrin protein web
  19. 19. Blood Clotting: Platelets• Platelets dontstick to intactendotheliumbecause ofpresence ofprostacyclin(PGI2--aprostaglandin) &NO– Keep clots fromforming & arevasodilators13-20QuickTime™ and aTIFF (LZW) decompressorare needed to see this picture.
  20. 20. Consequences of Blood Clottingin Normal Vessels
  21. 21. Blood Clotting: Platelets• Damage to endotheliumallows platelets to bind toexposed collagen– von Willebrand factorincreases bond bybinding to bothcollagen & platelets– Platelets stick tocollagen & releaseADP, serotonin, &thromboxane A2• = platelet releasereaction13-21Damaged blood vessel wall
  22. 22. Blood Clotting: Platelets• Some chemicals (serotonin& thromboxane A2)stimulate vasoconstriction,reducing blood flow towound• Other chemicals (ADP &thromboxane A2) causeother platelets to becomesticky & attach & undergoplatelet release reaction– This aggregationcontinues until plateletplug is formed13-22Platelet aggregation
  23. 23. Blood Clotting: Fibrin• Next, calcium and phospholipids (from theplatelets) convert prothrombin to the activeenzyme thrombin, which convertsfibrinogen to fibrin.
  24. 24. Blood Clotting: Fibrin• Fibrinogen is converted to fibrin via one oftwo pathways:1. Intrinsic: Activated by exposure to collagenor glass which activates a cascade of otherblood factors.
  25. 25. Blood Clotting: Fibrin2. Extrinsic: Initiated by tissue factor (factor III).This is a more direct pathway.• Vitamin K is needed for both pathways.
  26. 26. 13-25Intrinsic: Activated byexposure to collagenExtrinsic: Initiated by tissuefactor (factor III).
  27. 27. • Platelet plug becomes infiltrated by meshwork of fibrin• Clot now contains platelets, fibrin & trapped RBCs– Platelet plug undergoes plug contraction to form morecompact plugRole of Fibrin13-23
  28. 28. Blood Clotting: Fibrin
  29. 29. Anticoagulants• Clotting can be prevented with certaindrugs:– Calcium chelators (sodium citrate or EDTA)– Heparin: blocks thrombin– Coumarin: inhibits vitamin K
  30. 30. Blood Clotting
  31. 31. Dissolution of Clots• When damage is repaired, activatedfactor XII causes activation of kallikrein– Kallikrein converts plasminogen to plasmin• Plasmin digests fibrin, dissolving clot13-26
  32. 32. II. Structure of the Heart
  33. 33. Structure of the Heart• Right atrium: receivesdeoxygenated blood from thebody• Left atrium: receivesoxygenated blood from thelungs• Right ventricle: pumpsdeoxygenated blood to thelungs• Left ventricle: pumpsoxygenated blood to the body• Chambers separated byfibrous skeleton
  34. 34. Pulmonary and Systemic Circulations• Pulmonary: between heartand lungs– Blood pumps to lungs viapulmonary arteries.– Blood returns to heart viapulmonary veins.• Systemic: between heartand body tissues– Blood pumps to bodytissues via aorta.– Blood returns to heart viasuperior and inferiorvenae cavae.
  35. 35. • Resistance in systemic circuit > pulmonary– Amount of work done by left ventricle pumping to systemic is5-7X greater• Causing left ventricle to be more muscular (3-4X thicker)Pulmonary & Systemic Circulationscontinued13-34
  36. 36. Valves of the Heart• Atrioventricularvalves: locatedbetween the atriaand the ventricles– Tricuspid: betweenright atrium andventricle– Bicuspid: betweenleft atrium andventricle
  37. 37. Valves of the Heart• Semilunar valves:located betweenthe ventricles andarteries leaving theheart– Pulmonary:between rightventricle andpulmonary trunk– Aortic: between leftventricle and aorta
  38. 38. Valves of the Heart• Opening & closing ofvalves results frompressure differences– High pressure ofventricular contractionis prevented fromeverting AV valves bycontraction of papillarymuscles which areconnected to AVs bychorda tendinea13-37
  39. 39. Three Types of Muscle• Skeletal Muscle– Voluntary– Striated– Not interconnected– Long and not branched• Cardiac Muscle– Involuntary– Striated– Interconnected via intercalateddiscs (Gap junctions)– Functional syncytium• Smooth Muscle– Involuntary– Non-striated– Most have gap junctions
  40. 40. • Pericardial Sac:• Anchors theheart• Reduces frictionagainst the ribcageStructure of Heart Wall
  41. 41. III. Electrical Activity of the Heartand the Electrocardiogram
  42. 42. Electrical Activity of the Heart• Cardiac muscle cells are interconnected by gap junctionscalled intercalated discs.– Once stimulation is applied, it flows from cell to cell.– The area of the heart that contracts from onestimulation event is called a myocardium.– The atria and ventricles are separated electrically bythe fibrous skeleton.
  43. 43. Electrical Activity of the HeartAutorhythmicity: Rhythmic beat of heartproduced by producing its own actionpotentialsAuthorhythmic cells: Special cardiomyocytesthat initiate and conduct action potentialsAt −40mV, voltage-gated Ca2+channels open, triggeringaction potential andcontraction.Repolarization occurs with theopening of voltage-gated K+channels
  44. 44. Electrical Activity of the Heart• Sinoatrial node: “pacemaker”; located inright atrium– Pacemaker potential: slow, spontaneousdepolarization
  45. 45. Electrical Activity of the Heart• Pacemaker cells in the sinoatrial nodedepolarize spontaneously, but the rate atwhich they do so can be modulated:– Epinephrine and norepinephrine increase theheart rate.– Parasympathetic neuron slows heart rate.
  46. 46. Electrical Activity of the Heart• Myocardial action potentials– Cardiac muscle cells have a resting potential of−90mV.– They are depolarized to threshold by action potentialsfrom the SA node.Voltage-gated Na+channelsopen, and membrane potentialplateaus at 15mV for 200−300msec.Due to balance betweenslow influx of Ca2+andefflux of K+More K+are opened, andrepolarization occurs.
  47. 47. Electrical Activity of the Heart– Action potentialsspread viaintercalated discs(gap junctions).– AV node at base ofright atrium andbundle of Hisconduct stimulationto ventricles.
  48. 48. Electrical Activity of the Heart– In the interventricularseptum, the bundleof His divides intobundle branches.– Branch bundlesbecome Purkinjefibers, whichstimulate ventricularcontraction.
  49. 49. Electrical Activity of the Heart– Action potentials from the SAnode spread rapidly.• 0.8–1.0 meters/second– At the AV node, APs slowdown.• 0.03−0.05 m/sec• This accounts for half ofthe time delay betweenatrial and ventricularcontraction.– The speed picks up in thebundle of His, reaching 5m/sec in the Purkinje fibers.– Ventricles contract 0.1–0.2seconds after atria.
  50. 50. Spread of Excitation
  51. 51. Refractory Periods• Because the atria andventricles contract assingle units, they cannotsustain a contraction.• Because the actionpotential of cardiac cellsis long, they also havelong refractory periodsbefore they can contractagain.
  52. 52. Electrocardiogram• This instrument records the electricalactivity of the heart by picking up themovement of ions in body tissues inresponse to this activity.
  53. 53. Electrocardiogram• P wave: atrial depolarization• QRS wave: ventriculardepolarization• S-T segment: plateau phase• T wave: ventricularrepolarization
  54. 54. Electrocardiogram
  55. 55. Heart Sounds• Produced by closing valves- “Lub” = closing of AV valves• Occurs at ventricular systole- “Dub” = closing of semilunar valves• Occurs at ventricular diastole
  56. 56. ECG and Heart Sounds• Lub occurs afterthe QRS wave.• Dub occurs at thebeginning of theT wave.
  57. 57. Heart Murmur• Abnormal heart sounds produced byabnormal blood flow through heart.– Many caused by defective heart valves.• Mitral stenosis: Mitral valve calcifies andimpairs flow between left atrium andventricle.– May result in pulmonary hypertension.
  58. 58. Heart Murmur• Incompetent valves: do notclose properly– May be due to damagedpapillary muscles• Septal defects: holes ininterventricular or interatrialseptum– Blood crosses sides.
  59. 59. IV. Cardiac Cycle
  60. 60. Cardiac Cycle• Repeating patternof contraction andrelaxation of theheart.– Systole: contractionof heart muscles– Diastole: relaxationof heart muscles
  61. 61. Cardiac Cycle1. Ventricles begin contraction, pressurerises, and AV valves close (lub).2. Pressure builds, semilunar valves open,and blood is ejected into arteries.1. Pressure in ventricles falls; semilunarvalves close (dub).
  62. 62. Cardiac Cycle4. Pressure in ventricles falls below that ofatria, and AV valve opens. Ventricles fill.5. Atria contract, sending last of blood toventricles
  63. 63. Cardiac Cycle and Pressures
  64. 64. V. Blood Vessels
  65. 65. Blood Vessels• Arteries• Arterioles• Capillaries• Venules• Veins
  66. 66. Parallel Arrangement of Blood FlowAllows:All organs to receive blood of same compositionBlood flow through an organ system to be adjusted according to needBlood constantly reconditionedReconditioning organs (digestive organs, Kidneys, Skin) receive more bloodthan their own need
  67. 67. Blood Vessels
  68. 68. 73Table 13.8
  69. 69. Blood Vessels• Innermost layer of all vessels isthe endothelium• Capillaries are made of onlyendothelial cells• Arteries & veins have 3 layerscalled tunica externa, media, &interna– Externa is connective tissue– Media is mostly smoothmuscle– Interna is made ofendothelium, basementmembrane, & elastin• Although have same basicelements, arteries & veins arequite different
  70. 70. Arteries• Large arteries are muscular & elastic– Contain lots of elastin so very elastic– Expand during systole & recoil during diastole• Helps maintain smooth blood flow during diastole• Serve as rapid transit pathway to the tissues and pressurereservoir during diastole13-67
  71. 71. Arterioles• Small arteries & arterioles are muscular– Provide most resistance in circulatory system– Arterioles cause greatest pressure drop– Mostly connect to capillary beds• Some connect directly to veins to form arteriovenousanastomoses13-68
  72. 72. Physical Laws Describing BloodFlow• Blood flows through vascular system when there is pressuredifference (∆P) at its two ends– Flow rate is directly proportional to difference (∆P = P1 - P2)14-33
  73. 73. Physical Laws Describing BloodFlowFlow rate is inversely proportional to resistanceFlow = ∆P/RResistance is directly proportional to length of vessel (L) & viscosity ofblood (η) and inversely proportional to 4th power of radiusSo diameter of vessel is very important for resistance becauseviscosity and length of the vessel do not changeMean Arterial Pressure:Diastolic Pressure (80) + 1/3rdPulse Pressure (13.33)Pulse Pressure = Systolic Pressure (120) – Diastolic Pressure (80)So MAP for a normal BP is 80 + 13.33 = 93.3314-34
  74. 74. Relationship between blood flow,radius & resistance14-35Relationship between blood flow,radius & resistance
  75. 75. Vasoconstriction andVasodilation
  76. 76. Intrinsic Regulation of Blood Flow(Autoregulation)• Maintains fairly constant blood flow despite BPvariation• Myogenic control mechanisms occur in sometissues because vascular smooth musclecontracts when stretched & relaxes when notstretched– E.g. decreased arterial pressure causes cerebral vessels todilate & vice versa. Brain requires a constant supply ofblood14-39
  77. 77. • Metabolic control mechanism matches bloodflow to local tissue needs• Low O2 or pH or high CO2, adenosine, or K+from high metabolism cause vasodilation whichincreases blood flow (= active hyperemia)• Reactive hyperemia: a local vosodilation inresponse to stopping or constriction of bloodflow to the area.Intrinsic Regulation of Blood Flow(Autoregulation) continued14-40
  78. 78. • Local Histamine Release: In injuries orallergies local histamine release causesvasodilation• Local Heat or Cold: Used therapeutically toreduce vasodilation by applying cold packs toaffected areasIntrinsic Regulation of Blood Flow(Autoregulation) continued14-40
  79. 79. • Sympathoadrenal activation (Neural Control)causes increased CO & resistance in periphery& viscera– Blood flow to skeletal muscles is increased• Because their arterioles dilate in response to Epi & theirSymp fibers release ACh which also dilates theirarterioles• Thus blood is shunted away from visceral & skin tomusclesEndocrine control: Many hormones affect the radii ofarterioles; e.g., epinephine, angiotensin and vasopressincause vasoconstrictionExtrinsic Regulation of Blood Flow14-36
  80. 80. Paracrine Regulation of Blood Flow• Endothelium produces several paracrineregulators that promote relaxation:– Nitric oxide (NO), bradykinin, prostacyclin• NO is involved in setting resting “tone” of vessels– Levels are increased by Parasymp activity– Vasodilator drugs such as nitroglycerin or Viagra act thru NO• Endothelin 1 is vasoconstrictor produced byendothelium14-38
  81. 81. Aerobic Requirements of the Heart• The coronary arteries supply blood to amassive number of capillaries (2,500–4,000 per cubic mm tissue). Heart is themost perfused tissue in human body– Unlike most organs, blood flow is restrictedduring systole. Cardiac tissue therefore hasmyoglobin to store oxygen during diastole tobe released in systole.
  82. 82. Circulatory Changes During Exercise• Cardiac outputcan increase5X due toincreasedcardiac rate.• Stroke volumecan increasesome due toincreasedvenous return.
  83. 83. Cerebral Circulation• The brain cannot tolerate much variationin blood flow.– At high pressure, vasoconstriction occurs toprotect small vessels from damage andstroke.– When blood pressure falls, cerebral vesselsautomatically dilate.
  84. 84. • Provide extensive surface area for exchange• Blood flow through a capillary bed is determined by state ofprecapillary spincters of arteriole supplying itCapillaries13-69
  85. 85. • In continuous capillaries, endothelial cells are tightly joinedtogether– Have narrow intercellular channels that permit exchange ofmolecules smaller than proteins– Present in muscle, lungs, adipose tissue• Fenestrated capillaries have wide intercellular pores– Very permeable– Present in kidneys, endocrine glands, intestines.• Discontinuous capillaries have large gaps in endothelium• Are large & leaky• Present in liver, spleen, bone marrow.Types of Capillaries13-70
  86. 86. Exchange across capillary wall
  87. 87. Exchange of Fluid betweenCapillaries & Tissues• Distribution of ECF between blood & interstitialcompartments is in state of dynamic equilibrium• Movement out of capillaries is driven byhydrostatic pressure exerted against capillarywall– Promotes formation of tissue fluid– Net filtration pressure= hydrostatic pressure incapillary (17-37 mm Hg) - hydrostatic pressure ofECF (1 mm Hg)14-19
  88. 88. Fig 14.914-22
  89. 89. Cutaneous Blood Flow• The skin can tolerate the greatest fluctuations inblood flow.• The skin helps control body temperature in achanging environment by regulating blood flow =thermoregulation.– Increased blood flow to capillaries in the skin releasesheat when body temperature increases.– Sweat is also produced to aid in heat loss.– Vasoconstriction of arterioles keeps heat in the bodywhen ambient temperatures are low.
  90. 90. Cutaneous Blood Flow• Thermoregulationis aided byarteriovenousanastomoses,which shunt bloodfrom arteriolesdirectly to venules.
  91. 91. • Contain majority of blood in circulatory system• Capicitance vessels• Very compliant (expand readily), but not elastic• Contain very low pressure (about 2mm Hg)– Insufficient to return blood to heart– Have valves for one way flowVeins13-71
  92. 92. Venous Return continued• Veins hold most ofblood in body (70%) &are thus calledcapacitance vessels– Have thin walls &stretch easily toaccommodate moreblood withoutincreased pressure(=highercompliance)• Have only 0-10 mm Hgpressure14-16
  93. 93. Venous Return• Is return of blood toheart via veins• Controls EDV & thus SV& CO• Dependent on:– Blood volume &venous pressure– Vasoconstrictioncaused by Symp– Skeletal musclepumps– Pressure drop duringinhalation14-15
  94. 94. • Blood is movedtoward heart bycontraction ofsurrounding skeletalmuscles (skeletalmuscle pump)– & pressure dropsin chest duringbreathing– 1-way venousvalves ensureblood moves onlytoward heartVenous Return13-72
  95. 95. VI. Lymphatic System
  96. 96. Functions of the Lymphatic System• Transports excess interstitial fluid (lymph) fromtissues to the veins• Produces and houses lymphocytes for theimmune response• Transports absorbed fats from intestines toblood
  97. 97. Lymphatic System continued• Lymphatic capillariesare closed-end tubesthat form vast networksin intercellular spaces– Very porous, absorbproteins,microorganisms, fat13-88
  98. 98. Vessels of the Lymphatic System• Lymphatic capillaries: smallest;found within most organs– Interstitial fluids, proteins,microorganisms, and fats canenter.• Lymph ducts: formed frommerging capillaries– Similar in structure to veins– Lymph is filtered throughlymph nodes• Tonsils, thymus, spleen– Sites for lymphocyteproduction
  99. 99. Organs of the Lymphatic System
  100. 100. Edema• Normally filtration, osmotic reuptake, & lymphatic drainagemaintain proper ECF levels• Edema is excessive accumulation of ECF resulting from:– High blood pressure– Venous obstruction– Leakage of plasma proteins into ECF– Myxedema (excess production of glycoproteins inextracellular matrix) from hypothyroidism– Low plasma protein levels resulting from liver disease– Obstruction of lymphatic drainage14-23
  101. 101. 107
  102. 102. 108Table 14.2
  103. 103. Blood Pressure (BP)• Is controlled mainly by HR, SV, & peripheralresistance– An increase in any of these can result in increasedBP• Sympathoadrenal activity raises BP via arteriolevasoconstriction & by increased CO• Kidney plays role in BP by regulating bloodvolume & thus stroke volume14-54
  104. 104. VII Cardiac Output14-3
  105. 105. • Is volume of blood pumped/min by eachventricle• Stroke volume (SV) = blood pumped/beat byeach ventricle• CO = SV (`70 ml/min) x HR (`70 beats/min)=4900ml/min• Total blood volume is about 5.5LCardiac Output (CO)14-4
  106. 106. Fig 14.514-14
  107. 107. Regulation of Cardiac Rate• Without neuronal influences, SA node will driveheart at rate of its spontaneous activity• Normally Symp & Parasymp activity influenceHR (chronotropic effect)• Autonomic innervations of SA node is maincontroller of HR– Sympathetic NS increases heart rate by releasingepinephrine and Nor-epinephrine– Parasympathetic NS innervates at the SA nodeand releases Acetylcholine. The affect is to reducethe heart rate14-5
  108. 108. Stroke Volume• Is determined by 3 variables:– End diastolic volume (EDV) = volume of blood inventricles at end of diastole– Total peripheral resistance (TPR) = impedance toblood flow in arteries– Contractility = strength of ventricular contraction14-9
  109. 109. • EDV is workload (preload) on heart prior tocontraction– SV is directly proportional to preload & contractility• Strength of contraction varies directly with EDV• Total peripheral resistance = afterload whichimpedes ejection from ventricle• Ejection fraction is SV/ EDV– Normally is 60%; useful clinical diagnostic toolRegulation of Stroke Volume14-10
  110. 110. Frank-Starling Law of the Heart• States that strengthof ventricularcontraction variesdirectly with EDV– Is an intrinsicproperty ofmyocardium– As EDVincreases,myocardium isstretched more,causing greatercontraction & SVFig 14.214-11
  111. 111. Frank-Starling Law of the Heart continued• (a) is state of myocardial sarcomeres just before filling– Actins overlap, actin-myosin interactions are reduced &contraction would be weak• In (b, c & d) there is increasing interaction of actin & myosinallowing more force to be developed14-12
  112. 112. Extrinsic Control of Contractility• At any given EDV,contraction dependsupon level ofsympathoadrenalactivity– NE & Epi produce anincrease in HR &contraction (positiveinotropic effect)• Due to increasedCa2+insarcomeres14-13
  113. 113. 14-14
  114. 114. VIII Blood Pressure14-51
  115. 115. Blood Pressure (BP)• Arterioles play role in blood distribution & control of BP• Blood flow to capillaries & BP is controlled by aperture ofarterioles• Capillary BP is decreased because they are downstream ofhigh resistance arterioles14-52
  116. 116. Blood Pressure (BP)• Capillary BP is also low because of large totalcross-sectional area14-53
  117. 117. Blood Pressure (BP)• Is controlled mainly by HR, SV, & peripheralresistance– An increase in any of these can result in increasedBP• Sympathoadrenal activity raises BP via arteriolevasoconstriction & by increased CO• Kidney plays role in BP by regulating bloodvolume & thus stroke volume14-54
  118. 118. Baroreceptor Reflex• Is activated by changes in BP– Which is detected by baroreceptors (stretchreceptors) located in aortic arch & carotid sinuses• Increase in BP causes walls of these regions to stretch,increasing frequency of APs• Baroreceptors send APs to vasomotor & cardiac controlcenters in medulla• Is most sensitive to decrease & suddenchanges in BP14-55
  119. 119. Fig 14.2614-56
  120. 120. 14-57
  121. 121. Atrial Stretch Receptors• Are activated by increased venous return & actto reduce BP• Stimulate reflex tachycardia (slow HR)• Inhibit ADH release & promote secretion ofANP14-58

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