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Flashcards in Oxygen Transport Deck (13)
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what happens to DlCO in patients with severe anemia?

DlCO will decrease, b/c patient breathes faster
-cardiac output increases b/c want more O2 to get to more organs
-decreased Hb


what is the usual extraction of dissolved O2 from blood to tissues?

-this dissolved O2 alone is not enough to meet O2 consumption needs of the body
-thus, need O2 carried on Hb


how much O2 is bound to blood? (found by Hb and O2 bound to Hb)

Hb = 15 g/dL
O2 bound/g of Hb = 1.34 mL
so 20.1 mL O2 per 100 mL blood


what is the shape of the O2 dissociation curve?
-what happens if PO2 = 100 mmHg, 40 mmHg, and 26 mmHg?

sigmoid shape
-100 mmHg, there is 97-98% saturation, and dissolved O2 is only 1.5% of total O2
-40 mmHg, there is 75% saturation
-26 mmHg, there is 50% saturation (P50)


what are the 2 important features to remember about the oxygen dissociation curve/

1. sigmoid shape allows unloading of O2 to tissues without as large a change in PO2 as would occur if binding was not cooperative
-result is that PaO2 is maintained high, favoring diffusion of O2 to tissues where PO2 is low
2. plateau above 80 mmHg insures practically constant O2 content despite wide variations in PO2
-thus drop in PAO2 (in hypoxia) gives only 10% drop in CaO2


how does O2 carrying capacity (content) differ in polycythemia and anemia?

polycythemia = increased Hb (excessive production of RBC)
-the O2 content is higher
anemia = decreased Hb
-O2 content is lower

for both diseases, the saturation is the same at same pressures (around 100 mmHg = 100% saturation)


where is EPO made and how does it increase RBCs?

1. hypoxia causes increased hypoxia-inducible factor 1-alpha
2. induces renal fibroblasts to make EPO


how do PCO2, pH, temp, and 2,3-DPG/BPG (found in beta chain Hb) regulate O2 dissociation curve?

oxygen dissociation curve will shift right with:
-increased PCO2
-decreased pH
-increased temp
-increased 2,3-DPG (so more right if adult Hb, not fetal Hb)


what is hypoxic hypoxia characterized by? what can it be caused by?

low PaO2 (hypoxemia) and low CaO2 with normal extraction, thus low PvO2 (there isn't much O2 to be distributed)
-caused by high altitude, diffusion problems, and hypoventilation


what is stagnant hypoxia characterized by? what can it be caused by?

normal PaO2 and CaO2, increased extraction, thus low PvO2 (b/c more O2 is diffused to tissues)
-caused by sluggish circulation from low cardiac output, such as in CHF


what is histotoxic hypoxia characterized by? what can it be caused by?

normal PaO2 and CaO2 with reduced extraction and elevated PvO2 (b/c less O2 taken up by tissues)
-caused by poisoning of tissue metabolism by heavy metals, cyanide, or other toxins


what is anemic hypoxia characterized by? what can it be caused by?

normal PaO2 but low CaO2, with normal extraction thus low PvO2 (since even though PvO2 is low, CaO2 is low too, so extraction is normal)
-caused by Fe deficiency anemia or congenital hemolytic anemia like sickle cell anemia


what happens to the O2 dissociation curve during CO poisoning?

substitution of CO for O2 bound to Hb (higher affinity)
-thus, O2 binding capacity of Hb is reduced, and the O2 dissociation curve shifts to the left, decreasing O2 delivered to tissues

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