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Unit 4 - Cardiovascular and Respiratory Physiology

Shauna Ryner Physiology Unit 4 Englisch 200 Karten

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  1. 1Primary Function of the Cardiovascular SystemTransport
  2. 2Cardiovascular PhysiologyThe study of the function of the heart, blood vessels, and blood
  3. 3What is the medium for transport?Blood
  4. 4Modes of Transport: Bulk FlowBlood moving through the vessels (rapid, over long distances). For flow to occur there must be a pressure difference: pressure at one end is greater than pressure at the other end.
    Perfusion Pressure: difference in pressure that causes blood to flow through a blood vessel.
  5. 5What happens if the heart stops?Unconsciousness in approximately 30 seconds. Irreversible damage to brain and other organs and tissues. (Tissues/organs basically die because there is no oxygen transported to tissues/organs)
  6. 6IschemiaInadequate blood flow to any tissue
  7. 7Transient IschemiaDysfunction (Eg. neurological dysfunction because of lack of blood flow)
  8. 8Persistent IschemiaPermanent tissue damage (infarction) or cell death (necrosis)
  9. 9Primary Cardiovascular DysfunctionsDisturbance or disease process that affects the cardiovascular system directly (eg. hemorrhage, myocarditis).
    a) Congenital
    b) Acquired
  10. 10Congenital Primary Cardiovascular DysfunctionPresent at birth. Eg. valve defects: inability of the heart to pump an adequate amount of blood
  11. 11Acquired Primary Cardiovascular DysfunctionDeveloping after birth.
    Eg. Myocarditis (infection of the heart muscle)
    Eg. Parasites: Dirofilaria immitis (dogs) - Heartworm, or Strongylus vulgaris (horses) - similar to heartworm
  12. 12Secondary cardiovascular dysfunctionsCardiovascular system is NOT the primary target of the disease
  13. 13ShockSerious medical condition in which the organs and tissues are not receiving an adequate flow of blood, depriving organs and tissues of oxygen and allowing the building up of waste products.
    Shock is a type of secondary cardiovascular dysfunction
  14. 14Types of Shock: HemorrhagicCardiovascular failure due to severe blood loss
  15. 15Types of Shock: CardiogenicCardiovascular collapse caused by heart failure. (Eg. heart can't beat anymore)
  16. 16Types of Shock: SepticCaused by bacterial infections in the bloodstream
  17. 17Types of Shock: EndotoxicOccurs when endotoxins (bacterial cell wall fragments) enter the bloodstream (usually due to intestinal mucosal damange as a result of ischemia) that cause the body to produce substances that decrease pumping ability of the heart (failure)
  18. 18Substances transported by the Cardiovascular System (4)1) Metabolic substrates required for cellular function: oxygen, glucose, amino acids, fatty acids, lipids
    2) Metabolic Waste Products: Carbon dioxide, lactic acid, nitrogenous wastes (by-products of metabolism), heat
    3) Hormones: chemical messengers
    4) Water and Electrolytes: Primarily maintained by kidney
  19. 19Perfusion PressureDifference in pressure that causes blood to flow through a blood vessel
  20. 20Modes of Transport: DiffusionPrimary method by which dissolved substances move across the blood vessel walls from blood to interstitial fluid (and then to tissue) and vice versa. Movement occurs due to concentration gradient. Occurs across the capillaries to make diffusion faster. Because diffusion is slow, every metabolically active cell in the body must be close to a capillary carrying blood by bulk flow
  21. 21Functional Arrangement of the Cardiovascular System: HeartProvides force for blood flow. Functions coordinately as 2 independent pumps: 1) Left side: receives oxygenated blood from lungs & delivers it to systemic circulation 2) Right side: Receives deoxygenated blood from systemic circulation & sends it to lungs for gas exchange.
    Under normal conditions in both sides: pump exactly the same amount of blood/minute
  22. 22Cardiac OutputVolume of blood pumped each minute one ventricle. Increases during exercise, etc.
  23. 23Hematocrit (PCV)Fraction of cells in the blood
  24. 24If you have high plasma concentration and low cell concentration in the blood, this could indicate:Hemorrhage
  25. 25If you have low plasma concentration and high cell concentration, this could indicate:Dehydration
  26. 26BloodSuspension of cells in liquid
  27. 27Gas Transport99% of oxygen carried as oxyhemoglobin and only 1% carried as dissolved oxygen. Carbon dioxide is transported as bicarbonate (a buffer), or combines with hemoglobin or plasma proteins.
  28. 28What is the buffy coat in blood?White blood cells
  29. 29Cell Types of The HeartCardiomyocytes (muscle cells):
    a) Contractile cells
    b) Pacemaker Cells
    Non-Cardiomyocyte Cells (non-muscle cells):
    a) Fibroblasts
    b) Endothelial & Smooth Muscle Cells
    c) Neural Cells
  30. 30Cardiomyocytes: Contractile CellsMake up 99% of cardiac myocytes.
    Striated muscle cells with contractile proteins arranged into sarcomeres. Responsible for generating the force for myocardial contraction.
    (Mechanism is similar to skeletal muscle contraction)
  31. 31Cardiomyocytes: Pacemaker CellsMake up 1% of Cardiac myocytes.
    Autorhythmic
    Low abundance of contractile proteins, NOT arranged into sarcomeres. Responsible for estrablishing the rate/rhythm of myocardial contraction/relaxation
  32. 32AutorhythmicGenerating their own action potentials spontaneously independent of a synapse
  33. 33Non-cardiomyocyte Cells: Fibroblasts70% or more of all cells in the heart. Responsible for producing extracellular matrix essential for the structural integrity of the myocardium. Important in repair of injured heart after myocardial infarction
  34. 34Endothelial and Smooth Muscle CellsMake up coronary vasculature. Multiple capillaries per cardiac myofibril (works hard all the time; needs nutrients and waste removal)
  35. 35Neural CellsConvey sympathetic or parasympathetic drive
  36. 36When we die, our heart keeps beating for a while. What causes the actual cessation of our autorhythmic heart?Heart runs out of resources (oxygen and nutrients) and therefore cannot keep working
  37. 37Secondary Cardiovascular Dysfunctions: Pulmonary EdemaLife-threatening. Decreased movement of oxygen from alveoli to blood stream.
    Also occurs in shock-lung syndrome: toxic substanes cause increased lung permeability of lung blood vessels. Leads to accumulation of water, electrolytes, plasma proteins, etc. in the lung
  38. 38Secondary Cardiovascular Dysfunction: Anesthetic OverdoseDue to CNS depression of cardiovascular (and respiratory) centers. Leads to decreased blood pressure and cardiac output. Barbituates act directly on the heart to decrease pumping ability.
  39. 39Secondary Cardiovascular Dysfunctions: Burns or Persistent vomiting or diarrheaLoss of water and electrolytes leads to cardiac arrhythmias. If wrong fluid therapy is given: leads to edema
  40. 40SA node:The pacemaker (sets the rhythm of the heart)
  41. 41AV nodeLocated at base of right atrium near the atrioventricular ceptum
  42. 42AV bundle (Bundle of his)Originates at atrioventricular node, enters the septum
  43. 43Purkinje fibresSmall terminal fibers extending to ventricular myocytes for synchronous contraction.
  44. 44Left/Right bundle branchesTravel to the apex and curve upward
  45. 45Sympathetic Effects on the HeartAct on all cardiac cells. Predominates in exercise, stress. Norepinephrine, epinephrine. Adrenergic receptors. Increased intracellular calcium, decreased potassium conductance. Positive ionotropy (decreased contractility), positive chronotropy (increase HR)
  46. 46ChronotropyAffects the rate/speed of the heart; affects the timing. Chrono- means time, tropos means 'a turn'
  47. 47Parasympathetic Effects on the HeartPrimarily acts on SA node, AV node, & atria. Predominates at rest. Acetylcholine. Muscarinic receptors (where ACh acts). Decreased intracellular calcium. Increased potassium conductance. Negative ionotropy (mild) (decreased contractility). Negative chronotropy (decrease HR).
  48. 48Action potentials in pacemaker cellsPacemaker cells spontaneously depolarize to threshold and then form an AP. RMP constantly doing slow increase to threshold. Takes longer for AP to occur than skeletal/neuronal AP. Slower to get to peak in AP: No fast Na+ channels in pacemaker cells. Rounded shape due to opening of calcium channels.
  49. 49Pacemaker PotentialSpontaneous depolarization to threshold
  50. 50Pacemaking in the HeartUnder normal conditions: SA node (70-80bpm). If SA node damaged/diseased, other pacemaker cells establish heart rate, following conduction pathways (fail safes): AV node (40-55bpm); Bundle of His (25-40bpm); Bundle branches (25-40bpm); and Purkinje fibers (25-40bpm).
  51. 51Conduction System of the Heart1) AP arises in cell of SA node
    2) AP moves across L & R atria: atrial contraction
    3) AP travels to AV node (delay in conduction thru AV node and Bundle of His allows delay b/w atrial and ventricular contraction)
    4) Rapid conduction thru remainder of AV bundle to L & R bundle branches
    5) At apex, Purkinje fibers propagate AP into ventricular muscle fibers, then thru ventricular walls
  52. 52What does the extremely rapid conduction of an action potential allow for?A nearly synchronus contraction of all fibers in both ventricles
  53. 53Electrocardiogram (ECG)Graphical recording of electrical impulses propagating through the heart using electrodes on the skin (usually 6 leads are used in veterinary medicine). Measures total electricity across the heart, does NOT measure single AP's. Detection and dx of irregularity in HR and rhythm.
  54. 54Einthoven TriangleLeads on the Right and left forelimb and the left hindlimb. (An imaginary formation of 3 limb leads in a triangle used in electrocardiography, formed by the 2 shoulders and the pubis. Shape forms an inverted equilateral triangle with heart at the center that produces zero potential when the voltages are summed)
  55. 55Arrhythmias: Classification (2)Disorders of Rate
    and
    Disorders of rhythm
  56. 56Arrhythmias: Disorders of RateBradyarrhythmias (bradycardia) - slow HR
    Tachyarrhythmias (tachycardia) - fast HR
  57. 57Arrhythmias: Disorders of rhythmIrregular heart rhythms: Premature atrial (PACs) and ventricular complexes (PVCs), heart blocks, atrial fibrillation, ventricular fibrillation, etc.
    These affect QRS form on ECG.
  58. 58What does decreased cardiac output lead to?Decreased nutrients (eg. oxygen) reaching tissues, and increase of waste buildup in tissues
  59. 59Arrhythmia DefinitionDeviations from normal cardiac rate or rhythm
  60. 60Arrhythmias: CausesProblems with 1) formation of AP's or 2) propagation (conduction) of AP's
    Decreased efficiency of heart's pumping cycle. Abnormal conduction patterns (detect with ECG). Can be caused by electrolyte (ion) abnormalities, fever, hypoxia, stress, inf., drug toxicity, disease
  61. 61Arrhythmias: Problems with the formation of APsi) Sinus arrest: SA node completely fails to form AP
    ii) Sick Sinus Syndrome: SA node pacemaker cells form sluggish depolarizations (char. by bradycardia, insufficient increase in HR during exercise).
  62. 62Arrhythmias: Problems with the formation of APs - Treatmenta) drugs to block parasympathetic input (eg cholinergic muscarinic antagonist such as atropine) to incr. HR
    b) Drugs to incr. sympathetic nerve activity (eg beta adrenergic agonist such as isoproterenol)
    c) artifical cardiac pacemaker
  63. 63Arrhythmias: Problems with Propagation of APs AV node block- Definition and ClassificationsAV node block: does not allow conduction of APs from SA node
    a) 1st degree
    b) 2nd degree
    c) 3rd degree
  64. 64Arrhythmias: Problems with propagation of AP's: Atrial Conduction Abnormalitiesa) Premature atrial contractions or beats (PAC/PAB) - extra contraction or ectopic beats (due to irritable atrial muscle cells outside conduction pathway).
    b) Atrial Fibrillation rate >400bpm: Causes pooling of blood in atria causing a risk of thrombus formation. Loss of effective contraction, no P waves visible on ECG
  65. 65Cardiac CyclePeriod of time b/w 2 successive heart beats. 2 alternating phases: systole and diastole.
  66. 66SystolePeriod during which heart is contracting and emptying. Pressure devel'd by heart exceeds pressure in aorta & pulmonary artery allowing oxygenated blood to flow into aorta & pulmonary artery following ventricular contraction
  67. 67DiastolePeriod during which heart is relaxing and filling. Diastole is longer than systole (2/3 of cardiac cycle). Pressure in heart is lower than vasculature allowing deoxygenated blood to return to heart. Changes in HR primarily manifested by changes in diastolic interval: Increased HR decreases diastolic interval (heart relaxed, shorter interval). Decreased HR increases diastolic interval (heart relaxes longer)
  68. 68Stroke volume (SV)Volume of blood ejected by each ventricle during each contraction. [End diastolic volume - end systolic volume]
  69. 69Cardiac PhysiologyPeriod of time between 2 successive heart beats. 2 alternative phases: systole and diastole
  70. 70SystolePeriod during which heart is contracting and emptying. Pressure developed by heart exceeds pressure in aorta and pulmonary artery allowing oxygenated blood to flow into the aorta and pulmonary artery following ventricular contraction
  71. 71DiastolePeriod during which heart is relaxing and filling. Diastole is longer than systole (2/3 of cardiac cycle). Pressure in heart is lower than in the vasculature allowing deoxygenated blood to return to the heart. Changes in heart rate primarily manifested by changes in diastolic interval. Increased HR decreases diastolic interval (heart relaxed for shorter time)
  72. 72Cardiac Cycle1) Ventricles fill passively
    2) Atrial systole forces small amount of additional blood into ventricles
    3) Ventricular ejection: Blood ejected
    4) Neither filling nor emptying of the ventricle
  73. 73Factors Affecting cardiac output causing an increase in cardiac outputIncreased stroke volume. Increased heart rate. Increased end diastolic volume. Increased contractility. Increased sympathetic activity. Decreased parasympathetic activity. Decreased end systolic volume. Increased preload.
  74. 74ContractilityPumping ability of the ventricle. (All factors that cause an increase in contractility work by causing an increase in intracellular calcium concentration during systole
  75. 75Normal heart sounds (lub dub)1) Lub: Closure of AV valves at the beginning of ventricular systole
    2) Dub: Closure of aortic and pulmonic valves at the end of ventricular systole
  76. 76Cardiac MurmursAbnormal heart sounds caused by turbulent blood flow through heart defects (turbulent flow is noisy). Turbulent blood flow through a cardiac defect only occurs if there is a substantial pressure difference from one side to the other.
  77. 77Systolic MurmursOccur during ventricular systole. Due to problems with: AV valves - Mitral incompetence and tricuspid incompetence; Aortic valve &/or pulmonic valve - stenosis; Ventricular septal defect; Patent ductus arteriosis
  78. 78Diastolic MurmursOccur during ventricular diastole. AV valves - Mitral &/or Tricuspid stenosis; Aortic valve &/or pulmonic valve incompetence; Patent ductus arteriosis
  79. 79Patent ductus arteriosisOpening between aorta and pulmonary artery remains open after birth
  80. 80Cardiac Defects that cause murmurs usually lead to:1) Abnormally high or low blood flow to a region of the body
    2) Abnormally high or low BP in a region of the body
    3) Cardiac hypertrophy (enlargement of heart b/c its working much harder so increased CO in short term, but walls thicken and detrimental effects with decreased CO in long term.)
  81. 81Pathological Consequences of Cardiac Defects - Mitral Regurgitation:Mitral Regurgitation: Increased volume work of LV --> LV hypertrophy. Increased left atrial pressure--> increased pulmonary venous pressure-->pulmonary edema
  82. 82Pathological Consequences of Cardiac Defects - Patent DuctusIncreased volume of LV --> LV hypertrophy. Increased pulmonary artery pressure --> increased pressure work of RV --> RV hypertrophy
  83. 83Pathological Consequences of Cardiac Defects - Mitral StenosisIncreased left atrial pressure --> increased left atrial size leading to atrial fibrillation. Increased pulmonary venous pressure leading to pulmonary edema
  84. 84Systemic circulationPressure difference between aorta and vena cava forces blood to move. Pumping of blood by heart maintains pressure difference. If heart stops eventually there is no pressure difference b/w aorta (pressure decrease) and vena cava (pressure increase)
  85. 85ComplianceAbility of a vessel to distend when pressure or volume is added (how much force is needed to achieve distention. Veins: expand to increase volume; no change in venous pressure. Volume reservoirs.
    Arteries: far less compliant. Increase/decrease in blood volume changes pressure a lot! Function as pressure reservoirs.
  86. 86Vascular ResistanceResistance to flow. Factors influencing it: 1) size: larger vessels offer less resistance to blood flow 2) length: longer the vessels, the greater the resistance to blood flow
    3) Viscosity: more viscous the fluid, the greater the resistance to blood flow.
    Arterioles have highest vascular resistance
  87. 87ArteriolesVessels with highest vascular resistance. Resistance is adjustable. Main determinant of blood flow to tissues: increased arteriolar resistance leads to decreased local blood flow. Change radius by contraction/relaxation of smooth muscle in arteriole walls
  88. 88Blood flow to each organ is determined by1) Perfusion Pressure: All organs exposed to same perfusion pressure; dif's in blood flow due to:
    2) Vascular resistance: Primarily determined by arteriolar contraction/relaxation in one organ relative to another
  89. 89Pulmonary CirculationMuch less resistance to blood flow (compared to systemic circulation). All cardiac output must pass through lungs. Exercise requires increase in CO: increased pulmonary blood flow prevents large increase in pulmonary arterial pressure
  90. 90Mean Arterial PressureDiastolic pressure + 1/3 (Systolic pressure - diastolic pressure)
  91. 91Blood/Pulse Pressure CalculationBlood pressure = cardiac output x Peripheral resistance
  92. 92CapillariesSmallest blood vessels; single layer of epithelial cells. The microcirculation. 'Exchange vessels' due to exchange of water and solutes (and gases) between the blood and interstitial fluid
  93. 93Oncotic ForcesWater moves across capillary walls by 1) Osmosis: diffusion across a semi-permeable membrane from an area of low solute concentration to an area of high solute concentration (to dilute it). Depends on: osmotic pressure in interstitial fluid and plasma oncotic pressure/colloidal osmotic pressure
  94. 94Hydrostatic forcesWater moves across capillary walls by 2) Bulk flow: movement of water from capillary to interstitial fluid due to hydrostatic forces. Increase hydrostatic pressure at arteriolar end of capillary bed forces water out of the capillary to interstitial fluid (filtration)
  95. 95Onocotic and Hydrostatic forces under normal conditionsNet hydrostatic pressure difference and the net oncotic pressure dif is almost balanced but net hydrostatic pressure difference is slightly larger than net oncotic difference --> small excess of water in interstitial fluid: lymphatic system collects excess fluid and interstitial proteins and returns it to bloodstream via subclavian veins
  96. 96EdemaClinically noticeable excess of interstitial fluid caused by 1) excessive filtration of fluid, 2) depressed lymphatic function
  97. 97Safety Mechanisms that limit the degree of edema1) increased interstitial fluid pressure acts directly to oppose filtration
    2) Increase interstitial fluid pressure promotes lymph flow (remove more fluid)
    3) Decreased interstitital fluid protein concentration decreases filtration rate (due to decreased interstitial fluid oncotic pressure)
  98. 98What can lead to edema?Increased venous pressure
    Decreased plasma protein concentration
    Lymphatic obstruction
    Histamine Release
  99. 99Local Control of Blood FlowBlood flow through any organ determined by perfusion pressure and vascular resistance. Since all organs are exposed to same perfusion pressure, differences in blood flow due to differences in vascular resistance
  100. 100Control of Vascular Resistance: Intrinsic FactorsLocal mechanisms within a tissue to alter resistance. Dominate in critical tissues that require second to second control of blood flow. Predominate in control of arterioles in coronary circulation, brain, working skeletal muscle
  101. 101Control of Vascular Resistance: Extrinsic FactorsInvolves mechanisms that act from outside a tissue to alter resistance (nerves, hormones). Dominates in tissues that can withstand temporary reductions in bloodflow. Predominate in control of blood flow to kidneys, splanchic organs and resting skeletal muscle
  102. 1022 intrinsic factors in the control of vascular resistancea) Metabolic Control: matches blood flow to a tissue with metabolic rate. Tissues increase blood flow when metabolic rate increases
    b) Paracrine Actions: Local chemical signals not related to metabolism. Recall histamine: released fr 1 type of cell in tissue acts directly on arteriolar smooth muscle cells to cause vasodilation
  103. 103Metabolic ControlMost important local control mechanism. Works by means of chemical changes in the tissue. Also involves negative feedback when oxygen delivered and metabolic waste products removed.
  104. 104Metabolic Control of Blood Flow: Active HyperemiaIncrease in tissue blood flow in response to increased metabolic rate (all these chemical mediators/waste products)
  105. 105Reactive HyperemiaTemporary increase in tissue blood flow after a period when blood flow was restricted (eg hold hand tight, then let go and blood flows to area that had been deprived/restricted)
  106. 106Mechanical Compression (MC)Decreased blood flow in a tissue by squeezing down on all the blood vessels. Brief compression: reactive hyperemia. Prolonged compression: ischemia leading to irreversible tissue damage and cell death (infarction) Eg bed sores
  107. 107AutoregulationRelative constancy in blood flow in an organ when there have been no change in metabolic rate but blood pressure has increased/decreased.
    Metabolic mechanisms responsible for active and reactive hyperemia account for autoregulation
  108. 108Paracrine Signalsa) Endothelin-1
    b) Nitric oxide (NO)
    c) Thromboxane A2 and Prostacyclin
    d) Histamine
    e) Bradykinin
  109. 109Paracrine signals: Endothelin - 1Endothelial cells. Mechanical or chemical stimuli --> vasoconstriction
  110. 110Paracrine signals: Nitric Oxide (NO) (gas)Vascular smooth muscle. Released due to increased blood velocity --> vasodilation (negative feedback. Decreased velocity b/c capillary diffusion
  111. 111HistamineMast cells. Released in response to tissue injury antigen challenge --> vasodilation (via stimulating NO formation)
  112. 112BradykininGlobulin proteins and sweat glands. Vasodilation (via stimulating NO formation
  113. 113Neurohumoral Control of the Cardiovascular SystemNervous system and hormones. Extrinsic control mechanisms. Predominate over intrinsic mechanisms in control of blood flow to kidneys, splanchic organs, and resting skeletal muscle (non-critical organs that can withstand decrease in bloodflow). Also controls HR and contractility (heart muscle) allowing adjustment of CO (BUT coronary vasculature under local control)
  114. 114ANS controls of the CV systemNeural component of neurohumoral regulation. ANS conrols CV system via release of epinephrine, norepinephrine, and acetylcholine (Ach) which activate receptors on cardiac myocytes or vascular smooth muscle.
  115. 115BaroreceptorsPressure (stretch) sensitive nerve endings in aortic arch and carotid sinus. Send afferent impulses in vagus nerve (aortic arch) and glossopharyngeal nerve (carotid sinus) to the CNS (brainstem) --> appropriate ANS output. Essential for normal moment to moment stability of BP
  116. 116Baroreceptor ReflexBaroreceptor reflex essential for normal moment to moment stability of BP, but NOT the major mechanism responsible for setting long term levels of BP. Baroreceptors adapt slowly or 'reset' to the prevailing BP. Baroreflex responds quickly and powerfully to counteract sudden changes in BP but has little influence on long term level of BP
  117. 117Atrial Volume ReceptorsSensitive nerve endings in atrium that respond to stretch (caused by increased vol in atrium therefore called 'volume receptors'). Decreased blood flow at kidney --> activates renin-angiotensin-aldosterone system (RAAS)
  118. 118Renal PerfusionAmount of blood in kidney/reaching kidney
  119. 119Heart (pump) FailureAny condition in which decreased contractility limits ability of heart to deliver normal CO and unable to meet metabolic needs of body, or can do so only in presence of pathophysiological adaptive mechanisms. Can be bilateral heart failure, or left or right sided heart failure. Characterized by decreased CO: heart unable to pump sufficient blood to meet metabolic demands of body. Various compensation mechanisms maintain CO
  120. 120Bilateral Heart failureDecreased contractility affecting both sides of heart
  121. 121Left- or Right-sided heart failureDecreased contractility affecting left or right ventricle.
  122. 122When heart can't maintain pumping capability, 3 things occur:1) CO or stroke volume decrease: Less blood reaches various organs-->decreased cell function. Fatigue and lethargy
    2) Backup & congestion develop: Output fr ventricle less than inflow of blood-->Congestion in venous circulation draining into affected side of heart
    3) Other complications secondary to heart failure also develop
  123. 123Left-sided heart failureLV fails-->blood accumulates in lungs.
    Pulmonary congestion/edema: dyspnea, cough, excess fluid in lungs often leads to infections (eg pneumonia)
  124. 124Right-sided heart failureRV fail-->blood accumulates in vena cava. Systemic backup: edema in feet, legs. Increased pressure in jugular veins (= distention). Hepato- and speno-megaly (digestive disturbances). Ascites: fluid accumulation in peritoneal cavity (abd distention)
  125. 125Compensations of Heart failureCompensations allow BP to be maintained near normal when at rest (despite severe ventricular failure)
  126. 126Complications Secondary to Heart failureComplications include: exercise intolerance, decompensation (when heart failure reaches a certain degree of severity, the compensations made by the body to maintain CO make heart failure worse)
  127. 127Decompensation in LV failureBack up of blood in the LA -->increased preload-->increased stroke volume BUT increased preload leads to pulmonary edema
  128. 128Consequences and Compensations of Hemorrhage initiated by:Baroreflex and atrial volume reflex
  129. 129Behavioural and Hormonal Responses to HemorrhageBehavioural: drinking
    Hormonal: Decreased salt and water loss in the urine
  130. 130Muscle PumpDuring exercise the rhythmical contraction of the skeletal muscle squeeze venous blood back to the heart.
  131. 131Amphibian Cardiovascular System3 chambers (2 atria, 1 ventricle): mixed blood sent to systemic circulation. Pulmocutaneous circulation: the ability for oxygen exchange through the moist skin.
  132. 132Reptilian Cardiovascular System3 chambered heart (except for crocodilians - 4 chambers). 2 atrial, 1 ventricle with a partially divided septum --> little blood mixing occurs b/w deoxygenated and oxygenated blood.
  133. 133Respiratory functionsPrimary: To provide oxygen to support tissue metabolism and remove carbon dioxide.
    Others: thermoregulation (panting - heat loss), metabolism of endogenous and exogenous substances, protection against inhaled dusts, toxic gases, and infectious agents
  134. 134Basal metabolismMetabolism of the resting animal
  135. 135Basal Metabolic Rate (BMR)Rate of metabolism required to maintain cellular function. Function of body weight: smaller animals need more oxygen/kg body weight than larger animals
  136. 136Gas ExchangeRequirements: vary with metabolism. May increase 30x with exercise.
    Usually accomplished easily, with little energy cost. In animals with respiratory disease, energy cost increases which means less energy available for exercise and weight gain. May present as thin animals.
  137. 137Processes involved in gas exchange1) Lung ventilation
    2) Distribution of gas within lung
    3) Diffusion at alveoli-capillary membrane
    4)Diffusion of gases b/w blood and tissue
    5) Transport of oxygen in blood from lungs to tissue and carbon dioxide in the opposite direction.
  138. 138VentilationMovement of gas into and out of the lung. Oxygen needs of metabolism require that an animal take in a certain volume of air into the lung (alveoli each minute).
  139. 139VEMinute ventilation. Total volume of air breathed/min. Must increase when an increase in metabolic rate demands increased oxygen. Determined by tidal volume (VT) and respiratory frequency (f)
  140. 140VT f VA VDVT: Volume of each breath
    f: number of breaths/min
    VA: Portion of VT that enters alveoli
    VD: Portion of VT that enters dead-space
  141. 141Conducting airwaysNares, nasal cavity, larynx, pharynx, trachea, bronchus, bronchioles. NO gas exchange occurs in these pathways, therefore also known as 'anatomic dead space'
  142. 142Types of Dead-SpaceGet rid of dead space so volume of air with each breath make it to alveoli (don't want to add additional deadspace).
    Equipment deadspace: any equipment in our airway where air is conducted through
    Anatomic deadspace: fr equipment to alveoli
    Alveolar deadspace: Volume of air in a poorly perfused alveoli (how much capillary around alveoli - decreased fr fluid, inf, scarring, etc.
  143. 143Physiological deadspaceSum of anatomic and alveolar deadspace
  144. 144Dead space/tidal volume ratio (VD/VT)Fraction of each breath ventilating the dead-space. Varies among species: smaller (eg dog) approx. 30%, larger (eg cattle) approx. 50-70%. Deadspace relatively constant, so changes in VT and/or f alter amount of air tha tventilates alveoli and deadspace.
  145. 145InhalationUses diaphragm, external intercostal muscles, abdominal muscles
  146. 146ExhalationPrimarily abdominal muscles and internal intercostal muscles but also uses elastic energy, stored in the stretched lung and thorax.
    During exercise, resp muscle activity increases to generate the increased VE required to meet metabolic oxygen demand
  147. 147In running animals, ventilation is synchronized with gait. During inhalation and exhalation:Inhalation: Forelimbs are extended and hind limbs are accelerating the animal forward (elongates trunk, increases size of thorax)
    Exhalation: Forelimbs are in contact with the ground
  148. 148Pulmonary SurfactantPrevents the lung from collapsing by reducing surface tension. Produced by type II alveolar cells. Composed of lipids and proteins. Surfactant apoproteins: aid in surfactant secretion, maintenance of surface films, reuptake of surfactant, antimicrobial properties. As lung vol decreases, surfactant molecules become concentrated on the alveolar surface: leads to decreased surface tension and promotes stability
  149. 149Lung complianceRefers to how easy a lung is to inflate. Compliant lung: easy to inflate. Lung with low compliance: difficult to inflate.
  150. 150Pleural fluidFluid b/w visceral and parietal pleura. Mechanically links lungs to thorax which allows resp system to act as single unit. Allows lungs to expand during inhalation. Ensures lungs don't deform hen animal exhales beyond FRC
  151. 151AtelectasisMore likely to occur in animals with compliant thoraces (reason lung collapse is more common in newborn animals than adults)
  152. 152Frictional Resistance of the AirwaysProvided by tubes of the upper airway (nose, pharynx, larynx) and tracheobronchial tree. Nasal turbinates warm air, humidify. Branches have lots of smooth muscle in airway. Resistance can be decreased by 1)dilation of nares 2)vasoconstriction. Resistance caused by branching decreased by: increased radius (dilation) of airway passages)
  153. 153Control of airway diameterSmooth muscle: regulates airway diameter in response to neural and other stimuli. PNS activation: bronchoconstriction: activation of PNS: ACh release -->smooth muscle contraction. Can occur in response to irritants, inflammatory mediators (eg histamine and leukotrienes released fr mast cells). SNS: bronchodilation activation of SNS-->catecholamines (Epi, NE), which acts on beta 2 adrenergic -->smooth muscle relaxation
  154. 154Dynamic CompressionSince walls of the airways are not rigid, airways can be compressed or expanded. Understanding when dynamic compression is likely to occur can provide diagnostic clues to location of airway obstruction. Upper airway: dynamic compression occurs during inhalation. Eg laryngeal hemiplegia
  155. 155Collateral ventilationProvides air to alveoli when their main parent bronchus is obstructed. Determined by degree to which lungs are sub-divided into secondary lobules. Varies by species: pigs/cattle: complete separation. Dogs/cats: no separation. Horses/sheep: partial separation. Gas exchange abnormalities that are the result of airway obstruction are more serious in the pig than dogs.
  156. 156Air distribution in the lungDepends on mechanical properties of the lung. Optimal gas exchange requires the matching of ventilation and blood flow. Ideally each region of the lung shoul drecieve equal amounts of ventilation BUT this never occurs (and uneven distribution becomes worse in disease). Uneven distribution can be caused by: local decrease in lung compliance (pneumonia), local airway obstructions (mucus, bronchospasm), recumbent large animals (compresses lowermost areas, sometimes to extent of no ventilation).
  157. 157Intrathoracic airwaysDynamic compression occurs during exhalation. Eg cough: forced exhalation during which dynamic collapse narrows the airways (high air velocity through narrowed airway helps get rid of foreign material). Eg collapsing trachea in toy breeds: Weakened intrathoracic trachea dynamically collapses during forceful ventilation of exercise which results in honking noise
  158. 1582 circulatory Systems for blood flow to the lung1) Bronchial circulation: branch of systemic circulation that provides a nutritional blood supply to the airways and other structures within the lung (supplies tissues of lung)
    2) Pulmonary circulation: Receives total output of right ventricle. Perfuses alveolar capillaries (site of gas exchange)
  159. 159Bronchial CirculationProvides blood supply to airways, large vessels, & visceral pleura (some sp: cattle, sheep, horses). Receives ~2% LV output. Provides nutrient blood flow to lung structures (if bronchial blood flow obstructed, lung structures won't die due to presence of anastomose - usu at capillary & venular level) with pulmonary circulation)
  160. 160Pulmonary CirculationBlood only passes through lung (differs fr systemic circulation). Control mechanisms regulate distribution of blood within lung so blood preferentially perfuses well oxygenated regions. Blood flow regulated by smooth muscle in walls of small pulmonary arteries
  161. 161Pulmonary CapillariesForm extensive branching network almost covering entire alveoli. Not all pulmonary capillaries are perfused when animal is at rest but can be recruited (used if needed)
  162. 162Pulmonary VeinsAlso form a reservoir of blood for LV which can be used to initiate a change in CO (eg burst of exercise)
  163. 163Alveolar capillariesThin walled capillaries that perfuse alveolar septum. From alveoli to bloodstream: diffusion; lipophilic so easy mvmnt.
  164. 164Distribution of Pulmonary Blood Flow influenced by 2 main factors1) Gravity-dependent distribution (bipeds). Vertical gradient of perfusion (blood flow per unit of the lung increases from top to the bottom)
    2) Gravity-independent distribution (quadrupeds). Preferential distribution of blood flow to dorsocaudal region of lung. Accentuated by exercise. Due to branching pattern of pulmonary arteries & arterioles & the relative resistance of each
  165. 165Pulmonary Vascular Resistance (PVR)Resistance in pulmonary vascular bed against which the right ventricle must eject blood. Pulmonary blood vessels offer a low resistance to blood flow. Low in resting animal, even lower when pulmonary blood flow or pulmonary arterial pressure incr. due to recruitment of un-perfused vessels, and distension of all vessels. Capillaries provide majority of resistance blood flow
  166. 166In systemic circulation what provides the majority of resistance blood flow?Arterioles
  167. 167Transmural PressureBlood vessel diameter function of transmural pressure: Dif in pressure b/w inside of vessel and outside of vessel. Incr blood vol in vessel: incr transmral pressure-->vasodilation
    Decreased pressure surrounding vessel -->incr transmural pressure -->vasodilation
    (occurs in lrg pulmonary arteries/veins as lung inflates)
  168. 168Vascular Smooth MuscleNeural and humoral factors act on pulmonary smooth muscle to relax or contract vessels --> alters blood flow. Depends on amount of smooth muscle in pulmonary arteries (varies w species) and initial vascular tone. Neural: SNS and PNS innervation to pulmonary arteries
    Humoral: chemical mediators
  169. 169Alveolar Hypoxia and Vascular ResistancePoorly ventilated alveolus: air has low partial pressure of oxygen, so little benefit to send blood there. Alveolar hypoxia: causes vasoconstriction of pulmonary artery --> decreased blood flow to poorly ventilated alveoli and redistributes blood to better ventilated lung regions. Magnitude of response varies among sp: among of vascular smooth muscle and enviro. (eg altitude)
  170. 170Hypoxic VasoconstrictionBeneficial when alveolar hypoxia localized (eg pneumonia). Serious consequences when alveolar hypoxia generalized. eg cattle grazing at high altitudes: generalized hypoxic vasoconstriction -->pulmonary pressure incr-->incr work for RV-->right-sided CHF (so systemic edema). Brisket dz: clinical syndrome describing edematous fluid accumulation in brisket (trunk/abd)
  171. 171Exercise and Pulmonary CirculationExercise leads to incr pulmonary blood flow b/c pulmonary blood vessels dilate (decrease PVR).
    Exercise induced pulmonary hemorrhage: seen in horses during strenuous exercise. Leakage of RBC's fr pulmonary capillaries due to incr pulmonary arterial pressure
  172. 172Partial Pressure/Fractional CompositionDescribes composition of gas mixture. Oxygen is 21% in Kingston and Mt. Everset but hypoxia develops in altitude. Partial pressure of oxygen takes into account fraction of oxygen and how tightly oxygen molecules packed which depends on barometric pressure
  173. 173Alveolar Gas CompositionDetermined by alveolar ventilation (VA) and exchange of oxygen/carbon dioxide.
  174. 174Alveolar HypoventilationDecrease in alveolar ventilation (VA) in relation to carbon dioxide production. Results in incr PAcarbon dioxide and decreased PAoxygen
  175. 175Alveolar HyperventilationCauses decreased PAcarbondioxide b/c ventilation incr in relation to carbon dioxide production (causing inr PAoxygen). Caused when need to ventilate incr by: hypoxia, incr production of H+ and incr body temp
  176. 176Causes of alveolar hypoventilation1. Damage to CNS (drugs, trauma)
    2. Peripheral nerve injury
    3.Damage to pump (eg muscle paralysis, trauma to chest, resp muscles, bloated abd)
    4. Lung resisting inflation (eg airway obstruction
  177. 177Rate of Gas movement (Voxygen) b/w alveolus and blood determined by 4 things:1) Physical property of gas (D)
    2) Alveolar surface area avail for diffusion (A)
    3) Thickness of air-blood barrier (x) <1um thick
    4) driving pressure gradient b/w alveolus and capillary blood (PAoxygen - -PcapO2
  178. 1781) Physical property of gas (D)Determined by molecular weight of gas and solubility of gas
  179. 1792) Alveolar surface area avail for diffusion (A)Occupied by perfused pulmonary capillaries. Incr during exercise b/c more capillaries are perfused
  180. 1803) Thickness of air-blood barrier (x)Very thin (<1um), diffusion also occurs for gas movement to RBC. Diffusion b/w alveolus and capillary, must also occur b/w plasma and RBC
  181. 1814) Driving pressure gradientDifference b/w PAoxygen (alveolar oxygen tension) and Pcapoxygen (capillary oxygen tension) If PAoxygen>Pcapoxygen, oxygen moves from alveolus to capillary. B/c capillary blood is mixed venous blood (has returned fr veins fr all parts of circulation) it has lower oxygen tension than alveolar oxygen tension. Driving pressure gradient: oxygen moves fr alveoli to capillary and is taken up by Hb
  182. 182Gas exchange b/w blood and tissueAlso occurs by diffusion & is dependent on difference b/w PAoxygen, PAco2, & tissue oxygen and CO2 tension. Tissue oxygen tension: determined by rate of oxygen delivery relation of rate of tissue oxygen consumption. Tissue CO2 tension: determined by rate of tissue CO2 production in relation to rate of CO2 removal. Tissues w high O2 demand have more capillaries/gram of tissue which 1) provides incr surface area for diffusion 2) Decrease max distance b/w tissue and nearest capillary
  183. 183Gas Exchange b/w blood and tissue during exerciseCapillary recruitment --> 1_ bring blood closer to tissue and 2) decrease rate blood flow through tissue (allowing incr time for diffusion equilibrium)
  184. 184V/Q ratioRatio b/w ventilation (V) and perfusion (Q). Ideally V and Q should be matched (alveoli should receive air and blood in amounts that are optimal for gas exchange). V and Q always mismatched due to: 1) branching patterns of bronchi and blood vessels
    2) gravitational forces
    In dz: V/Q mismatching becomes more extreme, leading to hypoxia
  185. 185Oxygen TransportSmall amount in plasma due to poor solubility in water. Majority in combination with hemoglobin (Hb)
  186. 186Hemoglobin (Hb)Oxygen carrying pigment that takes oxygen to tissues. Consists of 4 units, each w 1 heme and 1 associated protein (globin). Heme: contains 1 ferrous iron which can reversibly bind 1 oxygen molecule. Globin: critical to oxygen binding (cradles heme prevents oxidation of ferrous iron). Each molecule of Hb can combine w 4 molecules of oxygen
  187. 187Hemoglobin Affinity for Oxygen (1)Depends on: 1) Temperature: incr temp decreases Hb oxygen affinity --> release of oxygen fr Hb --> oxygen moves to tissues
    Decreased temp: Incr Hb oxygen affinity --> less release of oxygen fr Hb --> oxygen doesn't move to tissues as easily (so tissue Poxygen must be lower than usual for oxygen to be released fr Hb
  188. 188Hemoglobin Affinity for Oxygen (2)Pco2 (Co2 tension) called the Bohr shift. Principle: Hb oxygen binding affinity is inversely related both to pH and to the [Co2]. Incr in [Co2]-->decreased blood pH-->decreased Hb oxygen affinity-->release of oxygen from Hb-->oxygen moves to Hb picks up more oxygen
  189. 189Hemoglobin Affinity for Oxygen (3)pH: alters oxygen binding by changing structure of Hb. Acidic pH: decrease oxygen affinity of Hb (assists in unloading of oxygen to tissues). Alkaline pH: incr oxygen affinity of Hb (holds tightly to oxygen)
  190. 190Hemoglobin Affinity for Oxygen (4)Organic phosphates: regulates binding of oxygen to Hb. Presence of organic phosphates-->decreased oxygen affinity of Hb (assists in unloading of oxygen)
  191. 191Hb colourRed= Hb bound to oxygen
    Blue (Cyanosis): Hb depleted of oxygen
  192. 192Carbon monoxide affinity for Hb200x the affinity that oxygen has. Therefore, carbon monoxide can saturate Hb and displace oxygen--> death. Tx of CO poisoning: Remove source of CO and administer oxygen
  193. 193Carbon Dioxide transportCarbon dioxide transported in several forms (differs fr oxygen). 5% transported as carbon dioxide in plasma, majority enters RBC
  194. 194Gas transport during exercise1) incr CO which incr blood flow/min to lung-->incr oxygen uptake fr lungs
    2) redistribution of CO to exercising muscles
    3) Incr # of circulating RBC's which incr amount of Hb (contraction of spleen, hct incr to 50% fr 35%
    4) incr oxygen extraction
    5) Small amount of oxygen released by myoglobin
  195. 195During exercise, what is increased oxygen extraction due to?-Decreased muscle Poxygen (due to incr metabolism --> oxygen diffusion gradient
    -incr muscle temp ->decreased Hb affinity for oxygen
    -Decreased pH (due to CO2 production) decreased Hb affinity for oxygen
  196. 196Regulation of ventilationControl mechanisms monitor:
    1) Chemical composition of blood
    2) Effort being exerted by resp muscles
    3) Presence of foreign materials in resp tract
    This info integrated w other nonresp activities such as thermoregulation, vocalization, parturition, eructation to produce breathing pattern to maintain gas exchange
  197. 197Central Control of RespirationPneumotaxic centre: Modulates resp frequency
    Apneustic centre: promotes inspiration (stimulates dorsal resp group)
    Dorsal resp group: Active during inhalation, regulate diaphragm
    Ventral resp group: Active during inhalation, exhalation (regulates expiratory and accessory inspiratory muscles)
    Cranial pons and caudal pons: Modifies resp rhythmicity
    Medulla: Responsible for resp rhythmicity
  198. 198Types of Pulmonary Airway Receptors: Slow adapting stretch receptorsAssociated w smooth muscle of trachea and bronchi, stimulated by deformation of wall (lung inflation), cause adjustments in rate and depth of breathing
  199. 199Types of Pulmonary Airway Receptors: Irritant Receptors (rapidly adapting stretch receptors)In larynx, trachea, bronchi, and intrapulmonary airways. Stimulated by deformation that occurs w lung inflation, bronchoconstriction, and mechanical irritation of airway. Stimulation causes cough, bronchoconstriction, mucus secretion, rapid shallow breathing, designed to clear irritant materials fr resp system
  200. 200Types of Pulmonary and Airway Receptors: C FibresAssociated pulmonary interstitium close to pulmonary capillaries. Monitor blood composition or degree of interstitium distention

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Physiology Unit 4 Karteikarten am Unit 4 - Cardiovascular and Respiratory Physiology, erstellt von Shauna Ryner am 22/02/2017.
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Shauna Ryner
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