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Pulmonology > Waters and Sinclair - Physiology > Flashcards

Waters and Sinclair - Physiology Flashcards

1
Q

Which intrinsic lung disease causes of hypoxemia are reversible via administration of 100% PiO2?

A
  • V/Q mismatch
  • Diffusion limitation
  • NOT R-to-L shunt
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2
Q

Inspiratory reserve volume (IRV)

A

Add’l amt that can enter in forced inspiration = 3 L

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3
Q

Why do cyanotic patients appear blue?

A
  • Unsaturated hemoglobin is purple
  • Low Hb saturation in surface capillaries causes a bluish color – cyanosis (lips, ears, nail beds, tongue)
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4
Q

What is the alveolar ventilation equation? What are PACO2 levels determined by?

A
  • PACO2 is determined by the ratio of CO2 production to alveolar ventilation
    1. PACO2 = k(VCO2/Valv) where VCO2 = rate of CO2 production in the body
  • CO2 production in the body and alveolar ventilation because there is virtually no CO2 in the inspired gas
  • Note: k is a constant (863 mmHg at BTPS - body temp and ambient pressure, saturated with water vapor)
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5
Q

Describe the O2-Hb dissociation curve. Why does it look like this?

A
  • Flat at the top (above P02 60 mmHg; below this # in arterial circulation, respiratory center kicks in): changes in PO2 cause relatively little change in Hb saturation

􏰀1. 120 mmHg, Hb sat = 98.2%

  1. 80 mmHg, Hb sat = 95.9%
  2. 60 mmHg, Hb sat = 90%
    - This is true until you get to a PO2 below 40 mmHg
    - Remember: small amount of O2 unloaded in the tissue capillaries (venous Hb still about 75% saturated)
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6
Q

What is the respiratory quotient? What does the gas exchange during one minute in a resting individual look like (image)?

A
  • Ratio of CO2 produced to O2 consumed:

RQ = VCO2/VO= 200 ml/min / 250 ml/min ~ 0.8

  • RQ depends upon what we eat and burn. RQ = 1 for carbohydrates, 0.7 for fat, and 0.8 for protein. For fat and protein, it takes more O2 to produce one CO2
  • The attached image shows the gas exchange during one minute in a resting individual
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7
Q

Why is the alveolar gas equation important (4)?

A
  • Allows us to estimate the alveolar PAO2.
  • Necessary for correct interpretation of arterial blood gases
  • Helps determine if hypoxemia is due to lung disease or not
  • Helps us determine the cause(s) of hypoxemia.
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8
Q

How does O2 bind to hemoglobin? What is cooperativity?

A

􏰀- Each of the four heme groups in a hemoglobin molecule contains one atom of ferrous iron (Fe2+) to which oxygen binds -> adult hemoglobin has α2β2 subunits

  • Cooperativity: the reactions of the four subunits occur sequentially, with each combination facilitating the next one – gives S-shape to the curve
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9
Q

What is the normal A-aDO2? How is it affected by age?

A
  • (Age + 4)/4
  • Lung function decreases with aging -> decreased O2 transfer to the blood
    1. Arterial O2 tension decreases with age, but since alveolar O2 tension stays the same, the A-aDO2 increases with age
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10
Q

What is the partial pressure of H2O at 37 degrees C? Why does this matter?

A
  • 47 mmHg (this pressure is going to be the same regardless of barometric pressure)
  • In gas phase, partial pressure is proportional to dry gas concentration
    1. Partial pressure = P(B) x F(I)Gas
  • As air is inspired, it is rapidly warmed and 100% saturated with H2O
    1. Partial pressure = (P(B) - P(H2O)) x F(I)Gas
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11
Q

How does COPD/emphysema lead to collapse of large airways during forced expiration?

A
  • INC lung compliance due to loss of elastic fibers
  • Alveolar airway pressure lower than normal due to diminished elastic recoil, causing collapse of large airways during forced expiration
  • Not able to generate as (-) an IP pressure. In exhalation, pressure reduced as air closer to release -> eventually less pressure than in IP space. Smaller areas do not have tendency to stay open, so they collapse more easily in exhalation. These pts purse their lips to keep airway pressure high, and prevent collapse
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12
Q

Residual volume (RV)

A

Amt. of air remaining in lung at max expiration = 1 L

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13
Q

What are compliance and elastance? How are they related?

A
  • Degree to which transpulm pressure results in lung expansion depends on compliance, or stretchability, of the lung (INVERSE of elastance)
    1. Compliance relates change in volume of a system to the pressure distending
    2. Can be obtained from pressure-volume curve
  • Increased compliance: small change in pressure will lead to a larger change in volume
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14
Q

What is hypoxemia? How does it happen?

A
  • Decreased O2 tension in circulating blood compared to normal
  • Defective exhange of O2 in the lungs OR decreased delivery of O2 to the alveolus in the absence of lung disease
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15
Q

Forced expiratory volume in 1 sec (FEV-1)

A

Maximal inspiration then forced expiration; normal is 80% of FVC

Obstructive disease: less than 70%

Restrictive disease: normal or increased

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16
Q

What is normal dead space? What % of tidal volume? Is it static (be specific)?

A
  • Normal V(D) = 150 - 180 mL (about lean body weight in pounds)
  • About 25-30% of tidal volume (V(D)/V(T) ratio)
  • Dead space is NOT STATIC
    1. V(D:anatomical) increases with increasing lung volume
    2. V(D:alveolar) decreases with exercise (INC V(T) + INC perfusion)
    a. INC V(D:alveolar) is ALWAYS PATHOLOGIC (ex: pulmonary embolism)
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17
Q

What determines the alveolar O2 balance (be specific)?

A
  • O2 delivery to the alveolus by ventilation
  • O2 removal from alveolus by capillary blood, determined by tissue O2 consumption (about 250 mL/min -> commit this # to memory)
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18
Q

How do obstructive and ventilatory defects affect the flow-volume curve (image)?

A
  • Note the characteristic SCOOPING of the exhalation curve in obstructive disease
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19
Q

What is asthma? What are some of its defining characteristics?

A
  • An inflammatory disease primarily of the airways in which the airway smooth muscle contracts strongly, markedly increasing airway resistance
  • Leukotrienes/histamine -> bronchial constriction, inflammation, increased production of mucous. markedly increasing airway resistance
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20
Q

What are the 5 steps of respiration?

A
  • See image (mvmt of O2 from atmosphere to mito in tissues)
  • At steady state, O2 uptake = O2 consumption, and CO2 production = CO2 excretion
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21
Q

What are the pressures at the end of an unforced expiration (image)?

A
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22
Q

What is physiologic dead space?

A
  • V(D:physio) = V(D:anatomic) + V(D:alveolar)
  • Sum of anatomic and alveolar dead space
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23
Q

What are the normal values for partial pressures (image)?

A
  • Note: alveolar partial pressures (PAO2 and PACO2) levels determine the systemic arterial partial pressures (PaO2 and PaCO2)
  • O2 diffuses out to the cells due to the lower partial pressure there (these conc differences drive gas flux)
  • KNOW THESE #’s
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24
Q

How does gravity affect the ventilation-perfusion ratio? Describe the graph.

A
  • This is the key - remember that there is variation in the V(A)/Q ratio from bottom to top of the lung
  • Clicker question: 72-y/o male with COPD most likely to have both increased and decreased V/Q ratio. In other words, this ratio will vary based on where in the lung you are measuring
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25
Q

Provide a potential clinical scenario for each of these images.

A
  1. Normal: V/Q = 0.8
  2. Pulmonary embolus
  3. Decreased perfusion
  4. Decreased ventilation
  5. Airway obstruction
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26
Q

How do obstructive ventilatory defects affect flow (use formula)?

A
  • They reduce flow (see image)
  • You can also have both of these things happening, i.e., in a patient with both emphysema and chronic bronchitis
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27
Q

Why are ratios of exercise:rest for minute vol and alveolar ventilation different?

What percent of minute ventilation is dead space ventilation for healthy person?

A
  • Dead space ventilation DEC as % of minute volume:
    1. Rest: (dead vol. Vent.)/minute vol = (150 x 15)/7500 = 30% of minute vol
    2. Exercise: (150 x 20)/40,000 = 7.5% of minute vol
  • For healthy individual, dead space ventilation about 25-30% of the minute ventilation
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28
Q

What is a tension pneumothorax?

A
  • Buildup of air in the pleural space, usually due to lung laceration (air leaks out, but cannot get back in; may be exacerbated by positive pressure ventilation)
  • Obstructs venous return to the heart, leading to circulatory instability, and even arrest in some cases
  • Post-mortem chest x-ray of left tension pneumothorax: 1) deviation of trachea away from side of tension, 2) shift of mediastinum, 3) depression of the hemi-diaphragm
  • Tachycardic, tachypneic, hypoxic patient
  • Tx with needle thoracostomy or chest tube/drain
  • Note: can also be bilateral
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29
Q

What do you see here?

A

Normal alveoli

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30
Q

What are the pressure changes and air flow during a typical respiratory cycle (diagram)?

A
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31
Q

What is incentive spirometry? How is it related to surfactant?

A
  • Strategy to ensure deep breathing -> teach them this before they go into surgery
  • Atelectasis is a common complication of sx procedures, esp. those requiring general anesthesia, due to impaired surfactant activity and the corresponding effects on alveolar compliance
    1. Reduced surfactant = decreased compliance and decreased vital capacity
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32
Q

Which of the following is not true regarding V/Q mismatch?

a) V/Q > 1 are called High V/Q or dead space-like units
b) V/Q < 1 are called Low V/Q or shunt-like units
c) Most lung diseases cause V/Q mismatch
d) V/Q mismatch is unresponsive to O2 Rx

A

d) V/Q mismatch is unresponsive to O2 Rx

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33
Q

What is ventilation?

A

Volume of air moving into or out of the lungs in a given time -> exchange of gases between atmosphere and alveoli

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34
Q

How does the “extra” ventilation at the top of the lung affect its “infectability”?

A

Some organisms that thrive in high O2 environments (i.e., TB) fluorish in the apex

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35
Q

What is pulmonary hypertension? What are some primary and secondary causes?

A
  • >25 mmHg at rest
  • Primary: inactivating mut in BMPR2 gene (promotes vascular smooth muscle cell proliferation, causing more constriction of the pul vessels)
  • Secondary: COPD, mitral stenosis, recurrent thrombo-emboli, auto-immune disease, left-to-right shunt, etc.
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36
Q

What is surface tension? What does T = for water?

A
  • A physical “constant” that is characteristic for any pair of liquid/gas interfaces

T = F/L where F = force and L = length

  • For water, T = 72 dyne/cm
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37
Q

Total pressure (Dalton’s law)

A

Sum of partial pressures of all the gases in a mixture

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38
Q

Where does most of the gas exchange in the pulmonary capillary occur? How does this determine perfusion or diffusion-limited transfer? Provide some examples.

A
  • Virtually all of the gas exchange is completed in the initial region of the pulmonary capillary
    1. Gas transfer perfusion-limited bc all blood leaving capillary has reached equilibrium with alveolar gas; true for O2 under normal conditions & for CO2, N2O
  • Diffusion-limited transfer: gases do not equilibrate bt capillaries and alveolar gas
    1. Example: CO binds avidly to Hb, so PaCO does not INC much -> transfer depends on diffusion of CO, not on the amt of blood flow
    2. O2 is diffusion-limited in fibrosis (thickened barrier), emphysema (decreased surface area), high altitude, intense exercise
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39
Q

How do you calculate the O2 content of the blood?

A
  • O2 content = (amt of O2 bound to hemoglobin) + (amt of O2 dissolved in plasma) = (O2 binding capacity x % saturation) + dissolved O2 􏰀
    1. 􏰀 O2 delivery to tissues = cardiac output x O2 content of blood
  • Normal O2 binding capacity ~ 20.1 ml O2/dL
  • Decreased Hb causes decreased O2 content of blood, but does not affect O2 saturation or arterial PO2
    1. For this reason, being anemic will decrease O2 content, but not necessarily O2 saturation
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40
Q

Why are the alveoli ideal for diffusion? What kinds of things can compromise this?

A
  • Mass (vol) flux = SA/thickness x Diff constant x Conc (PP) difference

Gas flow (volume/time) = (A/z) x D x (P1 – P2)

  • Vol flux in alveoli INC by large SA for exchange (size of tennis court) and short distance for diffusion (0.2 to 0.6 􏰄m)
  • Efficient exchange can be compromised by factors leading to DEC area (emphysema, obstruction) or I_NC diffusion distance_ (fibrosis, pulmonary edema - INC diffusion distance AND DEC amt of air coming in, or SA)
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41
Q

How much CO2 is produced per minute? By what 3 methods is CO2 transported out of tissues?

A
  • At rest, body produces 200 ml/min CO2 that has to be eliminated -> exercise may increase this by 20 fold
    1. Dissolved CO2: amount of CO2 dissolved in blood is determined by Henry’s law; CO2 dissolves better in water than O2 (think club soda), amounting to 28 ml/L blood:
    a. 5-10% of the total CO2 carried in the blood
    2. Protein carbamylation - carbaminohemoglobin: CO2 binds to amine (-NH2) groups of proteins -> Hb-NH2 + CO2 =􏰇􏰆 Hb-NHCOO- + H+ (not just Hb; lots of proteins)
    a. Plasma 7% protein, and 30% of RBC protein is Hb
    b. This accounts for 10-20% of the total CO2 carried in blood (binding to Hb accounts for ~5%)
    3. Formation of bicarbonate (HCO3-): CO2 undergoes hydration in RBC’s: carbonic anhydrase + CO2 + H2O (slow) 􏰇========􏰆 H2CO3 􏰇==􏰆 HCO3- + H+ (fast)
    a. M​ajor mechanism of CO2 transport (80-90%)
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42
Q

How does bronchiectasis affect flow and resistance?

A
  • Higher resistance because they are no longer able to have laminar flow (dilatation of terminal bronchioles)
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43
Q

What two terms describe the adequacy of ventilation (define them in terms of CO2)?

A
  • Hypoventilation: INC in PACO2 bc alveolar ventilation can’t keep up with CO2 production

􏰀- Hyperventilation: DEC in PACO2 when alveolar ventilation excessive for normal CO2 production

  1. Arterial PCO2 is normally the driving stimulus for respiration, so hyperventilation attenuates the stimulation of respiration
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44
Q

How do O2 and CO2 levels vary at a steady state?

A
  • Volume of oxygen transferred to the blood in the lungs per unit time is equal to the volume of oxygen consumed by the cells in the body during that same period of time
  • Production rate of carbon dioxide by the cells is equal to the rate of excretion in the lungs
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45
Q

How does exercise impact PO2?

A

􏰀- In exercise, the muscle consumes more oxygen, creating a larger PO2 gradient -> more oxygen is then extracted from the blood

  • There is also an increased blood flow to provide more oxygen
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46
Q

Total lung capacity (TLC)

A

Vital capacity + residual volume = 6-7 L

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47
Q

What is Fick’s Law?

A
  • O2 moves from alveolus to capillary blood via diffusion down pressure gradient
  • O2 flux = V(O2) = D(L)O2 x (PAO2 - PaO2)
  • D(L)O2 is the diffusion capacity
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48
Q

What are the steps in inspiration (7)?

A
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49
Q

What is the equation for pulmonary vascular resistance (PVR)?

A
  • PVR = (PPA - PLA)/cardiac output where PPA = pulmonary artery pressure and PLA = left atrial pressure (pulm wedge pressure)
  • PVR is very low, and so is pulm vascular pressure (10 - 14 mmHg) compared to the systemic circulation
  • Pulmonary blood vessels are highly compliant, and can be recruited or de-recruited in response to changes in pressure
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50
Q

On a basic level, how does surfactant reduce surface tension (image)?

A
  • Reduces air:water surface tension
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51
Q

What are two factors that affect the O2 content of the blood?

A
  • Carbon monoxide poisoning: CO binds 250x more strongly to Hb than oxygen (color of HbCO is cherry red). CO DEC maximum O2 capacity, but also increases affinity (left shift) making unloading more difficult in tissues (note curve shifted to the left in the attached graph)

􏰀- Anemia: as the number of red blood cells decreases, the concentration of Hb in the blood decreases. Reduced Hb decreases the maximum oxygen capacity of blood

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52
Q

How is intrapleural pressure estimated?

A

By esophageal pressure, i.e., placing a balloon catheter into the esophagus

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53
Q

Are expiration and inspiration typically active or passive processes in normal breathing?

A

Inspiration = active muscle contraction

Expiration = passive

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54
Q

What are the main pressures/pressure differences involved in ventilation (image)?

A
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55
Q

How do alveolar ventilation and CO2 production affect PACO2? What are some factors that can affect these 2 values?

A
  • Alveolar ventilation: increased alveolar ventilation will DEC PACO2 b/c fresh inspired air dilutes alveolar gas

􏰀- CO2 production: INC production of CO2 will INC PACO2 b/c more CO2 will enter alveoli from blood per unit time.

  • Key point: If CO2 production is constant, then PACO2 is determined by alveolar ventilation
  • Fever, exercise, other things that INC metabolism will INC CO2 production -> going to cause INC ventilation, except in cases where pt is grossly hypoventilated
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56
Q

What are some additional functions of the pulmonary circulation?

A
  • Functions as a filter, removing small clots

􏰀- Pulmonary endothelial cells:

  1. Convert angiotensin I to angiotensin II
  2. Inactivate bradykinin
  3. Remove other prostanoids and leukotrienes
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57
Q

What is happening here?

A
  • Right alveolus obstructed to some degree
  • Giving supplemental O2 will overcame this -> it will fully corrected (shunt would NOT correct)
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58
Q

What is flow (formula)?

A

F = DeltaP/R

  • F = flow, DeltaP = pressure difference, R = resistance
  • Air moves into and out of lungs by bulk flow, from region of high pressure to low
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59
Q

Tidal volume (TV)

A

Volume of normal breath = 500 mL

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60
Q

Example of decreased PiO2?

A
  • Barometric pressure decreases with altitude
  • F(i) of gases unchanged, but PiO2 DECREASES
  • PaO2 decreases, but A-aDO2 DOES NOT INCREASE
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61
Q

Why does the O2-Hb association curve have a sigmoid shape? Why is this shape important?

A
  • Sigmoid shape is due to positive cooperativity, and is the result of the change in affinity of the heme groups
    1. Plateau region provides a safety factor for the supply of oxygen: large range of PO2 levels leads to similar Hb saturation

􏰀- Lower part of the curve is steep -> relatively small change in PO2 causes large changes in saturation

􏰀 1. 20 to 60 mmHg causes a 60% change, while from 60 to 100 mmHg causes only a 10% change

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62
Q

What is respiratory distress syndrome (RDS) of the newborn?

A
  • Little or no surfactant production (occurs late in gestation), so infant lungs are difficult to inflate – DEC compliance; requires mechanical ventilation
  • Causes unstable alveoli that collapse on expiration (atelectasis)
  • Often helped by surfactant replacement therapy
63
Q

Expiratory reserve volume (ERV)

A

Difference b/t tidal end volume and forceful expiration end volume = 1 L

64
Q

What are some causes of hypoventilation?

A
  • Abnormal respiratory mechanics: increased airway resistance, decreased compliance, muscle disease
  • Normal A-a gradient
65
Q

What are the expiratory muscles? How is expiration different than inspiration?

A
  • Expiratory muscles: abdominal muscles (rectus abdominus, internal and external obliques, transverse abdominus) and internal intercostal muscles
  • Expiration is passive at rest (unlike inspiration); during exercise, however, expiratory muscle contraction becomes important
66
Q

What is minute ventilation? How is this different from effective/alveolar ventilation?

A
  • MINUTE VENTILATION (V(E)): V(E) = V(T) x RR = tidal volume x respiratory rate
    1. Total ventilation per minute, or volume exhaled per minute (V(E); liters/min)
  • EFFECTIVE/ALVEOLAR VENTILATION (V(A)): V(A) = V(E) - V(D:physio)
    1. Effective/alveolar vent = minute ventilation - physio dead space
67
Q

What is the A-a difference? What if it is widened? How is PaO2 measured?

A
  • A-aDO2 = PAO2 - PaO2
  • A widened difference signifies the presence of lung disease, while a normal gradient excludes it
  • PaO2 is measured by an arterial blood gas test
68
Q

What is diffusion?

A
  • Movement of gas molecules from areas of greater partial pressures to areas of lesser partial pressures; i.e. down partial pressure gradients (high conc to low conc)
  • Gas exchange between alveolar gas and blood and between blood and tissues is entirely by diffusion
69
Q

What are the factors affecting hemoglobin saturation that cause a shift to the right?

A
  • Decreased affinity for O2:

↑PCO2 􏰀

↓pH

↑ temperature

↑ 2,3-DPG

  • Want shift to the right when you want to unload O2 (i.e., release it in the tissue)
  • Both sets of things can also happen in other places in other ways
70
Q

How are PACO2 and V(A) related? Why is this important?

A
  • PACO2 = 1/V(A)
  • PACO2 (and thus PaCO2) is inversely proportional to V(A) -> PaCO2 is a good measure of alveolar ventilation
  • So, if PaCO2 is high (due to hypoventilation), PAO2 and PaO2 will be low -> A-aDO2 DOES NOT INCREASE (no intrinsic lung disease)
71
Q

What is the effect of hemoglobin on O2 transport and PO2?

A
  • Oxygen diffusion is governed only by the dissolved portion in blood -> O2 bound to hemoglobin does NOT contribute directly to the PO2 of the blood

􏰀- Hemoglobin does determine the total amount of oxygen that will diffuse by acting as a sink for the O2 -> diffusion is driven by the gradient of PO2

  1. In the lungs, diffusion gradient favoring O2 mvmt into blood maintained despite the very large transfer of oxygen; reverse is true in tissue capillaries
72
Q

What are the 5 causes of hypoxemia? A-aDO2?

A
  • Normal A-aDO2: NO LUNG DISEASE
    1. Decreased PiO2
    2. Hypoventilation
  • Widened A-aDO2: LUNG DISEASE
    1. Diffusion limitation
    2. R-to-L shunt
    3. Ventilation/perfusion (V/Q) mismatch
73
Q

What is surfactant? Where is it stored? What stimulates its release?

A
  • Reduces surface tension and increases lung compliance, reducing work of expanding the lungs
  • Complex mixture of phospholipids (incl. dipalmitoyl phosphatidylcholine, or lecithin, and sphingomyelin), cholesterol, and specific proteins, all of which are produced by type II alveolar epithelial cells and stored in lamellar bodies
  • Deep breath (large expansion of the lungs) stretches T2 cells and stimulates surfactant production
74
Q

Is V/Q static in the lungs? What is the overall V/Q? What is V/Q mismatch?

A
  • MOST COMMON CAUSE OF HYPOXEMIA IN HOSP PTS
  • Normally V & Q are NOT perfectly matched
  • Ventilation, perfusion vary from lung apices to bases
  • Both are higher at the bases than apices but by different mechanisms and to different degrees
  • A range of V/Q ratios exist from apex to base
  • Overall V/Q of the WHOLE LUNG is ~0.8
75
Q

During general anesthesia, a pt’s PACO2 levels are continuously monitored. What happens if PACO2 levels increase two-fold (from 40 to 80 mmHg)?

A

Assuming that CO2 production is constant, the alveolar ventilation must be increased two-fold by adjusting the ventilator to compensate

76
Q

What is the formula for pressure?

A

P = F/A

  • Pressure in a liquid or gas is independent of direction
  • Magnitude is determined by the number of gas molecules in a closed area
  • Common terminology of pressures refers to pressure relative to atmospheric pressure (760 mmHg)
77
Q

What happens to air when it is inspired?

A

It is warmed to 37o C and humidified

78
Q

Functional residual capacity (FRC)

A

Volume of air in the lungs after normal respiration = Expiratory reserve volume + Residual volume = 2.5 L

Measured by helium dilution or body plethysmograph

79
Q

Fractional concentration

A

Fraction of a given gas in a mixture (fractional % = fractional concentration x 100)

80
Q

Is pleural pressure higher at the apex or the base of the lungs? Why is this important?

A
  • Lungs hang from pleural cavity, and weight pulls at top and pushes at base -> apical pressure is more subatmospheric than at the base
  • Because pleural pressure is more (-) at apex, regional alveolar volume is larger
    1. Compliance is non-linear (higher at base than apex) -> alveolar ventilation higher at base
    a. Basal alveoli: volume changes more with a given change in pressure (b/c more compliant)
81
Q

How is diffusion affected by transit time? What are the normal values? Provide an example. Does administering 100% FiO2 help?

A
  • RBC pulmonary capillary transit time: 0.75 seconds
    1. If D(L)O2 normal, PAO2/RBC equilibrium takes about 0.25 seconds
  • Hypoxemia only occurs if:
    1. D(L)O2 severely decreased (<1/3rd of normal) OR
    2. Transit time decreased (<0.25 seconds)
  • Abnormal diffusion ALMOST NEVER causes hypoxemia at rest (may contribute lower PaO2 during exercise)
    1. Ex: pulmonary fibrosis -> normally not hypoxemic at rest, but rather with exertion. If you exert yourself, cardiac output goes up, making capillary time faster and reducing transit time
  • 100% FiO2 ELIMINATES effects of diffusion limitation, reversing hypoxemia and correcting A-aDO2
82
Q

How is CO2 eliminated from the body (if it is not converted to something else)?

A

Solely via VENTILATION

83
Q

What are the gravitational effects on pulm blood flow?

A
  • Distribution of pulm blood flow uneven due to gravity
  • Pulm blood pressure low (34/11 cmH2O at the heart); pulmonary arteries are collapsible
    1. Heart midway between apex and base of lungs, and lungs approx 40 cm long -> significant diff in pressure at apex (lower pressure) and base (higher pressure) in the standing position

􏰀- Apex receives less blood flow than base in upright lung (higher pressure = higher flow)

84
Q

Partial pressure

A

Pressure created by each type of gas in a mixture

85
Q

Why do regions of the lung that are not being perfused by the pulmonary system not necrose?

A
  • They are still supplied by the systemic circulation
  • Bronchial arteries: supply lg extrapulmonary conducting airways (from ascending aorta)
  • Dual blood supply: from the intrapulmonary airways to the terminal bronchioli – systemic + pulm circulation
  • Pulmonary arteries and veins: deliver and return blood relative to the heart.
  • Pulmonary capillaries: exclusively supply alveoli
86
Q

What factors affect airway resistance (5)?

A
  1. Anatomic factors: mouth resistance < nose resistance
  2. Lateral traction: elastic connective tissue fibers attach to the airway exterior and pull outward, tending to hold open the airways (compromised in emphysema)
  3. Lung volume: as it increases, airway diameters INC, and resistance goes down -> pts w/INC airway resistance (asthmatics) often breathe at high lung volumes, which helps keep airway resistance lower
  4. Relaxation/contraction of bronchial smooth muscle: esp important in asthma, bronchitis, emphysema. Epinephrine and other β2- adrenergic agonists cause dilation, while leukotrienes and acetylcholine cause constriction
  5. Density and viscosity of inhaled gas
87
Q

How is FEV-1 affected by restrictive/obstructive lung disease? Provide examples of each.

A
  • Obstructive: FEV1 usually < 70% of FVC – difficult to expire rapidly through narrowed airways; limitation of airflow; results in air trapping
    1. Ex: asthma, emphysema, chronic bronchitis, bronchiectasis
  • Restrictive: reduced FVC (and TLC), and normal or increased FEV1 to FVC ratio; reduced expansion of lung parenchyma
    1. Ex: poor breathing mechanics via obesity, weak inspiratory muscles, neuromuscular disorder; or interstitial lung disease like pulmonary fibrosis, ARDS, sarcoidosis, hypersensitivity pneumonitis
88
Q

How does surfactant prevent alveolar collapse? How is this related to Laplace’s Law?

A 
- In the absence of surfactant, the attraction between
water molecules (H-bonds) can cause alveolar collapse
  • By reducing the surface tension of water, surfactant helps prevent alveolar collapse
  • Transmural pressure to keep open an average-sized alveolus = 2T/r ~ 30 cmH2O, but in reality, PTM ~ 5 cmH2O due to surfactant
89
Q

What is hysteresis?

A
  • Compliance changes during lung expansion
  • Inhalation portion of the curve will always look different than the exhalation portion -> this is due to a difference in surface tension (when exhaling, lung stays open more)
90
Q

Describe the factors that shift the O2-Hb curve to the left.

A
  • Decreased PCO2 and increased pH: Bohr effect; DEC tissue metabolism = DEC CO2 production and H+ conc (increased pH) – leads to an increase in Hb affinity
  • Decreased temperature: INC affinity facilitates loading
  • Decreased 2,3 diphosphoglycerate (2,3-DPG): reflects decreased tissue metabolism; increased affinity
  • Fetal hemoglobin (Hbf): slightly different structure from adult Hb (has α2γ2 subunits) and shows a higher affinity for O2. This is an adaptation to lower placental PO2 (~30 mmHg): can still saturate to 75% at this low PO2
91
Q

What happens to pulmonary capillaries during exercise? Why?

A
  • During exercise many pulmonary capillaries are opened due to increased pulmonary vascular pressures
  • Pulmonary pressures are generally very low
92
Q

What is going on here? How might this cause hypoxemia?

A
  • Interstitial lung disease (broken-glass appearance)
  • Low V/Q (harder to inflate; also decreased diffusion)
93
Q

What is a pneumothorax?

A

Chest wall pierced due to trauma or surgery -> intrapleural pressure goes to 0 mmHg, and lung collapses

94
Q

What is going on here? How might this cause hypoxemia?

A
  • Pulmonary edema
  • Low V/Q
  • Shunt (depending on how full of fluid the alveolus is)
95
Q

What is alveolar dead space?

A
  • Alveoli ventilated, but NOT perfused cannot participate in gas exchange
  • Acts as DEAD SPACE VENTILATION
  • Ventilation to areas with REDUCED but not absent perfusion act as if a portion is normal and a portion is dead space
96
Q

What is going on here? How might you fix this?

A
  • Right alveolus obstructed to some degree
  • Giving supplemental O2 will overcome this -> it will fully correct (unlike shunt)
97
Q

Why is 60 mmHg an important number to remember?

A

\When you get below this number, the O2-sensing part of your respiratory control kicks in

98
Q

What are the inspiratory muscles? Describe the mvmt of the diaphragm (be specific).

A
  • Diaphragm: moves 1 cm at tidal breathing and 10 cm at forced inspiration
    1. Innervation by phrenic nerve
  • Accessory muscles: scalene, sternocleidomastoids
  • Increase the volume of the thoracic cage
99
Q

What are the factors affecting hemoglobin saturation that cause a shift to the left?

A
  • Increased affinity for O2.

􏰀 ↓ PCO2 􏰀

↑pH

↓ temperature 􏰀

Fetal Hb (Hbf) 􏰀

↓ 2,3-DPG

  • Things that shift to the left are things that are advantageous for O2 binding
  • These are things that occur in the pulmonary circulation
  • Both sets of things can also happen in other places in other ways
100
Q

How are most lung volumes measured? What are they (list them)?

A
  • Spirometer
  • Total lung capacity (TLC; a capacity is the sum of 2 or more volumes)
  • Tidal volume (TV)
  • Functional residual capacity (FRC)
  • Residual volume (RV)
  • Forced vital capacity (FVC)
  • Inspiratory reserve volume (IRV)
  • Expiratory reserve volume (ERV)
  • Forced expiratory volume in 1 second (FEV-1)
101
Q

What are the typical volumes and flows for 70 kg man at rest?

(TV, anatomic dead space, alveolar gas vol, alveolar ventilation, pulm cap blood vol, pulm blood flow, minute vol, RR)

A
  • Tidal volume: 500 mL
  • Anatomic dead space: 150 mL
  • Alveolar gas vol: 3 L
  • Alveolar ventilation: 5250 mL
  • Pulm cap blood vol: 70 mL
  • Pulm blood flow: 5 L (CO)
  • Minute volume: 7.5 mL
  • RR: 15
102
Q

In terms of alveolar ventilation, is increasing depth of breathing or breathing rate more effective?

A
  • Depth of breathing
  • EX: 3 breathing patterns w/same minute ventilation (6000 ml/min):

A. Normal breathing (500 ml/breath, 12 breaths/min) dead space vent. = 150 x 12 = 1800 ml/min alveolar vent. = 4200 ml/min

B. Slow, deep breaths (TV = 1000 ml/breath, 6 breaths/min) dead space vent. = 150 x 6 = 900 ml/min alveolar vent. = 5100 ml/min

C. Rapid, shallow breathing (TV = 150 ml/breath, 40 breaths/min) dead space vent. = 150 x 40 = 6000 ml/min alveolar vent. = 0 ml/min

103
Q

What is the equation for estimating resistance to air flow? What is MOST IMPORTANT about this equation?

A
  • Resistance to air flow is est. by Poiseulle’s equation:

R = 8nl/􏰁r4

where n = viscosity of air, l = length of segment, and r = radius of segment

  • Air flow is dependent on pressure difference and resistance (INC resistance = more energy required)
  • Resistance inversely proportional to r4, suggesting major resistance would be in small airways. But, due to branching, overall cross-sectional area increases, and major resistance is in upper, medium-size airways. MOST IMPORTANT factor in resistance of a segment is tube radius (tubes get small quickly, but don’t grow in # as fast)
104
Q

What is normal compliance in the human lung? What might INC or DEC it? Characterize the physiological effects of these diseases.

A

􏰀- Normal: 0.2 L/cmH2O (takes about 2.5 cmH2O to stretch lungs to inhale 0.5 L in tidal volume breathing)

􏰀- DEC in diseases that lead to stiffer lungs (fibrosis, pulmonary edema), or restrictive lung disease (RLD)

  1. Pts must generate larger than normal forces to expand lungs; work of breathing is greater. Patients have reduced capacities and volumes (FVC, TLC, RV, FRC). Difficulty getting air IN. Lower FRC.

􏰀- Increased compliance if reduced elastic recoil (flabby lungs), causing obstructive ventilatory defect

  1. Emphysema: destruction of alveolar walls, leading to INC in airspace size and DEC elastic fibers of lung (also in normal aging) – causes barrel-shaped chest
  2. INC compliance = lungs prone to collapse: can’t stay open. Patients have increased FRC, TLC, RV, but normal or reduced FVC. Takes longer to empty the lungs (decreased FEV1). Difficulty getting air OUT. Higher FRC – patients breathe at higher lung vols
105
Q

By what two mechanisms is O2 carried to the tissues?

A
  1. Physically dissolved in blood (plasma & RBC cytosol)
    a. O2 solubility very low: 0.003 ml O2/L/mmHg 􏰆 yields 3 ml O2/L blood -> accounts for only 1.5% of O2 carried by blood
    b. Partial pressure (PO2) a measure of dissolved O2
  2. O2 binding to hemoglobin (Hb): one Hb binds 4 molecules of oxygen -> 14.7 g Hb/L blood, so each liter of blood is capable of binding ~ 197 ml O2.
    a. Accounts for 98.5% of O2 carried by blood
106
Q

What is the ventilation-perfusion ratio? Why is it important?

A
  • Can be defined by alveolus, region, or whole lung
  • For ideal gas exchange, ventilation and perfusion should be matched, i.e., V/Q = 1
    1. Ex: 5L/min gas exchange, 5L/min cardiac output
107
Q

How is pulmonary blood flow regulated?

A
  • Most important mech involves vasoconstriction of small pulm blood vessels in response to low PO2: hypoxia-induced pulmonary vasoconstriction (you don’t want blood to go where there is no oxygen)

􏰀1. Opposite effect of hypoxia on systemic arterioles

  1. Hypoxia thought to depolarize pulm vascular smooth muscle cells, opening voltage-gated Ca2+ channels, leading to Ca2+ entry and cell contraction.

􏰀- Alveolar PO2 is major factor regulating pulm blood flow

􏰀1. This protective mechanism can fail if lung disease is widespread.

  • Gravity affects regional blood flow in the lungs
108
Q

What is Dalton’s Law?

A
  • States that in a mixture of gases, the pressure exerted by each gas is independent of the pressure exerted by the other gases. Gas molecules do not generally interact with one another
  • The total pressure of the mixture is the sum of the individual “partial pressures”
109
Q

What is the P50 on the Hb-O2 saturation curve?

A
  • The PO2 at which hemoglobin is 50% saturated (approx. 2 molecules of oxygen per molecule of hemoglobin)
  • Used to determine changes in affinity of hemoglobin for oxygen (i.e., a shift of the O2 curve -> shift to the right would cause increase in P50; shift to the left would cause a decrease)
110
Q

Why does O2 move from the RBC’s to the tissues?

A
  • Very low PO2 in the mitochondria, so there is a gradient for O2 to move in there and be consumed
  • This allows for mass O2 diffusion from RBC to tissues (because it is being consumed in mito; similar to Hb effect for Alveolar to arterial movement)
111
Q

What is the alveolar gas equation? What are the typical values at sea level?

A

PAO2 = PiO2 - (PaCO2/R) =

((P(B) - PH2O)xFiO2) - (PaCO2/R), where

R = V(CO2)/V(O2)

  • If R<1, then more O2 removed than CO2 added
  • At sea level: R = 0.8, PAO2 = 100 mmHg, VCO2 = 40 mmHg, and PiO2 = 150 mmHg
112
Q

What are V(O2) and V(CO2)?

A

O2 consumption and CO2 production

113
Q

What is anatomic dead space? How does this relate to gas exchange?

A
  • Air that remains in conducting airways at end of inspiration
  • DOES NOT participate in gas exchange
  • At end exhalation, alveolar gas (w/CO2 added and O2 partially removed) fills anatomic dead space and re-enters alveoli with next breath
114
Q

Describe the factors that shift the O2-Hb saturation curve to the right.

A
  • Increased PCO2 and decreased pH: linked; metabolic activity INC CO2 production and H+ concentration – both molecules can bind to Hb and lead to a decrease in Hb affinity for O2; this is called the Bohr effect

􏰀- Increased temperature: heat produced in working muscle; conformational change decreases Hb affinity, facilitates unloading

􏰀- Increased 2,3 diphosphoglycerate (2,3-DPG): metabolite of the glycolytic pathway in RBC’s; increased in hypoxia. Binds strongly to deoxygenated Hb, causing a rightward shift in the dissociation curve, lowering its affinity for oxygen, and helping oxygen unloading in tissues

  • Facilitate unloading of O2; TAP mnemonic
115
Q

Why is Boyle’s Law important?

A
  • PV = nRT
  • So, at a constant temperature and constant number of molecules, P1V1 = P2V2
  • If you change the volume, you will change the pressure in an equal and opposite way
116
Q

How saturated in Hb when it is leaving the tissue capillaries?

A

􏰀- In most tissues under resting conditions, Hb is still 75% saturated as blood leaves the tissue capillaries􏰆

  1. There is an enormous reserve for oxygen as activity increases
117
Q

If unarousable patient on drugs comes in with big O2 difference and lower lung infiltrate, what should you be thinking about?

A

This patient may have aspirated

118
Q

Describe the blood flow, alveolar ventilation, V/Q ratio, and pressures driving blood flow at each of the 3 lung levels (chart). How is this impacted by exercise?

A
  • Wasted ventilation at the top
  • Wasted perfusion at the bottom
  • Exercise: cardiac output increases, capillaries are recruited (opened more), and V/Q approaches 1
119
Q

What is minute ventilation (formula)? How does it vary at rest v. during exercise?

A
  • Total ventilation per minute: mL/min
  • V(mv) = V(i) x f where V(i) = tidal vol (mL/breath) & f = RR (breaths/min)
  • Rest, V(mv) = 500 ml x 15/min = 7500 ml/min
  • Exercise: V(mv) = 2000 ml x 20/min = 40,000 ml/min
  • Ratio of exercise/rest = 40,000/7500 = 5.3 fold INC
120
Q

How does ARDS cause hypoxemia? What are some of the pathological changes that occur?

A
  • Alveolar flooding and collapse cause large physiological shunt – leads to decreased oxygenation (blood flow going into areas with very little O2, i.e., pulm edema)
  • Leakage of fluid from capillary space into air space. T2 pneumocytes also damaged. These pts will not recover unless the edema is cleared, and the epithelium is recovered
121
Q

What are the A-a gradient and PaO2/FiO2?

A

􏰀- A–agradient=PAO2 –PaO2

  1. Difference b/t PO2 in alveolar gas and arterial blood. Measure of whether oxygen has equilibrated b/t alveolar gas and pulmonary capillary blood. Useful tool for examining causes of hypoxemia
    - PaO2/FiO2
  2. Ratio of arterial PO2 to fraction of inspired O2 is used as measure of acute lung injury (ALI); e.g., used to define severity of ARDS (Berlin criteria; <300); normal value is 100 mmHg/0.21 = 476 mmHg
122
Q

What is R-to-L shunt? Provide some examples. Does it help these patients to give them 100% FiO2?

A
  • Fraction of venous blood bypasses gas exchange units
  • Mix of venous blood & O2 blood causes hypoxemia (venous admixture) -> EXAMPLES:
    1. 5% “physiologic” shunt
    2. Cardiac shunts: ASD/VSD (Eisenmenger’s)
    3. Pulmonary shunts: unventilated alveoli with preserved perfusion or A-V malformations (blood does not even go past an alveolus)
  • Hypoxemia DOES NOT CORRECT with 100% FIO2
123
Q

What are the 3 types of dead space?

A
  • Anatomic: vol of conducting airways not available for gas exchange ~ 150 ml
  • Alveolar: vol of alveolar space not available for gas exchange b/c of limited blood supply (i.e., embolus); vol of non-perfused alveoli
  • Physiologic: anatomic + alveolar dead space; can be estimated as fraction of TV by measuring end-tidal PCO2 and arterial PCO2
124
Q

How can we measure the diffusing capacity of the lung?

A

Using single breath inhalation of carbon monoxide (CO) - DLCO

125
Q

What are hypoxemia, hypoxia, and hypercapnia?

A
  • Hypoxemia: lower than normal arterial PO2 (normal is 100 mmHg); can be due to high altitude, low alveolar ventilation (hypoventilation), diffusion defect (e.g., fibrosis), ventilation/perfusion defect, or R-to-L shunt

􏰀- Hypoxia: DEC in O2 delivery to, or utilization by, tissues. Can be due to DEC blood flow or DEC O2 content of blood (hypoxemia, anemia, CO poisoning, cyanide poison)

􏰀- Hypercapnia: higher than normal arterial PCO2 (normal is 40 mmHg). Most often due to low alveolar ventilation (hypoventilation)

126
Q

What are the steps in expiration (8)?

A
127
Q

What are some diseases associated with V/Q mismatch (low or high)?

A
  • Low:
    1. Obstructive diseases (asthma, COPD)
    2. Pulmonary edema
    3. Most extreme low V/Q is shunt (NO VENTILATION)
  • High:
    1. Pulmonary embolism (ventilation for days, but NO perfusion)
    2. Most extreme high V/Q is dead space (NO BLOOD FLOW)
128
Q

What is this?

A

Normal chest x-ray

129
Q

A 15 year old boy with congenital heart disease has a PaO2 of 30mmHg breathing room air. The PaO2 increases to 80mmHg after 15 minutes Of breathing 100% oxygen. The PaCO2 in both cases is 40mmHg.

What is the cause of hypoxemia?

A

R-to-L shunt

130
Q

How might this cause hypoxemia?

A
  • Low V/Q (interstitial edema) -> it will eventually become shunt
  • NOTE: cardiogenic edema -> ARDS (see a lot of shunt; laying on back, lung tissue under dorsal diaphragm caudally will have the most severe air-space disease)
131
Q

What is the alveolar gas equation? What factors determine PAO2?

A

PAO2 = PIO2 – PACO2/R where R = CO2 production/O2 consumption (normal is ~0.8)

  • Combined measure of alveolar ventilation and oxygen consumption
  • Determined by:
    1. PIO2: at high altitude, PO2 in air lower = DEC PAO2
    2. Alveolar ventilation: lower alveolar ventilation INC PACO2 and DEC PAO2
    3. Cellular oxygen consumption: if cell consumption INC, PAO2 will decrease, i.e., more O2 will leave the alveoli and enter blood (higher conc gradient)
132
Q

Forced vital capacity (FVC)

A

Amt of air exhaled in forceful expiration = Tidal volume + Inspiratory reserve volume + Expiratory reserve volume = 5 L

133
Q

How does emphysema affect V/Q? Why?

A
  • Severe ventilation-perfusion inequality -> wide range of V/Q
  • Destruction of lung tissue and obstruction of airways causes some areas of lung to receive large amounts of air while others receive none
  • When alveolar walls are destroyed, some capillaries are lost, and little blood flow goes to those regions
134
Q

What is the most important mechanism for moving CO2 out of tissues?

A
  • Formation of bicarbonate (HCO3-): carbonic anhydrase + CO2 + H2O (slow) 􏰇========􏰆 H2CO3 􏰇==􏰆 HCO3- + H+ (fast)
  • First rxn is the rate-limiting step, and is catalyzed by carbonic anhydrase (CA), which is present in RBC’s (and other cells) but not in plasma
  • CO2 moving by concentration gradient in the attached image -> high concentration produced in the tissues, so it moves into the capillaries, then into the RBC’s
135
Q

What happens to R when FiO2 = 100%?

A

R = 1 when FiO2 = 100%

REMEMBER THIS

136
Q

If 500 mL breath taken, how much fresh gas will be delivered to alveoli?

A

500 mL - anatomic dead space

137
Q

How is edema fluid cleared in ARDS?

A
  • Most likely, both T1 and T2 cells perform this function to reduce edema. Certain amount of water does flow through aquaporins, but you can actually knock these out, and it does not affect alveolar fluid clearance
  • Sodium moves out, and water follows. The details are not quite worked out yet - there is a lot of discussion about chloride transport, and the role that it plays in this
138
Q

What is alveolar ventilation (formula)? How does it vary at rest v. during exercise?

A
  • Total vol of fresh air entering alveoli per min; true portion available for gas exchange
  • V(alv) = (TV - dead space) x RR
  • Rest: Valv = (500 – 150) ml/breath x 15/min = 5250 ml/min
  • Exercise: Valv = (2000 – 150) ml/breath x 20/min = 37,000 ml/min
  • Ratio of exercise/rest = 37,000/5250 = 7.0 fold INC
139
Q

What is Henry’s Law, and why is it important?

A
  • Relates conc of gas x (Cx) in a solution to its partial pressure (Px): Cx = 􏰃alpha x Px where alpha 􏰃is the solubility of the gas in solution
  • Two different gases at the same partial pressure can have different concentrations in the liquid depending on solubility -> CO2 has a much greater solubility in water than O2 (23 fold higher)
  • Note: this relationship depends on the gas dissolved in solution – does not include gas in the bound form (for example, gas bound to hemoglobin)
140
Q

What determines lung compliance?

A
  1. Tissue properties: lungs contain lg amts of collagen and elastin connective tissue fibers that generate elastic forces -> accounts for approx. 1/3 of elastance of the lung
    a. Alveolar structure supported by tissue “interdependence,” based on many connections of similar alveoli surrounded by one another. If one alveolus has tendency to collapse, it will be counteracted by expanding forces due to the fact that the surrounding alveoli are expanded
  2. Surface forces: the role of pulmonary surfactant
    a. Surface tension: molecular cohesive (attractive) force b/t liquid molecules leads to devo of a macroscopic force; force that pulls surface molecules together at an air-liquid interface.
    - Expansion of the lung must overcome both the elastic tissue forces as well as the surface tension due to the water lining the alveoli
141
Q

What pressures drive blood flow at the 3 different levels of the lung in a person who is standing?

A
  • Alveolar pressure may compress capillaries in Zone 1
  • Blood flow driven by difference between arterial and alveolar pressure in Zone 2
  • Blood flow driven by difference between arterial and venous pressure in Zone 3
142
Q

What is the normal human pH?

A

7.35 - 7.45

143
Q

What is the driving force for air flow into and out of the lungs? What is the first step?

A
  • Pressure difference from alveoli to the mouth (usually atmospheric)
    1. P(alv) < P(atm) = air in
    2. P(alv) > P(atm) = air out
  • First step in ventilation involves a change in the dimensions (volume) of the lungs, leading to changes in P(alv) that drive air flow
  • Trans-respiratory system pressure: P(rs) = P(alv) - P(atm)
144
Q

How does diffusion of CO2 compare to that of O2 in gas and in tissue/fluid? Why?

A
  • Diffusion about the same in gas: 0.85 (CO2:O2 based on molecular weight)
  • In tissue/blood: CO2 diffuses 20x faster than O2 (b/c solubility of the gases becomes important)
  • The diffusion coefficient is based on solubility and molecular weight
145
Q

Barometric pressure

A

760 mmHG (at sea level; varies with altitude, but always use this unless you are given something else)

Total kinetic energy of all molecules in the atmosphere

146
Q

How does gravity affect the ventilation and perfusion of the lung (image)? Why is this important?

A
  • Apical alveoli are relatively overinflated, while the base of the lung is overperfused
  • Ventilation-perfusion ratio = amount of air available for gas exchange per unit of blood
    1. Determines gas exchange – low ratio causes poor oxygenation
147
Q

What happens to PiO2, PaCO2, PAO2, and R when the patient is hypo- or hyperventilating?

A
  • Hypo: 64 and 70
  • Normal: 40 and 100
  • Hyper: 20 and 125
  • R = 0.8 and PiO2 = 150 in all of these cases
148
Q

Why are diffusion capacity tests suspect?

A
  • O2 in alveoli diffuses across alveolar-capillary mem, through plasma & RBC membrane, & binds hemoglobin
  • Gas diffusion across membrane affected by surface area, mem thickness, driving pressure, gas molecular weight and solubility -> method of measuring diffusion is affected by all these + lung volume, ventilation, RBC volume, and perfusion
  • An abnormal Diffusion Capacity test can’t separate these mechanisms
149
Q

What do you see here? How might this cause hypoxemia?

A
  • Pulmonary fibrosis
  • Low V/Q and diffusion limitation
150
Q

What are some examples of V/Q mismatch (visual)?

A
  • Anything that can cause ventilation to be non-homogeneous
  • Changes in elasticity: emphysema (usually in the apices with smokers)
  • Dynamic compression: emphysema (airways that flop close on exhalation)
  • Regional limitation to expansion: pulmonary fibrosis (less expansile character of some alveoli)
  • Air is going to go down the path of least resistance
151
Q

What are some hemoglobin variants?

A
  • Methemoglobin: iron in the ferric state (Fe3+) does not bind O2; oxidation caused by nitrites and sulfonamides
    1. Shifts O2 dissociation curve to the left (harder for RBC’s to release O2); turns blood a dark blue/brown
    2. Caused by G6PD, pyruvate kinase deficiency, and the drugs listed above

􏰀- Fetal hemoglobin (HbF): has a higher affinity for O2; has α2γ2 subunits.

  • Hemoglobin S: abnormal variant that causes sickle cell
152
Q

What is the transpulmonary/transmural pressure, and what does it determine?

A

P(tp) = P(alv) - P(ip)

  • It determines the inflation of the lungs
153
Q

Why is transit time important to the alveolar blood:gas exchange? What factors can impact this?

A
  • At rest, blood spends about 0.75 seconds in the lung capillary, and it takes about 0.3 seconds for the gases to equilibrate by diffusion
    1. Even at the peak of the hardest exercise, blood spends >0.3 sec in the lung capillaries

􏰀- As blood leaves the pulmonary capillaries, the PO2 and PCO2 levels are about the same as alveolar air.

  • A lot lower partial pressure difference driving the exchange at high altitude, so slower
  • 􏰀 This efficient exchange can be impaired by disease
154
Q

What are the atmospheric air fractional percentages?

A

Pulmonology (18 decks)

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