Respiration2 upload


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Respiration2 upload

  1. 1.
  2. 2. Spirogram<br />
  3. 3. Volumes & Capacities<br />Tidal volume x frequency of breaths = Total ventilation (L/min)<br />
  4. 4. Factors affecting Vol & Capacities<br />Inspiratory reserve volume (IRV)<br />Current lung volume<br />Lung compliance<br />Muscle strength<br />Comfort<br />Flexibility of skeleton<br />Posture<br />Expiratory reserve volume (ERV)<br />Same as above + strength of abdominal M<br />
  5. 5. Why have RV?<br />Airways would collapse<br />Would take an unusually high pressure to inflate them during inspiration<br />Modest RV minimizes airway collapse, thereby optimizing ventilation efficiency <br />Would affect blood oxygenation<br />Blood flow to the lungs and other parts of the body is continuous<br />During collapse – Po2 will plummet <br />
  6. 6. Expiratory Flow<br />Spirometry yields FVC in 2 ways:<br />Spirogram (Volume-time)<br />Provides*: <br />FVC<br />FEV1<br />FEV1/FVC<br />**FEF25-75 (also called MMEF***)<br />Flow-volume loop<br />
  7. 7. Normal Values<br />FVC = 5.0 L<br />FEV1 = 3.8 L<br />FEF25-75 = 3.25 L/sec<br />FEV1/FVC = 0.76<br />PEFR = 10 L/sec<br />
  8. 8. FEV1<br />Volume of air that can expired in the 1st second of a forced maximal expiration<br />Normally 80% of vital capacity, expressed as:<br />FEV1/VC = 0.8<br />Obstructive lung disease (asthma) – FEV1 is reduced more than VC (FEV1/VC decreased)<br />Restrictive lung disease (fibrosis) – both FEV1 & VC are reduced (FEV1/VC normal or increased – since their elastic recoil is more aggressive!)<br />
  9. 9. Helium Dilution Method(for TLC & FRC)*<br />[He]initial = 10%<br />VS(initial) = 2 L<br />[He]final = 5% (assume)<br />Final Vol = VS + VL<br />C1xV1 = C2xV2<br />[He]initial x VS= [He]final x (VS +VL)<br />
  10. 10. Dead Space<br />Volume that does not participate in gas exchange<br />Anatomical & Physiological<br />Anatomical DS<br />Nose (and/or mouth), trachea, bronchi, and bronchioles<br />Volume = 150 ml <br />Hence out of VT only 350 ml reaches gas exchange areas<br />First air expired – DS air <br />To sample alveolar air - sample end-expiratory air<br />
  11. 11. Dead Space<br />
  12. 12. Anatomical DS: Fowler’s Method<br />Assuming:<br />Gray area: 30 sq. cm <br />Pink area is 70 sq. cm<br />Total volume expired = 500 ml<br />DS would be:<br />
  13. 13. Physiological DS: Bohr’s Method<br />Based on:<br />Measurement of Pco2 of mixed expired air (PeCO2) AND<br />3 assumptions:<br /> (1) All of CO2 in expired air comes from exchange of CO2 in functioning (V & Q) alveoli; <br /> (2) There is no CO2 in inspired air<br /> (3) Physiologic DS neither exchanges nor contributes any CO2<br />If Physiologic DS = 0 then,<br />PeCO2 = alveolar Pco2<br />If Physiologic DS = x then,<br />PeCO2 < alveolar Pco2<br />Diluted by physiologic DS<br />
  14. 14. Physiological DS: Bohr’s Method<br />Hence, by comparing PeCO2 with PaCO2, dilution factor can be measured<br />This dilution factor reflects Physiologic DS<br />Problem: alveolar air cannot be sampled directly<br />Solution: arterial PaCO2 (PaCO2)reflects alveolar PaCO2<br />Fraction is dilution factor<br />
  15. 15. Ventilation Rates<br />Volume of air moved into & out of lungs per unit time<br />Ventilation rate can be expressed in 2 ways:<br />Minute ventilation<br />Total rate of air movement into & out of lungs/minute<br />VTx breathes/min = 500 x 12 = 6L/min<br />Alveolar ventilation<br />Total rate of air movement into & out of lungs/minute (corrected for DS)<br />(VT – VD) x breathes/min <br />(500 – 150) x 12 = 4200 ml/min<br />
  16. 16. Example: Calculating Ventilation Rates<br />A man who has the following data: <br />Tidal volume = 550 mL<br />Breathing rate = 14 breaths/min<br />Pco2 (arterial blood) = 40 mm Hg<br />Pco2 (expired air) = 30 mm Hg. <br />What is his minute ventilation? <br />What is his alveolar ventilation? <br />What percentage of each tidal volume reaches functioning alveoli? <br />What percentage of each tidal volume is dead space?<br />
  17. 17. Alveolar Ventilation Equation<br />Fundamental relationship of respiratory physiology<br />Describes the inverse relationship b/w VA & alveolar Pco2 (PaCO2)<br /> or<br />
  18. 18. Effect of Variations in Respiratory Rate and Depth of Alveolar Ventilation<br />
  19. 19. Pulmonary Circulation (Perfusion)<br />
  20. 20. Pulmonary Circulation<br />Pulmonary artery (differences from systemic arteries)<br />Thinner<br />Larger in diameter<br />Highly distensible<br />Less no. of arterioles<br />Overall VERY COMPLIANT (7 ml/mm Hg = entire systemic arterial tree!)<br />Accommodate 2/3 of SV of right ventricle<br />Pulmonary veins<br />As distensible as systemic veins<br />Bronchial vessels<br />1-2 % of total C.O.<br />Oxygenated blood<br />Supplies lung tissue<br />Bronchial veins empty into the left atrium<br />Bronchial (& coronary) vessels causing slight shunting of blood<br />Physiological shunt (PO2 of arterial blood is 2 mm Hg < than pulmonary vein blood)<br />
  21. 21. Pulmonary Circulation<br />Pressures in pulmonary system<br />Right ventricle<br />Systolic 25 mm Hg<br />Diastolic 0-1 mm Hg<br />Pulmonary artery<br />Systolic 25 mm Hg<br />Diastolic 8 mm Hg<br />Mean 15 mm Hg<br />Pulmonary arteriolar P (mean) – 12 mm Hg<br />Pulmonary capillary P (mean) – 10.5 mm Hg<br />Pulmonary venous P (mean) – 9 mmHg<br />
  22. 22. Pulmonary Circulation<br />Left atrial P & pulmonary venous P<br />Mean P in left atrium and major pulmonary veins – 2 mm Hg (recumbent)<br />Pulmonary Wedge Pressure<br />5 mm Hg<br />Role in estimating pulmonary capillary P & left atrial P<br />Blood flow through the lungs and its distribution<br />Blood flow through lungs = C.O.<br />Poorly aerated areas – vasoconstriction<br />Diversion of blood to better aerated areas<br />Time spent by RBC in navigating pulmonary capillary – 0.75 sec (total amount 75 ml)<br />During exercise – 200 ml with time shortened<br />
  23. 23. Distribution of Pulmonary Blood Flow<br />Pulmonary circ. is low pressure/low resistance<br />Hence gravity affects it more<br />This effect causes ‘uneven’ perfusion in lungs<br />Blood flow increases from apex to base (upright posture)<br />Recumbent posture: flow > in posterior than anterior<br />Supine: flow equalizes<br />In stress (excercise)<br />All areas even out!<br />
  24. 24. Distribution of Pulmonary Blood Flow<br />Hydrostatic Pressure (HP) difference in lungs<br />Difference between highest & lowest point in lung – 30 cm apart<br />This causes a pressure gradient of 23 mmHg<br />15 mmHg above heart level<br />8 mmHg below heart level<br />Another way to look at it:<br />Every 1 cm that an artery has to ‘ascend’ the lung<br />A change in HP of 0.74 mmHg (1 cm H2O) occurs<br />So an ‘ascend’ of 10 cm above heart level<br />Induces HP change of 7.4 mmHg <br />HP at heart level = 14 mmHg<br />So, 14 <minus> 7.4 = 6.6 mmHg (arterial P in upper areas)<br />
  25. 25. Distribution of Pulmonary Blood Flow<br />Gravity affects arteries & veins alike throughout lung fields<br />This also affects ventilation (V/Q ratios)<br />Meaning, perfusion affects ventilation<br />Conversely, alveolar pressure also influences perfusion<br />Meaning, ventilation affects perfusion<br />
  26. 26. Distribution of Pulmonary Blood Flow<br />PA = pulmonary alveolar pressure<br />Pa = pulmonary arterial pressure<br />PV = pulmonary venous pressure<br />
  27. 27. Lung Zones<br />Zone 1<br />No blood flow during any part of cardiac cycle<br />PA > Pa > PV<br />Occurs in abnormalities such as:<br />Positive pressure ventilation (Palv >>>)<br />Hemorrhage (Ppc <<<)<br />Zone 2<br />Pa > PA > PV<br />Going down into zone 2<br />Hydrostatic P increases increasing Pa<br />Zone 3<br />Pa > PV > PA<br />
  28. 28. Normally,<br />Zone 2 present in 10 cm above heart level to upper lung areas<br />Zone 3 present in 10 cm above heart level to lower lung areas<br />During exercise – entire lung may become – Zone 3!<br />In vivo<br />During respiratory cycle:<br />PA b/c –ve during inspiration (promoting dilation of capillaries)<br />During expiration it becomes +ve (constricting capillaries)<br />During cardiac cycle<br />P in arterioles & capillaries is >>> during systole<br />Thus promoting dilation of pulmonary capillaries<br />And is lowest during diastole<br />Thus promoting dilation of pulmonary capillaries<br />Thus blood flow through an alveolar vessel would be greatest when inspiration coincides with systole!!<br />
  29. 29. Ventilation-Perfusion Ratio (V/Q)<br />Defined as ratio of ventilation to blood flow<br />Can be defined for:<br />Single alveolus (VA / capillary flow)<br />Group of alveoli<br />Entire lung (Total VA / C.O.)<br />Normal lung<br />Overall V/Q = 0.8<br />Total VA = 4 L/min, CO = 5 L/min<br />This value is averaged – differs in various zones<br />
  30. 30. Ventilation-Perfusion Ratio (V/Q)<br />V/Q only describes the nature of relationship b/w V & Q<br />So a normal V/Q only means the relation is normal*<br />
  31. 31. Integrating Lung Zones & V/Q Concept<br />V & Q are both gravity-dependent; both increase down the lung<br />Q shows about a 5-fold difference b/w the top & bottom of lung<br />V shows about a 2-fold difference<br />This causes gravity-dependent regional variations in the V/Q <br />Ranging from 0.6 (base) - 3 or higher (apex)<br />Q is proportionately greater than V at the base, and <br />V is proportionately greater than Q at the apex<br />
  32. 32. V/Q Affects Gas Exchange<br />Three scenarios<br />Va/Q = 0<br />Alveolar air equilibrates with venous blood<br />Va/Q = infinity<br />Alveolar air equilibrates with inspired air<br />Va/Q = normal<br />
  33. 33. Ventilation-Perfusion Ratio (V/Q)<br />Physiological Shunt (V/Q= less than normal)<br />Some blood may not get oxygenated due to poorly ventilated alveoli – shunted blood<br />This, along with bronchial & coronary blood – Physiological Shunt<br />Measurement: <br />analyzing the concentration of O2 in both mixed venous blood and arterial blood, along with simultaneous measurement of cardiac output.<br />Greater the physiologic shunt - greater the amount of blood that fails to be oxygenated!<br />
  34. 34. Ventilation-Perfusion Ratio (V/Q)<br />Physiological Dead Space (V/Q= greater than normal)<br />Ventilation ‘wasted’<br />Ventilation is also wasted in anatomical DS<br />Together : Physiological DS<br />Measurement:<br />appropriate blood and expiratory gas measurements into the following:<br />When the physiologic dead space is great - much of the<br />work of ventilation is wasted<br />
  35. 35. Abnormalities of V/Q ratio<br />Abnormal V/Q - Upper and Lower in Normal Lung<br />Normal person – upright position<br />Lung upper regions: Va/Q higher (Physio. DS)<br />Lung lower regions: Va/Q lower (Physio. Shunt)<br />In both cases – lung’s effectiveness for gas exchange decreases<br />In exercise – situation improves!<br />
  36. 36. Abnormalities of V/Q ratio<br />Abnormal V/Q in COPD<br />various degrees of bronchial obstruction occurs<br />Emphysema occurs resulting in 2 scenarios:<br />Small bronchioles obstructed – alveoli unventilated – V/Q=0<br />Other areas – wall destruction causes loss of blood vessels – ventilation wasted – V/Q = infinity<br />
  37. 37. Alveolar-Arterial Difference (AaDO2)<br />Relationship b/w PAO2 and PaO2<br />Even in normal people – there is a slight difference b/w the two<br />Difference is called AaDO2<br />This slight difference is caused bu mixing of venous blood (thebesian + broncial veins) into oxygenated blood<br />Increased AaDO2 is indicative of impaired gas exchange<br />
  38. 38. GAS TRANSPORT<br />
  39. 39. Pulmonary Capillary Dynamics<br />
  40. 40. Pulmonary Edema<br />Any factor – causing pulmonary interstitial fluid pressure to rise from : -ve to +ve<br />Left-sided heart failure or mitral valve disease<br />Damage to the pulmonary blood capillary membranes caused by infections (pneumonia) or noxious material<br />Pulmonary Edema Safety Factor<br />Pulmonary Capillary Pressure must rise - 7 mm Hg to > 28 mm Hg to cause pulmonary edema <br />This provides an acute safety factor against pulmonary edema of 21 mm Hg<br />
  41. 41. Respiratory Membrane<br />Respiratory Unit(also called “respiratory lobule”)<br />Composed of:<br />Respiratory bronchiole <br />Alveolar ducts <br />Atria<br />Alveoli<br />
  42. 42. Respiratory Membrane<br />
  43. 43. Forms of Gases in Solution <br />In alveolar air:<br />There is one form of gas (expressed as a partial pressure) <br />In solutions (blood):<br />Gases are carried in additional forms:<br />Gas may be dissolved<br />It may be bound to proteins<br />It may be chemically modified.<br />Hence total gas concentration in solution= dissolved gas + bound gas + chemically modified gas<br />Partial pressure of gas in a solution is exerted only by dissolved form!!<br />
  44. 44. Gas Transfer & Transport<br />Two types of gas movements in lungs<br />Bulk flow (trachea to alveoli)<br />Diffusion (alveoli to blood)<br />Henry law states<br />At equilibrium, amount of gas dissolved in a liquid (at a given temperature) is directly proportional to parital P & solubility of a gas<br />Fick law states<br />Volume of gas diffusing per minute across a membrane is directly proportional to:<br />membrane surface area<br />diffusion coefficient of the gas <br />partial pressure difference of the gas <br />And is inversely proportional to membrane thickness<br />
  45. 45. Capillary blood flow & gas uptake<br />Perfusion-limited vs Diffusion-limited gases*<br />Difference b/w N2O, O2 and CO<br />
  46. 46. O2 Transport in Blood <br />O2 is carried in 2 forms in blood: <br />Dissolved<br />Bound to Hb<br />Dissolved form<br />Free in solution <br />Approx. 2% of total O2 content of blood<br />The only form of O2 that produces a partial pressure<br />At normal PaO2 = 100 mm Hg, <br />Concentration of dissolved O2 = 0.3 mL O2/100 mL<br />Insufficient to meet tissue demands*<br />
  47. 47. Bound with Hb<br />Remaining 98% of the total O2 content of blood is reversibly bound to Hb<br />Hemoglobin<br />Globular protein consisting of four subunits<br />Each subunit can bind one molecule of O2 - total of four molecules of O2 per molecule of Hb<br />For the subunits to bind O2, iron in the heme moieties must be in the ferrous state (i.e., Fe2+)<br />
  48. 48. O2-binding Capacity, O2Content&O2Saturation<br />O2-binding capacity – max. amount of O2 that can be bound to Hb per volume of blood<br />1 g Hb = 1.34 mL O2<br />Normal conc. of Hb = 15 g/100 mL<br />O2-binding capacity of Hb= 20.1 mL O2/100 mL blood<br />O2content - actual amount of O2 per volume of blood<br />
  49. 49. Problem<br />An arterial blood gas reveals:<br />PaO2 = 60 mmHg <br />O2 saturation (SaO2) = 90%<br />Patient's Hb = 14 g/dl <br />What is the total (Hgb-bound +dissolved) O2 content? <br />
  50. 50. O2 content = (14gm/dl x 1.34) x 90/100 + 0.3ml/dl<br />O2 content = 17.18 ml/dl<br />(normal = 20 ml/dl)<br />The patient is treated with 30% supplemental O2, and a repeat arterial blood gas reveals:<br />PaO2 of 95 mmHg <br />O2 saturation of 97% <br />What is the total O2 content now? <br />18.49<br />
  51. 51. O2 Transport in Blood <br />Quaternary structure of Hb determines its O2 affinity:<br />T (tense) configuration: Hb in deoxygenated blood<br />R (relaxed) configuration: Hb in oxygenated blood<br />R statehas 500-fold more affinity for O2 than T state<br />Positive cooperativity<br />
  52. 52. O2 Transport in Blood<br />Hb –O2 Dissociation Curve<br />Studies the relation between PO2 and hemoglobin % saturation or O2 content of blood (O2 volume %)<br />At arterial PO2 = 95 mmHg (resting conditions)<br />Hb % saturation = 97%<br />O2 volume % = 19.4 ml (~ 20 ml)<br />At venous PO2 = 40 mmHg (resting conditions)<br />Hb % saturation = 75 %<br />O2 volume % = 14.4 ml<br />P50 – partial pressure of O2 at which ½ Hb is saturated<br />Basis of shape of the curve being sigmoid<br />Positive cooperativity<br />
  53. 53. Hb –O2 Dissociation Curve<br />Maximum amount of O2 that can combine with Hb<br />Normal conc. of Hb in blood = 15 gms/dl<br />1 gm Hb can bind = 1.34 ml O2<br />15 gm Hb can bind = 19.4 ml O2 (~20 volume %)<br />In other words every 100 ml (dl) delivers ~ 20 ml of O2<br />Amount of O2 released from Hb to tissues<br />Arterial blood status<br />PO2: 95 mmHg<br />Hb% saturation: 97%<br />O2: 19.4 volume %<br />Venous blood status<br />PO2: 40 mmHg<br />Hb% saturation: 75%<br />O2: 14.4 volume %<br />
  54. 54. Hb – Tissue Oxygen Buffer<br />‘Based on tissue need’<br />Under basal conditions<br />Tissue O2 requirements = 5 ml/dl<br />Change in Po2 = 55 mmHg<br />O2 release = 5 ml/dl<br />Under heavy exercise<br />Extra 15-25 mmHg change in Po2 achieves – large release of O2 to tissues<br />Reason: Po2 < 40 mmHg lies on STEEP part of curve – LESS change in Po2 results in MORE O2 release<br />
  55. 55. Hb – Tissue Oxygen Buffer<br />‘Buffering action at fluctuating Alveolar Po2’<br />Alveolar Po2 fluctuates:<br />At high altitudes: alveolar Po2 DECREASES<br />In deep sea: alveolar Po2 INCREASES<br />If alveolar Po2 falls to 60 mmHg – <br />Blood Hb% - 89% (only 8% less than max. saturation)<br />Hb%= 89 (5 ml O2 taken away – resting Po2 in venous blood 35 mmHg)<br />If alveolar Po2 rises to 500 mmHg – <br />Blood Hb% - 100% (only 3% above max. saturation)<br />Hb%= 100 (5 ml O2 taken away – resting Po2 in venous blood is only slightly higher)<br />
  56. 56. Shift of Hb – O2 Dissociation Curve<br />Temperature<br />Increase – right shift<br />Decrease – left shift<br />High temperature decreases Hb affinity for O2<br />Excercising muscle!<br />Skin in cold temperature!<br />2,3-DPG<br />@ rest – right shift in systemic circulation (beneficial)<br />May cause difficulty in O2 pickup in lungs (if conc. Increases)<br />Exercise<br />Right shift<br />
  57. 57. Shift of Hb – O2 Dissociation Curve<br />Acid (Bohr pH effect)<br />Metabolically active tissues – H+ production – displaces O2 from incoming Hb – Right shift<br />Lungs – increased Po2 – displaces H+ - left shift<br />CO2 (Bohr CO2 effect)<br />Hypercapnia in tissues – right shift<br />CO poisoning, HB-F<br />Left shift<br />
  58. 58. CO Poisoning <br />Hb binding site for O2 and CO is the same!<br />Binding capability of CO with Hb is 250 folds more than O2<br />Alveolar pressure of 0.4 mmHg (1/250 of normal Po2) <br />CO competes equally with O2 for hemoglobin<br />causes 1/2 Hb to bind with CO instead of with O2<br />Alveolar pressure of 0.6 mmHg – Lethal<br />Clinical scenario<br />Patient comes in with nervous signs <br />No obvious signs of hypoxemia (no cyanosis, bright red blood,)<br />Po2 is normal – body does not detect hypoxia!<br />Treatment<br />Pure O2 with 5% CO2<br />