Anesthesia-Respiratory Exam 1

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Anesthesia-Respiratory Exam 1
2013-03-01 14:09:34
CRNA Respiratory Exam

NU490 Exam 1 Spring 2013
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  1. Oxygen is carried in the blood in two
    forms.  What are they?
    • The greater part is in reversible
    • chemical combination with hemoglobin, while a smaller part is in physical
    • solution in plasma and intracellular fluid.
  2. O2 + Hb -->
    O2 + Hb--> HbO2 (oxyhemoglobin)

    this is a reversible reaction
  3. When is Oxygen Capacity is reached?
    • Oxygen Capacity is reached when the
    • maximal amount of oxygen is combined with hemoglobin  i.e. all binding sites are occupied
  4. Oxygen saturation of hemoglobin  =
    • O2 with hemoglobin
    • oxygen capacity

    then multiple by 100
  5. For each 1 mmHg of PO2, there is
    •    0.003ml O2 
    • 100ml of blood.
  6. Why is it important to look at concentration of oxygen (or oxygen content) in blood instead of SaO2 and PaO2?
    Because you can have a normal SaO2 and PaO2 but if you do not have enough Hemoglobin, there is not enough oxygen being carried to the tissues.
  7. How do measure the amount of delivered oxygen?
    DO2 = Qt (CaO2 x10)   

    • Q=flow (or cardiac output) and 10 because
    • referring to oxygen content as deciliter (ex:2ml O2 per 100ml of blood).
  8. What is the first sign of low oxygen content?
    • ACIDOSIS.  
    • No Oxygen so anaerobic metabolism, thus creating lactate and acidosis because oxygen delivery is so low.
  9. Why does cyanosis have different degrees?
    • It depends on how much hemoglobin they have. Ex: If someone has Hb of
    • 30 (polycythemic), will have large amount of reduced hemoglobin and will look cyanotic even though they have 15 of saturated hemoglobin.
  10. What are the physiologic advantages of the oxygen dissociation curve?
    • on high flat end of curve,
    • even is PO2 decreases, there is not effect on hemoglobin saturation. The steep
    • portion of curve is advantageous, because at lower PO2s, saturation drops. Say
    • venous pO2 of 40, on very steep portion of curve. Meaning at tissue level where
    • pO2 is 40, less affinity for oxygen and oxygen is given up to tissues.
  11. What does the oxygen association curve describe?
    the affinity for oxygen to the hemoglobn
  12. What is the normal curve of oxygen dissociation curve?
    The normal is when hemoglobin is 50% saturated then the PO2 is 27.5mmHg.
  13. When does the oxygen dissociation curve shift to the right and why?
    • In right shift, there is less affinity between oxygen and hemoglobin (low saturation). And we like this because if patient is hypothermic or acidotic, want hemoglobin to release oxygen more readily which is what happens in right shift. 
    • acidosis, hypothermic, increased DPG, increased CO2
  14. When does the oxygen dissociation curve shift to the left and why?
    • During Left shift, (hyperthermia, alkalosis, and decreased DPG) there is a
    • greater affinity for oxygen to hemoglobin. Oxygen less likely to be given up to
    • tissues. In blood transfusions (if not fresh, been refrigerated) if you transfused 5-6 units of blood, could have decreased 23 DPG.
  15. What is the Bohr effect?
    • describes the effect of CO2 on the oxygen
    • dissociation curve.
    • •Increase in CO2 or Increase in H+ cause
    • a Right shift, i.e. lower affinity of hemoglobin for oxygen 
    • Advantageous
    • in human body, because if higher CO2 at
    • tissues, less affinity, O2
    • given up to tissues more readily. In venous blood, the curve is right shifted,
    • and oxygen is given up. Perfect for tissue level.
  16. What are the three forms carbon dioxide is carried in the blood?


  17. What is the Hamburger effect (or chloride shift)?
    • Bicarbonate left cell, to maintain
    • electric neutrality, chloride moves into cell (chloride shift). This was
    • discovered and named by Dr. Hamburger so it’s also called Hamburger effect as
    • well as chloride shift.
  18. This slide is showing what’s happening at tissue level.

    CO2 + H20 <-> H2CO3 <-> HCO3 + H+ 

    • CO2 is going into cell. Meets up with
    • water, becomes carbonic acid, then dissociates into bicarb and H+. Bicarb leaves the cell going into plasma and tissues. The H+ becomes attached to Hb. (making HHb) Reduced hemoglobin is weaker acid than oxyhemoglobin. More willing to pick up H+. Bicarb left cell, to maintain electric neutrality, Cl- moves into cell
  19. What is the basis  Haldane effect?
    • the fact that reduced hemoglobin is more capable of picking up acid.
    • Saying reduced Hb can carry more hydrogen and more CO2, so it carries more acid.
    • Refers to different in amount of CO2 carried in Oxygen and de-oxygenated blood.
  20. Reduced hemoglobin is ______ as effective
    in carrying PCO2 compared to oxyhemoglobin.
    3.5 x
  21. The Haldane Effect– describes
    • the effect of oxygen on the CO2 Dissociation curve
    • •Low PO2 (peripheral tissues) shifts CO2 to the left..more affinity for CO2
    • •High PO2 (lungs) shifts CO2 to the right..less affinity for CO2
  22. Henderson—Hasselbach equation
    the pH resulting from the solution of CO2 in blood and the consequent dissociation of carbonic acid

    pH =  pKa +  log  (HCO3) / 0.03PCO2

    As long as bicarbonate and CO2 stays normal, the pH will stay normal.
  23. Muscles of inspiration:
    •Diaphragm—most important

    • •Intercostals muscles
    • •Accessory muscles of inspiration
    • •Scalene muscles (raise 1st
    • two ribs)
    • •Sternamastoid muscle (raises sternum)
  24. Muscles of expiration:
    • rectus abdominus

    • internal and external obliques

    • transverse abdominus
  25. Lung compliance is defined as....
    the change in lung volume per unit change in transmural pressure gradient (i.e. between the alveolus and the pleural space)
  26. Factors affecting Lung Compliance
    • -Posture 
    • -Pulmonary blood volume (if pulmonary congestion, decrease compliance)
    • -Restriction of chest expansion
    • -Bronchial smooth muscle tone

    *Disease (BIGGEST FACTOR)*
  27. Usual value for lung compliance is
  28. If you have low lung compliance, the lungs are....
    • STIFF! 
    • you have poor or low lung compliance, it will take a great deal of pressure to move lungs at all (lot of pressure to move a certain tidal volume)
  29. Pulmonary fibrosis has increased or decreased lung compliance?
  30. Emphysema, increased or decreased lung compliance?
    INCREASED! There is a loss of elastin, think of elastin as a rubber band, it is the collagen that makes up lung. Allows for expansion and then release of pressure from the lungs. Elastin likes to get the lungs to return to baseline. They inhale, inhale, inhale, and lung gets bigger, giving barrel chest. You keep stretching and nothing is bringing it back.
  31. What is hysteresis and what is the cause?
    • The lung is more compliant on exhalation than inhalation.
    • The surface tension of alveoli is greater during inspiration than during expiration.
  32. Where is surfactant formed?
    in Type 2 cells
  33. Surfactant is released in response to....
    • High inflation. It’s also part of fight or flight response. Released in response to endocrine
    • secretions/stimulation.
  34. Surfactant is made early or late in fetal maturation?
    LATE! (32-34 weeks?)
  35. Surfactant is made of..
    Phospholipid, fatty acids at one end, trap gas molecules. Fatty acids are lipophilic, they like the gas phase. The other end of the molecule, glycerol/phosphate, likes the  water phase, hydrophilic. The molecule is trapped at the gas liquid interface. Lipophilic and hydrophilic traps the molecule at this gas/liquid interface.
  36. Physiologic Advantages of Surfactant
    Lowers surface tension in alveoli, increases lung compliance and decreases work of breathing

    Promotes stability of Alveoli

    Helps to keep alveoli dry
  37. P = 2T        
    La Place’s law for one surface involving liquid-lined spherical alveolus.

    T  is surface tension and r is radius. P is pressure. (If one surface, then it’s 2 if it’s more than the numerator is 4)
  38. According to La Place's law, if the radius is smaller, the pressure is higher and air will leave the small bubble and go into a larger bubble (collapsing small bubble). Why doesn't this happen in the lung?
    Because of surfactant! The alveoli in dependent area of lung is smaller, this doesn’t happen because of surfactant.
  39. Anatomic factors that influence the
    compliance of the thoracic cage include:
    •The ribs and the state of ossification of the costal cartilages

    •Obesity or abdominal distention

    •Pathological skin conditions (Burn over chest)
  40. What happens in a pneumothorax?
    • No longer have visceral & parietal pleura attached and intrapleural pressure is now  atmospheric or 0. 
    • The lung springs in and the chest wall springs out. Equilibrium positions between lung and chest wall are different. Lung wants to be small and chest wants to be big. Chest likes big volume & this creates negative pressure.
  41. What are the two types of resistance we must overcome to breathe?
    Elastic and airway resistance.

    • Elastic disease (emphysema/pulmonary fibrosis)
    • Airway resistance disease (COPD/Asthma)
  42. Flow is equal to....
    • change in pressure
    •      resistance
  43. In laminar flow what is most important?
    • The viscosity of gas!
    • Can’t change length of tube, or really change resistance. So the only factor in this resistance is the viscosity of the flow.
  44. In laminar flow, the gas flow rate is....
    directly proportional to the pressure gradient along the tube.
  45. In turbulent flow at high rates results in...
    result in a breakdown of the orderly flow of gas. (particularly through branched or irregular tubes)
  46. In turbulent flow the driving  pressure is
    proportional to the density of the gas and is independent of its viscosity

    and is proportional to the square of the gas flow rate.

    P ~KV2
  47. The nature of gas flow (whether it will be laminar or turbulent) maybe predicted from
    the Reynolds’ number!

    • Re  = 
    • linear velocity of gas  X  tube diameter 
    • X (gas density/gas viscosity)

    • Re over 2000, flow is turbulent.
    • Re less than 2000, flow is laminar.
  48. Four grades of increased airway resistance
    Grade 1: Slight Resistance 

    Grade 2 : Moderate Resistance  

    Grade 3: Severe Resistance

    Grade 4 : Respiratory Obstruction
  49. Causes of Increased Airway Resistance
    • -Material within the lumen 
    • -Thickening or contraction of the wall of the passage (Mucosal swelling, secretions, bronchospasm)
    • -Intraluminar obstruction of the lower respiratory tract (tumor,edema)
  50. As lung volume increases airway resistance....
    • Help patients to increase lung volume by giving them PEEP so we can lower the airflow resistance and keep airways open. CPAP and BiPAP. We use pressure to keep airways open
  51. Closing capacity is...
    • The lung volume at which dependent airways close.
    • Airway closure begins at certain volume. When airway resistance goes up up up, at somepoint it’s going to collapse.
    • Closing volume is same concept.Closing volume is closing capacity minus the residual volume.
  52. How are FRC and closing capacity related?
    If FRC is less than the point at which airways would close, then airways are closing.

    Normally, during normal TV, at end of expiration, we’re breathing at FRC & breathing at volume higher than at which airways would close.

    If FRC is lower, same TVs, but closing & developing atelectasis.

    It’s the relationship between FRC and closing capacity that determines airway patency.

    Now closing capacity increases with lung disease and with normal aging. FRC decreases with change in position (standing to supine) decreases FRC.
  53. Closed alveoli are....
    SHUNT! venous admixture, why in pathological conditions you have the PAO2-PaO2 gradient.
  54. As we age, closing capacity...
    • increases...explains why the normal PAO2-PaO2 gradient is higher. 
    • Expect more shunt when placing patient supine for anesthesia.
  55. Flow rate is limited by....
    • airway compression. 
    • For the majority of exhalation, the rate of exhalation is due to airway  compression.
    • Regardless of effort, expiratory curves end in final common pathway which is independent of effort.
  56. Muscular control of airway diameter

    The four pathways involved in controlling muscle tone in small bronchi and
    bronchioles are:
    • 1.Neural pathways (efferent
    • nerves release Ach, causes smooth muscle contraction)

    2.Humoral control (Beta2 receptors in  bronchial mucousa)

    3.Direct physical and chemical effects  (cold, ETT, gastric acid)

    4.Local cellular mechanisms (Mast cell degranulation & histamine release)
  57. Time constant has to do with...
    resistance and compliance. TC=R x C.

    If resistance or compliance is abnormal, lung will not fill and empty as a unit.
  58. During quiet breathing, Work of breathing is performed entirely by the _______ ______.
    inspiratory muscles.
  59. The actual work performed by the respiratory muscles is very ____in the healthy resting subject.
  60. In increased elastic resistance (pulmonary fibrosis) the patient will breathe at a ____ rate.
    FASTER (and lower TV)
  61. In increased airway resistance, the patient should breathe at at ____ rate.
    SLOWER. (and increased TV)
  62. Respiratory center divided into three major collections of neurons:
    a) the dorsal respiratory group (involved with inspiration). *Has most fundamental role in respiration*

    • b) the ventral respiratory group (expiration
    • and inspiration)

    c) the pneumotaxic center.
  63. What three things transmit signals to the dorsal group?
    • peripheral chemoreceptors
    • baroreceptors 
    • lung receptors

    (transmits signals over two pathways, one is glossopharyngeal nerve and the other is the vagal)
  64. The dorsal group neurons emit a signal to the...
    • diaphragm causing diaphragm to contract
    • (inspiration)
  65. Explain the inspiratory ramp signal
    In normal respiration, a signal to diaphragm that begins weakly, and increases steadily in a ramp manner for about two seconds. Then there’s a pause for about 3 sec where expiration occurs, then again you get a ramp signal from dorsal group of neurons.
  66. What are the two ways the inspiratory ramp in controlled?
    • 1) rate of increase of the ramp.
    • (ramping up signal as time goes on, starts weak and increase) 

    2)the limiting point where the ramp ceases.
  67. How does the pnuemotaxic center decrease the duration of inspiration?
    it inhibits the dorsal group neurons. 

    • A strong pneumotaxic signal increases the RR (inhibits the ramp of dorsal group so increased RR).
    • Whereas a weak signal, weakly inhibiting the dorsal and reducing RR.
  68. The ventral group is _____ during
    normal quiet respiration
    inactive. But becomes active in exercise.
  69. How do the lung inflation signals work?
    • lung receptors sending signals to dorsal group (aka neuronal control)
    • Also, sensory nerves in the lungs that help control resp. -stretch receptors in the lungs, send signals through the vagal nerve to the dorsal group.
    • *NOT a part of normal breathing* When the lungs become over inflated (over 1L) the stretch receptors switch off the inspiratory ramp.
  70. The Hering-Breuer Reflex
    If in abnormal situation, taking in huge TV over 1L, then stretch receptors will send signal to switch off inspiratory ramp and stop further inspiration
  71. Ventilation is controlled in three ways, what are they?
    1) Central Chemical Control of Respiration

    • 2) Direct chemical control by carbon dioxide
    • and hydrogen ions

    3) Response of the chemoreceptor neurons to hydrogen ions
  72. Oxygen acts on _____ chemo receptors.

    In carotid and aortic bodies.
  73. There is chemosensitive area near dorsal group. Only ____ can effect this area directly but _____ drives the process and has profound effect.
    Hydrogen ions. CO2.

    H+ being potent ion can  not cross BBB. CO2 crosses, and mixes with water to become carbonic acid, which dissociates into hydrogen and bicarb.
  74. Excitation of respiratory center by CO2
    is ______ in first few hours.
    • When CO2 increased, we know the effect doesn’t last more than a few days (has renal compensation)
  75. As CO2 increases, alveolar ventilation will ____.
  76. Peripheral chemoreceptors respond to PO2 less than ____ but not to oxygen in normal range.
  77. How do peripheral chemoreceptors send signals?
    have efferent nerve fibers that pass through the vagus nerve to the dorsal group.

    When PO2 drops below 70, the peripheral chemorecepoters transmit nervous signals to dorsal group to increase respiration
  78. What happens if you have a bilateral carotid resection?
    Lose hypoxic ventilatory drive.
  79. PCO2, pH, and PO2 have ____ _____on Alveolar Ventilation
    composite effects. If have low PO2. If patient is acidotic and hypoxic, there is greater  increase in alveolar ventilation
  80. Anesthesia ______ FRC
    DECREASES. Anesthesia effects it because it relaxes the diaphragm, pressure is more easily transmitted through a relaxed  diaphragm get upward abdominal pressure and that decreases FRC. The obese patients are most effected by this.
  81. Respiratory _____ is effected by anesthesia.
    • Pattern
    • Depends on what type of anesthesia you're using and also how deep (anestheticized)
    • is the patient
  82. What is the reason for the jerky irregular respiration of deep anesthesia?
    lack of active intercostal muscle contribution. Diaphragm is strong muscle, still working under anesthetic, but the intercostal muscles are out. The diaphragm descends but the intercostals not working, get descending but not expanding, This is called paradoxal respiration.
  83. How does anesthesia effect minute ventilation?
    • As ETCO2 increases, ventilation increases. But with anesthesia the patient is less sensitive to CO2.
    • The response curve is flatter, as CO2 increases, there is a smaller increase alveolar ventilation.
  84. What is the mechanism of cheyne stokes breathing?
    1) heart failure. Low blood flow but gas changes still occurring. by the time the blood reaches brain) there is a higher level of CO2, and the body responds to that by increasing ventilation. Get excessive ventilation and then long apnea periods.

    2) brain damage, brain edema. The dorsal group is not functioning normally.The brain damage turns off respiratory drive entirely for a few seconds. Too much CO2 builds up, and then there’s excessive ventilation
  85. Are pulmonary function tests diagnostic?
    • NO. 
    • They are used to follow progress of patients and to assess results of treatment.
  86. When do we consider vital capacity abnormal?
    if it falls below a percent predicted value (less than 80% of predicted value).
  87. A decreased vital capacity may result from:
    Lung Pathology (pneumonia, atelectasis, and pulmonary fibrosis)

    Loss of distensible lung tissue (following  surgical excision)

    Causes other than Lung Disease (muscle weakness, abdominal swelling, or pain)
  88. What is the normal FEV/FVC ratio?
  89. In obstructive disease, the FEV/FVC ratio is....
    • low. The FEV is low compared to FVC. Because
    • of obstruction and gas trapping makes the volume exhaled in first second so low.
    • So you could give bronchodilator or give patient longer time to exhale.
  90. In restrictive disease, the FEV/FVC ratio is...
    higher. FVC is low because there is a problem with inhalation but will have large FEV.
  91. What is maximum breathing capacity?
    • have expiratory volume measured over 1min. Breathe in/out as much as possible.
    • Normal value is 150-175L/min in healthy adult male. Depends again on body size, muscle mass, etc so looking at percent predicted.
    • (less than 80% predicted is an abnormal)
  92. What does maximum breathing capacity indentify?
    • tolerance to stress/activity.
    • *Non-specific*can not ID where it is.
    • Pre-op workup- will know some info about lung function, motivation, etc.
  93. How do you measure inspiratory muscle strength?
    • Measured just before inspiration starts. When lung volume is very low. Will measure the tension in your muscles.
    • Near residual volume, inspiration is about to start
    • In young adult males, the normal inspiratory pressure is -100cmH20.
    • NIF, occlude circuit and tell patient to  breath, look at negative insp. Pressure, want at least -25 before extubation.
  94. How do you measure expiratory muscle strength?
    • (abdominal measure)
    • measuring at high volume. Take a deep breath and just before take a deep breath out.
    • (normal PE max is =250cmH2O).
    • If you don’t have exp. Pressure of at least +40, there will be impaired coughing ability post-op. Will get pneumonia.
  95. Physiologic Determinants of Maximum Flow Rates
    1.Degree of effort, or the driving pressure generated by muscle contraction

    2. The elastic recoil pressure of the lung

    3. Airway Resistance
  96. In _____, flow rate is low in relation to lung volume.
    Obstructive disease. (Get scooped out pattern on flow/volume curve).
  97. Ficks law of diffusion states
    that the amount of gas that moves across a sheet of tissue is proportional to the area of the sheet but inversely proportional to its thickness.
  98. Darlton's law states
    The partial pressure of a gas is found by  multiplying its concentration by the total dry gas pressure
  99. Oxygen and CO2 move between lungs and
    blood by
    simple diffusion
  100. The Extrinsic muscles:
    infrahyoid group consists of......

    and these muscles pull the larynx and hyoid bone _____ to a ____ position in the neck
    the sternohyoid, sternothyroid, thyrohyoid, and omohyoid muscles

     down, lower
  101. The extrinsic muscles: the suprahyoid group consists of....

    and these muscles pull the hyoid bone ____, ____, & _____.
    The suprahyoid group consists of the stylohyoid, myohyoid, digastric, geniohyoid, and stylopharyngeus muscles.

    forward, upward, and backward
  102. Posterior Cricoarytenoid Muscles pull _____ on the ____ ____ of the arytenoids (two bumps).

    This causes the vocal
    folds to move ____.
    inferiorly on the lateral angles

    causes vocal cords to move apart (abduct) and allows air to pass through
  103. Lateral Cricoarytenoid muscles pull _____ on the lateral angles of the arytenoids, causing the vocal folds to _____.
    laterally, move together (adduct).
  104. Transverse Arytenoid Muscles  _____ the arytenoid cartilages ____ and thereby position the two vocal folds so that they _____ as air passes
    between them during exhalation.
    pull, together vibrate.

    Thus the sounds for speech or singing are generated.
  105. Thyroarytenoid Muscles lie in the vocal folds _____ to the vocal ligaments.

    Contraction of the thyroarytenoid
    muscles ____ the arytenoid cartilage ____.
    lateral, pulls, forward, allowing a lower frequency of phonation
  106. Cricothyroid Muscle are located on the  ____ surface of the larynx, can swing the entire thyroid cartilage _____.

    This action provides an additional way to ____ the vocal folds and thereby change the ____ ___ ______.
    anterior, anteriorly,frequency of phonation
  107. Larynx primary function is to
    ensure free flow of air in to and from lungs.
  108. What is the second function of the larynx?
    vasalva maneuver, massive adduction of vocal cords so glottis is sealed and air can not escape. Helpful for lifting, coughing and defecation
  109. When is the best time to extubate?
    At the END of INSPIRATION when the glottis is most open.
  110. List the  parts of the conducting zone in order of biggest to smallest.
    trachea, main stem bronchi, lobar bronchi, segmental bronchi, subsegmental bronchi, bronchioles, and terminal bronchioles
  111. What is the function of the conducting zone? What does it represent?
    • to lead inspired air to gas exchange area of lung.
    • Represent anatomic dead space
  112. List the areas of the respiratory zone from biggest to smallest.
    respiratory bronchioles, alveolar ducts, and alveolar sacs.
  113. What is the function of the respiratory zone?
    sites of gas exchange.

    Respiratory zone is also called terminal respiratory units or acinus
  114. Is the respiratory zone cartilaginous or non-cartilaginous?
  115. Is the conducting zone cartilaginous or non-cartilaginous?
  116. What are the cartilinaginous areas or the airway?

    •Main Stem Bronchi

    •Lobar Bronchi

    •Segmental Bronchi

    •Subsegmental Bronchi
  117. Where are the canals of lambert and what do they do?
    • between the lining of terminal bronchiole and alveoli.
    • It is believed these tiny pathways may be important secondary routes for collateral ventilation in patients with COPD.
    • In normal respiration, gases are not flowing between these but is possible for gas to do this.
  118. After terminal bronchioles,  the movement of gases is by _____.
  119. EPIthelium is composed of two cell types, what are they?
    • Type 1 cells are squamous pneumocytes.
    • Type 2 cells are granular pneumocytes.
  120. _____forms 95% of the alveolar
    surface. It is very thin (0.5micrometers) and the major site of gas exchange
    Type 1 cells
  121. represent 5% of the alveolar
    surface and are believed to be the primary source of pulmonary surfactant.
    Type 2 cells
  122. What are the small pores in the alveoli called and what do they do?
    • pores of Kohn.
    • These pores permit gas to move between adjacent alveoli(in normal lungs).
  123. What are type 3 cells called and what do they do?
    Alveolar Macrophages. Which remove bacteria or foreign particles that are deposited in the respiratory zone
  124. Interstitium has two parts. Name each one and it's location, why are they important?
    • 1) tight space is the site of gas
    • exchange. It’s between the alveolar  epithelium and the endothelium of the pulmonary capillary.

    • 2) The loose space surrounds the
    • bronchioles, alveolar ducts & sacs. Neuro fibers are found in this area.
  125. What it the mean PA pressure? What is the normal pulmonary blood flow?
    15mmHg. 5-6L/min.

    It is very low pressure for that amount of flow. The resistance of pulmonary circulation is very small and the pressure is much lower.
  126. What is the Hilum?
    the part of the lung where vessels, main stem bronchi, and nerves enter.
  127. Both arteriole and venule have three layers of tissue, what are they?
    The inner layer is called the tunica intima (endothelium).

    The middle layer is called the tunica media (middle layer). The artery has more of the middle layer (more muscle).

    The outer later is called the tunica adventitia (collagen).
  128. How long does a red blood cell spend in a pulmonary capillary?
  129. Pulmonary capillaries also play an important biochemical role in the production and destruction of a broad range of biologically active substances. Give an example.
    Convert Angiotension I to Angiotension II. 

    Where sertonin and epinephrine are destroyed.

    Some prostaglandins are produced and synthesized in the pulmonary capillaries
  130. The walls of the capillaries are less than .1 micrometer thick and their external diameter is about 10 micrometers. Why is this important?
    The thinness of capillary means it can also be easily damaged. (ex: by large inspiratory pressures)
  131. Why are the venules called capacitance vessels?
    • because they are capable of collecting a large amount of blood with very little pressure change.
    • The veins have thinner walls and contain less smooth muscle and elastic tissue than the arteries.
  132. What percent of cardiac output is the bronchial circulation? Can the lungs function without it?
    • normal bronchial arterial blood flow is ~1% of the cardiac output.
    • The lung can function without this, and doe after lung transplantation
  133. Why is bronchial circulation important to us (venous blood)
    ~2/3 of the bronchial venous blood drain into the pulmonary veins via bronchial  pulmonary anastomoses,pulmonary veins flow into the LA. This bronchial venous blood (low oxygen, high CO2) mixes with oxygenated blood. This is why there is a small percentage of venous admixture.
  134. Why is someone more likely to a get a pleural effusion on the R than the left?
    Lymphatic system is larger and more numerous in the Left lower lung than in the right lower  lung
  135. DEAD space equation:
    • Vd = PaCO2-PeCO2
    • Vt           PaCO2
  136. What are the three things you can not measure by spirometry?
    Residual Volume, Functional Residual Capacity, and Total Lung Capacity
  137. What are the two ways to measure FRC?
    1) Helium dilution (measures communicating gas)

    2)Body plethysmography *uses Boyle's  law to measure total FRC* (including gas trapped behind closed airways)
  138. Total ventilation is....
    tidal volume x frequency
  139. Alveolar ventilation is....
    (Tidal volume-dead space) x frequency
  140. Is it more efficient to raise TV or respiratory rate?
    Raising TV is more efficient because you will always have ~150ml of dead space
  141. If alveolar ventilation decreases by half....CO2 will
  142. Fowler's method measures
    ANATOMIC dead space. (Breathe in oxygen, measure nitrogen concentration coming out....
  143. Bohr's method measures...
    • PHYSIOLOGIC dead space. measures
    • volume of lung that does not eliminate CO2. 

    Dead space equation is listed on another flashcard....
  144. Which areas have greater ventilaton?
    Dependent areas (usually the base of lung) Alveoli are smaller and more compliant.
  145. Pulmonary diffusion capacity may be affected by 3 major mechanisms, what are they?
    Changes in the effective surface area of gas exchange. (# of alveoli ventilated)

    Changes related to the uptake of gases by the RBC (oxygen dissociation curve)

    • Change in the physical properties of the
    • membrane (thickened in pulm. fibrosis)
  146. When there is a diffusion limitation why can someone will have a normal PO2 until they start to exercise?
    The RBC has 0.75seconds in the capillary but normally it only needs 0.25seconds for gas exchange. In disease, it may take up to the entire 0.75s. Once you exercise, the amount of time the RBC is in capillary decreases and so it will not have enough time to for gas exchange and will see lower PO2.
  147. Why is diffusion limited in high altitudes?
    The driving pressure gradient is lower. Starting with a lower PO2 .
  148. CO is _______ limited.
    Diffusion limited. Never builds up pressure because it is very soluble.
  149. N20 is ______ limited.
    perfusion. Builds up partial pressure in blood very quickly.
  150. Under normal conditions, oxygen is _____ limited.
  151. Pressures within the pulmonary circulation may be expressed in three different forms. Name them.
    • 1. Intravascular pressure—The pressure at
    • any point in the circulation relative to atmosphere. (usual way of expressing pressures in the systemic circulation and is  common method of indicating the pulmonary vascular pressures)

    2. Transmural pressure—The difference in pressure between the inside of a vessel and the tissue surrounding the vessel.  

    3. Driving pressure--- The difference in pressure between one point in the circulation and another point downstream
  152. Driving pressure of pulmonary circulation is...
    PAp -LAp
  153. PVR (pulmonary vascular resistance) is....
    pulmonary driving pressure / cardiac output

    Usual is 1.7 mmHg/min
  154. What vessels are involved in active control of PVR?
    • Pulmonary arteries and arterioles, with
    • muscular vessel walls, are mostly extra-alveolar and involved in active control
    • of PVR
  155. Effect of Increased Pulmonary  Blood Flow
    Recruitment----Recruitment of previously unperfused pulmonary vessels may occur in response to increased pulmonary blood flow.     

    • Distention---It is likely that capillaries never close completely and that passive distention
    • is an important adaptation to increased flow.
  156. ___ vessles are compressed at high lung volume and increase PVR.
    • The small vessels (alveolar vessels or
    • capillaries)
  157. _____ vessels increase at lung volumes and PVR decreases.
    Large vessels.
  158. Blood flow is ____ at the bottom of
    the lung, and ___ at the top (apex) of the lung. (when standing)
    highest, lowest
  159. What is Zone 1?
    PA > Pa > Pv

    • Not normal, think high PEEP in septic pt. Alveolar squishing capillary. 
    • Usually enough pressure to get blood to flow to apex of lung.
  160. What is zone 2?
    Pa> PA> Pv
  161. What is zone 3?
    Pa>Pv> PA 

    vessels compress on alveolus
  162. Usually passive factors dominate the PVR and determine distribution of blood flow. 

    Sometimes active responses occur...when?
    when PO2 of alveolar gas is reduced…. called  HYPOXIC PULMONARY VASOCONSTRICTION—contraction of smooth muscle in the walls of arterioles in the hypoxic region.
  163. Hypoxic pulmonary ventilation curve shows...
    When alveolar PO2 drops below 70, large vessels constrict, resistance  increases, and blood flow decreases. Blood will be directed away from hypoxic region. This helps to normalize the V/Q ratio. Want blood to go where there is oxygen.
  164. Fluid exchange across the capillary endothelium obeys Starlings Law. Explain this..
    Net fluid out = K [ (Pc – Pi) – reflection coefficient (colloid osmotic pressure in the blood – colloid osmotic pressure of the interstitium)]
  165. Explain what happens in pulmonary edema.
    There is critically opening pressures of alveoli, once this pressure is exceeded, fluid rushes in and floods alveoli.
  166. Name causes of pulmonary edema. (Think starlings law)
    • Increased hydrostatic pressure.
    • Increased capillary permeability.
    • Reduced Lymph drainage.
    • ?Decreased interstitial pressure
    • Decreased colloid osmotic pressure
  167. Alveoli with no ventilation have V/Q of....
    (V=0) then (V/Q = 0 ) will have PO2 and PCO2 values that are the same as those of mixed venous blood, because the trapped air in the alveoli will equilibrate with mixed venous blood.
  168. Alveoli with no perfusion have V/Q of....
    (Q=0) then (V/Q = infinity) will have PO2 and PCO2 values that are the same as those of the inspired gas, because there is no gas exchange to alter the composition of the inspired gas.
  169. Therelationship between the fall in PO2 and the increase in PCO2 that occurs in hypoventilation can be calculated from the Alveolar Gas  Equation which is....
    • PAO2 =PiO2 – PACO2 + F
    •                         R

    Therefore large increases in PACO2 readily produce hypoxemia at room air but not at high FiO2. This is why hypoventilation is easy to correct with Oxygen.
  170. the PA-Pa gradient is normally...
    In healthy person, this gradient does not exceed 15mmHg. In an older person, with health lungs, this does not exceed 37mmHg.
  171. What is venous admixture?
    • Venous admixture refers to the degree of
    • admixture of MV blood with pulmonary capillary blood that would be required to produce the observed difference between the arterial and the pulmonary end-capillary PO2 (alveolar PO2 )

    Admixture is a most important cause of arterial hypoxemia
  172. What are the different forms of venous admixture?
    • Thesbian Veins
    • Bronchial Veins  
    • Congenital Heart Disease*
    • Pulmonary Pathology*
    • Scatter of V /Q ratios*

  173. Shunt flow calculation:
    •  Qs   =   CcO2 - CaO2
    •  Qt        CcO2 – CvO2
  174. A small amount of shunted blood ___reduces the PaO2 and ____ increases PCO2
    Greatly, barely
  175. Is perfusion or ventilation a bigger factor in the V/Q ratio as you move to the dependent areas of the lung?
    • Perfusion! .
    • Because the gradient for perfusion is much higher than the gradient for ventilation. As you go down the lung, to the dependent area of the lung, the V/Q decreases