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Pulmonary a p s10
- 1. Structure and Functionof the Pulmonary System Reference: Pathophysiology by Kathryn McCance Chapter 32 Mindy Milton, MPA, PA-C July 13, 2010
- 2. Structures of the Pulmonary System Airways Blood vessels Chest wall Lungs – Lobes – Segments – Lobules break down of branching. 2
- 3. Structures of the Pulmonary System Conducting airways – Upper airways Nasopharynx Oropharynx Laryngopharynx – Larynx Connects upper and lower airways - three cartillage. – Lower airways Trachea Bronchi Terminal bronchioles Conducting air way: 3 carry air only.
- 4. Conducting Lower Airways Text 26 generations of branching. 4
- 5. Structures of thePulmonary System Gas-exchange airways every bronchus h own venule and a – Respiratory bronchioles Every sac has its cap bed. – Alveolar ducts – Alveoli Epithelial cells – Type I alveolar cells Alveolar structure – Type II alveolar cells Surfactant production 5
- 6. Structures of thePulmonary System 6
- 7. Respiratory Mucosa Respiratory Mucosa – Lines the conducting portion of the respiratory tree – Lined by a mucous membrane that contains both epithelium and areolar tissue – Structure of the epithelium changes from the upper to lower respiratory system – Upper airway to larger bronchi Pseudostratifiedciliated columnar epithelium with large number of goblet cells and submucosal glands 7
- 8. Surface View ofthe Respiratory Epithelium: Dense Cilia Hella cilia. 8
- 9. Sectional View: Pseudostratified Ciliated Columnar Epithelium 9
- 10. Respiratory Mucosa Lower respiratory system: – Cuboidal epithelium with scattered cilia Alveolus – Lined by simple squamous epithelium Specialized cells – Lamina Propria Underlyinglayer of areolar tissue Upper airway: contains large number of mucous cells Lower conduction airway: smooth muscle 10
- 11. Structures of thePulmonary System GOod example 11
- 12. Respiratory Defense System Components Innate immunity – Mucosal membrane Gobletcells in the epithelial layer Mucous cells in lamina propria Cilia – All work together to sweep mucous and trapped particles to the oropharynx for expulsion – Alveolar macrophages important in Addaptie im clearing foreign material and bacteria the lower airway – Irritant receptors - sensitive to noxious Nose, carina (sneeze, cough) 12
- 13. Gas Exchange Alveoli – Primary gas exchange unit Pores of Kohn – Air passes through septa from alveolus to alveolus Collateral ventilation and even air distribution deep Only work with breath. especially during illness 13
- 14. Pulmonary and Bronchial Circulation Pulmonary circulation has a lower pressure than systemic circulation (mean = 18 mmHg) – Only one third of vessels filled with blood at any given time – Increased pressure can increase recruitment – Automatic distribution of blood to area of increased ventilation. – Gas Exchange – delivers nutrients to lung tissues, acts as a reservoir for the left side of the heart, and filters out clots, air, and other debris from the circulation. Bronchial circulation is part of systemic circulation – Supplies nutrients to conducting airways, nerves, lymph nodes, large pulmonary vessels, and pleurae 14
- 15.
- 16. Pulmonary Circulation Pulmonary artery divides and enters the lung at the hilus Each bronchus and bronchiole has an accompanying artery or arteriole 16
- 17. Pulmonary Circulation Alveolocapillary membrane – Formed by shared alveolar and capillary walls – alveolar epithelium – alveolar basement membrane – interstitial space – capillary basement membrane 17
- 18. Pulmonary Lymphatic System Lymph capillaries keep the lung free of fluid – Deep Begin at the Terminal bronchioles, exit at the hillus. NOT in the acini. – Superficial Pleural membrane - 18
- 19. Chest Wall andPleura Chest wall – Skin, ribs, and intercostal muscles, diaphragm – Thoracic cavity Pleura – Serous membrane – Parietal and visceral layers – Pleural space (cavity) – Pleural flui – **they stay connected!!! 19
- 20. Main Lung Functions Gas exchange – Supply oxygen – Eliminate CO2 - gaseous form of carbonic acid. Maintain pH Eliminate water Maintain normal body temperature 20
- 21. Requirements for Ventilation, Perfusion, and Diffusion Adequate inspired O2 – (FiO2) (21% at sea level, rest is nitrogen.) Ventilation (V) and perfusion(Q) of alveoli A permeable alveolocapillary membrane Adequate blood flow Ability to transport O2 and CO2 Ability of cell to use O2 and eliminate CO2 Dissolved part of GAS is considered Partial Pressure. 21
- 22. Requirements for Ventilation, Perfusion, and Diffusion Adequate inspired O2 – (FiO2) Barometric pressure is 760 at sea level 21% x 760 = partial pressure of O2 at sea level = ~160 mmHg Barometric pressure is 600 at Salt Lake City (much lower on Mt. Everest) 21% x 600 = partial pressure of O2 at SLC = ~126 mmHg Why we give oxygen at high altitude 22
- 23. Function of thePulmonary System Ventilation – Mechanical movement of gas or air into and out of the lungs – Minute volume Ventilatory rate multiplied by the volume of air per breath – Alveolar ventilation Movement of air in and out of alveolus Adequacy determined by arterial blood gas analysis only! 23
- 24. Principles underlying Ventilation Air flows from an area of higher pressure to an area of lower pressure Visceralpleura that lines the outside of the lung remains in contact with parietal pleura that lines the chest cavity 24
- 25. Principles underlying Ventilation Enlargement of the chest cavity by muscle contractions will affect pressure changes When the diaphragm contracts, the lung cavity volume increases and the pressure decreases and air enters since the lung pressure is lower than atmospheric pressure Quiet breathing = DIAPHRAM. 25
- 26. Ventilation Principles Recoil CHest wa Lung wan Elastic recoil: tendency of lungs to return to resting state after inspiration is responsible for passive exhalation Compliance: measure of chest wall and lung distensibility: reciprocal of elastic recoil Airway Resistance: determined by the length, Compli recoil. radius, and cross sectional of the airway and the density, viscosity, and velocity of the gas Work of breathing is determined by the muscular effort required for breathing. Increased work of breathing will increase markedly the oxygen needs and metabolic demands 1/2 - 2/3 resistance t air is in the nose. 26
- 27. Pulmonary volumes Volume Relationships – Resting Tidal Volume Vt: amount of air you move in and out of your lungs in one respiratory cycle (500 ml) – Forced Vital Capacity: maximum amount of air you can move in and out of your lungs during one respiratory cycle sum of tidal volume and inspiratory and expiratory reserves 27
- 28. Pulmonary volumes Volume Relationships – Expiratory Reserve: amount of air you can voluntarily expel after you completed normal quiet respiratory cycle – Residual Volume: amount of air left after maximum expiration - dead space left over: conducting part, prevent collapse. 28
- 29. Pulmonary Volumes Volume Relationships – Inspiratory reserve: amount of air you can inhale over and above a quiet respiratory cycle – Functional residual capacity: (FRC) is the amount of air remaining in your lungs after you have completed a quiet resting cycle; expiratory reserve volume + residual volume. 29
- 30.
- 31. Lung Volumes andCapacities Based on Age, Gender, Height Dead space: oropharynx to division 16 of bronchioles – volume about equal to ideal body weight Tidalvolume VT (per breath) 400-800 ml IRV 3000 ml additional air that could be inhaled 31
- 32. Lung Volumes andCapacities Based on Age, Gender, Height ERV 1000 ml remaining air – Can be forcefully expired after normal expiration FEV1 - athma and emphysema. – Why abdominal thrusts work; expel VT plus ERV Forced vital capacity (theoretical) – VT + IRV + ERV ~4500-5000 ml Residual volume constant ~1200 ml – Air remaining in alveoli 32
- 33. Example using Formulas Minute ventilation (or volume/min) – RR x VT – RR 16, VT 500 – 16 x 500 = 8000 ml/min Effective minute volume (happening down at alvioli): RR x (VT -DS) – 100 lb, RR 16, VT 500 ml – 16 (500-100) = 6400 ml/min 33
- 34. Control of Ventilation ANS - automatic. – Stimulates smooth muscle Airway lumen diameter – Sympathetic - muscle relaxation – Parasympathetic – muscle contraction Main controller under normal conditions Bronchial smooth muscle tone – Depends on equilibrium Equal stimulation of contraction & relaxation – Constriction occurs with irritant receptor stimulation (epithelium) Inspired air irritants (pollen, toxic vapors) Endogenous substances – inflammatory chemical mediators such as histamine, prostaglandins Drugs 34
- 35. Control of Ventilation Chemoreceptors – Central receptors Reflects PaCO2 Stimulated by H+ in cerebrospinal fluid (pH) – CO2 diffuses into CSF until equilibrium is reached – Combines with H2O = H2CO3 – H2CO3 dissociates into H+ + HCO3- (￬ – Peripheral receptors Aortic arch and carotid bodies Primarily stimulated by hypoxemia (PaO2) – Also sensitive to changes in PaCO2 and pH Sends efferent signals to DRG (Dorsal respiratory group). – Increase respiratory rate and depth Major stimulus to ventilation in chronic hypoventilation – Central chemoreceptors become insensitive – Renal compensation with HCO3 diffusion into CSF 35
- 36. Ventilation Neurochemical control – Respiratory center Dorsal respiratory group - sets basic rythm. Ventral respiratory group - deep breath, quicker expiration. Pneumotaxic center Modulators Apneustic center 36
- 37. Ventilation Neurochemical control – Lung receptors Irritant receptors Stretch receptors J-receptors - capillaries. – Chemoreceptors Central chemoreceptors Peripheral chemoreceptors 37
- 38. Overview: Mechanics ofBreathing Mechanical aspects of inspiration and expiration – Major and accessory muscles – Elastic properties Lungs Chest wall – Resistance of airflow Conducting airways 38
- 39. Mechanics of Breathing Major and accessory muscles – Major muscles of inspiration Diaphragm inhale External intercostals – Accessory muscles of inspiration Sternocleidomastoid exhale and scalene muscles – Accessory muscles of expiration Abdominal and internal intercostal 39
- 40. Mechanics of Breathing Alveolar surface tension – Function of surfactant Elastic properties of lung and chest wall – Elastic recoil – Compliance Airway resistance (normally low) – Airway size; smaller – Gas velocity (Poiseuille’s law) R = ∆P/F, 40
- 41. equal in opposite Mechanics of Breathing direction. 41
- 42. Laplace’s Law Thesmaller a sphere’s radius (alveoli) the greater the surface tension and the more difficult (work) to expand the alveoli P = 2t/r – P = pressure inside a sphere (alveoli) – t = surface tension – r = radius of a sphere Surfactant reduces fluid surface tension lining the alveoli and decreases tendency to collapse, preventing atelectasis – Also keeps fluid out of alveoli – Participates in host defense against pathogens 42
- 43. Compliance A measure of lung and chest wall distensibility or “stiffness” ― volume of air moved ― force to move the air Low: increased work of inspiration – Stiff lungs High: increased work of expiration – Baggy lungs 43
- 44. Measurement of GasPressure Barometric pressure – Partial pressure Partial pressure of water vapor 44
- 45. Measurement of GasPressure 45
- 46. Gas Transport –Four Steps Oxygen Carbon Dioxide – Ventilation of the – Diffusion of CO2 out lungs of cells and into – Diffusion of oxygen systemic capillaries obviuse from the alveoli into – Perfusion of the the capillary blood pulmonary capillary – Perfusion of bed by venous systemic capillaries blood with oxygenated – Diffusion of CO2 blood from the lungs into – Diffusion of oxygen the alveoli from systemic – Removal of CO2 capillaries into the from the lung by cells ventilation 46
- 47. Distribution of Ventilationand Perfusion Gravity and alveolar pressure Ventilation-perfusion ratio – Normal V/Q = 0.8 - perfusion is just a little hier! 47
- 48. Gas Transport: O2 Oxygen transport – Diffusion across alveolocapillary membrane Large total surface area Very thin High concentration gradient – Determinants of arterial oxygenation Hemoglobin concentration (15g/dl) SaO2 (97% on RA at sea level) PaO2 (100 mm Hg) 48
- 49. Gas Transport: O2 Oxygen Transport – Transported by combination with Hgb (19.7 ml/dl) or dissolved in plasma (0.3 ml/dl) – Diffusion across the alveolar membrane Amount of oxygen in the alveolus depends upon the amount of oxygen in the inspired air as well as the amount of physiologic dead space Oxygen diffuses across the membrane and binds with Hgb 49
- 50. Summary of GasTransport: O2 100 --> 40 50
- 51. Gas Transport: O2 Oxygen Transport – Hgb binds with oxygen and forms oxyhemoglobin – Hgb binding with oxygen in the lungs is called Hgb saturation (SaO2); Oxygen release from Hgb occurs in the tissues and is called Hgb desaturation – Can plot this process on a graph called the oxyhemoglobin dissociation curve 51
- 52. Oxyhemoglobin Dissociation Curve FLat - arterial portion (association side) Steep - venous (disassociation side). 52
- 53. Oxyhemoglobin Association and Dissociation Oxygen Transport – Factors that change the association between oxygen and Hgb Decreased affinity of Hgb for oxygen will be depicted as a shift to the right of the oxyhemoglobin dissociation curve – Acidosis Increased DPG – Increased PCO2 – Elevated temperature or hyperthermia Increasedaffinity of Hgb for Oxygen will be depicted as a shift to the left of the oxyhemoglobin dissociation curve – Alkalosis Hypothermia – Decreased PCO2 Decreased DPG 53
- 54. Oxyhemoglobin Association and Dissociation BOHR EFFECT: – Increased PaCO2 and H+ Result of cellular metabolism shift to the right with less affinity of Hgb for O2 and can be given up at the tissue level easier – Decreased PaCO2 Result of gas moving from blood to alveoli shift to the left: increased affinity of Hgb for O2 which promotes association in the lungs 54
- 55. Effects of pHand Temperature on Hemoglobin Saturation 55
- 56. Gas Transport: CO2 Carbon dioxide transport – Dissolved in plasma – Bicarbonate - 90%!!! – Carbamino compounds (Hb) Haldane effect – O2 effect on CO2 transport Lungs – oxygen binds to Hgb Tissues – oxygen dissociates from Hgb 56
- 57. Summary of GasTransport: CO2 Mostly binds to Hb. Buffers. Travels in the blood as 57 bicarb.
- 58. Control of PulmonaryCirculation Hypoxic pulmonary vasoconstriction – Caused by low alveolar PO2 – Blood is shunted to other, well-ventilated portions of the lungs Better ventilation and perfusion matching If alveolar hypoxia affects all segments of lungs, the vasoconstriction can result in pulmonary hypertension – Reversible if not chronic Acidemia also causes pulmonary artery constriction Other biochemical factors affect vessel caliber – Histamine, prostaglandins, endothelin, 58 serotonin, nitric oxide, bradykinin
- 59. Aging and thePulmonary System 59
- 60. Questions? Thanks Breakandthen on to pulmonary pathophysiology 60
Editor's Notes
- #2 \n
- #3 Larynx is what devides Upper from Lower. \nBronchial circ vs Pulmonary circ.\nPulm ART carry deoxygenated.\nBronchial circ capillaries add mixture, some dump into pulm vein. \nRight lobe is wider, Left lobe is longers. \n
- #4 Larynx - false and true chords. PHARYNX make the sound of the voice. \n
- #5 \n
- #6 \n
- #7 redundant\n
- #8 \n
- #9 \n
- #10 Pseudostrativied - every cell touches the basement membrane. \n
- #11 \n
- #12 \n
- #13 \n
- #14 Single lobule - good illustration. \nSee: blood, nerve, lymph (not all the way down!) requires Macrophage migrations. \n
- #15 ONly 1/3 of vessels are being perfused at any time. Protects lungs agains pulm htn in the case of increased CO. \nActs like a pressure valve. \n
- #16 \n
- #17 \n
- #18 Basement membranes fuse. \n
- #19 Pluged = Pulmonary edema\n
- #20 \n
- #21 \n
- #22 \n
- #23 \n
- #24 \n
- #25 \n
- #26 Accessory muscles - SCM and scalenes --> direct chest out!\n
- #27 \n
- #28 \n
- #29 \n
- #30 \n
- #31 Know this.\n
- #32 \n
- #33 \n
- #34 Slow down. \nUsually breath 1L less than we could. \n
- #35 Usually involuntare. \nBronchial smooth muscle tone a balance of ANS:\nSympathetic fibers innervate lumen of bronchial tubes --> relaxation.\nParasym, cholinergic --> Contraction. \nbeta blockers with asthma, need to be careful of HTN ptnt has Asthma\n
- #36 Take home:\nChronic hypovent - central lose sensitivity to pCO2, get “reset”, so peripheral get more important. \nCOPD - drive to breath by peripheral. THerefore, too much O2 stops drive to breath.\nTheory - bicarb reabsorbed from kidneys, goes into CSF and prevents sensitivity to H+. \n
- #37 \n
- #38 Figure out receptors\n
- #39 \n
- #40 \n
- #41 Surface tension happens on any gas, water interface. \nSurfactant - lipid protein, breaks molecules that cause ST.\n
- #42 Great Picture.\nMuscle contraction wins. \n
- #43 NOT in the objectives.\n\nSurfactant - might be antioxident, attract M0.\n\n
- #44 Compliance = stiff lungs. That’s it!\n
- #45 Pp - % of that gas in the air. \nWater vapor has nothing to do with Pressue, temp only. \n\n
- #46 Note average values of 02, CO2, and N. \nCO2 IS 20 X MORE SOLUBLE than O2, gradient isn’t strong, but the solubility helps it move. \n
- #47 Bhor effect - in the lungs, co2 leaves Hb, makes more affinity to load O2.\nHaldan effect - in the tissues. \n
- #48 Orthopnea,\nParoxysmal nocturnal dyspnea.\n
- #49 Diffusion taks .25 sec.\nCells in lungs for .75 sec. \n
- #50 \n
- #51 \n
- #52 \n
- #53 \n
- #54 \n
- #55 \n
- #56 \n
- #57 \n
- #58 \n
- #59 Control of hypoxia - pulmonary art constrict to got to perfused part of the lung. \n
- #60 X-ray: air trapping, consolidation, nodules. \n\nage: loss of recoil, stiffen chest wall, alt gas exchange. \nGreater risk of respiratory risk from medications, have lower tolerance from exercise. \n
- #61 \n