Mkgrady8 Mos3 West Blood Gas Transport

Front 1

the concentration of O2 in dry air

Back 1

21% so FO2=0.21 (the fractional concentration (keep in mind that all of the fractional concentrations add up to 1))

Front 2

the partial pressure of O2 in air

Back 2

multiply 0.21 by the atmospheric pressure which is 760 mmHG; so PO2=0.21(760)=160 mmHg

Front 3

the effect of water vapor on PO2

Back 3

the partial pressure of water pressure ONLY depends on the temp (so not on pressure) and at room temp PH2O=47 mmHg; so why do we need to take this into account? we moisten air when we breath it in; ok so do 760-47=713 and then P)2 must be 0.21(713)=150 mmHg and this is the partial pressure that we are actually dealing with

Front 4

the PO2 and [O2] in air and the water that is next to it

Back 4

if you allow them to come to equilibrium then the PO2 is the same in each (so 150 mmHg) but the [O2] will be much different with air being 21 and water being 0.45; this is because O2 is a lot less soluble in water than it is in air; so solubility in blood is 0.003 (because 0.45/150=0.003)

Front 5

is this enough if we said blood instead of water?

Back 5

no; the O2 dissolved in the blood wouldn't be enough for the tissues it travels to so we need an O2 carrying molecule (enter hemoglobin)

Front 6

the structure of hemoglobin

Back 6

there are 2 alpha chains and 2 beta chains; on each chain there is a heme which is an iron porphorin ring that can bind 4 O2 each; remember that Hbf is in babies and it hold O2 tighter (because of the low O2 levels); Hbs is in sickle cell anemia and the heme crystalizes causing the sickle shape and making occlusion likely

Front 7

the O2 dissociation curve

Back 7

it is shaped like it is (s shape) because of the change in configuration of Hb with O2 binding; it is a lot harder to get the first O2 to bind than the last one to bind

Front 8

in arterial blood with a PO2 of 100 mmHg what will be O2 saturation %

Back 8

almost 100% (almost fully saturated)

Front 9

in venous blood with a P02 of 40 mmHg what will be O2 saturation %

Back 9

about 75%

Front 10

the P50 (the partial pressure of O2 for 50% saturation) is what

Back 10

under normal conditions it is 27 mmHg

Front 11

how to calculate the total O2 in blood

Back 11

it is the sum of Hb bound and dissolved O2; total [O2]=1.39([Hb])(% saturation/100)+0.003(PO2); [Hb] is usually about 15 and percent saturation is usually about 97%

Front 12

effects of changing Hb concentration

Back 12

if we increase the Hb concentration (above 15) then the O2 concentration in blood is greater for the same 100% O2 saturation in blood (it has more Hb to bind to); in the case of anemia (decreased Hb concentration) it is the opposite

Front 13

shifting of the O2 dissociation curve to the right

Back 13

aka reduce the O2 affinity for Hb; increases in temp, DPG, PCO2, and H+; all of these things increase with exercise and this is advantageous because you can unload more oxygen for a given PO2 which is what you need

Front 14

CO effect on the O2 dissociation curve

Back 14

CO has a way higher affinity for Hb than O2 so at very low partial pressures of CO the saturation is 100%; this means that there is a lot less O2 available for metabolism; curve is shifted to the left meaning that any O2 still on the Hb has a harder times letting go (its affinity is increased too) and so it doesn't drop off in the periphery where it is needed

Front 15

CO2 is carried in the blood in what forms

Back 15

dissolved, as bicarbonate, and as carbamino compounds

Front 16

solubility of CO2 in blood

Back 16

0.067 so much larger than O2 which is 0.003; this means that there is more dissolved O2 in the blood than dissolved CO2

Front 17

formation of bicarbonate

Back 17

CO2+H20 <--> H2CO3 with the help of carbonic anhydrase; H2CO3 then immediately dissociates into H+ and HCO3- but it's reversible

Front 18

formation of carbamino compounds

Back 18

CO2 can combine with the terminal amine groups of proteins and hemoglobin is a big one it attaches to; so Hb.NH2+CO2 <--> Hb.NH.COOH; it is much easier to combine CO2 with the Hb when the Hb doesn't have the O2 on it (aka when it is reduced) so that means that areas where the O2 has been released are better able to pick up CO2 (this is called the haldane effect)

Front 19

uptake of CO2 in systemic caps

Back 19

so CO2 is made by cells and it dissolves across the cap wall into the cap where it can either dissolve into the blood or be taken up into the RBC; in the RBC some of it dissolves, some of it binds to Hb (carbamino compounds), and some combines with H2O with the help of carbonic anhydrase to form H2CO3 which dissociates into H+ and HCO3-; some of the HCO3- moves out of the RBC into the cap; H+ combines with carbamino Hb; because the H+ cannot move out there is an increase + change in the cell so Cl- moves in from the cap to offset it (this is called the chloride shift); because of the build up of ions water will also move into the cell

Front 20

% carriage of CO2 in its various forms in arterial blood

Back 20

5% carbamino, 90% HCO3-, and 5% dissolved

Front 21

% carriage of CO2 in its various forms in venous blood

Back 21

30% carbamino, 60% HCO3-, and 10% dissolved

Front 22

CO2 dissociation curves

Back 22

steep and almost linear in form; the curve is shifted up (can pick up more CO2) when there is less binding of O2 to Hb (when it has fallen off); the partial pressure of CO2 in venous blood is about 47 and the partial pressure of CO2 in arterial blood is about 40 so not a huge difference