Kaplan respiration/circulation question

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Mantis Toboggin

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There is an accompanying passage to this, but the question is pretty much a discrete.

"If a native of the peruvian andes came down to sea level for the first time, what would be the net effect on his blood PCO2 levels?"

A. It would decrease B. It would increase C. It would increase and acidify the blood D. There would be no net effect

No one I've asked this question to has given me a reasonable expalantion for Kaplan's answer.

The correct answer to this question is D (no change).

Also, please mention what happened to respiratory rate upon descent, and mention why/how the Bohr and Haldane effects might affect this. Thanks.

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There is an accompanying passage to this, but the question is pretty much a discrete.

"If a native of the peruvian andes came down to sea level for the first time, what would be the net effect on his blood PCO2 levels?"

A. It would decrease B. It would increase C. It would increase and acidify the blood D. There would be no net effect

No one I've asked this question to has given me a reasonable expalantion for Kaplan's answer.

The correct answer to this question is D (no change).

Also, please mention what happened to respiratory rate upon descent, and mention why/how the Bohr and Haldane effects might affect this. Thanks.
I really don't think the Bohr or Haldane effect is necessary to answer this question. This is how I reasoned it: If I'm not mistaken, people who live in upper elevations where PO2 is considerably lower are able to acquire sufficient oxygen supply due to increase production in RBC's. By increasing RBC's, these individuals have more hemoglobin readily available, which in turn allows for more oxygen to be captured at a lower PO2. Compare this to someone at lower elevations with a smaller amount of hemoglobin. At higher elevations, these individuals would have to increase respiration to achieve adequate oxygen supply.

At lower elevations, where PO2 is higher, the peruvian (due to more Hb) would attain higher blood 02 levels (compared to the normal population). However, O2 is essentially a nutrient and so there's no need to adjust the body's metabolic rate to dispose of it. Oxygen diffuses from hemoglobin to tissues (where myoglobin is readily available); because there is a fixed amount of myoglobin, I suppose at some point myoglobin will be saturated and thus, the remaining O2 will remain bound to hemoglobin. The rate of respiration for this individual should remain the same and therefore, CO2 blood levels should remain constant as well.

By contrast, this is entirely different when comparing an individual who consciously (or unconsciously) alters their rate of respiration. For example, breathing rapidly causes more CO2 to be expelled from the blood. This displaces the equilibrium achieved in our body. If you recall the equilibrium between CO2 dissolved in water (CO2 + H2O --> H2CO3 --> HCO3- + H+), a reduction in CO2 levels will shift the equilibrium causing both HCO3- and H+ to be consumed; higher pH blood levels (alkalosis). If the individual inhaled less, CO2 levels would build up (excess) and result in the accumulation of H+ (acidosis).

The Haldane and Bohr effect play an important role in regulating hemoglobin affinity for O2. In a nut shell, near tissues, where H+, CO2, and O2 is low, Hemoglobin has low affinity for O2 (tense state) and thus O2 bound to hemoglobin is readily released to metabolically active tissues where it's needed. In the lungs where O2 is freely available and CO2 is low, hemoglobin has high affinity for O2 (relaxed state; more O2 to Hb) and CO2 is able to readily diffuse down its concentration gradient (exhalation).
 
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Hey, thanks for the reply but I don't think that explanation is correct. The Kaplan answer specifically states that breathing rate does, in fact, decrease. The following is my logic of the answer though I'm not sure if I'm right:

Due to the Haldane effect, po2 would be higher in the blood initially. Subsequently pco2 would initially be lower (decreased affinity of HB for co2), so the body would decrease breathing rate to counteract this, thereby increasing pco2 to metabolically constant values.

And just for my own knowledge, is it correct to say that in the presence of more o2, more o2 will be more tightly bound to hemoglobin, and more co2 will be unloaded into the blood plasma (making bicarbonate and h+)? I know this is normally the case in the lungs, like you mentioned, but is it the case when overall blood o2 levels are higher (as with this example)?
 
I'm not entirely sure I agree with their reasoning, but then again it's difficult without passage information.

And just for my own knowledge, is it correct to say that in the presence of more o2, more o2 will be more tightly bound to hemoglobin, and more co2 will be unloaded into the blood plasma (making bicarbonate and h+)? I know this is normally the case in the lungs, like you mentioned, but is it the case when overall blood o2 levels are higher (as with this example)?
You're partly right. Very little CO2 exists in blood plasma though (because it is nonpolar); Immediately after it's released from tissues, it diffuses into a RBC where it can either bind to Hb to form a carbamate; this stabalizes the deoxy Hb form, causing O2 release. CO2 in the presence of H2O and Carbonic Anhydrase enzyme in RBC's converts to bicarbonate and H+. H+ can also bind to Hb to reduce H+ blood content (also stabilizes deoxy Hb form). HCO3- is an important constituent of blood plasma to maintain optimal blood pH of 7.35-7.4.
 
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Just want to contribute to this discussion because I don't quite understand what is going on myself. I agree with Czarcasm that people who live at high altitudes have made long-term accommodations to the smaller pO2 at higher altitudes (higher RBC count, more 2,3 BPG).

I guess, now that you told me, that it makes sense that their breathing rate decreases when they move to a lower altitude. My reasoning is that they have more hemoglobin and more 2,3-BPG (which decreases hemoglobin's affinity for O2) and can take up more oxygen per breath that someone with less. But I don't understand the effect this will have on CO2 levels.
 
I'm not entirely sure I agree with their reasoning, but then again it's difficult without passage information.

You're partly right. Very little CO2 exists in blood plasma though (because it is nonpolar); Immediately after it's released from tissues, it diffuses into a RBC where it can either bind to Hb to form a carbamate; this stabalizes the deoxy Hb form, causing O2 release. CO2 in the presence of H2O and Carbonic Anhydrase enzyme in RBC's converts to bicarbonate and H+. H+ can also bind to Hb to reduce H+ blood content (also stabilizes deoxy Hb form). HCO3- is an important constituent of blood plasma to maintain optimal blood pH of 7.35-7.4.


That was actually my answer, though I can give you their answer word for word if you want. Their explanation didn't help me though. They did mention that normal homeostatic functions such as the Bohr effect would contribute to no change in pco2, though I think they're referring more to the Haldane effect. If anyone else can give a better answer please let me know.

Also to the poster above, doesn't increasing bpg cause a right shift on the HB curve? If anything wouldn't we expect a left shift?
 
That was actually my answer, though I can give you their answer word for word if you want. Their explanation didn't help me though. They did mention that normal homeostatic functions such as the Bohr effect would contribute to no change in pco2, though I think they're referring more to the Haldane effect. If anyone else can give a better answer please let me know.

Also to the poster above, doesn't increasing bpg cause a right shift on the HB curve? If anything wouldn't we expect a left shift?
The Bohr effect is essentially the decreased affinity for Hb due to Oxygen due to the presence of H+. As I mentioned, the H+ binds to Hb, stabilizing the deoxygenated form (causing O2 release). 2,3-BP as mentioned above also stabilizes the deoxy form of Hb, thus enabling more H+ to bind to Hb. In either case, binding H+ allows more CO2 to be dissolved in the blood in the form of HCO3- (LeChatlier's Principle); This is the haldane effect. However, neither are really relevant to answering this question. Given that we're being told this person's respiratory rate is decreased, I'm a little confused myself as to why PCO2 levels wouldn't rise. Ultimately, blood CO2 levels is regulated by our respiratory rate; the amount of CO2 dissolved in blood (as HCO3-) is in large part controlled to how much CO2 is being exhaled at any given moment. This is why people who breath less frequently have higher blood CO2 levels, causing an increase in blood H+ (acidosis). The only appropriate reasoning for no change in CO2 levels given a decreased respiratory rate is if somehow this persons metabolic rate also decreased proportionally.

What was their reasoning for why the respiratory rate was decreased? If it's not too much trouble for you, I'd be interested in reading their explanation.
 
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The Bohr effect is essentially the decreased affinity for Hb due to Oxygen due to the presence of H+. As I mentioned, the H+ binds to Hb, stabilizing the deoxygenated form (causing O2 release). 2,3-BP as mentioned above also stabilizes the deoxy form of Hb, thus enabling more H+ to bind to Hb. In either case, binding H+ allows more CO2 to be dissolved in the blood in the form of HCO3- (LeChatlier's Principle); This is the haldane effect. However, neither are really relevant to answering this question. Given that we're being told this person's respiratory rate is decreased, I'm a little confused myself as to why PCO2 levels wouldn't rise. Ultimately, blood CO2 levels is regulated by our respiratory rate; the amount of CO2 dissolved in blood (as HCO3-) is in large part controlled to how much CO2 is being exhaled at any given moment. This is why people who breath less frequently have higher blood CO2 levels, causing an increase in blood H+ (acidosis). The only appropriate reasoning for no change in CO2 levels given a decreased respiratory rate is if somehow this persons metabolic rate also decreased proportionally.

What was their reasoning for why the respiratory rate was decreased? If it's not too much trouble for you, I'd be interested in reading their explanation.

I don't have access to my computer right now but check back tomorrow, I'll post it here.

Also you touched upon what I said in my answer. Up in the mountains this person has a basal metabolic pco2 and po2 level. Only pco2 and the carbonic anhydrase determine the breathing rate-- namely the medulla oblangata does so.

So we know, for a fact, that the Peruvian's breathing rate will only decrease if pco2 levels are below BASAL metabolic rates.

Given that he breathes in more oxygen, intuitively we'd say that his breathing rate shouldn't be affected. However, the Haldane effect results in more pco2 in the form of h+ and bicarb present in the blood plasma since its affinity for HB decreased, so by conjunction more pco2 is being breathed out.

The effect is that pco2 levels are lowered (similar to the Bohr effect lowering our total blood po2 levels).

The question asks for the *net* effect, so breathing rate would have to decrease to increase pco2. So the net result is that pco2 is the same as the metabolic original rate. That's my reasoning if it makes more sense.
 
I don't have access to my computer right now but check back tomorrow, I'll post it here.

Also you touched upon what I said in my answer. Up in the mountains this person has a basal metabolic pco2 and po2 level. Only pco2 and the carbonic anhydrase determine the breathing rate-- namely the medulla oblangata does so.

So we know, for a fact, that the Peruvian's breathing rate will only decrease if pco2 levels are below BASAL metabolic rates.

Given that he breathes in more oxygen, intuitively we'd say that his breathing rate shouldn't be affected. However, the Haldane effect results in more pco2 in the form of h+ and bicarb present in the blood plasma since its affinity for HB decreased, so by conjunction more pco2 is being breathed out.

The effect is that pco2 levels are lowered (similar to the Bohr effect lowering our total blood po2 levels).

The question asks for the *net* effect, so breathing rate would have to decrease to increase pco2. So the net result is that pco2 is the same as the metabolic original rate. That's my reasoning if it makes more sense.


Does this mean that his pO2 is the same as well? Also, could we simarily reason that the pco2 for someone who goes from normal altitude to the peruvian mountains would maintain normal pco2 levels long term?
 
I believe it's because the body breathes depending on CO2 levels not O2 levels so the body would make adjustments to keep CO2 constant...although if the breathing rate stayed constant as if it were in high altitude then CO2 would go up cause there would be more O2 to use (I think).
 
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Does this mean that his pO2 is the same as well? Also, could we simarily reason that the pco2 for someone who goes from normal altitude to the peruvian mountains would maintain normal pco2 levels long term?


With regards to pO2, I do believe that they would also be at metabolically constant values. My reasoning is that breathing rate decrease means a concomitant decrease in pO2 levels that were initially high (due to the Bohr effect and increased levels of pco2). Feel free to correct me if I'm wrong, since my review books never went into great detail on the Bohr/Haldane effects besides the effects on the HB sat curve.

And for a person who goes up, breathing rate would increase (fewer o2 molecules, higher amount of pco2 in blood so body acclimates by increasing breathing rate, thereby decreasing pco2/h+ levels). In the long term, I do think that the levels of both are metabolically constant. This seems to make sense since people who get mountain sickness suffer from respiratory alkalosis( breathing in too much o2, pH increases too much).
 
With regards to pO2, I do believe that they would also be at metabolically constant values. My reasoning is that breathing rate decrease means a concomitant decrease in pO2 levels that were initially high (due to the Bohr effect and increased levels of pco2). Feel free to correct me if I'm wrong, since my review books never went into great detail on the Bohr/Haldane effects besides the effects on the HB sat curve.

And for a person who goes up, breathing rate would increase (fewer o2 molecules, higher amount of pco2 in blood so body acclimates by increasing breathing rate, thereby decreasing pco2/h+ levels). In the long term, I do think that the levels of both are metabolically constant. This seems to make sense since people who get mountain sickness suffer from respiratory alkalosis( breathing in too much o2, pH increases too much).

Yeah I think everyone is overthinking this. I think the body would just long term adjust to its homeostatic levels
 
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