How does hyperventilation lower Oxygen levels?

[deleted647690]

Berkeley Review has a question, "In order to hold their breath for a longer duration, swimmers hyperventilate before swimming. This can be dangerous because:"

Answer was that lows pCO2 permits one to hold their breath, but it may lower PO2 levels and cause unconsciousness.'


How does hyperventilation lower PO2? After looking at another thread about hyperventilation, it looks like plenty of people would disagree with this. Instead, the other thread I looked at had people saying that pO2 would be increased.

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[studyingtoo714]

Anyone? Ill take a stab at it but man I am grasping at straws. So if the total pressure of gases comprises of PCO2 and PO2 wouldn't that mean that less of one gives you more room for the other? Help guys...please

 

[aldol16]

Use the bicarbonate buffer system in conjunction with the Bohr effect. Can you explain it using those two key concepts?

 

[mw18]

In the brain, oxygen is provided where there is CO2. If you get rid of CO2, you recruit less oxygen to the brain and you pass out.

And I haven't looked at pulm in a while, but these things are true. A decrease in CO2 raises pH. A rise in pH causes more tight binding with hemoglobin (shift left). This would create less free oxygen in the blood. Hence, lower PO2. The bottom line is the left shift. The x axis is pO2, so if it shifts to the left, you have less PO2.

 

[ohioishome]

So hypo ventilation would cause an increase in pCO2 and decrease in pH? How would that affect the affinity for O2 on Hb

 

[aldol16]

So hypo ventilation would cause an increase in pCO2 and decrease in pH? How would that affect the affinity for O2 on Hb

Again, look up the Bohr effect. It's a pretty important principle.

 

[studyingtoo714]

In the brain, oxygen is provided where there is CO2. If you get rid of CO2, you recruit less oxygen to the brain and you pass out.

And I haven't looked at pulm in a while, but these things are true. A decrease in CO2 raises pH. A rise in pH causes more tight binding with hemoglobin (shift left). This would create less free oxygen in the blood. Hence, lower PO2. The bottom line is the left shift. The x axis is pO2, so if it shifts to the left, you have less PO2.

That makes so much more sense now. Thank you. I still need to go over my shift but this can certainly explain it better than what I was thinking earlier

 

[5words]

That makes so much more sense now. Thank you. I still need to go over my shift but this can certainly explain it better than what I was thinking earlier

careful, that's only true for coronary blood flow, i believe it;s called local autoregulation where coronary blood vessel build up waste to dilate the vessel around them to acquire more O2. I am still not understanding the question since it pertains to the brain. Hyper ventilation as a rule always decrease PCO2 whilst indirectly increasing the PO2. (because you are breathing out CO2 and breathing in O2) .. So, their PO2 might be decreasing because you dont gain additional O2 under water? and since they are using ATP (exercising) , cellular respiration is probably using up the reserve of O2?

So as a rule, HyperVentilation always increases PO2 whilst decreasing PCO2.

I wonder what @aldol16 think.. am i right pal?

 

[5words]

nvm i was right, So hyperventilation does indeed increase the PO2 whilst decreasing the PCO2, however because they are experiencing and not gaining any additional oxygen under water... Their O2 reserve prior diving in is tremendously decreasing. Not be confused with Local autoregulation which only pertains to coronary Blood Flow.

 

[Sammyj98]

That makes so much more sense now. Thank you. I still need to go over my shift but this can certainly explain it better than what I was thinking earlier

Hey I see your question already got answered but I'll throw in my own two cents for a little more perspective.
Yeah, all about the Bohr effect. Protons are hemoglobin inhibitors, which means the lower your blood pH the less tightly hemoglobin binds to oxygen. This may seem like a bad thing but actually it's pretty key. The partial pressure of oxygen in the pulmonary capillaries is so high that a lowered affinity doesn't have a very significant effect on saturation. So even when your blood is on the acidic side of the spectrum pretty much all your arterial hemoglobin are bound to O2. However! when it reaches the tissues is different. At lower pO2 there is way more variability in saturation. The end effect is that if the hemoglobin are tightly bound to O2 they just don't let it go. So you have hypoperfusion not because O2 isn't getting into circulation but because it isn't getting out.

The phenomenon that ties all this together is the bicarbonate buffering system. CO2 is converted to carbonic acid to make it easier to transport in liquid (an acid should dissolve better in water than a gas, right?). Well, you make CO2 into carbonic acid, it dissociates into bicarbonate (it's conjugate base) and a proton and whammo, acidification. So the more CO2/bicarbonate in your blood the more protons, the lower the pH, the more inhibited the hemoglobin, the lower the affinity for O2, the less tightly bound, the more easily donating O2 to tissues, and the better the perfusion. Also, since hemoglobin are already essentially saturated with O2 hyperventilating doesn't do much for O2 transport. It DOES however effect CO2 release. The more you exhale the less CO2. This is why hyperventilation causes you to lose O2 in tissues.

cheers!

 

[5words]

Hey I see your question already got answered but I'll throw in my own two cents for a little more perspective.
Yeah, all about the Bohr effect. Protons are hemoglobin inhibitors, which means the lower your blood pH the less tightly hemoglobin binds to oxygen. This may seem like a bad thing but actually it's pretty key. The partial pressure of oxygen in the pulmonary capillaries is so high that a lowered affinity doesn't have a very significant effect on saturation. So even when your blood is on the acidic side of the spectrum pretty much all your arterial hemoglobin are bound to O2. However! when it reaches the tissues is different. At lower pO2 there is way more variability in saturation. The end effect is that if the hemoglobin are tightly bound to O2 they just don't let it go. So you have hypoperfusion not because O2 isn't getting into circulation but because it isn't getting out.

The phenomenon that ties all this together is the bicarbonate buffering system. CO2 is converted to carbonic acid to make it easier to transport in liquid (an acid should dissolve better in water than a gas, right?). Well, you make CO2 into carbonic acid, it dissociates into bicarbonate (it's conjugate base) and a proton and whammo, acidification. So the more CO2/bicarbonate in your blood the more protons, the lower the pH, the more inhibited the hemoglobin, the lower the affinity for O2, the less tightly bound, the more easily donating O2 to tissues, and the better the perfusion. Also, since hemoglobin are already essentially saturated with O2 hyperventilating doesn't do much for O2 transport. It DOES however effect CO2 release. The more you exhale the less CO2. This is why hyperventilation causes you to lose O2 in tissues.

cheers!

I am not understanding your last sentence, i thought Hb affinity for O2 was low in tissue no matter the condition? because of myoglobin having a greater affinity for O2 than Hemoglobin..

"This is why hyperventilation causes you to lose O2 in tissues." did you meant, the tissue are gaining O2 ? or?

 

[aldol16]

careful, that's only true for coronary blood flow, i believe it;s called local autoregulation where coronary blood vessel build up waste to dilate the vessel around them to acquire more O2. I am still not understanding the question since it pertains to the brain. Hyper ventilation as a rule always decrease PCO2 whilst indirectly increasing the PO2. (because you are breathing out CO2 and breathing in O2) .. So, their PO2 might be decreasing because you dont gain additional O2 under water? and since they are using ATP (exercising) , cellular respiration is probably using up the reserve of O2?

The immediate effect might increase the amount of O2 available in your bloodstream, but you have to consider the bicarbonate buffer mechanism. Decreasing CO2 also raises pH, which raises the binding affinity of hemoglobin. So basically, you offload less O2 in your tissues, due to the so-called Bohr effect.

Remember that in this case, you're not only hyperventilating but you're doing it right before you hold your breath to swim. That leaves your blood in an alkaline state which shifts the hemoglobin binding curve, as per the Bohr effect. If you're unloading less O2 to the tissues, that means you have O2 in your body, but your tissues just aren't getting them. This is, of course, bad. Take a look at this:

http://courses.washington.edu/conj/resp/BreathHolding.htm

 

[aldol16]

I am not understanding your last sentence, i thought Hb affinity for O2 was low in tissue no matter the condition? because of myoglobin having a greater affinity for O2 than Hemoglobin..

It's always relatively low in the tissue - but that doesn't mean you're unloading the same amount of O2 all the time. Shifting the binding curve for hemoglobin to the left means that hemoglobin now has a greater affinity for O2 and thus will retain more of it.

 

[5words]

The immediate effect might increase the amount of O2 available in your bloodstream, but you have to consider the bicarbonate buffer mechanism. Decreasing CO2 also raises pH, which raises the binding affinity of hemoglobin. So basically, you offload less O2 in your tissues, due to the so-called Bohr effect.

But should the increase in Hb affinity for O2 really matters? Increase affinity just means that more O2 are being taken up by the blood at the aveali, When it comes to the tissue, the affinity of Myoglobin is so great that it' will always take all of Hb hemoglobin from it regardless of Hb affinity for it;s O2s. So, if you think about it, The increase Affinity just allow hemoglobin to load more O2 at the lungs , thereby increase the amount of O2 in your Tissue because of Mb affinity to O2. or am i missing something?

It's always relatively low in the tissue - but that doesn't mean you're unloading the same amount of O2 all the time. Shifting the binding curve for hemoglobin to the left means that hemoglobin now has a greater affinity for O2 and thus will retain more of it.

think i am starting to get this.. but i just dont undertsand why the minute decrease in CO2 ought to overide the effect of Mb.

 

[aldol16]

But should the increase in Hb affinity for O2 really matters? Increase affinity just means that more O2 are being taken up by the blood at the aveali, When it comes to the tissue, the affinity of Myoglobin is so great that it' will always take all of Hb hemoglobin from it regardless of Hb affinity for it;s O2s. So, if you think about it, The increase Affinity just allow hemoglobin to load more O2 at the lungs , thereby increase the amount of O2 in your Tissue because of Mb affinity to O2. or am i missing something?

It's not all taken up by myoglobin. Look up hemoglobin binding curves that have % O2 bound at the alveoli and the % O2 bound at the tissues. The % O2 bound at the alveoli isn't going to change much by the shift because it's close to 100% at most times. But it's the % O2 bound after the Hb goes through the tissues that matters. The difference is how much is offloaded. Please look up the Bohr effect. I can't reproduce all the graphs here due to time, so I think you'll get a more fulfilling experience from reading it. And look at the link I posted above with the data in it. It's bolded.

 

[5words]

It's not all taken up by myoglobin. Look up hemoglobin binding curves that have % O2 bound at the alveoli and the % O2 bound at the tissues. The % O2 bound at the alveoli isn't going to change much by the shift because it's close to 100% at most times. But it's the % O2 bound after the Hb goes through the tissues that matters. The difference is how much is offloaded. Please look up the Bohr effect. I can't reproduce all the graphs here due to time, so I think you'll get a more fulfilling experience from reading it. And look at the link I posted above with the data in it. It's bolded.

This paper is confirming what you just said : https://www.ncbi.nlm.nih.gov/pubmed/1909316

So i am confused.. So which is it? Hyperventillation doesnt increase PO2? is that final?

 

[5words]

@aldol16 what about he following .. Hyperventilating decrease PCO2 levels in blood, increases (insignificant increase) PO2 level in the Blood but decreases those of the tissues? is that correct?

 

[aldol16]

So i am confused.. So which is it? Hyperventillation doesnt increase PO2? is that final?

@aldol16 what about he following .. Hyperventilating decrease PCO2 levels in blood, increases (insignificant increase) PO2 level in the Blood but decreases those of the tissues? is that correct?

Well, I'm not sure I understand how much O2 is in the blood under hyperventilation conditions and non-hyperventilation conditions. All you're doing when you're breathing really quickly is improving movement through your alveolar space. But that doesn't necessarily force more O2 into the blood. That is, it allows equilibrium between your blood gas concentration and alveolar O2 concentration to be reached quicker because of the greater movement, but I can't see chemically how it would force more O2 into the blood.

I do know that given the bicarbonate buffer system and the so-called Bohr effect, the amount of O2 offloaded in the tissue decreases when you're hyperventilating, which is dangerous.

 

[mw18]

careful, that's only true for coronary blood flow, i believe it;s called local autoregulation where coronary blood vessel build up waste to dilate the vessel around them to acquire more O2. I am still not understanding the question since it pertains to the brain. Hyper ventilation as a rule always decrease PCO2 whilst indirectly increasing the PO2. (because you are breathing out CO2 and breathing in O2) .. So, their PO2 might be decreasing because you dont gain additional O2 under water? and since they are using ATP (exercising) , cellular respiration is probably using up the reserve of O2?

So as a rule, HyperVentilation always increases PO2 whilst decreasing PCO2.

I wonder what @aldol16 think.. am i right pal?

That's not only true for coronary blood flow. (https://www.ncbi.nlm.nih.gov/books/NBK53082/) But CO2 definitely isn't the only reason for it.

All three of these articles indicate a decrease in both pco2 and po2 with hyperventilation, albeit they aren't perfect articles or this situation. But it makes sense. Look at the graph.

https://www.ncbi.nlm.nih.gov/pubmed/8051307
https://www.ncbi.nlm.nih.gov/pubmed/1909316
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1343723/

At every level of oxygen saturation, having a lower CO2 leads to a lower PO2. This process is generally thought about in a kind of reverse way, that for each level of po2, what is the O2 saturation at that point.

 

[deleted647690]

Alright, so essentially, the blown off CO2 via hyperventilation prevents release of the available O2 into the tissues, and that is why hyperventilation before going underwater is bad? Thank you for clearing that up guys, I really appreciate all the help that people on this board provide

 

[studyingtoo714]

In the brain, oxygen is provided where there is CO2. If you get rid of CO2, you recruit less oxygen to the brain and you pass out.

And I haven't looked at pulm in a while, but these things are true. A decrease in CO2 raises pH. A rise in pH causes more tight binding with hemoglobin (shift left). This would create less free oxygen in the blood. Hence, lower PO2. The bottom line is the left shift. The x axis is pO2, so if it shifts to the left, you have less PO2.

Best explanation ever

 

[studyingtoo714]

For sure. Thank you for everyone's input. It was very helpful