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Hyperventilation

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Yes, brief pre-dive hyperventilation may be a good compromise between comfort and safety. Ama divers and Polynesian native divers also use different levels of hyperventilation. It shows it may remain relatively safe, while allowing for efficient serial diving. It does not tell much about whether less comfortable dives would not allow for longer times, or what ventilation is needed for maximal performances.
 
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if I see the local spearo again (!, pls. ignore smart ass comment opportunity) I'll ask him why no more than three breaths (I know why, I just want his explanation).

I agree with Wes that repetitive dives are tiring, and surface relaxation is often surface tension, wave/current fighting etc that never seems to unload the last dives effort. I now never do the 3 deep breaths and dive, mainly 'cause I've been told not to here rather than find my own way. The closest i get is the 3 to 5 big purges (hyperventilations) with the mouth and airway very open, via the snorkel, and then rest another minute breathing slowly before diving. This is very similar to what Wes mentions. It helps me relax, and is never enough to get me "tingly". The normal breathing after helps my heart slow back down, and I can almost feel in my stomach/throat, a very light yawn type sensation (impossible to describe), something that tells me when I'm ready to do the final full inhalation before the dive.

Just a beginners perspective, for what it's worth.
 
Eric: did you hyperveltilate before your recent -67m dive at the blue hole?
Howard

I am starting my dives on relatively low CO2. Although I do not do 'purges', the length of my breathe-up lowers my CO2 quite a lot. However I never get tingling in my extremities or signs of very low CO2.

I also know that my method of breathing does not increase my heart rate hardly at all, compared to normal breathing, so this large increase in heart rate that trux keeps talking about is absent for me. Also, changing the bohr effect may actually be beneficial, since I want to deprive my body of oxygen at the start of the dive for as long as possible, until the full dive reflex has kicked in near the bottom. Then and only then do I want O2 to start to become available. Until then it is fine to keep it locked up in the blood.

Further, diving somewhat hypocapnic can create a huge advantage at the end of the dive, as it becomes possible to take a single inhale and hold it (single hook breath). Upon surfacing I inhale, and hold my breath, crunch my abs. That's it, no more breaths. I don't need to take any more breaths because I don't have that much CO2 to get rid of. During high CO2 dives, one must basically breathe extremely rapidly upon surfacing because it is almost impossible to take one breath and hold it.

Further, there is the factor of enjoyment. During recreational diving, if I'm getting contractions on every dive, why would I even want to be in the water? I'd rather go skiing or something. Similarly if you teach a beginner to dive and they get horrid contractions on every dive (early in the dive), do you really think they will stick with the sport?

Certainly high CO2 can result in good performances. Diving on moderate CO2 can reach similar performances with greater comfort, if done properly. Diving on very low CO2, where one feels tingling in the extremities, I think is very bad, very dangerous and leads to very poor performances.

In addition, the amount of burn in the lungs varies not only with the CO2 you start with, but also the lung volume you start with. Starting on less than a full inhale or FRC, you get much less burn in your lungs on a dive, because you don't generate much CO2 on the descent and so there is no CO2 to compress. For this reason, an FRC dive is always much more comfortable in terms of feelings in the lungs. Occasionally I try a full inhale or packing dive, and it feels awful, it reminds me of the old days.
 
I agree that starting your dive slightly hypocapnic means a more comfortable dive as the contractions start later ,but i have also noticed that when i start my dive with high co2, contractions(normaly) start ealier but are milder and easier to cope with.

I am starting my dives on relatively low CO2. Although I do not do 'purges', the length of my breathe-up lowers my CO2 quite a lot. However I never get tingling in my extremities or signs of very low CO2.

I also know that my method of breathing does not increase my heart rate hardly at all, compared to normal breathing, so this large increase in heart rate that trux keeps talking about is absent for me. Also, changing the bohr effect may actually be beneficial, since I want to deprive my body of oxygen at the start of the dive for as long as possible, until the full dive reflex has kicked in near the bottom. Then and only then do I want O2 to start to become available. Until then it is fine to keep it locked up in the blood.

Further, diving somewhat hypocapnic can create a huge advantage at the end of the dive, as it becomes possible to take a single inhale and hold it (single hook breath). Upon surfacing I inhale, and hold my breath, crunch my abs. That's it, no more breaths. I don't need to take any more breaths because I don't have that much CO2 to get rid of. During high CO2 dives, one must basically breathe extremely rapidly upon surfacing because it is almost impossible to take one breath and hold it.

Further, there is the factor of enjoyment. During recreational diving, if I'm getting contractions on every dive, why would I even want to be in the water? I'd rather go skiing or something. Similarly if you teach a beginner to dive and they get horrid contractions on every dive (early in the dive), do you really think they will stick with the sport?

Certainly high CO2 can result in good performances. Diving on moderate CO2 can reach similar performances with greater comfort, if done properly. Diving on very low CO2, where one feels tingling in the extremities, I think is very bad, very dangerous and leads to very poor performances.

In addition, the amount of burn in the lungs varies not only with the CO2 you start with, but also the lung volume you start with. Starting on less than a full inhale or FRC, you get much less burn in your lungs on a dive, because you don't generate much CO2 on the descent and so there is no CO2 to compress. For this reason, an FRC dive is always much more comfortable in terms of feelings in the lungs. Occasionally I try a full inhale or packing dive, and it feels awful, it reminds me of the old days.
 
Yes, I agree, these numbers may sound very impressive - The difference between 120 and 130 is roughly 8%! Who would not want improving his/her PB by 8%!.

The values are misleading, though. The normal atmospheric pressure at sea level is 760 mmHg (the normal O2 partial pressure in dry air is ~21% which equals to the partial pressure of ~160 mmHg, much less in alveoli). So by increasing the alveolar pressure from 120 mmHg to 130 mmHg, it makes 10 mmHg difference, which then represents 1.3%, and is already not as impressive as the 8%.

This 1.3% represents roughly 100 ml of oxygen at lungs of 8 l of total capacity. The nominal resting O2 consumption is 250 ml/min, and only part of the oxygen available in lungs can be used, let's assume it is 50%. That would mean we can use 50 extra ml of O2 which could increase the apnea by 12 seconds. And I am not even sure that the alveolar oxygen saturation (exhale air) can drop as deep as 50%. I think values around 70% - 80% of the original level are more realistic. That vould mean gain of some 5-7 s.
I disagree with your numbers. We're already talking ppO2, so why are you dividing by atmospheric a second time? Also, you're talking about quantities of oxygen in the lungs, whereas this is talking about the quantity of O2 aready taken up by the alveoli. In other words, you're suggesting that the performance improvement is (1.3 / 2)/8 times smaller than I am reading it. It may be that the actual improvement won't be as big as eight percent, but that eight percent would take me from six to six and a half minutes in statics. Even half that would be worth considering.

Also, your assumption that that extra O2 storage 'replaces' CO2 is flawed. As you can read from my original post, this increase comes with little or no affect on CO2 stores. Unbound hemoglobin is where this O2 appears from, there is no replacement or displacement of CO2.
 
I disagree with your numbers. We're already talking ppO2, so why are you dividing by atmospheric a second time? Also, you're talking about quantities of oxygen in the lungs, whereas this is talking about the quantity of O2 aready taken up by the alveoli. In other words, you're suggesting that the performance improvement is (1.3 / 2)/8 times smaller than I am reading it. It may be that the actual improvement won't be as big as eight percent, but that eight percent would take me from six to six and a half minutes in statics. Even half that would be worth considering.

Also, your assumption that that extra O2 storage 'replaces' CO2 is flawed. As you can read from my original post, this increase comes with little or no affect on CO2 stores. Unbound hemoglobin is where this O2 appears from, there is no replacement or displacement of CO2.

I am sorry, but you are wrong in all points. My calculation is correct. PAO2 is partial alveolar oxygen pressure and represents the part of oxygen in the 760 mmHg of the total atmospheric pressure of the air inside the alveoli. That's unlike PaO2 (lowercase 'a'), which is partial arterial oxygen pressure which then describes the pressure of oxygen in arteries leaving the alveoli. However, the values are very close to each other, so even if your values were for the PaO2 and not PAO2 as you previously quoted, the math would be the same.

In my calculation, the value is divided only once. It is a quite simple math - I compare normal resting pressure you mentioned (120 mmHg) with the one after hyperventilation (130 mmHg). It makes pressure difference of 10 mmHg of pure oxygen. The alveoli are not filled with pure oxygen though, and definitely not with any gas of pressure of 130 mmHg. They are filled with air (well, air + CO2 + water vapor) at the atmospheric pressure - hence with 760 mmHg of gas pressure. Please note, that I do not even assume any packing or forced inhalation. If your values were measured after packing or forced inhalation, I would then need to use significantly higher value than the normal atmospheric pressure of 760 mmHg, and that would reduce the result even much more!

So the result of 1.3% of difference (100% * 10 mmHg / 760 mmHg) is perfectly OK, and in fact even overestimated, because I am practically sure your data do not come from tidal inhalation, but from a forced or even packed inhalation. In such case the value could be even below 1%.

Furthermore your calculation assuming 6% to 8% performance increase from the 10 mmHg PAO2 difference, assuming it would make ~30s at 6 minutes is very wrong too even if it really were 6% - 8% (which is definitely not the case). You do not hold your breath (only) thanks to the air you have in your lungs. Primarily it is the oxygen that is already stocked in your blood that allows for it. So if you only manage to increase the O2 content in your lungs, you won't manage saturating your venous blood without a good level of hyperventialtion (which then has many more side effects limitating the O2 intake). So even if it were 6% - 8% of increase of O2 in lungs (which it is not), it could make effect of only less than half of this value on the breath-hold length. However, as I wrote, the value is completely wrong anyway.

You are also absolutely wrong that the O2 does not replace any CO2. What else could it then replace if not CO2 in the alveoli??? The part of oxygen in air is 21% and constant. That represents 160 mmHg of PO2. In alveoli the 160 mmHg of PO2 are reduced by increased content of water vapor and especially by CO2, so normally it is just above ~100 mmHg.

So when you breathe air, you can only increase the PAO2 (and the content of oxygen in alveoli) by washing out the excess CO2. And that's indeed what happens with hyperventilation (or a purge breath) - in air there is 0.03% - 0.06% of CO2, in the normal alveolar air, there is around 5%-6%, so by increased ventilation you reduce the CO2 content and increase the partial pressure of oxygen (and the partial pressure of nitrogen, of course, too).

It means the 100 ml of difference in O2 and CO2 are perfectly correct. Additionally, as already mentioned, it assumes achieving the difference of 120 to 130 mmHg by only a single purge breath. You wrote about several hyperventilation breaths - that would wash out accordingly more CO2.

So, I am sorry to play a smart ass, but my calculation is all right, and the resulting difference of 5s to 12s is even highly overshot, because in reality the value would be even further lowered by several already mentioned but not calculated effects, and quite likely the result may be then negative.
 
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Eric, I do agree with most of your views, and I am not trying to deny the hyperventilation the right to exist. I am just trying to change the traditional opinion on hyperventilation. Most people avoid hyperventilation because of safety concerns, while being persuaded it allows for performance enhancements.

While I do not exclude there may be some schema where the benefits of moderated hyperventilation overweight its negative effects, I see that the possible positive outcome is much smaller than generally expected, and often inexistent. In most cases the result of hyperventilation may have rather serious negative impact on the maximal possible length of apnea.

When I spoke about the shifted Bohr effect, I knew it has also advantages. Its down side is though that it makes more difficult the oxygenation of cells and most importantly also of myoglobin (see the links to studies showing it, in my earlier post). So paradoxically, when hyperventilating you may bring your organism into certain level hypoxemia (not only cerebral hypoxemia). Well, that's extreme case, and I am sure it does not fully apply to the degree of hyperventilation you use, but I hope that everyone understands what message I am trying to pass - the performance enhancement effects of hyperventilation are much, much, much less than they appear to be, and often they are even negative.

Now the comfort and safety are quite different topics, that I actually did not really want to argue about here in this thread. However, the worst is that even if you explain beginners that they should avoid hyperventilation and why, they will hyperventilate anyway subconsciously. If you allow them certain level of hyperventilation, they will subconsciously do more, soon get accustomed to it, overdo it even more (especially when in stress) and can get themselves into big troubles very easily.
 
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Trux
I know you are right about the use of hyperventilation and stress. At the end of a cold water day (most days up here), and having been in the water for a couple of hours, I can't help but hyperventilate some. I'm breathing harder because I am tired and I'm breathing harder because I'm cold, and I still want to try just a few more drops before giving up and getting back into the boat. It's at those times I have the hardest time with it. On the safe side, I must say that by then, dives are (very) short and shallow. I simply can't do more. ; )

On another note: What about individual biolgoical variation?
I know that there is a lot of variability in human physiology, so where does that play into divers learning their limits?
For this, I'm referring not to training beginners, but rather to more experienced divers learning their own limits. There is a normal range for physiological processes, with some are more basic, and others acidic, just like some are more tolerant of hypoxia or hypercapnea than others.
This occurred to me this morning, and am wondering about how much as been done with it.

Howard
 
Trux: Read the DAN Workshop report.

The alveoli are filled with gas at atmospheric pressure, otherwise they collapse. You're suggesting they're at less than one fifth atmospheric and that's just crazy. Even if they weren't it's still a partial pressure of oxygen. To get the partial pressure of oxygen, you don't divide by atmospheric pressure a second time.

And trux, these aren't my numbers. They are from John R. Feiner, MD. As I suggested, read the report.
 
The alveoli are filled with gas at atmospheric pressure, otherwise they collapse. You're suggesting they're at less than one fifth atmospheric and that's just crazy.
Where did I suggest that? Quite oppositely, I wrote you have to go out from the atmospheric pressure of 760 mmHg (where the part of the oxygen is 120 resp 130 mmHg). I only told that when forcing inhalation or packing, the total alveolar pressure will be higher (may be more than 20% higher than atmospheric pressure). At higher pressure the alveoli will certainly not collapse.

Even if they weren't it's still a partial pressure of oxygen. To get the partial pressure of oxygen, you don't divide by atmospheric pressure a second time.
Exactly. And I also do not do it second time anywhere. I do it only once. I do not want to offend you, but since I do not know about the background you have, and see that you probably do not understand what the total and partial pressures exactly mean, I did the following diagram to demonstrate it:
hyperventilation.gif

As you can see, by increasing the oxygen part by 10 mmHg, you blow of CO2, and the difference makes 1,3% of the total of 760 mmHg. You can imagine the rectangles as being the volume of 7.6 liter lungs (10x760ml). The difference of 10 mmHg would then represent 100 ml of pure oxygen (or CO2), which is then 1.3% of the lung volume.

If you still see some double division in the formula, please let me know.

And trux, these aren't my numbers. They are from John R. Feiner, MD. As I suggested, read the report.
I do not really care from who it comes. I believe the numbers he gives are correct, but they simply do not show any significant advantage. Just the difference of the PAO2 is impressive for someone who does not understand what it really represents, that's all. As you can easily calculate, the effect on the breath-hold is negligible. You'd really need much higher difference of PAO2, or much higher SvO2 (venous oxygen saturation) to get some interesting difference. But as discussed earlier, that already requires more hyperventilation and has many negative side-effects that will eliminate the advantages either partially, or even the negatives totally override the positives.
 
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I have a BSc in Computer Science, with what would effectively be minors in Chemistry and Physics (the university I went to does not give minors for science degrees). I understand partial pressures.

And yes, 10mmHg is 1.3 % of atmospheric. But that is not relevant. The concentrations of other gasses are irrelevant when it comes to working out how much extra oxygen one is taking in. All that matters is that the partial pressure of oxygen increases by 8%. Taking diving as an example, if you dive with Nitrox 38, you're diving with 80% higher partial pressure of oxygen. Your calculation, which is difference divided by total pressure, would give 17% difference. I hope you can see where this goes wrong.

Lets take this the other way. Let's say you start a static on the summit of everest. Here, the ppO2 is 40mmHg, which by my calculations is 25% of the ppO2 at sealevel (159mmHg), or a 75% drop. Your calculation, which is ppO2 delta / atmospheric pressure, would give just a 15% drop. This would imply that a static with such a low ppO2 would still give a very satisfactory result, while mine implies a very bad one. Which do you consider to be correct?
 
I am sorry Chrismar, but you still do not understand what I mean. By increasing the partial pressure by 10 mmHg, you increase the volume of O2 in ~8 liters lungs by 100 ml, nothing else. Do you agree with that? If you do, then what exactly you do not agree with in the further calculation? It does not matter that it is 1.3% of the total volume, and ~8% of the oxygen volume - both is true (and I never denied it). But it is still the very same 100 ml.

You won't increase the arterial saturation by the higher alveolar pressure, since it is already practically saturated after some period of rest. And since you do not get the SaO2 higher, you won't get the SvO2 higher either, unless you increase cardiac output. In other words to get more O2 into the system you need to saturate the venous blood with all the side-effects. If you don't, all you have is the 100 ml of extra oxygen in lungs.

Your example with Everest is irrelevant, because on Everest your SaO2 won't be saturated, and likely you will need more than just one breath (or couple of them). If we speak about an hour on the Everest, and an hour of hyperventilation, then you can compare the two cases better, but not after a single purge breath (or a few of them)! Or if you start on the Everest, then drop to the sea level to get a single breath, and then come back again, OK, in that case we can better compare the two cases (though it will be still quite irrelevant).

Do not forget that the body can make apnea not because of the air in lungs, but especially thanks to the oxygen that is already in the blood. For this reason, the percentage of oxygen in lungs is not what is the most important. What pays is especially the saturation of hemoglobin in blood and that won't change in the same percentage as the PAO2!

EDIT: yet in other words: in your assumptions you simply consider the lung/blood system to be connected tanks, where the pressure and volume in one part (lungs) immediately translates into identical changes in the other part (blood). You completely ignored that there is a serious bottleneck between the two systems which is the blood saturation (the maximum of oxygen hemoglobin can bind), and that the exchange of oxygen between the two systems is not immediate.

You assumed that by a single deep breath (or a few of them) you increase the oxygen by 8% in your lungs and in the same time in the entire blood system. That's simply wrong. Arterial part is already saturated and cannot take any more. As Eric already wrote earlier in this thread, you only start increasing O2 in blood when the venous part of blood begins to be saturated above normal.
 
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Ah, we're closer to the same page here. Now, I have never studied medicine, so I don't know the rate at which O2 is taken up by the arteries, so I won't comment on that. My disagreement comes in how you calculate the percentage improvement as the increased quantity of O2 over total lung volume. This is where our disagreement lies. Let me try to clarify my understanding and see how this fits in with you.

The percentage increase in paO2 is what's important in the lungs, correct? This is 8%. This means, assuming we only used the O2 in our lungs for apnea, that the performance increase, assuming no other changes, would be 8%. Now of course neither of those two assumptions are correct. Eric or someone similar would have better numbers than me, but from the performances on exhale statics that I have seen, the percentage of O2 within the blood that is used in apnea is between 1/3 and 1/2 of the total used. Taking those numbers, that 8% difference would equate to between 4 and 5.5 percent performance increases. As for the second assumption, the good doctor that took the numbers stated that little change to CO2 levels was recorded. I have done my own experiments with a heart rate monitor during statics and have noticed no increased cardiac output when performing less than three deep breaths prior to apnea. As far as I am concerned, this suggests that the performance increase using this style of breathe-up should be around 4-5%, or 15 seconds in my case.

I hope we're back on the same page now.
 
Now if you have that one worked out, how about this? Start with 120 in lungs, end with say 60. Start with 130 and end with 60. 70/60 used is an 16% increase. If half the O2 used is in the lungs, that comes out to 8% on an 8 minute hold or 40". Sorry about the edit.
 
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You guys are overcomplicating things. 100ml of O2 equates to about 30 seconds of static time, as you consume about 200ml of O2 per minute during static.

This is assuming you can actually access & consume those 100ml of O2.
 
only part of the oxygen available in lungs can be used, let's assume it is 50%. That would mean we can use 50 extra ml of O2 which could increase the apnea by 12 seconds. And I am not even sure that the alveolar oxygen saturation (exhale air) can drop as deep as 50%.

I was about to bring this up... there is a difference between saying that half the oxygen in the lungs can be used (above) and saying that the transfer of oxygen to the blood stops at a certain pp02 (say half of .21, which is .105).

If you take Trux's statement literally, you could breathe pure O2 and black out with a pp02 of .5. Presumably this is not how it was intended to be read (?) and it is actually the absolute pp02 value that causes you to blackout rather than the proportion of 02 you've used. If this is the case, you would have access to 100% of any extra oxygen you gain from hyperventilation.
 
You guys are overcomplicating things. 100ml of O2 equates to about 30 seconds of static time, as you consume about 200ml of O2 per minute during static.
Yes, that's exactly what I claim from the beginning. With the small difference that I use the value 250 ml/min for resting consumption. 200 ml/min is the CO2 production during rest. Those values come from P. Lindberg's thesis. Of course, it may differ at individuals and during the apnea.

As Eric tells, all the percentage values are completely unimportant. I used them solely to get the volume of the extra oxygen from the PAO2 values. The volume difference is the only value that matters. Percentage of pure oxygen increase (8%) are not usable to get the volume, hence I had to use the percentage of the total volume (1.3%) wich was known (8 l).

I stress that all this is strongly simplified, because we are ignoring many other side-effects of hyperventilation (even if it is so short), and the real outcome may differ from this simplified hypothetical calculation.
 
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If you take Trux's statement literally, you could breathe pure O2 and black out with a pp02 of .5. Presumably this is not how it was intended to be read (?) and it is actually the absolute pp02 value that causes you to blackout rather than the proportion of 02 you've used. If this is the case, you would have access to 100% of any extra oxygen you gain from hyperventilation.
What I meant is that during apnea you can absorb some oxygen from lungs only to certain level, which is influenced by the gradient between PvO2 (venous oxygen tension) and PAO2 (alveolar oxygen tension), and the affinity of hemoglobin that decreases with the progressing apnea and increasing hypercapnia. With the progressing apnea you can only get some more oxygen from lungs only thanks to dropping venous PO2, which means higher hypoxemia and coming close to blackout. 50% desaturation at the end of apnea is already pretty serious, but the alveolar partial pressure (PAO2) would need to be considerably higher to still allow some diffusion through the alveoli and the intake of oxygen.

It means you can pull only part of the oxygen available in lungs. So yes, you are right, it is more matter of absolute values, than percentage (with pure oxygen in lungs you would use percentually more). The problem with hyperventilation is that the minimal PvO2 also changes.
 
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Where did I suggest that? Quite oppositely, I wrote you have to go out from the atmospheric pressure of 760 mmHg (where the part of the oxygen is 120 resp 130 mmHg). I only told that when forcing inhalation or packing, the total alveolar pressure will be higher (may be more than 20% higher than atmospheric pressure). At higher pressure the alveoli will certainly not collapse.


Exactly. And I also do not do it second time anywhere. I do it only once. I do not want to offend you, but since I do not know about the background you have, and see that you probably do not understand what the total and partial pressures exactly mean, I did the following diagram to demonstrate it:
hyperventilation.gif

As you can see, by increasing the oxygen part by 10 mmHg, you blow of CO2, and the difference makes 1,3% of the total of 760 mmHg. You can imagine the rectangles as being the volume of 7.6 liter lungs (10x760ml). The difference of 10 mmHg would then represent 100 ml of pure oxygen (or CO2), which is then 1.3% of the lung volume.

If you still see some double division in the formula, please let me know.


I do not really care from who it comes. I believe the numbers he gives are correct, but they simply do not show any significant advantage. Just the difference of the PAO2 is impressive for someone who does not understand what it really represents, that's all. As you can easily calculate, the effect on the breath-hold is negligible. You'd really need much higher difference of PAO2, or much higher SvO2 (venous oxygen saturation) to get some interesting difference. But as discussed earlier, that already requires more hyperventilation and has many negative side-effects that will eliminate the advantages either partially, or even the negatives totally override the positives.

Hi Trux

I am sure that it is just a number fault but pls if you agree and it is posible to corect the number of co2 at hyperventilated alveolar from 54mmHg to 34mmHg to avoid any misunderstanding in such a serious matter and also for the next that will read this topic.

Tolis
 
I am sure that it is just a number fault but pls if you agree and it is posible to corect the number of co2 at hyperventilated alveolar from 54mmHg to 34mmHg to avoid any misunderstanding in such a serious matter and also for the next that will read this topic.
Yes, thanks for the heads up, that was an oversight. The rectangle is smaller, the CO2 level is lower, and the PACO2 value should be smaller too. I am going to change the chart. EDIT: it is changed now, so if you reload the page, the image should contain the right value.
 
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