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  • *coloured blue parameters are already done**forced expiratory flow from 25-75% VC***mid-maximal expiratory flow: The third measure made by the spirogram is the average flow rate over the middle section of the vital capacity. This test has several names, including the MMEF (mid-maximal expiratory flow) and the FEF25-75 (forced expiratory flow from 25 to 75% of the vital capacity). It can be calculated from the spirogram by dividing the vital capacity into quarters, dropping a line from the first (25%) and third (75%) quartiles, and then connecting the lines and measuring the slope. Volume/time is a flow rate and thus the slope is a flow rate (the only real flow rate that can easily be obtained from the spirogram).
  • *VL corresponds to the lung volume at the instant we open the mouth valve and allow the He to beginequilibrating. If we wish to measure FRC, we open the valve just after the subject has completed a quietexpiration. If the subject has just completed a maximal expiration, then the computed VL is RV.
  • The constant, K, equals 863 mm Hg for conditions of BTPS and when Va and Vco2 are expressed in the same units (e.g., mL/min). BTPS means body temperature (310 K), ambient pressure (760 mm Hg), and gas saturated with water vapor. Using the rearranged form of the equation, alveolar Pco2 can be predicted if two variables are known: (1) the rate of CO2 production from aerobic metabolism of the tissues, and (2) alveolar ventilation, which excretes this CO2 in expired air.  A critical point to be understood from the alveolar ventilation equation is that if CO2production is constant, then PaCO2 is determined by alveolar ventilation. For a constant level of CO2 production, there is a hyperbolic relationship between PaCO2 and Va. Increases in alveolar ventilation cause a decrease in PaCO2; conversely, decreases in alveolar ventilation cause an increase in PaCO2. Another way to think about the alveolar ventilation equation is to consider how the relationship between PaCO2 and Va would be altered by changes in CO2 production. For example, if CO2 production, or Vco2, doubles (e.g., during strenuous exercise), the hyperbolic relationship between PaCO2 and Va shifts to the right. Under these conditions, the only way to maintain PaCO2 at its normal value (approximately 40 mm Hg) is for alveolar ventilation to double also. The graph shows that if CO2 production increases from 200 mL/min to 400 mL/min, PaCO2 is maintained at 40 mm Hg if, simultaneously, Va increases from 5L/min to 10L/min.
  • * Doesn’t mean that ventilation and perfusion to the entire lung is normal ! E.g. in lobar pneumonia, V to the affected lobe is affected, and perfusion isnt….but since hypoxia causes vasoconstriction – eventually perfusion too is affected….so V/Q remains ‘normal’ though both V and Q are in fact abnormal
  • The effect of regional V/Q on blood gases is shown in the above table. Because overventilation relative to blood flow occurs in the apex, the PaO2 is high and the PaCO2 is low at the apex of the lungs. Oxygen tension (PO2) in the blood leaving pulmonary capillaries at the base of the lungs is low because the blood is not fully oxygenated as a result of underventilation relative to blood flow. Regional differences in V/Q tend to localize some diseases to the top or bottom parts of the lungs. For example, tuberculosis tends to be localized in the apex because of a more favorable environment (i.e., higher oxygen levels for Mycobacterium tuberculosis).
  • In continuation of the last table showing effects of V/Q in various lung zones on blood gases
  • *transit time
  • *For example, in a person at rest, O2 consumption is about 250 mL O2/min. If O2 delivery to the tissues were based strictly on the dissolved component, then 15 mL O2/min would be delivered to the tissues (O2 delivery = Cardiac output × dissolved O2 concentration, or 5 L/min × 0.3 mL O2/100 mL = 15 mL O2/min). Clearly, this amount is insufficient to meet the demand of 250 mL O2/min. An additional mechanism for transporting large quantities of O2 in blood is needed-that mechanism is O2 bound to hemoglobin.
  • Volume% is ml/dl
  • Transcript

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