Pulmonary Physiology S1M3

  1. What fraction of a breath is in dead space
  2. In what branches is there no gas exchange, and in which is there gas exchange
    • 1-16 no gas exchange
    • 17-23 gas exchange
  3. What is FRC and what is its normal vol
    • Functional residual capacity 3L
    • This is the air left after a normal expiration includes the residual volume and the Expiratory reserve vol
  4. What is tidal volume and what is its normal vol
    Normal quite breathing with a vol of about 500ml
  5. What is anatomical dead space and how does it differ from physiological dead space
    • It is the amount of air that is located in spaces where no oxygen exchange is happening
    • Physiological includes areas that normally have gas exchange but are damaged
  6. What Ig's are found in abundance on the surface of respiratory epithelium
    A and G
  7. What is the Residual Vol (RV), how large is it
    This is the amount of air that cannot be expired, 1.5 L
  8. What is the ERV, and how large is it (vol)
    • Expiratory reserve volume 1.5 L
    • The max amount of air that can be expired beyond tidal volume
  9. What is IRV and how large is it (vol)
    • Inspiratory reserve volume 2.5 L
    • The amount of air that can be inspired beyond tidal vol
  10. What is the VC
    Vital capacity, the largest amount of air that can be inspired and expired including tidal volume
  11. What happens to the lung volumes as one ages
    The vital capacity decreases after age aprox. 58 (increases till then) while the total lung capacity continually increases, and residual vol increases
  12. What are two very important variables to lung volume
    Temp and Pressure
  13. What happens to the TLC and RV values in Obstructive lung disease and Restrictive lung disease respectively
    • Obstructive (Emphysema, COPD) an increase in TLC and a large increase in RV
    • Restrictive lung disease (Pulmonary fibrosis) a decrease in both
  14. What lung capacities require the helium addition
    • RV
    • TLC
    • FRC
  15. Transmural pressure
    Pressure across a wall
  16. Recoiling force is opposite of
  17. A flat curve and a steep curve indicate what on a Vol/transmural pressure difference curve
    • Flat = decrease compliance
    • Steep = Increase compliance
  18. Max inspiration is resisted by
  19. Expiration is limited by
    Chest wall
  20. What makes up 50% of the compliance in the lungs, and what make up the other 50%
    • Elastic fibers and their arrangement
    • Surface Tension
  21. What affects does a small radius have on the aveoli
    There is larger inside pressure, and tendency to colapse
  22. What are the effects of surfactant
    • Reduces surface tension
    • Increase compliance of the lung
    • Minimizes tendency to collapse aveoli
    • Helps alveoli expand in equal amounts
    • Reduces recoiling force
    • Keeps inside of lungs dry
  23. What percent of surfactant is recycled, and where does the rest go
    • 50% is recycled by type II Pneumocytes (some is destroyed by them as well)
    • Removed by macrophages
  24. What is the resting volume of the lung
    Minimal lung volume of 500ml, FRC 3L
  25. When does the respiratory system have its greatest compliance
    At Functional Residual Capacity FRC
  26. Expiration above, and below FRC is
    • Passive
    • Active (energy required)
  27. Where is the least resistance located in the airways, and the greatest resistance
    • Least, in the respiratory zone from 17-23 due to the total diameter increasing
    • Greatest, first 7 branches (80%)
  28. Why is the measurement of resistance in a lung not a good indicator of small airway obstructions
    Because the major site of resistance is in the upper airways
  29. What happens to lung compliance as the volume increases
    It decreases
  30. If the lung volume increases, what happens to the recoiling force
    It increases
  31. What factors affect the airway resistance
    • Density and viscosity of air
    • Concentration of CO2
    • Sympathetic/Parasympathetic innervation
    • Local metabolites
    • Lung Volume
  32. What metabolites constrict the airway
    • Histamine
    • Acetylcholine
    • Thromboxane A2
    • Prostaglandin F2
    • Leukotrienes
  33. How do patients with emphysema lungs expand in relation to a healthy individual
    They don't breath from the FRC but from a higher lung volume do to the decrease in resistance
  34. What is an easy test a physician can perform to assess restrictive or obstructive lung disease
    Forced expiration test
  35. What parameters are measured in a forced expiration test
    • Forced expiratory volume after 1 second
    • Forced vital capacity
  36. In a forced expiration test what is the normal vol expired in the first second
    80% of the total volume
  37. Obstructive lung disease will show what result in a Forced expiration test
    Decreased expiration volume in the first second, and a decrease percentage in the first second compared to the overall expiration
  38. What results would be seen in a forced expiration test with someone with restrictive lung disease
    A decrease in the FEV1 and a decrease in FVC, but a normal or high FEV1/FVC
  39. Expiratory muscles have an optimal length when
    When the vol of the lungs is increased
  40. In restrictive lung diseases the lung volumes are affected how
    All lung volumes are proportionally smaller, but the compliance is reduced, and therefore the recoiling force increased
  41. What happens to extralveolar capillaries upon inspiration
    They dilate as pulmonary capillaries constrict
  42. What is the only active control of pulmonary resistance
  43. How are the effects of hypoxia in the alveolar different from those in the vessels
    Hypoxia in the alveolar causes constriction of the vessels surrounding them, low CO2 in the vessels themselves causes dilation
  44. What is the mechanism that causes constriction of alveolar during hypoxia
    Hypoxia inhibits K+ channels, the cell depolarizes, Ca++ channels open, and the muscle contracts
  45. When is generalized hypoxia good
    During fetal development, but bad following birth
  46. High altitude pulmonary edema (HAPE)
    • Caused by greater hypoxic vasoconstriction response
    • that causes pulmonary hypertension
  47. What happens to capillaries in the lungs that are above the heart
    The alveolar pressure exceeds that of the pulmonary artery pressure disallowing blood air exchange
  48. What are some anatomical shunts that are found in a normal adult
    • Thebesian veins taking deoxygenated blood from coronary arteries to left atrium and ventricle
    • Bronchial veins contributing to pulmonary veins
  49. How much oxygen is dissolved in the blood
    About 15 ml/min during normal cardiac output of 5L/min
  50. What is the saturation of Hb with O2 at 40 and 100 mmHg in the blood respectively
    75% and 98%
  51. A decrease in the amount of red blood cells like in an anemic patient would have what affects on Hb saturation and Oxygen blood concentration
    • Saturation would not be affected
    • Concentration of blood would be decreased (PaO2 isn't effected though)
  52. What happens to the intrapleural pressure during inspiration and why
    It is more negative do to the effects of the recoiling force
  53. What is the definition of hypo and hyperventilation
    Hypo is an increase in PaCO2 Hyper is a decrease
  54. CO, NO, and O2 are limited how
    • CO diffusion limited
    • NO is perfusion limited
    • O2 is perfusion limited normally
  55. How does pulmonary vascular resistance compare to TPR
    It is 16x smaller
  56. Decrease alveolar O2 has what effect on the blood vessels
    Constriction of pulmonary blood vessels
  57. High altitude has what affect on the arterial CO2 pressure
  58. Where is the V/Q ratio highest
    Apex of the lung
  59. Diffusion limitation only happens when
    • High Altitudes
    • Lung Disease
  60. What are the three ways CO2 can be carried in the blood
    • Diffused in blood
    • Bicarbonate
    • Carbamate (much lower concentration)
  61. Bronchopulmonary sequestration
    Lung lobes or segments without connection to airways, but has its own blood supply from the aorta
  62. What are the three classes of atelectasis
    • Resorption - Complete obstruction of airways
    • Compressive - Fluid or air in plueral cavity
    • Patchy - Often found in RDS
  63. What are the two subcategories of pulmonary edema
    • Hemodynamic causes - pressure increase
    • Microvascular - capillary damage
  64. Adult respiratory distress syndrome (ARDS) aka. Diffuse Alveolar Damage (DAD)
    • Alveolar capillary damage due to inflammation
    • May cause cyanosis, organ failure, pulmonary adema, 50% mortality
  65. Why are small embolims of the lung rare
    Lungs have a double blood supply
  66. What is the difference between exudate and transudate
    • Exudate is fluid from the circulatory system usually RBC, platelets, plasma proteins
    • Transudate is extravascular fluid w/ low protein content
  67. Terminal respiratory unit
    Final stage of bronchiole tree containing bronchiole, alveolar ducts and sacs
  68. What are the two primary types of Emphysema
    • Panacinar - enlargement of acinus uniformly
    • Centriacinar - elargement of the central parts of the acinus, not the ends
  69. Acinus
    Respiratory segment of bronchioles
  70. Alpha 1 antitrypsin and emphysema relate how
    It's inactivation is beleived to cause it
  71. Honeycomb lungs is caused by
    Pulmonary fibrosis (Restrictive disease)
  72. Pneumoconiosis
    Fibrosis (restrictive) of lungs via inhilation of certain inorganic dusts
  73. What are the different types of hypoxia
    • Stagnant
    • Anemic
    • Histotoxic
    • Arterial
  74. Stagnat hypoxia
    Blood flow reduced
  75. Anemic Hypoxia
    O2 capacity of blood is low such as Hb availability low, or CO poisoning
  76. Histotoxic hypoxia
    Tissues aren't using O2, cyanide or hydrogen sulfide poison can cause it
  77. Arterial hypoxia
    Reduction in blood O2 saturation, only hypoxia where PO2 is diminished (altitude is a common cause)
  78. Anoxia
    Complete absence of O2 in tissue
  79. Why are anemic patients unlikely to get cyanosis
    Because they have such a small amount of RBC's, to reach the deoxyhemoglobin 5g/100ml blood required for cyanosis signs to be expressed, they would be dead
  80. What is a common cause of peripheral cyanosis
    A low perfusion, meaning the blood has more time to diffuse O2 into the tissues
  81. What is a normal arteriole/alveoli O2 concentration difference
    3-10 mm Hg
  82. Why doesn't a PCO2 difference have much of an effect
    It takes a very large concentration difference to effect the CO2 partial pressure
  83. How can you tell the difference between a mismatch or a Diffusion problem
    A diffusion problem will show a decrease in CO when tested, a mismatch will not
  84. When trying to decide the reason for a patient having arterial hypoxia (low PaO2), what would be the best set of steps
    • If increased PaCO2 it is hypoventilation, decreased Low PIO2 (altitude)
    • If PaCO2 is normal try 100% O2, if it doesn't fix the problem it is a shunt if it does try the last step
    • Do a CO diffusion test, if they show a low capacity it is diffusion problems, if not, it is a mismatch
  85. What are the two causes of hypercapnia
    • Hypoventilation
    • Ventilation perfusion inequality
  86. What is the only hypoxemia that will not be effected by 100% oxygen treatment
  87. The oxygen concentration is highest where in the lung and why
    At the top of the lung, because the ventilation to perfusion ratio is high. Meaning, there is less blood flow and therefore less oxygen exchange leaving leftovers
  88. How can the alveolar prefusion be measured
    By measuring the alveolar-arterial PO2 differences
  89. Sensory information for breathing is coordinated where
    • Medulla (Ventral respiratory group, Dorsal respiratory group)
    • Pons (Pneumotaxic center)
  90. What is the job of the Pneumotaxic center in the brain
    It controls inhibitory effects and regulates inspiration volume and respiratory rate
  91. What is the job of the Dorsal respiratory group
    Inspiration and generates the basic rhythm for breathing
  92. The dorsal group receives input from where and output is sent where
    • Vagus N. (peripheral chemoreceptors and mechanoreceptors from lungs)
    • Glossopharyngeal N. (peripheral chemoreceptors)
    • Output to phrenic nerve to diaphragm
  93. The ventral group is primarily responsible for
    Expiration, not active in quiet breathing, active in exercise
  94. Slow adapting stretch receptors are located where, and have what function
    • Airway smooth muscles (inn. by vagal n.)
    • Terminates inspiration and expiration
  95. Rapidly adapting stretch receptors are located where and have what function
    • Airway epithelium (inn. by vagal n.)
    • Cough reflex and gasping
  96. Where are C-fiber and J-receptors found, and what is their function
    • Near capillaries (non myelinated vagal)
    • These are activated by disease conditions and cause shallow breathing, bronchoconstriction, and cardiovascular depression
  97. Central chemosensitive regions are found where and have what function
    • On the ventral lateral surface of the medulla
    • They are stimulated by H+ and inhibited by cold or anesthetics
    • They will increase respiration when Ph is low
    • Not triggered by Hypoxia
  98. Where are peripheral chemoreceptors found and what is there job
    • They are found in the junction of the carotid arteries and on the aortic arch.
    • Triggered by Hypoxia, PCO2 and Ph levels stimulating breathing and raising blood pressure
  99. An increase in CO2 will effect what receptor most and how
    The central receptors will be the only ones effected, and it responds 80% to the lower Ph as a result of the high CO2
  100. What is the difference of effect of ventilation with someone with acute hypercapnia and chronic
    • Acute will immediately trigger a response of increased ventilation trying to compensate for the low O2 and high CO2.
    • Chronic elevation in CO2 will only exhibited a slightly higher ventilation due to the renal compensation of low Ph. PCR is operating independently after renal compensation
  101. Hypoxia will cause what chain of events
    • Increase ventilation
    • Decrease PCO2
    • Large Ph decrease if chronic
    • Compensatory Ph by kidneys
  102. How does ventilation change with acute vs chronic hypoxia (high elevation)
    Acute is a short change of ventilation due to is being brought back after normal oxygen levels return from hyper ventilation

    Chronic will cause alkylosis due to hyperventilation inhibiting the CO2 and Ph receptors in both the PCR and CCR. Ph will be compensated for by the kidneys and then normal breathing will return at the higher ventilation
Card Set
Pulmonary Physiology S1M3