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
capnia and ventilation relationship
hypercapnia (hypovent) | hypocapnia (hypervent)
26
causes of hypercapnia
``` VA = VE - VD hypoventilation from: low VE (sedatives, paralysis) high VD (COPD, restrictive) or combo ```
27
causes of hypocapnia
hyperventilation from: anxiety fever aspirin (salicyclics) poisoning
28
hyperpnea
increased ventilation to match increased metabolic demand (exercise)
29
blood gas values
``` pH (7.35-7.45) PaCO2 (35 - 45) PaO2 (85-95) SaO2 (94-98%) (pulse ox) HCO3 (22-28) - Henderson-Hasselbach ```
30
Acid base conditions
``` normal acute/chronic respiratory/metabolic acidosis/alkalosis 9 all together ```
31
compensation defenses
1st: chemical buffering (seconds) 2nd: resp (minutes) 3rd: renal (days)
32
Henderson-Hasselbach eq
pH = pK + log [HCO3]/0.3[PaCO2] | usually ratio = 20 --> pH 7.4
33
resp acidosis mech
retain CO2 HH down pH down
34
causes of retaining CO2 (resp acid)
VA down V/Q mismatch diffusion defect ex: obstruction, resp depressant, NM impairment
35
resp acidosis buffer
can't use HCO3 (resp failure) | use non-bicarb (Hb in RBC)
36
resp acidosis compensation
Renal can't change PaCO2 (resp problem) so up HCO3 PCO2 up stim kidney to conserve HCO3 and excretes H+
37
resp alkalosis mech
low CO2 HH up pH up
38
causes of low CO2 (resp alk)
increase VA | ex: anxiety, fever, altitude, acute asthma, CHF
39
resp alkalosis compensation
renal can't change PaCO2 so lower HCO3 kidney secretes less H and generates less new HCO3
40
sign of compensation
HCO3 and PCO2 rise or fall together and pH is normal | part comp if pH still abnormal
41
Resp acidosis values
PCO2 up pH down HCO3 norm
42
Resp alkalosis values
PCO2 down pH up HCO3 norm
43
Metabolic acidosis values
PCO2 norm pH down HCO3 down
44
Metabolic alkalosis values
PCO2 norm pH up HCO3 up
45
metabolic acidosis causes
``` bicarb down (loss or used up against acids) ex: diabetes (ketoacidosis), diarrhea, strenuous exercise, uremic acidosis ```
46
metabolic acidosis compensation
1st: pulm - up RR to down PaCO2 2nd: renal - eliminate ketones or H+
47
metabolic alkalosis causes
up HCO3 ex: volume depletion - vomiting, furosemide, K or Cl loss no volume depletion - hyperaldosteronism, cushings
48
metabolic alkalosis compensation
pulm: down RR to up PaCO2 renal: conserve H+, excrete excess HCO3
49
O2 content eq
(Hb x 1.34 x SaO2) + PaO2 x 0.003)