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IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
IVMS-Respiratory  Anatomy and Physiology Global Overview / Review
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IVMS-Respiratory Anatomy and Physiology Global Overview / Review

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IVMS-Respiratory Anatomy and Physiology Global Overview / Review

IVMS-Respiratory Anatomy and Physiology Global Overview / Review

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  • 1. Respiratory Anatomy and Physiology Global Overview / Review Compiled and Presented by Marc Imhotep Cray, M.D. Basic Medical Sciences Professor Pulmonary Pathology IVMS Respiratory Pathology and Pathophysiology and Clinical Presentation
  • 2. Respiration The term respiration includes 3 separate functions:  Ventilation:  Breathing.  Gas exchange:  Between air and capillaries in the lungs.  Between systemic capillaries and tissues of the body.  02 utilization:  Cellular respiration. 2
  • 3. Ventilation Mechanical process that moves air in and out of the lungs. [O2] of air is higher in the lungs Insert 16.1 than in the blood, O2 diffuses from air to the blood. C02 moves from the blood to the air by diffusing down its concentration gradient. Gas exchange occurs entirely by diffusion:  Diffusion is rapid because of the large surface area and the small diffusion distance. 3
  • 4. Alveoli Polyhedral in shape and clustered like units of honeycomb. ~ 300 million air sacs (alveoli).  Large surface area (60–80 m2).  Each alveolus is 1 cell layer thick.  Total air barrier is 2 cells across (2 mm). 2 types of cells:  Alveolar type I:  Structural cells.  Alveolar type II:  Secrete surfactant. 4
  • 5. Respiratory Zone Region of gas exchange between air and blood. Includes respiratory bronchioles and alveolar sacs. Must contain alveoli. 5
  • 6. Conducting Zone All the structures air passes through before Insert fig. 16.5 reaching the respiratory zone. Warms and humidifies inspired air. Filters and cleans:  Mucus secreted to trap particles in the inspired air.  Mucus moved by cilia to be expectorated. 6
  • 7. Thoracic Cavity Diaphragm:  Sheets of striated muscle divides anterior body cavity into 2 parts. Above diaphragm: thoracic cavity:  Contains heart, large blood vessels, trachea, esophagus, thymus, and lungs. Below diaphragm: abdominopelvic cavity:  Contains liver, pancreas, GI tract, spleen, and genitourinary tract. Intrapleural space:  Space between visceral and parietal pleurae. 7
  • 8. Intrapulmonary and Intrapleural Pressures Visceral and parietal pleurae are flush against each other.  The intrapleural space contains only a film of fluid secreted by the membranes. Lungs normally remain in contact with the chest walls. Lungs expand and contract along with the thoracic cavity. Intrapulmonary pressure:  Intra-alveolar pressure (pressure in the alveoli). Intrapleural pressure:  Pressure in the intrapleural space.  Pressure is negative, due to lack of air in the intrapleural space. 8
  • 9. Transpulmonary Pressure Pressure difference across the wall of the lung. Intrapulmonary pressure – intrapleural pressure.  Keeps the lungs against the chest wall. 9
  • 10. Intrapulmonary and Intrapleural Pressures (continued) During inspiration:  Atmospheric pressure is > intrapulmonary pressure (-3 mm Hg). During expiration:  Intrapulmonary pressure (+3 mm Hg) is > atmospheric pressure. 10
  • 11. Boyle’s Law Changes in intrapulmonary pressure occur as a result of changes in lung volume.  Pressure of gas is inversely proportional to its volume. Increase in lung volume decreases intrapulmonary pressure.  Air goes in. Decrease in lung volume, raises intrapulmonary pressure above atmosphere.  Air goes out. 11
  • 12. Physical Properties of the Lungs Ventilation occurs as a result of pressure differences induced by changes in lung volume. Physical properties that affect lung function:  Compliance.  Elasticity.  Surface tension. 12
  • 13. Compliance Distensibility (stretchability):  Ease with which the lungs can expand. Change in lung volume per change in transpulmonary pressure. DV/DP 100 x more distensible than a balloon.  Compliance is reduced by factors that produce resistance to distension. 13
  • 14. Elasticity Tendency to return to initial size after distension. High content of elastin proteins.  Very elastic and resist distension.  Recoil ability. Elastic tension increases during inspiration and is reduced by recoil during expiration. 14
  • 15. Surface Tension Force exerted by fluid in alveoli to resist distension.  Lungs secrete and absorb fluid, leaving a very thin film of fluid.  This film of fluid causes surface tension.  Fluid absorption is driven (osmosis) by Na+ active transport.  Fluid secretion is driven by the active transport of Cl- out of the alveolar epithelial cells. H20 molecules at the surface are attracted to other H20 molecules by attractive forces.  Force is directed inward, raising pressure in alveoli. 15
  • 16. Surface Tension (continued) Law of Laplace:  Pressure in alveoli is Insert fig. 16.11 directly proportional to surface tension; and inversely proportional to radius of alveoli.  Pressure in smaller alveolus would be greater than in larger alveolus, if surface tension were the same in both. 16
  • 17. Surfactant Phospholipid produced by alveolar type II cells. Insert fig. 16.12 Lowers surface tension.  Reduces attractive forces of hydrogen bonding by becoming interspersed between H20 molecules.  Surface tension in alveoli is reduced. As alveoli radius decreases, surfactant’s ability to lower surface tension increases. Disorders:  RDS. 17  ARDS.
  • 18. Quiet Inspiration Active process:  Contraction of diaphragm, increases thoracic volume vertically. Parasternal and external intercostals contract, raising the ribs; increasing thoracic volume laterally. Pressure changes:  Alveolar changes from 0 to –3 mm Hg.  Intrapleural changes from –4 to –6 mm Hg.  Transpulmonary pressure = +3 mm Hg. 18
  • 19. Expiration Quiet expiration is a passive process.  After being stretched by contractions of the diaphragm and thoracic muscles; the diaphragm, thoracic muscles, thorax, and lungs recoil.  Decrease in lung volume raises the pressure within alveoli above atmosphere, and pushes air out. Pressure changes:  Intrapulmonary pressure changes from –3 to +3 mm Hg.  Intrapleural pressure changes from –6 to –3 mm Hg.  Transpulmonary pressure = +6 mm Hg. 19
  • 20. Pulmonary Ventilation Insert fig. 16.15 20
  • 21. Pulmonary Function Tests Assessed by spirometry. Subject breathes into a closed system in which air is trapped within a bell floating in H20. The bell moves up when the subject exhales and down when the subject inhales. Insert fig. 16.16 21
  • 22. Terms Used to Describe Lung Volumes and Capacities 22
  • 23. Anatomical Dead Space Not all of the inspired air reached the alveoli. As fresh air is inhaled it is mixed with air in anatomical dead space.  Conducting zone and alveoli where [02] is lower than normal and [C02] is higher than normal. Alveolar ventilation = F x (TV- DS).  F = frequency (breaths/min.).  TV = tidal volume.  DS = dead space. 23
  • 24. Restrictive and Obstructive Disorders Restrictive disorder:  Vital capacity is reduced. Insert fig. 16.17  FVC is normal. Obstructive disorder:  Diagnosed by tests that measure the rate of expiration.  VC is normal.  FEV1 is < 80%. 24
  • 25. Pulmonary Disorders Dyspnea:  Shortness of breath. COPD (chronic obstructive pulmonary disease):  Asthma:  Obstructive air flow through bronchioles.  Caused by inflammation and mucus secretion.  Inflammation contributes to increased airway responsiveness to agents that promote bronchial constriction.  IgE, exercise. 25
  • 26. Pulmonary Disorders (continued)  Emphysema:  Alveolar tissue is destroyed.  Chronic progressive condition that reduces surface area for gas exchange.  Decreases ability of bronchioles to remain open during expiration.  Cigarette smoking stimulates macrophages and leukocytes to secrete protein digesting enzymes that destroy tissue. Pulmonary fibrosis:  Normal structure of lungs disrupted by accumulation of fibrous connective tissue proteins.  Anthracosis. 26
  • 27. Gas Exchange in the Lungs Dalton’s Law:  Total pressure of a gas mixture is = to the sum of the pressures that each gas in the mixture would exert independently. Partial pressure:  The pressure that an particular gas exerts independently. PATM = PN2 + P02 + PC02 + PH20= 760 mm Hg.  02 is humidified = 105 mm Hg.  H20 contributes to partial pressure (47 mm Hg).  P02 (sea level) = 150 mm Hg.  PC0 = 40 mm Hg. 2 27
  • 28. Partial Pressures of Gases in InspiredAir and Alveolar Air Insert fig. 16.20 28
  • 29. Partial Pressures of Gases in Blood When a liquid or gas (blood and alveolar air) are at equilibrium:  The amount of gas dissolved in fluid reaches a maximum value (Henry’s Law). Depends upon:  Solubility of gas in the fluid.  Temperature of the fluid.  Partial pressure of the gas. [Gas] dissolved in a fluid depends directly on its partial pressure in the gas mixture. 29
  • 30. Significance of Blood P0 and PC0 2 2 Measurements At normal P0 arterial 2 blood is about 100 mm Hg. P0 level in 2 the systemic veins is about 40 mm Hg. P is 46 mm Hg in the systemic veins. C02Provides a good index of lung function. 30
  • 31. Pulmonary Circulation Rate of blood flow through the pulmonary circulation is = flow rate through the systemic circulation.  Driving pressure is about 10 mm Hg. Pulmonary vascular resistance is low.  Low pressure pathway produces less net filtration than produced in the systemic capillaries.  Avoids pulmonary edema. Autoregulation:  Pulmonary arterioles constrict when alveolar P0 2 decreases.  Matches ventilation/perfusion ratio. 31
  • 32. Pulmonary Circulation (continued) In a fetus:  Pulmonary circulation has a higher vascular resistance, because the lungs are partially collapsed. After birth, vascular resistance decreases:  Opening the vessels as a result of subatmospheric intrapulmonary pressure.  Physical stretching of the lungs.  Dilation of pulmonary arterioles in response to increased alveolar P0 . 2 32
  • 33. Lung Ventilation/Perfusion Ratios Functionally: Insert fig. 16.24  Alveoli at apex are underperfused (overventilated).  Alveoli at the base are underventilated (overperfused). 33
  • 34. Disorders Caused by High Partial Pressures of Gases Nitrogen narcosis:  At sea level nitrogen is physiologically inert.  Under hyperbaric conditions:  Nitrogen dissolves slowly.  Can have deleterious effects.  Resembles alcohol intoxication. Decompression sickness:  Amount of nitrogen dissolved in blood as a diver ascends decreases due to a decrease in PN . 2  If occurs rapidly, bubbles of nitrogen gas can form in tissues and enter the blood.  Block small blood vessels producing the “bends.” 34
  • 35. Brain Stem Respiratory Centers Neurons in the reticular formation of the medulla Insert fig. 16.25 oblongata form the rhythmicity center:  Controls automatic breathing.  Consists of interacting neurons that fire either during inspiration (I neurons) or expiration (E neurons). 35
  • 36. Brain Stem Respiratory Centers (continued) I neurons project to, and stimulate spinal motor neurons that innervate respiratory muscles. Expiration is a passive process that occurs when the I neurons are inhibited. Activity varies in a reciprocal way. 36
  • 37. Rhythmicity Center I neurons located primarily in dorsal respiratory group (DRG):  Regulate activity of phrenic nerve.  Project to and stimulate spinal interneurons that innervate respiratory muscles. E neurons located in ventral respiratory group (VRG):  Passive process.  Controls motor neurons to the internal intercostal muscles. Activity of E neurons inhibit I neurons.  Rhythmicity of I and E neurons may be due to pacemaker neurons. 37
  • 38. Pons Respiratory Centers Activities of medullary rhythmicity center is influenced by pons. Apneustic center:  Promotes inspiration by stimulating the I neurons in the medulla. Pneumotaxic center:  Antagonizes the apneustic center.  Inhibits inspiration. 38
  • 39. Chemoreceptors 2 groups of chemo- receptors that monitor changes in blood PC0 , 2 Insert fig. 16.27 P0 , and pH. 2 Central:  Medulla. Peripheral:  Carotid and aortic bodies.  Control breathing indirectly via sensory nerve fibers to the medulla (X, IX). 39
  • 40. Effects of Blood PC0 and pH on 2 Ventilation Chemoreceptor input modifies the rate and depth of breathing.  Oxygen content of blood decreases more slowly because of the large “reservoir” of oxygen attached to hemoglobin.  Chemoreceptors are more sensitive to changes in PC0 . 2 H20 + C02 H2C03 H+ + HC03- Rate and depth of ventilation adjusted to maintain arterial PC0 of 40 mm Hg. 2 40
  • 41. Chemoreceptor Control Central chemoreceptors:  More sensitive to changes in arterial PC0 . 2 H20 + C02 H2C03 H+ H+ cannot cross the blood brain barrier. C02 can cross the blood brain barrier and will form H2C03.  Lowers pH of CSF.  Directly stimulates central chemoreceptors. 41
  • 42. Chemoreceptor Control (continued) Peripheral chemoreceptors:  Are not stimulated directly by changes in arterial PC0 . 2 H20 + C02 H2C03 H+ Stimulated by rise in [H+] of arterial blood.  Increased [H+] stimulates peripheral chemoreceptors. 42
  • 43. Chemoreceptor Control of Breathing Insert fig. 16.29 43
  • 44. Effects of Blood P0 on Ventilation 2 Blood P0 affected by breathing indirectly. 2  Influences chemoreceptor sensitivity to changes in PC0 . 2 Hypoxic drive:  Emphysema blunts the chemoreceptor response to PC0 . 2  Choroid plexus secrete more HC03- into CSF, buffering the fall in CSF pH.  Abnormally high PC0 enhances sensitivity of carotid 2 bodies to fall in P0 . 2 44
  • 45. Effects of Pulmonary Receptors on Ventilation Lungs contain receptors that influence the brain stem respiratory control centers via sensory fibers in vagus.  Unmyelinated C fibers can be stimulated by:  Capsaicin:  Produces apnea followed by rapid, shallow breathing.  Histamine and bradykinin:  Released in response to noxious agents.  Irritant receptors are rapidly adaptive receptors. Hering-Breuer reflex:  Pulmonary stretch receptors activated during inspiration.  Inhibits respiratory centers to prevent undue tension on lungs. 45
  • 46. Hemoglobin and 02 Transport 280 million hemoglobin/RBC. Insert fig. 16.32 Each hemoglobin has 4 polypeptide chains and 4 hemes. In the center of each heme group is 1 atom of iron that can combine with 1 molecule 02. 46
  • 47. Hemoglobin Oxyhemoglobin:  Normal heme contains iron in the reduced form (Fe2+).  Fe2+ shares electrons and bonds with oxygen. Deoxyhemoglobin:  When oxyhemoglobin dissociates to release oxygen, the heme iron is still in the reduced form.  Hemoglobin does not lose an electron when it combines with 02. 47
  • 48. Hemoglobin (continued) Methemoglobin:  Has iron in the oxidized form (Fe3+).  Lacks electrons and cannot bind with 02.  Blood normally contains a small amount. Carboxyhemoglobin:  The reduced heme is combined with carbon monoxide.  The bond with carbon monoxide is 210 times stronger than the bond with oxygen.  Transport of 02 to tissues is impaired. 48
  • 49. Hemoglobin (continued) Oxygen-carrying capacity of blood determined by its [hemoglobin].  Anemia:  [Hemoglobin] below normal.  Polycythemia:  [Hemoglobin] above normal.  Hemoglobin production controlled by erythropoietin.  Production stimulated by PC0 delivery to kidneys. 2 Loading/unloading depends:  P0 of environment. 2  Affinity between hemoglobin and 02. 49
  • 50. Oxyhemoglobin Dissociation Curve Graphic illustration of the % oxyhemoglobin saturation at different values of P0 . 2  Loading and unloading of 02.  Steep portion of the sigmoidal curve, small changes in P0 2 produce large differences in % saturation (unload more 02). Decreased pH, increased temperature, and increased 2,3 DPG:  Affinity of hemoglobin for 02 decreases.  Greater unloading of 02:  Shift to the curve to the right. 50
  • 51. Oxyhemoglobin Dissociation Curve Insert fig.16.34 51
  • 52. Effects of pH and Temperature The loading and unloading of O2 influenced by the Insert fig. 16.35 affinity of hemoglobin for 02. Affinity is decreased when pH is decreased. Increased temperature and 2,3-DPG:  Shift the curve to the right. 52
  • 53. Effect of 2,3 DPG on 02 Transport Anemia:  RBCs total blood [hemoglobin] falls, each RBC produces greater amount of 2,3 DPG.  Since RBCs lack both nuclei and mitochondria, produce ATP through anaerobic metabolism. Fetal hemoglobin (hemoglobin f):  Has 2 g-chains in place of the b-chains.  Hemoglobin f cannot bind to 2,3 DPG.  Has a higher affinity for 02. 53
  • 54. Inherited Defects in Hemoglobin Structure and Function Sickle-cell anemia:  Hemoglobin S differs in that valine is substituted for glutamic acid on position 6 of the b chains.  Cross links form a “paracrystalline gel” within the RBCs.  Makes the RBCs less flexible and more fragile. Thalassemia:  Decreased synthesis of a or b chains, increased synthesis of g chains. 54
  • 55. Muscle Myoglobin Red pigment found exclusively in striated muscle. Insert fig. 13.37  Slow-twitch skeletal fibers and cardiac muscle cells are rich in myoglobin.  Have a higher affinity for 02 than hemoglobin.  May act as a “go- between” in the transfer of 02 from blood to the mitochondria within muscle cells.  May also have an 02 storage function in cardiac muscles. 55
  • 56. C02 Transport C02 transported in the blood:  HC03- (70%).  Dissolved C02 (10%).  Carbaminohemoglobin (20%). ca H20 + C02 H2C03 High PC02 56
  • 57. Chloride Shift at Systemic Capillaries H20 + C02 H2C03 H+ + HC03- At the tissues, C02 diffuses into the RBC; shifts the reaction to the right.  Increased [HC03-] produced in RBC:  HC03- diffuses into the blood.  RBC becomes more +.  Cl- attracted in (Cl- shift).  H+ released buffered by combining with deoxyhemoglobin. HbC02 formed.  Unloading of 02. 57
  • 58. Carbon Dioxide Transport andChloride Shift Insert fig. 16.38 58
  • 59. At Pulmonary Capillaries H20 + C02 H2C03 H+ + HC03- At the alveoli, C02 diffuses into the alveoli; reaction shifts to the left. Decreased [HC03-] in RBC, HC03- diffuses into the RBC.  RBC becomes more -.  Cl- diffuses out (reverse Cl- shift). Deoxyhemoglobin converted to oxyhemoglobin.  Has weak affinity for H+. Gives off HbC02. 59
  • 60. Reverse Chloride Shift in Lungs Insert fig. 16.39 60
  • 61. Respiratory Acid-Base Balance Ventilation normally adjusted to keep pace with metabolic rate. H2CO3 produced converted to CO2, and excreted by the lungs. H20 + C02 H2C03 H+ + HC03- 61
  • 62. Respiratory Acidosis Hypoventilation. Accumulation of CO2 in the tissues.  Pc02 increases.  pH decreases.  Plasma HCO3 increases. - 62
  • 63. Respiratory Alkalosis Hyperventilation. Excessive loss of CO2.  Pc02 decreases.  pH increases.  Plasma HCO3 decreases. - 63
  • 64. Effect of Bicarbonate on Blood pH Insert fig. 16.40 64
  • 65. Ventilation During Exercise During exercise, breathing becomes deeper and more rapid. Insert fig. 16.41 Produce > total minute volume. Neurogenic mechanism:  Sensory nerve activity from exercising muscles stimulates the respiratory muscles.  Cerebral cortex input may stimulate brain stem centers. Humoral mechanism:  PC0 and pH may be different 2 at chemoreceptors.  Cyclic variations in the values that cannot be detected by blood samples. 65
  • 66. Lactate Threshold and EnduranceTraining Maximum rate of oxygen consumption that can be obtained before blood lactic acid levels rise as a result of anaerobic respiration.  50-70% maximum 02 uptake has been reached. Endurance trained athletes have higher lactate threshold, because of higher cardiac output.  Have higher rate of oxygen delivery to muscles.  Have increased content of mitochondria in skeletal muscles. 66
  • 67. Acclimatization to High Altitude Adjustments in respiratory function when moving to an area with higher altitude: Changes in ventilation:  Hypoxic ventilatory response produces hyperventilation.  Increases total minute volume.  Increased tidal volume. Affinity of hemoglobin for 02:  Action of 2,3-DPG decreases affinity of hemoglobin for 02. Increased hemoglobin production:  Kidneys secrete erythropoietin. 67
  • 68. Selected Online Resources about Asthma: http://www.nlm.nih.gov/hmd/breath/asthma.html 68

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