Resp - Gas Exchange Flashcards
things affecting diffusion rate
- PP gradient (same)
- SA (same)
- thickness of membrane (opp)
- diffusion constant (solubility of gas/mw) (same)
- blood flow (same)
diffusion limited exchange
ex: CO
binds to Hb so strong that PP gradient never changes
limited by amt that can diffuse
perfusion limited
ex: N2O
doesn’t bind to Hb
as diffuses across, PP gradient goes down
limited by blood flow to keep gradient up
O2 diffusion/perfusion limited
usually perfusion limited (like N2O)
equillibrate 1/3 way along cap
if disease makes it not equilibrate in time - now diffusion limited
O2 forms in blood and how much in each
dissolved (0.3 ml/100 ml blood)
Hb bound (19.7)
total: 20 ml O2/100 ml blood
PO2 measures…
dissolved O2 in blood
Hb - when to take up or release O2
take up when PO2 is high
release when PO2 is low
SO2
% saturation of Hb
SO2 = HbO2 content/HbO2 capacity
Hb cooperative binding
binding an O2 makes Hb more likely to bind another
O2 diss curve: plateau
reflects loading zone
saturate in lungs where theres high PO2
not much change in Hb sat from 60 - 100 (wiggle room)
O2 diss curve: steep section
reflects unloading zone
gives up O2 easily w/ small changes in PO2
unload in tissue with low PO2
Hb helps diffusion how
in lungs: acts as storage of O2 so that gradient stays higher for longer and O2 can come in
O2 diss curve: right shift consequences
DECREASE O2 affinity
decrease Hb binding at given PO2
increase P50
–> unload
P50
PO2 when Hb is 50% saturated
O2 diss curve: right shift causes
up acid up CO2 up temp up 2,3 DPG (all from exercise)
O2 diss curve: left shift consequences
INCREASE O2 affinity
increase Hb binding at a PO2
decrease P50
–> uptake
Bohr effect
acid up (pH down) –> up unloading (and reverse)
due to:
CO2 bound to Hb decreases affinity
H+ bound to Hb does same
CO2 forms in blood
bicarb (60%)
dissolved in plasma (10%)
carbamino proteins (Hb) (30%)
bicarb steps in RBCs
- .CO2 goes into RBC
- .CO2 + H2O –CA–> H2CO3 –> H + HCO3
- HCO3 goes out and Cl- comes in
- H binds to Hb (downs O2 affinity)
chloride shift
for each bicarb leaves RBC, a Cl comes in
maintains electroneutrality of RBC
Haldane effect
(low PO2 –>) Hb release O2 –> take up CO2 more easily
bohr/haldane together
(low PO2 –>) Hb release O2 –> take up CO2 more easily –> CO2/H lower affinity –> Hb drop more O2
effects of CO2 being more soluble
more dissolved in plasma
lungs can remove large amount of CO2 w/ small changes in PP
CO2 binding to Hb
bind to globin (not heme)
deoxy binds more CO2 than oxy
capnia and ventilation relationship
hypercapnia (hypovent)
hypocapnia (hypervent)
causes of hypercapnia
VA = VE - VD hypoventilation from: low VE (sedatives, paralysis) high VD (COPD, restrictive) or combo
causes of hypocapnia
hyperventilation from:
anxiety
fever
aspirin (salicyclics) poisoning
hyperpnea
increased ventilation to match increased metabolic demand (exercise)
blood gas values
pH (7.35-7.45) PaCO2 (35 - 45) PaO2 (85-95) SaO2 (94-98%) (pulse ox) HCO3 (22-28) - Henderson-Hasselbach
Acid base conditions
normal acute/chronic respiratory/metabolic acidosis/alkalosis 9 all together
compensation defenses
1st: chemical buffering (seconds)
2nd: resp (minutes)
3rd: renal (days)
Henderson-Hasselbach eq
pH = pK + log [HCO3]/0.3[PaCO2]
usually ratio = 20 –> pH 7.4
resp acidosis mech
retain CO2
HH down
pH down
causes of retaining CO2 (resp acid)
VA down
V/Q mismatch
diffusion defect
ex: obstruction, resp depressant, NM impairment
resp acidosis buffer
can’t use HCO3 (resp failure)
use non-bicarb (Hb in RBC)
resp acidosis compensation
Renal
can’t change PaCO2 (resp problem) so up HCO3
PCO2 up stim kidney to conserve HCO3 and excretes H+
resp alkalosis mech
low CO2
HH up
pH up
causes of low CO2 (resp alk)
increase VA
ex: anxiety, fever, altitude, acute asthma, CHF
resp alkalosis compensation
renal
can’t change PaCO2 so lower HCO3
kidney secretes less H and generates less new HCO3
sign of compensation
HCO3 and PCO2 rise or fall together and pH is normal
part comp if pH still abnormal
Resp acidosis values
PCO2 up
pH down
HCO3 norm
Resp alkalosis values
PCO2 down
pH up
HCO3 norm
Metabolic acidosis values
PCO2 norm
pH down
HCO3 down
Metabolic alkalosis values
PCO2 norm
pH up
HCO3 up
metabolic acidosis causes
bicarb down (loss or used up against acids) ex: diabetes (ketoacidosis), diarrhea, strenuous exercise, uremic acidosis
metabolic acidosis compensation
1st: pulm - up RR to down PaCO2
2nd: renal - eliminate ketones or H+
metabolic alkalosis causes
up HCO3
ex: volume depletion - vomiting, furosemide, K or Cl loss
no volume depletion - hyperaldosteronism, cushings
metabolic alkalosis compensation
pulm: down RR to up PaCO2
renal: conserve H+, excrete excess HCO3
O2 content eq
(Hb x 1.34 x SaO2) + PaO2 x 0.003)
