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Physiology > Ventilation and gas transport > Flashcards

Ventilation and gas transport Flashcards

1
Q

Define: tidal volume

A

The volume of gas that flows into and out of the lungs in 1 breath

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2
Q

Define: total lung capacity. How would you calculate it?

A

The maximum value of gas that the lungs can contain

TLC= RV+ IRV+ TV+ ERV

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3
Q

Define: inspiratory reserve volume

A

the maximum volume of gas that can be inhaled from the end-inspiratory tidal volume position

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4
Q

Define: expiratory reserve volume

A

The maximum volume of gas that can be expired from the end-expiratory tidal volume position

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5
Q

Define: residual volume

A

The amount of gas contained in the lungs after a maximal forced expiration

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6
Q

Define: functional residual capacity

A

The volume of gas in the lungs after a normal expiration when the diaphragm and chest wall muscles are relaxed (Pc= -P(lungs))

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7
Q

Define: vital capacity. How would you calculate it?

A

The maximum volume of gas that can be exhaled after a maximal inspiration
VC= TLC- RV

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8
Q

Define: inspiratory reserve capacity. How would you calculate it?

A

The maximum volume of gas that can be inhaled from the resting expiratory position
IC= IRV+ VT
IC= TLC- FRC

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9
Q

How does increased compliance affect FRC? Why does this occur?

A

Increased C increases FRC b/c the lung is less stiff, so the chest wall (and it’s elastic outward recoil) dominates thus the lung hyperinflates and FRC increases

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10
Q

How does pulmonary compliance change with age?

A

It increases. This is the opposite of vascular compliance

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11
Q

How does the open circuit N washout method allow for measurement of FRC?

A

Generally, the fraction of N in the lung at the beginning (typically 80%) x FRC (volume) = fraction of N in the spirometer x volume of spirometer. You pump 100% O2 through the lungs so all N in the lungs goes into the spirometer
FRC= (frac of N in spirometer) x (Vol spirometer)/(Frac N in lung)

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12
Q

How does a body plethysmograph measure FRC?

A

Pt in telephone booth. Expires against a transducer which measures the change in pressure. The air outside the pt in the booth increases in volume (measured by a change in pressure). FRC= -(total dry gas pressure in lungs) x (change in V)/(change in P)

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13
Q

Does the nitrogen washout method measure the volume of trapped air in the lungs? How about the body plethysmograph?

A

Nitrogen washout- no

Body plethysmograph- yes

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14
Q

Why does the alveolar ventilation matter?

A

It sets the partial pressures of O2 and CO2 in alveoli (which are equal to the partial pressures of those gasses in the capillaries)

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15
Q

If a person hyperventilates, what happens in the alveoli? What about hyopventilation?

A

Hyperventilation- hyperoxia, hypocapnea and alkalemia

Hypoventilation- hypoxia, hypercapnea and acidemia

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16
Q

What is the usual alveolar partial pressure for oxygen? CO2?

A

100 mm Hg and 40 mm Hg

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17
Q

Using the alveolar gas equation for CO2, what happens to steady state CO2 with an increase in alveolar ventilation? What about after an increase in CO2 production?

A

Increase in alv vent- decreases CO2 PP

Increase in CO2 prod- increases CO2 PP

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18
Q

Using the alveolar gas equation for O2, how does steady state O2 change with an increase in alveolar ventilation? How about increased O2 consumption? Or increased PP O2 in inspired gas?

A

Increased alv vent- increased PP O2
Increased consumption- decreased PP O2
Increased PP O2 inspired- increased PP O2

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19
Q

How is total minute ventilation related to alveolar ventilation and dead space ventilation?

A

Total minute = alveolar + dead space

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20
Q

Why is oxygen therapy (i.e. ventilation) effective?

A

It increases the inspired PP O2 thus increasing alveolar PP O2

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21
Q

How does alveolar O2 change during 1 breath? How does CO2 change?

A

O2- transient decrease (since inspired O2 not to alveoli yet) then increase to about 102 mm Hg, then decreases during expiration to about 98-99 mm Hg
CO2- transient increase then falls to about 38 mm Hg before increasing on expiration to about 40.5 mm Hg

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22
Q

How does the single breath method assess anatomic dead space?

A

Pt inspires normal air then expires into a spirometer. The volume that corresponds to the midpoint in the rise of expired CO2 is the volume of dead space. This is because CO2 is only in the alveoli; not the dead space. All dead space air (low CO2 air) should be expired by this point, allowing for some mixing of air

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23
Q

How could you calculate the alveolar ventilation rate using the dead space volume and total volume?

A

(total vol- dead space vol) x freq of breathing= alveolar ventilation

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24
Q

Rapid, shallow breathing signifies a _____ in RR and a _____ in TV

A

Increased RR, decreased TV

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25
Q

What is the normal partial pressure for O2 in arterial blood? In venous blood? In alveoli?

A

100 mm Hg in arterial and alveoli

40 mm Hg in venous

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26
Q

What is the normal partial pressure for CO2 in arterial blood? In venous blood? In alveoli?

A

40 mm Hg, 46 mm Hg, 40 mm Hg

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27
Q

What three laws/principles are important for gas transfer in the alveoli?

A

Henry’s law for gas solubility, Fick’s law of diffusion and transit time in the capillary

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28
Q

What does Henry’s law for gas solubility tell us about the composition of blood? Does Henry’s law tell us anything else important?

A

The concentration of dissolved gas in blood is directly proportional to the partial pressure of the gas.
Yes, the partial pressure of a dissolved gas does not contribute to blood pressure. And partial pressure for a dissolved gas is only from the unbound form

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29
Q

What does Fick’s law of diffusion tell us about the flow of gas across a membrane? What variable has the greatest effect?

A

The movement of a gas = (surface area)x (partial pressure gradient) x [(solubility) / (square root of the molecular weight] x 1/ (thickness of the membrane)
The partial pressure gradient is the biggest determining factor of movement

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30
Q

How fast/slow does CO2 diffuse relative to O2? Why is this clinically important?

A

CO2 diffuses about 20x faster than O2

Pts with impaired diffusion develop hypoxemia before hypercapnea

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31
Q

What is the transit time of blood in pulmonary capillaries? When does most O2 and CO2 diffusion occur?

A

t= 0.75 sec

Most diffusion takes place in the first .4 seconds. Both gasses are in equilibrium by then

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32
Q

What does diffusion limited mean? How does this differ from being perfusion limited?

A

Diffusion limited gasses don’t reach equilibrium in the capillary. Thus, a change in membrane thickness which would increase their movement (i.e. Fick’s law) will increase their concentration in the blood. Perfusion limited gasses do reach equilibrium so a change in membrane thickness will just change the time it takes for them to reach equilibrium.

33
Q

Why does CO2 take longer than O2 to reach equilibrium?

A

Some CO2 in the blood reacts with water to form bicarbonate and H+. As CO2 diffuses out of the blood, some of that bicarbonate will be converted back to CO2, increasing the blood PP CO2. Eventually though, the partial pressures equilibrate

34
Q

Why does CO not reach equilibrium?

A

It has a very high affinity for hemoglobin and consequently binds it quickly. This keeps blood PP low and it never reaches equilibrium

35
Q

How does exercise change the transit time of blood in the pulmonary capillaries? Does this change the diffusion curves? How does this affect pts with diffusion problems?

A

It shortens it to about 0.25 s. O2 reaches equilibrium closer to the venous side of the capillary instead of on the arterial side. Patients with diffusion problems will likely become hypoxic b/c the O2 can’t equilibrate in this short time

36
Q

How does being at high altitude change the transit time of blood in the pulmonary capillaries? Does this change the diffusion curves?

A

The partial pressure gradient is lower but transit time remains the same. It takes O2 longer to equilibrate because the lung vasculature vasoconstricts causing an increase in pressure and some pulmonary edema. This slows the diffusion of gasses.

37
Q

What is lung diffusion capacity? How is it represented mathematically? What gas is used to measure it?

A

The overall ability of the lung to move gasses.
D(L)= D x A x 1/T where D= solubility/(sqrt molecular weight), A= surface area, T= thickness
CO b/c it does not reach equilibrium

38
Q

How can you determine lung diffusion capacity?

A

D(L) CO= movement of CO across the membrane/alveolar pressure of CO
You can measure alveolar pressure of CO and you can measure CO inspired and CO expired (difference b/wn them is CO mvt across the mem)

39
Q

How does DL for O2 relate to DL for CO? Why is this?

A

DL O2 is 1.23 DL. CO b/c O2 has a greater diffusion coefficient, D

40
Q

What are some things that increase D(L) CO? Some that decrease it?

A

Supine body position and exercise both increase blood flow to the lung which increase surface area and also DL. Diseases typically decrease DL (i.e. fibrosis increases thickness, tumors decrease surface area, anemia reduces Hb so less CO can move across the membrane)

41
Q

Why does O2 administration help patients with a diffusion problem?

A

Breathing gas with an increased PP O2 will increase the gradient between the alveoli and the blood and drive more O2 into the blood.

42
Q

Why do pulmonary vessels vasoconstrict at low PP O2s?

A

It’s a protective thing. If there is a region of the lung that isn’t getting enough air (and thus enough PP O2), the lung wants to shunt blood to an area that’s receiving better air flow. At altitude though, the whole lung is hypoxic so this mechanism isn’t particularly protective.

43
Q

How much O2 (% by volume) is normally dissolved in arterial blood? Venous blood? Does this meet tissue VO2 needs?

A

0.3% arterial, 0.12% venous. No

44
Q

How much O2 is bound to hemoglobin? Does this meet tissue VO2 needs?

A

20.1 ml O2/ 100 mL of blood. Yes

45
Q

What does the dissolved O2 curve look like?

A

It gradually increases from 0% O2 by volume to about .3% at 100 mm Hg partial pressure

46
Q

What does the oxygen dissociation curve (bound to hemoglobin) look like?

A

It’s a sigmoid curve that’s at 0 % by volume at 0 mm Hg; 10% by vol (50% saturated) at 26; 15% by vol (75% sat) at 40; and 20% by vol (97% sat) at 100

47
Q

What does the plateau of the oxygen dissociation curve permit? Why?

A

It allows the body to tolerate moderate hypoxemia. A big change in partial pressure corresponds to a small change in O2 content

48
Q

What does the sigmoid shape of the curve permit? Why?

A

It facilities unloading of O2 in tissues b/c it’s steepest around the venous partial pressure of O2

49
Q

Why is the venous curve shifted slightly to the R of the O2 curve?

A

In the veins, O2 binds Hb less strongly so more O2 is released into the tissues

50
Q

What is associated with a R shifted O2 curve?

A

Increased CO2, decreased pH, increased 2,3-DPG, increased temperature

51
Q

How does polycythemia or anemia change O2 content of the blood? O2 sat?

A

O2 content changes with hemoglobin concentration. With more Hb in polycythemia, there will be more O2 content. However, O2 sat is independent of Hb conc so all have the same O2 sat

52
Q

What is erythropoetin? What does it do?

A

It is a hormone that stimulates erythrocyte development. It is released under conditions of hypoxia

53
Q

What does Fick’s law of O2 transport tell us?

A

The rate of O2 delivered to the tissues = Rate of O2 used by the tissues + rate of O2 collected by the blood
(C arterial O2 x CO)= V(dot) O2 + (C venous O2 x CO)

54
Q

How can we use Fick’s law to measure CO?

A 
CO= V(dot) O2/ Extraction
Extraction= C arterial O2-C venous O2
55
Q

How does polycythemia alter O2 content, percent sat, extraction and PP O2 in arterial and venous blood?

A

Increased O2 content, same O2 sat, same extraction, high arterial and venous PP O2

56
Q

How does anemic hypoxia alter O2 content, percent sat, extraction and PP O2 in arterial and venous blood?

A

Decreased O2 content and arterial PP O2. Same percent sat and extraction. Decreased venous PP O2

57
Q

How does hypoxic hypoxia (i.e. high altitude) alter O2 content, percent sat, extraction and PP O2 in arterial and venous blood?

A

Decreased O2 content, percent sat and PP O2 arterial. Normal extraction so low PP O2 in venous blood

58
Q

How does stagnant hypoxia (i.e. CHF) alter O2 content, percent sat, extraction and PP O2 in arterial and venous blood?

A

Normal PP arterial O2, O2 content, and percent sat. Increased extraction so decreased venous PP O2

59
Q

How does histotoxic hypoxia (i.e. some muscle dies) alter O2 content, percent sat, extraction and PP O2 in arterial and venous blood?

A

O2 content, percent sat and arterial PP are normal. Decreased extraction so high venous PP O2

60
Q

How does CO poisoning alter O2 content, percent sat, extraction and PP O2 in arterial blood? Why does this occur?

A

Normal PP arterial O2, decreased O2 sat and content. Lower extraction.
CO binds Hb preferentially, so less O2 can bind to Hb. Additionally, CO shifts the O2 curve to the L so Hb doesn’t like to let go of O2 (reduced extraction)

61
Q

Will movement be faster with a large or small gradient?

A

Should be faster with a smaller gradient

62
Q

How is CO2 transported in the blood? How much of the total CO2 is transported in these forms?

A

Bicarbonate- 90%
Dissolved- 5%
Carbamino hemoglobin- 5%

63
Q

What forms contribute to CO2 partial pressure?

A

Only dissolved CO2

64
Q

What is the pH of the arteries? Of the veins? Why is the difference so small?

A

Arteries- 7.4
Veins- 7.38
Hemoglobin serves as a buffer (binds the released H+ formed when H2CO3 dissociates to form Bicarbonate)

65
Q

What is the % content by volume of CO2 in venous blood? The partial pressure? How about the % content and partial pressure of CO2 in arterial blood?

A

Venous- 55%, 46 mm Hg

Arterial- 50%, 40 mm Hg

66
Q

Describe what occurs in the Jabobs-Stewart cycle

A

CO2 leaves the tissues and diffuses into the blood where it enters RBCs and combines with water to make H2CO3 (via carbonic anhydrase sometimes). H2CO3 dissociates into HCO3- and H+ which binds to Hb. So H+ can bind, Hb releases O2 which goes to the tissues. The RBC also pumps out HCO3- for Na+ and Cl- causing the reactions to continue and the RBC to gain a little H2O and thus volume. CO2 can also react with Hb to form carbamino Hb

67
Q

How does the Jacobs-stewart cycle differ in the lungs?

A

All reactions go in reverse

68
Q

What is the chloride shift? The pH Bohr effect? The CO2 Bohr effect?

A

Cl- shift- When RBCs take up CO2, they also take up Cl-
pH- at low pH, the O2-Hb dissociation curve shifts to the R so more O2 is released b/c deoxyHb binds H+ better than HB-O2
CO2- at higher PCO2, more carbamino-Hb is formed and consequently less O2 is bound to Hb

69
Q

What AA does H+ bind to on Hb?

A

histidine

70
Q

Deoxygenation promotes (formation/breakdown) of carbamino-Hb and (promotes/does not promote) H+ binding to Hb

A

Deoxygenation promotes formation of carbamino Hb and binding of H+ to Hb

71
Q

Describe the CO2 absorption curve

A

As PCO2 increases, so does total CO2 but the increase isn’t linear b/c CO2 is also transported as HCO3- and bicarbonate

72
Q

What does the CO2 absorption curve look like in venous blood v. arterial blood? How about completely deoxygenated blood?

A

In venous blood, the curve is shifted up (for the same PCO2, the blood can hold more volume % CO2). In deoxygenated blood, it is shifted up even further

73
Q

What two things does the Haldane effect tell us?

A
  1. Total CO2 content increases with more deoxygenated blood
  2. This minimizes the change in pH b/wn arterial and venous blood (b/c CO2 is taken up by RBCs in deoxygenated blood to form bicarbonate)
74
Q

Describe the Bohr effect

A

At any given PO2, oxygen sat decreases as PCO2 increases

Increased CO2 and decreased pH shift the O2-Hb curve rightward so O2 dissociates more easily

75
Q

When Hb is bound to H+ it’s binding affinity for O2 is (greater/reduced)

A

Reduced

76
Q

What is the henderson-hasselbach eqn for blood pH?

A

pH= pK + Log ([Hco3-]/[CO2])

Where [CO2]= .03 x PCO2

77
Q

Describe the bicarbonate titration curve

A

It’s pK is 6.1 so it’s flat at physiologic pH thus a little change in the % acid (H2CO3) v. base (HCO3-) will cause a big change in pH

78
Q

Why is bicarbonate a good buffer?

A

Our circulatory+ respiratory system is an open system with a ventilatory response. An increase in acid (such as after eating a meal) will favor formation of CO2 from HCO3-. The CO2 can be let off by the lungs (where atmospheric and thus inspired PCO2 is low so we can let out as much as we need to) so more HCO3- can form CO2, thus pulling H+ out of the blood and reducing the acidemia

Physiology (13 decks)

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