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Pulmonary > Respiratory Phys: Exchange of Gases in Alveoli, Transport, Balance > Flashcards

Respiratory Phys: Exchange of Gases in Alveoli, Transport, Balance Flashcards

1
Q

How is gas exchanges between alveoli and blood?

A

diffusion (from areas of greater to lesser partial pressures)

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2
Q

What is the respiratory quotient?

A

ratio of CO2 produces to O2 consumed

RQ = VCO2 / VO2

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3
Q

How much O is carried in the blood per min? CO2?

A

1L

2.8L

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4
Q

What is the formula for partial pressure?

A

P = (atm pressure) x (fraction of molecules in dry air)

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5
Q

amt of gas dissolved (Cx) =

A

partial pressure x solubility

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6
Q

Why are alveoli kind of awesome for diffusion?

A

thin = short diffusion distance

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7
Q

The flow of gas across a membrane is directly related to:

A

area available for diffusion
diffusion constant
partial pressure of gas

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8
Q

The flow of gas across a membrane is inversely related to:

A

thickness of barrier

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9
Q

Diffusion coefficient is directly related to

A

molecular weight

solubility

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10
Q

Arterial partial pressures are determined by

A

alveolar partial pressures

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11
Q

The partial pressure of CO2 in alveoli is directly related to:

A

CO2 production

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12
Q

The partial pressure of CO2 in alveoli is inversely related to:

A

alveolar ventilation

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13
Q

How does increased alveolar ventilation affect the partial pressure of CO2 in alveoli?

A

decreases, because freshly inspired air dilutes alveolar gas

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14
Q

How does increased cellular metabolism affect the partial pressure of CO2 in alveoli?

A

increases, because more CO2 will enter blood per unit time

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15
Q

If the production of CO2 is constant, what determines the partial pressure of CO2 in alveoli?

A

alveolar ventilation

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16
Q

Describe hypoventilation in terms of PCO2

A

P-ACO2 increases because alveolar ventilation canot keep up with CO2 production

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17
Q

Describe hyperventilation in terms of PCO2

A

P-ACO2 decreases because alveolar ventilation is excessive for nml CO2 production

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18
Q

What is the driving stimulus for normal respiration?

A

arterial PCO2

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19
Q

What factors determine P-AO2 (alveolar)?

A
  1. PO2 of inspired air
  2. alveolar ventilation
  3. cellular oxygen consumption
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20
Q

Alveolar gas equation:

A

P-AO2 = P-IO2 - (P-ACO2 / R)

where R = CO2 production / O2 consumption (~0.8)

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21
Q

How does an increase in cellular consumption of O affect alveolar PO2?

A

decreases, greater concentration gradient so more O leaves alveoli

22
Q

Causes of hypoxemia?

A
  1. high altitude
  2. low alveolar ventilation
  3. diffusion defect
  4. ventilation/perfusion defect
  5. R to L shunt
23
Q

What is hypoxemia?

A

lower than nml arterial PO2

24
Q

What does A-a gradient measure?

A

measure of whether O has equilibrated between alveolar gas and pulm capillary bed

25
Q

What is hypoxia?

Causes?

A

decreased O2 delivery to tissues

  1. decreased blood flow
  2. decreased O2 in blood (hypoxemia, anemia, CO poisoning, cyanide)
26
Q

What is hypercapnia?

Most common cause?

A

higher than nml arterial PCO2

hypoventilation

27
Q

At rest, blood spends about ___ sec in the lung capillary. It takes about ___ sec for the gases to equilibriate by diffusion.

A

.75

.3

28
Q

How does exercise affect pulm capillaries?

A

increased pulm vasc pressure opens up “many” pulm capillaries

29
Q

As blood leaves pulm capillaries, the PO2 and PCO@ are about the same as:

A

alveolar air

30
Q

How is O carried in tissues?

A
  1. oxygen is physically dissolved (1.5% of O)

2. hgb bound

31
Q

What is cooperativity (in terms of hgb)?

A

reactions of 4 hgb subunits occur sequentially, with each binding facilitating the next

32
Q

What is cyanosis, in terms of hgb?

A

unsaturated hgb = purple; causes the bluish coloring in surface capillaries with low hgb sats

33
Q

Percent hgb saturation =

A

O2 bound to hgb / max capacity of O2 bound hgb

x100%

34
Q

What is demonstrated by hgb sat curve?

A

over 60 mmHg, changes in PO2 cause relatively little change in hgb sat
(e.g. 80mmHg ~ 95.9%; 60mmHg ~ 90%)

35
Q

Why is a hgb-O dissociation curve sigmoid shaped?

A
  1. positive cooperativity

2. for steep portion, relatively small change in PO2 causes large changes in saturation

36
Q

O diffusion is governed ONLY by

A

gradient of dissolved portion of O in blood

37
Q

How does O bound to hgb contribute to blood PO2?

A

it doesn’t directly; however, it maintains gradient by capturing O2
*determines the total amount of oxygen that will diffuse

(adding hgb = O binds, more can diffuse into space)

38
Q

How does exercise affect the release of O from hgb to tissues?

A
  1. increased blood floow

2. increased O2 demand creates a larger gradient, more O is extracted from the blood

39
Q

Decreased affinity of hgb for O causes a shift to the (right/left)
What factors facilitate unloading?

A

right

  1. increased PCO2
  2. decreased pH
  3. increased temp
  4. increased 2,3-DPG
40
Q

Increased affinity of hgb for O causes a shift to the (right/left)
What factors facilitate loading?

A

left

  1. decreased PCO2
  2. increased pH
  3. decreased temp
  4. decreased 2,3-DPG
  5. fetal hgb
41
Q

How does metabolic activity affect hgb saturation?

A

increased metabolic activity increases CO2 production and increases [H] (lowers pH)

this DECREASES hgb affinity for O

42
Q

How does heat affect hgb saturation?

A

working muscle produces heat, which causes a conf change in hgb and facilitates release of O

43
Q

How does RBC’s glycolytic pathway affect hgb saturation?

A

increased glycolysis = increased levels of 2,3-DPG; this binds strongly to deoxy-hgb and lowers its O affinity (more O released to tissue)

44
Q

How does CO affect oxygen content of blood? Anemia?

A

CO binds 250x more strongly to hgb than O; this decreases the max O2 carrying capacity of blood

anemia = less hgb = decreased hgb O capacity

45
Q

3 mechanisms for CO2 transport in the blood:

A
  1. dissolved in blood
  2. carbamylation of proteins (carbamino-hgb)
    * 3. formation of bicarb via hydration in RBCs
46
Q

How is CO2 transported out of tissues?

A
  1. CO2 is produced by tissues; it leaves cell and is dissolved in interstitial fluid
  2. CO2 diffused into plasma, then into RBC where it is converted to bicarb
  3. bicarb diffuses into plasma, and is exchanged for Cl- (maintains charge balance)
  4. Cl- entrance into cell drags in H2O, which causes cell to swell
47
Q

How are H ions carried in blood?

A

within RBC, buffered by deoxy-hgb

48
Q

What is the Bohr effect?

A
  • when tissues produce CO2, H and bicarb are produced by blood
  • H production lowers pH, which shifts the dissociation curve to the right (facilitates O unloading)
49
Q

What are the differences between O2 and CO2 dissociation curves?

A
  1. CO2 curve is much higher (more CO2 per L blood and more stored CO2)
  2. CO2 curve is linear; O2 curve is sigmoidal
  3. CO2 curve much steeper, big changes in CO2 content as PCO2 changes
50
Q

What is the Haldane effect?

A

When O2 sat of hgb is lower (more in deoxy form), H binding to hgb increased and CO2 carrying capacity increased

51
Q

pH =

H-H eq

A

6.1 + log [HCO3-]/0.03PCO2

Pulmonary (31 decks)

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