Lectures 1-4.txt

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Lectures 1-4.txt
2010-10-11 20:47:46
svetik Pulmonary

Pulmonary first 4 lectures
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  1. Lecture 1
    • Anatomic structures
    • Dynamics
    • Epidemiology
  2. Almost all of first week is physiology. Have to pass each of tests individually.
    • Pulmonary functions, arterial blood gas measurements
    • Partial CO2 pressure should be around 40
  3. Visceral and parietal pleura
    • Diaphragm moves the chest wall and separates the thoracic and abdominal cavities
    • High cervical fractures can affect the phrenic nerve. Whenever put needle into chest, need to go right above the rib, NOT right under rib.
  4. Have multople lobes, and multiple segments.
  5. Most important tests when diagnosing radiography – x-rays
  6. Clasically 5 densities can be distinguished on x-ray. Metal is white, and air is black, then tissue, bone, and liquid will be shades of grey in between.
  7. Done standard, PA view – x-rays pass through the back to the front. Minimizes cardiac magnification when x-rays are at a certain distance from the x-rays
  8. One side chest x-rays, the right costophrenic angle/margin looks larger because rays go from right to left.
  9. Have different lobes, and on x-rays can sometimes see fissures. Certain diseases happen in different locations.
  10. The lingula is the equivalent of the middle lobe on the left side.
  11. Diaphragm:
    • The diaphragm - sharply marginated domes
    • Peripheral margins of the diaphragm define the
  12. CT Scans:
    • “digital x-ray”
    • Differentiation is much clearer, can clearly see ribs, spine, the canals, the xcapula, different muscle groups, etc.
    • A lot better resolution and have a rapid way to scan
  13. Pulmonary function tests:
    • Long volumes – static properties
    • And flow volumes
    • Performed with pulmonary function instruments, can also use a “body box”.
    • Also look at how fast the air comes out of the lungs, with the most important test being FEV1

    Lecture 2
  15. During exercise:
    • Lungs can’t collapse completely
    • Breathe deeper
    • Interaction btw the lungs and “chest wall” (intercostals, diaphragm, etc. ) determine the volumes
  16. Lung volumes:
    • Tidal volume: normal breathing
    • Inspiratory Reserve Volume (IRV): What you can inspire past the tidal volume
    • Expiratory reserve volume (ERV): Maximum you can breathe out past tidal end expiration
    • Residual Volume: still have an amount of air remaining after breathing out down to ERV.
  17. Total Lung Capacity
  18. Vital Capacity
    • Amount at the maximum inspiration which you can blow out.
    • IRV+TV+ERV
  19. Functional residual capacity (FRC)
    • Amount of air in lungs at the end of the normal tidal breath
    • ERV+RV
  20. Inspiratory capacity (IC)
    • What you can breathe in at the end of a normal breath
    • TV+IRV
  21. Lung volumes change in disease: PFTs – restrictive pattern – lungs are “smaller than normal”
    • Pulmonary fibrosis
    • Muscle weakness
    • Chest wall deformity
    • Lung surgery – pneumonectomy
  22. Inspiration (Active)
    Negative pressure is generated
  23. Expiration (Passive)
    Muscles relax, the balloon of the lung recoils
  24. Airflow
    • Moving air from mouth, to the alveolus, etc. with no effort
    • Need to work efficiently
    • Airways are a branching system
    • The active cross sectional area of the lung effectively increases as you go from trachea to the alveoli
    • So effective resistance is a lot lower because have many more numbers of smaller ducts, but with a lot of a greater area (cross sectional area of alveoli size of a tennis court)
  25. Flow
    • Flow = Driving pressure/airway resistance
    • P/R
  26. PFTs
    • Try to get maximum driving pressure
    • Flow inversely related to resistance
    • If flow id decreased over time, infer that resistance is increased
  27. Forced Vital Capacity maneuver
    • Maximum inspiration
    • Maximum effort forced expiration
    • The total expired volume is FVC
  28. Forced expiratory volume in 1 s (FEV1)
    • Expressed as absolute value and as percent of predicted value
    • Expressed as percent of the FVC: FEV1/FVC %
  29. FEV1/FVC % Normal and abnormal
    • Normal: >/= 75% most; >/= 70 in pts >50 y.o.
    • Abnormal: < 70% - Obstructive pattern – increased airway resistance
    • Lower the value, greater the resistance
  30. FEF 25-75%
    • Average flow over midrange of FVC
    • Divide FVC into 4 parts
    • Draw line 25% exhaled to 75% exhaled
    • Slope of line (chord is average flow over midrange of FVC
  31. FEV1 is best test for
    • Obstruction
    • Declines linearly as disease worsens
    • Mortality increases as value worsens
    • Useful in predicting response to therapy
    • Predicts likelihood of surgical complications
  32. Measurement flow
    Flow-volume loops, etc.
  33. Peak flow from the flow volume loops
    • Correlates well with FEV1 so can use it as surrogate
    • And in disease it can be measured at home and be used for management of disease at home as well.
    • Peak flow, is measured during expiration
  34. Diffusing capacity
    • Measure rate of transfer of gas from lungs to blood
    • Use carbon monoxide (small amount – 0.3%)
    • Avidly taken up and bound by hemoglobin
    • So in the alveolus gets quickly across the membrane
  35. CO diffusing capacity
    • Measure amnt of CO taken up during breath – hold
    • Estimate pressure of CO in the alveolus across the membrane
    • Diffusing capacity (DLco) is amount of CO taken up by blood divided by the driving pressure
  36. Factors affecting diffusing capacity
    • 1)Delivery of CO to alveolar-capillary membrane: need normal capillaries and need normal SA for diffusion
    • 2)Ability of CO to cross the alveolar-capillary membrane: diffusion depends in part on thickness.
    • 3)Reaction rate: depending on the concentration/function of Hb
  37. Diseases with decreased diffusing capacity
    • Interstitial lung diseases: loss of SA / ? thickness of membrane
    • Emphysema:
    • Etc.
  38. Problems with PFTs
    • Reproducibility
    • Testing standards
    • Predicted values – what compared to?
    • Factors make PFTs unique
  39. Reproducibility
    • Vital capacity, FEV1: 2-5% variation on repeated testing
    • Diurnal variation: Lowest in early morning (3-6am)
    • Response to bronchodilators: At least twice expected variations; at least a 12% of dilation in response to be sure that it’s not just part of normal variation
  40. Standards and certification
    • Americal Thoracic Society Guidelines
    • No real quality controls
    • “Hope that PFTs are done correctly”
  41. NHANES III Findings:
    • Mexican-Americans – lower VC & FEV1 than age-matched Caucasians BUT same if compare height
    • African-Americans – lower VC & FEV1 than age-matched Caucasians: Smaller trunk:leg ratio than Caucasians
  42. PFTs and Racial/Ethnic Diversity
    Because don’t have good normals for certain different populations, the normal range
  43. Value of PFTs
    • Quantitative PFTs in those known to have disease
    • Predict morbidity and mortality
    • Follow course of disease and response
    • BUT have limited function because of low reproducibility and because of the predicted values based on limited populations
  44. Spirometer
    Breathe into an air space where some is filled with water the level of which is allowed to lower when you breathe into the air space
  45. Lung capacities
    • TLC = IRV + TV + ERV + RV
    • VC = IRV + TV + ERV
    • FRC = ERV + RV
    • IC = TV + IRV air in lungs at end of normal breath
  46. With a spirometer can measure:
    • TV - Tidal volume
    • IRC – Inspiratory residual capacity
    • ERC – Expiratory residual capacity
    • VC – Vital Capacity
  47. But CAN’T measure:
    • Those capacities that contain residual volume:
    • RV
    • Functional residual capacity (FRC)
    • Vital Capacity
  48. Measurement of lung volume by Helium Dilution
    • A patient has a certain amnt of air in his/her lungs
    • Helium distributed in the spirometer volume and tubing, remove the block, and let person breathe back and forth and let them equilibrate the helium
    • Now the concentration of He is lower, and Volume has increased
    • So since mass = concentration * volume, by conservation of mass, can calculate the change in the volume of helium
    • Helium mixed throughout spiromoter V1. And lungs V2
    • Helium has lower concentration now
    • Mass of helium = C2*(V1+V2)
    • C1*V1 = C2*(V1+V2)
    • So V2 = [(C1-C2)*V]/C2
  49. Helium dilution measurement:
    • Measure lung volume V1 at FRC ( at the end of a normal breath and let rebreathe)
    • So with helum dilution measurement really measure FRC
    • And measure the ERV and can then calculate the RV: RV=FRC-ERV
  50. Boyle’s law:
    • Valsalva maneuver: expire against a closed glottis
    • Muller maneuver: inspire against a closed glottis
  51. Muller maneuver
    • Inspire against a closed glottis
    • Pressure in lungs lowered
    • Volume of lungs expand
  52. Boyle’s law: Muller maneuver
    • Mass of gas in lungs hasn’t changed
    • Initial pressure times initial volume = P1*V1=P2*(V1+deltaV)
    • Can measure P1 and P2: Mouthpiece with closed shutter; measure pressure between mouth and closed shutter
    • If we can measure change in volume, can calculate V1
  53. If do Muller maneuver at FRC, can calculate RV:
  54. Measurement of lung volume Body Plethysmography (Box)
    • As inspire against closed shutter, pressure in lungs decreases
    • Small volume increase in thorax -- > compresses gas in box
    • Box pressure rises
    • Box calibrated so know change in volume from rise in box pressure
  55. Body Box measurement:
    • Breathe in and out against a closed shutter at FRC
    • Measure changes in pressure at mouth
    • Measure pressure (volume) changes in box
    • Calculate RV: RV=FRC-ERV
  56. Body Box measurement:
    FRC in box – Thoracic Gas Volume (TGV)
  57. Body Box vs. Helium
    • More accurate: Body Box is a lot faster, and can make many measurements in a short time and average
    • Body Box measures “true volume of gas in thorax at FRC”
    • In severe obstructive disease may not reach true equilibrium with He dilution – the blocked areas may not equilibrate with the rest of He in lungs
    • In Body Box can also measure flow and get the volume by integrating the flow over time
  58. Determinants of lung Volumes
    • Lung volumes determined by mechanical properties of respiratory tract as well as the chest wall
    • It’s their elastic properties that directly determine the volume and breathing
  59. Lung:
    • Size of lung
    • Distending pressure: pressure inside lung minus pressure outside of lung
    • To distend: P in lung(alveoli) > P outside of lung (pressure of pleural space)
    • Plung = Palveoli – Ppleura
    • Plung = Pa-Ppl
    • Lung Pressure volume curve – increases from minimum volume and goes flattening out to a maximum volume
    • Lungs act as a balloon
  60. Lung minimum volume:
    Lung collapses to 5-10% of maximum volume
  61. Compliance of lung
    • Compliance: = Change in volume / change in pressure
    • C = delta V / delta P
  62. Hysteresis
    • The volume at any given pressure is larger on deflation than inflation
    • At any given volume, pressure larger on inflation than deflation
    • Surfactant gives lungs this property, surface tension at the interface
  63. Role of Surfactant
    • Lowers surface tension
    • Surface tension changes as a function of area (volume of alveolus): greater effect at lower volume
    • Surface tension lower with deflation than inflation
  64. Effects of Surfactant
    • When inspire all the way, molecules are spread out
    • When expire, all surfactant molecules move closer together, and they lower surface tension
    • Some of the molecules will form micelles because in expiration they com so very close together and will no longer be at the air-alveolar interface, and therefore as you inspire, they won’t be available to lower the surface tension as much as in expiration. But as inspire, you recruit more and more surfactant from micells and then get back to a regular surfactant spreading over alveolar surface
  65. Surfactant’s effect
    • Start at maximum inflation
    • Molecules compressed on deflation
    • Molecules form micelles and leave surface as deflation ends
    • On inflation, new surfactant spread on surface
    • Near maximum inflation molecules spread out and lose some effect
  66. Surfactant Stabilizes Alveoli
    • Allows small and large alveoli to co-exist at same pressure
    • Without surfactant, small alveoli would have higher pressure and empty into large alveoli, and would end up with less surface area for exchange of gases
    • In smaller alveoli, surfactant will have a greater surface tension lowering effect
    • Lecture 4: Ventilation
    • Variables
    • Volume V
    • Concentration C
    • Gas Fraction F
    • Pressure P
    • Remember wheras pressures can be different and can have pressure gradient, with no partial pressure gradient. For diffusion, need a gradient of partial pressure!
  67. Gas Phase
    • Inspired – I
    • Expired E
    • Alveolar A
    • Tidal T
    • Dead space D – where there is no functioning gas exchange
    • a = arterial
    • v = venous
  68. Air is 70% Nitrogen (nitrogen and argon are inert, so are effectively the same for discussion)
  69. Dalton’s Law
    The sum of all partial pressures will equal the total pressure
  70. P(B) = P H2O + P O2 + P CO2 + PN2
    P N2 is effectively zero in inspired air
  71. Anatomic dead space
    • Under normal conditions you waste about 1/3 of your breath
    • Doesn’t change much – it does expand during exercise, but not by much
  72. In exercise
    The tidal volume increases tremendously, so wasted volume is only about 1/10 th of inspired gas
  73. Components of Tidal Volume (VT)
  74. Vd/Vt = Dead space/Tidal Volume
    Dead space at normal conditions = ~ 1ml/lb ideal body weight
  75. In ventilation, need to account for dead space when determining the tidal volume that is to be used
  76. Physiologic dead space
    • Anatomic + Alveolar
    • Alveolar dead space doesn’t occur much
    • BUT can supply ventilation in excess of what can be accommodated by the blood supply, then, effectively have increased volume that is wasted, because of effective dead space in the alveolus: this can lead to as much as 2/3 of Vt to be wasted
  77. At alveolar level, almost no relative air velocity because
    With greater area, almost no resistance to air flow, so in alveoli with VERY SMALL area, the air velocity is very very low, so the diffusion will happen faster than convective air flow. So when auscultate – can’t hear the air in alveoli
  78. If RQ = 1.0
    • Put out the same CO2 as take in O2
    • Means that the Inspired oxygen will be equal to the Partial oxygen in alveoli + Partial pressure of alveolar CO2
  79. In normal conditions R – respiratory exchange ratio
    • R is slightly less than 1
    • So the Alveolar oxygen is = inspired oxygen – alveolar CO2/ R
  80. Alveolar Air Equation in Western New York:
    • P AO2 = 148 – 1.2(P ACO2)
    • P AO2 = P iO2 – 1.2(P ACO2)
  81. When want to assess adequacy of air exhange and ventilation
    Look at P co2
  82. Oxygen Transport
    O2 terribly insoluble in aqueous solution, so need Hb! Which provides the vast amount of O2 transport
  83. HB doesn’t have a hyperbolic binding curve
    • Because it’s a tetramer, and as you bind each oxygen, O2 affinity changes
    • The vast amount of O2 is bound to Hb, and reach maximum at about 100 mmHg of PO2, so don’t really need to go higher than that because the only thing that will increase is the dissolved oxygen at that point
  84. Different organs need different O2 content
    • The heart – takes out the most O2, about 1/3 total
    • But, heart can’t use up all, because need to leave some for the muscle as well.
    • Can take out a lot of O2 with not a huge change in PO2 because the curve is pretty steep
  85. O2 saturation curve, P50
    Curve can shift to the right or to the left depending on Hb affinity to O2
  86. HB saturation %
    Oxygen content x 100 / Maximum Oxygen content
  87. Right O2 saturation shift caused by
    • Increased PO2 required to reach P50
    • Increased H+ (decreased pH)
    • Increased CO2
    • Increased 2,3-DPG
    • Increased Temperature – though not a very important factor normally
  88. Left O2 saturation shift caused by
    • Decreased H+
    • Decreased CO2
    • Decreased 2,3-DPG
    • Decreased temp – worry about only in severe hypothermia
  89. DPG will hold the molecule in reduced form, and will therefore shift the O2 curve to the right
    So will take a higher concentration of O2 to change the conformation of Hb
  90. H+ binds to Hb, will keep O2 in oxygenated form,
    • so will have less affinity for O2
    • And will need a higher O2 concentration
  91. CO2 Reactions will release huge amounts of H+
    • Major effect of Bohr effect: Prevents shift in pH as we go from arterial to venous blood
    • This change called Oxylabile change
    • So Hb will have some buffering ability for H+, can accommodate a change of about 8% in pH
  92. In the lung PO2 in the alveolus is the independent variable, determines how much O2 will be in the blood
    • If different alveoli oxygenate blood to their respective PO2, will later mix blood, and can’t get any more O2 into blood.
    • This means that you switch from PO2 being the independent variable, to another independent variable
  93. O2 Transfer depends on
    • 1.Diffusion of O2 from alveoli into plasma: Barrier thickness, Alveolar-capillary surface area, Partial pressure difference, Solubility of O2 in membrane ….diffusion will also be time-limited – the time that the air stays in the alveoli
    • 2.Simultaneous combination of O2 with Hb and diffusion inside the RBC
  94. CO2 Transfer depends on
    • 1.Dissolved CO2
    • 2.Bicarbonate
    • 3.Carbamate
    • 4.Haldane effect
  95. Mechanisms of Haldane effect
    • 1.Oxylabile carbamate formation
    • 2.Oxylabile buffering of H+ by Hb
    • About 40% of the O2 is excreted in the lungs because you shift from one curve to the other.
  96. Bicarbonate in plasma can’t contribute much to the O2 exchange
    • BUT the carbonic anhydrase that converts H2CO3 into CO2 and H2O and allows diffusion to occure (over msecs)
    • Also have transmembrane exchange of bicarbonate and chloride (carbonate is pumped into cell, where carbonic anhydrace converts it to O2 and H2O
  97. Processes in CO2 Transfer dependent upon O2 exchange
    • Oxylabile release of CO2 bound as carbamates
    • Oxylabile buffering of hemoglobin:
    • H+ used in HCO3- reaction
    • H+ used in carbamate reaction