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Physiology > Resp - Gas Exchange > Flashcards

Resp - Gas Exchange Flashcards

1
Q

things affecting diffusion rate

A
  1. PP gradient (same)
  2. SA (same)
  3. thickness of membrane (opp)
  4. diffusion constant (solubility of gas/mw) (same)
  5. blood flow (same)
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2
Q

diffusion limited exchange

A

ex: CO
binds to Hb so strong that PP gradient never changes
limited by amt that can diffuse

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3
Q

perfusion limited

A

ex: N2O
doesn’t bind to Hb
as diffuses across, PP gradient goes down
limited by blood flow to keep gradient up

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4
Q

O2 diffusion/perfusion limited

A

usually perfusion limited (like N2O)
equillibrate 1/3 way along cap
if disease makes it not equilibrate in time - now diffusion limited

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5
Q

O2 forms in blood and how much in each

A

dissolved (0.3 ml/100 ml blood)
Hb bound (19.7)
total: 20 ml O2/100 ml blood

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6
Q

PO2 measures…

A

dissolved O2 in blood

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7
Q

Hb - when to take up or release O2

A

take up when PO2 is high

release when PO2 is low

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8
Q

SO2

A

% saturation of Hb

SO2 = HbO2 content/HbO2 capacity

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9
Q

Hb cooperative binding

A

binding an O2 makes Hb more likely to bind another

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10
Q

O2 diss curve: plateau

A

reflects loading zone
saturate in lungs where theres high PO2
not much change in Hb sat from 60 - 100 (wiggle room)

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11
Q

O2 diss curve: steep section

A

reflects unloading zone
gives up O2 easily w/ small changes in PO2
unload in tissue with low PO2

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12
Q

Hb helps diffusion how

A

in lungs: acts as storage of O2 so that gradient stays higher for longer and O2 can come in

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13
Q

O2 diss curve: right shift consequences

A

DECREASE O2 affinity
decrease Hb binding at given PO2
increase P50
–> unload

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14
Q

P50

A

PO2 when Hb is 50% saturated

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15
Q

O2 diss curve: right shift causes

A 
up acid
up CO2
up temp
up 2,3 DPG
(all from exercise)
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16
Q

O2 diss curve: left shift consequences

A

INCREASE O2 affinity
increase Hb binding at a PO2
decrease P50
–> uptake

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17
Q

Bohr effect

A

acid up (pH down) –> up unloading (and reverse)
due to:
CO2 bound to Hb decreases affinity
H+ bound to Hb does same

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18
Q

CO2 forms in blood

A

bicarb (60%)
dissolved in plasma (10%)
carbamino proteins (Hb) (30%)

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19
Q

bicarb steps in RBCs

A
  1. .CO2 goes into RBC
  2. .CO2 + H2O –CA–> H2CO3 –> H + HCO3
  3. HCO3 goes out and Cl- comes in
  4. H binds to Hb (downs O2 affinity)
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20
Q

chloride shift

A

for each bicarb leaves RBC, a Cl comes in

maintains electroneutrality of RBC

21
Q

Haldane effect

A

(low PO2 –>) Hb release O2 –> take up CO2 more easily

22
Q

bohr/haldane together

A

(low PO2 –>) Hb release O2 –> take up CO2 more easily –> CO2/H lower affinity –> Hb drop more O2

23
Q

effects of CO2 being more soluble

A

more dissolved in plasma

lungs can remove large amount of CO2 w/ small changes in PP

24
Q

CO2 binding to Hb

A

bind to globin (not heme)

deoxy binds more CO2 than oxy

25
Q

capnia and ventilation relationship

A

hypercapnia (hypovent)

hypocapnia (hypervent)

26
Q

causes of hypercapnia

A 
VA = VE - VD
hypoventilation from:
low VE (sedatives, paralysis)
high VD (COPD, restrictive)
or combo
27
Q

causes of hypocapnia

A

hyperventilation from:
anxiety
fever
aspirin (salicyclics) poisoning

28
Q

hyperpnea

A

increased ventilation to match increased metabolic demand (exercise)

29
Q

blood gas values

A 
pH (7.35-7.45)
PaCO2 (35 - 45)
PaO2 (85-95)
SaO2 (94-98%) (pulse ox)
HCO3 (22-28) - Henderson-Hasselbach
30
Q

Acid base conditions

A 
normal
acute/chronic
respiratory/metabolic
acidosis/alkalosis
9 all together
31
Q

compensation defenses

A

1st: chemical buffering (seconds)
2nd: resp (minutes)
3rd: renal (days)

32
Q

Henderson-Hasselbach eq

A

pH = pK + log [HCO3]/0.3[PaCO2]

usually ratio = 20 –> pH 7.4

33
Q

resp acidosis mech

A

retain CO2
HH down
pH down

34
Q

causes of retaining CO2 (resp acid)

A

VA down
V/Q mismatch
diffusion defect
ex: obstruction, resp depressant, NM impairment

35
Q

resp acidosis buffer

A

can’t use HCO3 (resp failure)

use non-bicarb (Hb in RBC)

36
Q

resp acidosis compensation

A

Renal
can’t change PaCO2 (resp problem) so up HCO3
PCO2 up stim kidney to conserve HCO3 and excretes H+

37
Q

resp alkalosis mech

A

low CO2
HH up
pH up

38
Q

causes of low CO2 (resp alk)

A

increase VA

ex: anxiety, fever, altitude, acute asthma, CHF

39
Q

resp alkalosis compensation

A

renal
can’t change PaCO2 so lower HCO3
kidney secretes less H and generates less new HCO3

40
Q

sign of compensation

A

HCO3 and PCO2 rise or fall together and pH is normal

part comp if pH still abnormal

41
Q

Resp acidosis values

A

PCO2 up
pH down
HCO3 norm

42
Q

Resp alkalosis values

A

PCO2 down
pH up
HCO3 norm

43
Q

Metabolic acidosis values

A

PCO2 norm
pH down
HCO3 down

44
Q

Metabolic alkalosis values

A

PCO2 norm
pH up
HCO3 up

45
Q

metabolic acidosis causes

A 
bicarb down (loss or used up against acids)
ex: diabetes (ketoacidosis), diarrhea, strenuous exercise, uremic acidosis
46
Q

metabolic acidosis compensation

A

1st: pulm - up RR to down PaCO2
2nd: renal - eliminate ketones or H+

47
Q

metabolic alkalosis causes

A

up HCO3
ex: volume depletion - vomiting, furosemide, K or Cl loss
no volume depletion - hyperaldosteronism, cushings

48
Q

metabolic alkalosis compensation

A

pulm: down RR to up PaCO2
renal: conserve H+, excrete excess HCO3

49
Q

O2 content eq

A

(Hb x 1.34 x SaO2) + PaO2 x 0.003)

Physiology (22 decks)

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