Clarifying some stuff in the Haldane and Workman's papers?

[janosik]

I have started reading those papers with great interest, and I have a bunch of questions about some of the underlying assumptions. I would appreciate some hints. I apologize if these are obvious, I am not a physicist.

a) Haldane states that one need not be concerned about PCO2 in alveolar air because it remains constant regardless of the ambient pressure. I skimmed over his earlier paper, and I did not stumble upon any sort of clear explanation why this should be the case. It was perhaps sort of vaguely hinted (or not) that the excess CO2 would condensate in the lungs as a water vapor and exhaled. Is that correct?

b) Workman asserted that the 2:1 ratio was really a 1:56 ratio, but his argument is unclear. He seems to be comparing the partial pressure of nitrogen with an absolute ambient pressure. Henry's law, as I understand it, only talks about partial pressures of the same gas, and if the ambient pressure drops 2x, so does the partial pressure of Nitrogen. Clearly, he must be referring to some other gas law, for otherwise I do not see how the presence or absence of oxygen should affect the process of Nitrogen diffusion from tissues/blood into the expired air.

 

[Mod63]

as to b), Haldane played it simple and didn't bother with partial pressure. Workmann corrected/clrified this. Haldane gives you a ratio of 1:2, Workman says at 1bar ambient the tolerated pressure of nitrogen in the tissues is 1,58bar (0,79bar times 2).
The absence or presence of oxygen does effect the nitrogen diffussion, as the sum of all gases is always 1 (or 100%). So if there is a higher presence of oxygen there must be a lesser precence of nitrogen, resulting in a higher nitrogen diffusion from the tissue (that's we EANxx or oxygen can be used to accelerate decompression.

 

[janosik]

But that is precisely my concern, this assumption seems to go against Henry's law as it is usually stated; e.g., from Wikipedia "The solubility of a gas in a liquid at a particular temperature is proportional to the pressure of _THAT_ gas above the liquid.". So presumably, there is some other law that Workman is referring to.

 

[Doppler]

If you have not already searched Rubicon database, it is perhaps the best starting point.

Not clear what your concerns are but I believe Workmann and anyone else doing work in this field (and in the absence of consideration for dual phase influences) would have made some account for Daltons and Ficks.


Oh, and by the way, you do not need to be a physicist to understand the gas laws... they are chemistry not physics!

:0

 

[TSandM]

The alveolar pCO2 will remain constant because the body has an extremely powerful drive to keep it that way -- this is because pCO2 is an integral part of the pH buffering system in the body, and cellular processes are exquisitely sensitive to pH changes. Alveolar pCO2 is regulated entirely by alveolar minute ventilation, so as long as the diver is moving enough air per minute through the gas exchange portion of the lungs, the pCO2 will remain constant.

 

[Doppler]

And as Lynne has eloquently illustrated, gas behavior within the human body is neither Physics nor Chemistry, but Physiology...




and alchemy.

 

[janosik]

@Mod63: Haldane did bother with partial pressures, he was suggesting to reduce the absolute (and therefore partial) pressure by half; here is the relevant fragment from his paper (page 16):

"The process of desaturation can therefore be hastened very greatly by rapidly reducing the absolute pressure to half, (...) rate of discharge evidently depends on the difference in partial pressure of nitrogen between the venous blood and the alveolar air; and by keeping this difference at the maximum consistent with safety a great saving of time is effected."

Workman in his paper makes what appears to be an inaccurate account of Haldane's work (page 8):

"The limit (...) was to never allow the computed nitrogen pressure in the tissues to be more than twice the ambient pressure."

The way I am reading it, the whole section 2.1.6 seems to be making a moot point; he compared different things, and came up with a different number. I would ignore that were it not for the argument about oxygen. I do not understand how oxygen plugs into this equation.

@Doppler: Thanks for the hints, I will read up on Ficks. Sadly, I am not a chemist, physiologist or alchemist, either, which makes the whole subject all the more mysterious and exciting.

@TSandM: Let me see if I understand. So, in response to the increased PCO2, the rate of respiration slightly increases, which is imperceptible and does not affect other gases, but has an effect on PCO2 because it constitues such a tiny fraction of the alveolar air?

 

[gsk3]

@TSandM: Let me see if I understand. So, in response to the increased PCO2, the rate of respiration slightly increases, which is imperceptible and does not affect other gases, but has an effect on PCO2 because it constitues such a tiny fraction of the alveolar air?

In addition to respiratory control, excess CO2 gets buffered in the blood as carbonic acid. Your body's immediate reaction to excess CO2 is to increase respiratory rate (not necessarily imperceptibly even in normal situations, and quite perceptibly in disease states--look up Kussmaul respirations), and then over the course of hours the kidneys will start to play a role.

On the surface, it has an effect mainly on PCO2 because you're not breathing in more CO2. I'd have to think about the diving analogue but I assume it's similar.

 

[Doppler]

... Sadly, I am not a chemist, physiologist or alchemist, either, which makes the whole subject all the more mysterious and exciting.

You are asking the questions and are engaged by the topic... excited even... all good stuff!

Dive safe... Have fun!