Chap 37

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Chap 37

  1. 1. Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings. PowerPoint® Lecture Slide Presentation by Robert J. Sullivan, Marist College RESPIRATION Chapter 37 PULMONARY VENTILATION DR FARZANA MAJEED
  2. 2. Human Respiratory System Figure 10.1
  3. 3. Respiratory system extracts oxygen from the atmosphere , and the body utilizes the oxygen and produce CO2 as a result of metabolism. RESPIRATORY SYSTEM
  4. 4. Basic functions of the respiratory system 1. Breathing (Pulmonary Ventilation) – movement of air in and out of the lungs • Inhalation (inspiration) draws gases into the lungs. • Exhalation (expiration) forces gases out of the lungs.
  5. 5. Non –pulmonary functions: 2. Gas Conditioning – as gases pass through the nasal cavity and paranasal sinuses, inhaled air becomes turbulent. The gases in the air are • warmed to body temperature • humidified • cleaned of particulate matter 3. Protects respiratory surfaces 4. Site for olfactory sensation 5. Secretes pulmonary alveolar macrophages 6. Endocrine functions
  6. 6. 7. Immune function 8. Vocalization 9. Coughing and sneezing to eliminate irritants from respiratory tract 10. Production of surfactant
  7. 7. Respiration processes
  8. 8. Components of the Upper Respiratory Tract Figure 10.2
  9. 9.  Passageway for respiration  Receptors for smell  Filters incoming air to filter larger foreign material  Moistens and warms incoming air  Resonating chambers for voice Upper Respiratory Tract Functions
  10. 10. Components of the Lower Respiratory Tract Figure 10.3
  11. 11.  Functions:  Larynx: maintains an open airway, routes food and air appropriately, assists in sound production  Trachea: transports air to and from lungs  Bronchi: branch into lungs  Lungs: transport air to alveoli for gas exchange Lower Respiratory Tract
  12. 12. Mechanics of breathing Pulmonary ventilation is accomplished by two processes.  Inspiration is an active process and refers to inflow of air into the lungs. This occurs when the intrapulmonary pressure falls below the atmospheric pressure.
  13. 13.  Expiration is a passive process and refers to outflow of air from the lungs. This occurs when intrapulmonary pressure exceeds the atmospheric pressure.  Changes in intrapulmonary pressure which govern respiratory cycle are related to the changes in intrapleural pressure.  Changes in intrapleural pressure in turn depend upon the changes in size of thoracic cavity.
  14. 14.  Changes in size of thoracic cavity depend upon the respiratory muscles  Muscles of normal quiet inspiration are diaphragm and external intercostal muscles.  Muscles of forceful inspiration are sternocledomastoid, scalenes and parasternals
  15. 15.  Normal quiet expiration is due to elastic recoil of lungs  Muscles of forceful expiration are internal intercostals and abdominal recti
  16. 16. movements of inspiration  It is an active process  Normally produced by descent of diaphragm and contraction of inspiratory muscles  Therefore diaphragm and external intercostal muscles contract and cause increase in vertical, antroposterior and transverse diameters of thoracic cavity
  17. 17. Role of diaphragm  Helps in 70-75% expansion of chest during normal inspiration  During inspiration , diaphragm contracts and draw the central tendon part downwards by 1.5cm in quiet breathing and 7cm in deep respiration  Cause an increase in vertical diameter of the thorax
  18. 18.  Contraction of diaphragm also lifts the lower ribs causing thoracic expansion laterally and anteriorly (the bucket handle and pump handle movements respectively)
  19. 19. The respiratory muscles
  20. 20. Role of external intercostal muscles  Fibers of external intercostal muscles are attached to vertebral ends of upper and lower ribs  Contraction leads to elevation of ribs causing lateral and antro posterior enlargement of thoracic cavity  Bucket handle and pump handle movements.
  21. 21. movements of expiration  Passive phenomenon brought about by elastic recoil of lungs  Decrease in the size of thoracic cavity by relaxation of diaphragm and external intercostal muscles
  22. 22. mechanism of forced inspiration  Forceful contraction of diaphragm…..decent 7-10 cm as compared to 1-1.5 cm in quiet breathing  Forceful contraction of external intercostal muscles……..increasing transverse and AP diameter of thoracic cavity
  23. 23.  Contraction of accessory muscles  Sternocledomastoid contracts and lifts the sternum upwards  Anterior serrati and scaleni muscles contract and lift ribs upwards
  24. 24. mechanism of forced expiration  Contraction of abdominal muscles causes increase in vertical diameter of thoracic cavity  Downward pull on the lower ribs by contraction of internal intercostal muscles decreases AP and transverse diameter of thoracic cavity
  25. 25. Pressure and volume changes during respiratory cycle  Relationship between intrapulmonary pressure and atmospheric pressure determines direction of air flow  In quiet breathing , at end expiration and at end inspiration .no air is going in and out of the lungs as the intrapulmonary pressure and atmospheric pressures are equal i.e. 0 mmHg
  26. 26. Intra ALVEOLAR pressure (IAP) During normal quiet inspiration  IAP decreases to about -1 mmHg which is sufficient to suck in 500 ml of air into lungs within 2 sec.  At the end of inspiration IPP decreases again to 0 mmHg
  27. 27. During expiration  IAP swings slightly towards positive side (+1 mmHg) which forces 500 ml of air out of lungs in 3 sec  At the end of expiration IPP again decreases to 0 mmHg
  28. 28. Significance  Negative pressure in alveoli during inspiration causes the air to enter into alveoli but during expiration IAP becomes positive so air is expelled out of the lungs  Helps in exchange of gasses between air and lungs
  29. 29. Intrapleural pressure
  30. 30. During normal quiet inspiration  It is negative pressure  At the start of inspiration -5mmHg which is the minimum amount of pressure to hold the lungs open at resting level  During inspiration becomes more negative ( -7.5mmHg) During expiration  All the events are reversed during expiration
  31. 31. significance  As it is negative pressure so it prevents the collapse of lungs after elastic recoil  This also causes dilatation of larger veins and vena cava. So act as suction pump to pull venous blood from lower part of the body to increase venous return.
  32. 32. Transpulmonary pressure / recoil pressure  It is the difference between alveolar pressure and pleural pressure. SIGNIFICANCE  It is the measure of elastic forces of lungs that tend to collapse the lungs at each instant of respiration
  33. 33. Pressure changes during inhalation and exhalation
  34. 34.  Change in lung volume for each unit change in transpulmonary pressure = stretchiness of lungs  Transpulmonary pressure (TPP) is the difference in pressure between alveolar pressure and pleural pressure.  Value of compliance of both lungs in normal human adult =200ml of air/TPP in cm of H2O LUNG COMPLIANCE (Hysteresis)
  35. 35.  There are 2 different curves according to different phases of respiration.  The curves are called : Inspiratory compliance curve Expiratory compliance curve COMPLIANCE DIAGRAM
  36. 36.  Shows the capacity of lungs to “adapt” to small changes of transpulmonary pressure.  compliance is seen at low volumes (because of difficulty with initial lung inflation) and at high volumes (because of the limit of chest wall expansion)  The total work of breathing of the cycle is the area contained in the loop.
  37. 37.  Two forces try to collapse the lungs  Elastic forces of lungs  Thin layer of fluid  Two forces prevent collapse of the lungs  Intra pleural pressure  surfactant
  38. 38. Major determinants of compliance diagram A.A. Elastic forces of the lung tissue itself B. Elastic forces of the fluid that lines the inside walls of alveoli and other lung air passages (surface tension)
  39. 39. Elastic forces of the lungs This is provided by • Elastin and • Collagen interwoven in lung parenchyma Deflated lungs: fibers are contracted and in kinked state Inflated lungs: these fibers become stretched and unkinked exerting more elastic forces
  40. 40. Elastic forces caused by surface tension Is provided by the substance called surfactant that is present inside walls of alveoli.
  41. 41. Experiment:  By adding saline solution there is no interface between air and alveolar fluid. (B forces were removed)  surface tension is not present, only elastic forces of tissue (A)  Transpleural pressures required to expand normal lung = 3x pressure to expand saline filled lung.
  42. 42. Conclusion of this experiment:  Tissue elastic forces (A) = represent 1/3 of total lung elasticity  Fluid air surface tension elastic forces in alveoli (B) = 2/3 of total lung elasticity.
  43. 43. Surface tension  water molecules are attracted to one another.  The force of surface tension acts in the plane of the air-liquid boundary to shrink or minimize the liquid-air interface  In lungs = water tends to attract forcing air out of alveoli to bronchi = alveoli tend to collapse
  44. 44. Elastic contractile force of the entire lungs (forces B)
  45. 45. Forces affecting lung compliance  Deformities of thorax like  Kyphosis  Scoliosis  Fibrosis  Pleural effusion  Paralysis of respiratory muscles
  46. 46.  Surface agent which tend to decrease surface tension Synthesized by type II alveolar cells  Reduces surface tension (prevents alveolar collapse during expiration) Consists of apoproteins +phospholipid (dipalmitoylphosphatidylcholine) + calcium ions surfactant
  47. 47. Functions  Decreases surface tension in alveoli of the lungs  Stabilize the alveoli which have tendency to deflate  Prevents bacterial invasion  Cleans alveoli surface
  48. 48.  Plays important role in inflation of lungs during birth. In fetal life it starts producing after 3rd month and completes at 7 months. Till that time lungs remain collapsed. After birth inflation of lungs takes place with initiation of respiration due to CO2 induced activation of respiratory centers. Although respiratory movements are attempted again and again by the new born tend to collapse the lungs.
  49. 49. Effects of deficiency of surfactant  Infants: Collapse of the lungs called Respiratory distress syndrome (RDS) or hyaline membrane disease  Adults: Collapse of the lungs called Adult respiratory distress syndrome (ARDS)
  50. 50.  Surface active agent in water = reduces surface tension of water on the alveolar walls Pure water (surface pressure) 72 dynes/cm Normal fluid lining alveoli without surfactant (surface pressure) 50 dynes/cm Normal fluid lining alveoli with surfactant 5-30 dynes/cm
  51. 51. Respiratory volumes and capacities
  52. 52. Lung Volumes and Capacities  Tidal Volume (VT)  amount of air entering/leaving lungs in a single, “normal” breath  500 ml at rest, ↑ with ↑ activity IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  53. 53.  Inspiratory Reserve Volume (IRV)  additional volume of air that can be maximally inspired beyond VT by forced inspiration  3000 ml. at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  54. 54.  Expiratory Reserve Volume (ERV)  additional volume of air that can be maximally expired beyond VT by forced expiration  1100 ml. at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  55. 55.  Residual Volume (RV)  volume of air still in lungs following forced max. expiration  1200 ml. at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  56. 56.  Total Lung Capacity (TLC)  total amount of air that the lungs can hold  amt of air in lungs at the end a maximal inspiration  VT + IRV + ERV + RV  5800ml at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  57. 57.  Vital Capacity (VC)  max. amt. air that can move out of lungs after a person inhales as deeply as possible  VT + IRV + ERV  4600ml at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  58. 58.  Inspiratory Capacity (IC)  max amt. of air that can be inhaled from a normal end-expiration  breathe out normally, then inhale as much as possible  VT + IRV  3500ml at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  59. 59.  Functional Residual Capacity (FRC)  amt of air remaining in the lungs following a normal expiration  ERV +RV  2300ml at rest IC FRC VC TLC Lung Capacities Primary Lung Volumes IRV VT ERV RV Volume(ml) 0 6000
  60. 60. Forced Expiratory Volume (FEVt)  Amount of air forcibly expired in t seconds  FEVt = (Vt/VC) x 100%  Normally…  FEV1 = ~ 80% VC  FEV2 = ~ 94% VC  FEV3 = ~ 97% VC  Index of air flow through the respiratory air passages 0 1 2 3 5000 4000 3000 2000 1000 0 Time (sec)Volume(ml) FEV1 = (5000 ml -1000 ml) / 5000ml = 4000 ml / 5000 ml = 80%
  61. 61. Restrictive and Obstructive Disorders  Restrictive disorder:  Vital capacity is reduced.  FVC is normal.  Obstructive disorder:  VC is normal.  FEV1 is < 80%. Insert fig. 16.17 Figure 16.17
  62. 62. Air-Flow Disorders  Obstructive disorders  obstruction of the pulmonary air passages  air flow α radius4  slight obstruction will have large ↓ in air flow  bronchiolar secretions, inflammation and edema (e.g. bronchitis), or bronchiolar constriction (e.g. asthma)  reduced FEV, normal VC  Restrictive disorders  damage to the lung results in abnormal VC test  e.g. pulmonary fibrosis  reduced VC, normal FEV
  63. 63. Ventilation PULMONARY VENTILATION ALVEOLAR VENTILATION Cyclic process by which fresh air enters and leaves the lungs Air utilized for gaseous exchange Product of TV and RR Product of TV excluding dead space volume and RR PV=TV X RR 500ml X 12/min 600ml or 6L/min AV= (TV-DSV) X RR (500-150) X 12/min 4.200ml or 4.2 L/min
  64. 64. Dead space  Part of respiratory tract where gaseous exchange doesn’t take place  Types:  Anatomical dead space  Physiological dead space
  65. 65.  ANATOMICAL DEAD SPACE Volume of respiratory tract from nose up to terminal bronchiole  PHYSIOLOGICAL DEAD SPACE Includes anatomical dead space plus well perfused but non ventilated alveoli and well ventilated but non perfused alveoli
  66. 66.  NORMAL VALUE OF DEAD SPACE Under normal conditions ADS + PDS So DSV = 150 ml  MEASUREMENT BY N2 Wash method
  67. 67. Cough reflex  Stimulus irritants in the respiratory passages  Receptors in respiratory passageways  Afferents vagus nerve
  68. 68.  Centre medulla  Efferents neuronal circuits  Effectors / response  2.5 ml of air rapidly inspired  epiglottis gets closed
  69. 69.  vocal cords get approximated so air trapped in  abdominal muscles contract forcefully so that pressure exceeds 100 mmHg or more  Epiglottis suddenly gets open, air under high pressure in lungs exploded out with the velocity of 70-100 miles /hour

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