Oxygen solubility and half times

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The Iceni

Medical Moderator
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Location
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Dr Deco,

As usual I have a poser!

It is along time since I did any basic physiology but have been unsuccesful in finding the answers to the following basic questions and admit to simply wanting to save myself a lot more wasted time in the medical library of my nearest city.

Do you have access to the values in Kg or % for the avarage fit and reasonably healthy human body in terms of.

1) The circulating volume
2) The brain
3) The muscle bed
4) Tissue fluid other than active muscle
5) The contents of the visceral organs
6) Bone

The reason I am asking this is that I am trying to generate a model for oxygen toxicity for which I also I need a solubility coefficient and half times for oxygen for these tissues.

I am sure this has already been done for nitrogen in the various decompression models so it would save me a lot of time if you could let me know if you know these values, or provide me with a reference to them or to their equivalents?

many thanks,:)

Paul
 
Dear Paul:

This is a tricky problem. My first guess is that it related to the halftimes in terms of how they were assigned by Professor Buhlmann. That is, brain is 5 minutes, skin is 100 minutes, bone is 250 minutes (or something like that). These are nitrogen halftimes but are based on blood flows.

This would give the perfusion. However, oxygen toxicity appears to be related to oxygen utilization. The utilization by bone and fat is small and the partial pressure would become quite high in this tissue. The utilization by brain is very large and the partial pressure is never very high. The utilization rate is in Bennett and Elliott’s book (Dick Vann’s chapter, I believe). The CNS is a target and bone is not.

Brain and the CNS respond very profoundly to oxygen poisoning and bone does not. I would posit that some metabolic product is involved, and that it is associated with reactive oxygen intermediates. Free radicals are an example.

The data on the oxygen tolerance test (in Bennett and Elliott’s book) shows that the response is extremely variable from day to day. Pulmonary effects are apparently more regular. All in all it would not be an easy problem.

The final result is that I do not have the perfusion numbers handy but do not think that is the best way to get the half times.

:doctor:
 
Thanks Dr Deco,

Unfortunately I did not give you enough information for you to understand exactly why I am asking these questions.

I am trying to understand the physiology of closed circuit rebreather diving and the risks of oxygen toxicity to which these divers are exposed.

I believe it is generally accepted that a pp O2 of 1.4 bar at equilibrium is the maximum safe recommended level.

Rebreather diving is a whole new world, of course, and all the diver has to assess his exposure to oxygen is the pp O2 as recorded in the loop, which is seldom at the steady state. During descent this will increase, not because of compression of the loop but because oxygen will be added to the loop with the air which is normally used as the diluent.

If the loop volume is kept constant at all stages of the descent I postulate that the pp O2 in the loop will increase by 0.209 bar for every 10 metres of descent because this is the amount of oxygen added with the 1 bar of air needed to reinflate the loop to its constant working volume.

This model predicts that the oxygen pp O2 at the bottom of a 40-metre descent will be 0.8 bar greater than it was on the surface due to what I call "diluent enrichment". I have received a lot of flack from British rebreather divers who do not agree with this model on the basis that they never see oxygen spikes of this level. (Please see the attachment, if it works.)

Applying Henry's Law I have postulated that this is because this one-off excess oxygen is rapidly taken out of the loop by simple solution in the fast tissues so the brain will not exposed to toxic levels unless the pp O2 in the loop remains at the toxic level for a reasonably long time.

For example if the loop is 10 litres and the effective tissue volume of the body's fast tissues is as large as 5 litres (In other words it can dissolve 5 litres of oxygen per bar), a transient increase in the loop by 0.8 bar on descent, with a set point at 0.7 bar the loop pp o2 rises to 1.5 bar but it will rapidly be reduced by simple solution to a value of 2/3 of the difference; -

(1.5- 0.7) x 10/15 = 0.53 bar

0.7 + 0.53 = 1.23 bar.

Thus a spike from 0.7 to 1.5 bar, in my opinion, will not be problematic.

However, at depth with a set point of 1.3 bar a transient spike from equilibrium to 2.0 bar may be more of problem.

Although 2.0 bar is seen in the loop it will reach a maximum theoretical and transient equivalent of (2.0-1.3) x 10/15 + 1.3 = 1.76 bar only when the fast tissues, such as the brain, reach saturation. However this value is further reduced as this additional oxygen is simultaneously dissolved in the slower tissues of the body.

In addition, of course, metabolism further reduces the pp O2 at the affected tissues and it is the pp O2 at the brain and not the loop that matters, after all.

Does this sound like a reasonable hypothesis?

I am not up for a PhD but sounds like some work is needed!

Kind regards,
 
Dear Dr Thomas:

I do not believe that simple solubility could account for the reduction in the oxygen tension in the breathing circuit. The solubility of gases is not very great. Oxygen and nitrogen each are not very soluble. The body will dissolve about 1 liter of each per atmosphere of pressure at equilibrium (several hours) one would need to take into account a very large solubility in tissues to see the changes found in the circuit.

I do not however, have an answer as to where it goes.

Dr Deco
:doctor:
 
Why Dr Thomas, you rascal, I do believe you have a card up your sleeve. Would you be per chance, or by design, fashioning a theory concerning certain incidents among Inspiration users? I'm sure that K.N. is all ears.
 
Originally posted by Dr Deco
Dear Dr Thomas:

I do not believe that simple solubility could account for the reduction in the oxygen tension in the breathing circuit. The solubility of gases is not very great. Oxygen and nitrogen each are not very soluble. The body will dissolve about 1 liter of each per atmosphere of pressure at equilibrium (several hours) one would need to take into account a very large solubility in tissues to see the changes found in the circuit.

I do not however, have an answer as to where it goes.

Dr Deco
:doctor:

Both you guys have probably forgotten more physiology regarding this topic than I ever knew. But I should think that the biggest O2 sink in the body would be in the conversion of hemoglobin to oxyhemoglobin. That would account for far more than the simple solubility of O2 in the tissues.

I have also attached a few abstracts, which would seem helpful, although you guys are probably already aware of them.
 
Hi ET & DevJr,

The problem is that when a gas dissolves in a liquid not only does it take a considerable amount of time to reach saturation as Dr Deco rightly says, for more gas to dissolve or combine biochemically there has to be an increase in pressure at the gas-liquid interface, from the earlier steady state of saturation.

If you look at the oxygen dissociation curve for haemoglobin ET, you will see that it is far from linear and Hb is about 97% saturated when breathing air at 1 bar. The rest (3%) is largely combined with carbon dioxide as carbaminohaemoglobin. Haemoglobin (and presumably the myoglobin found in muscle) only becomes fully saturated when the partial pressure of oxygen approches 3 bar. This is why I do not believe there will be sufficient capacity for all the body's Hb and Mg to absorb very much more oxygen if the partial pressure is increased from 0.2 bar to 1.3 bar, for example.

However as Dr Deco confirms the soft tissues of the body, including the plasma, cytosol, and interstitial fluid could - IN THEORY AT LEAST - dissolve up to 1 litre of oxygen for each increase in pp O2 of 1 bar if the solubility coefficient of these tissues is about the same as plasma.

I understand it is generally accepted that the solubility coefficient of oxygen for blood @ 38 degrees C is 2.2 %. That is 22 mls of oxygen can be dissolved in every litre of plasma and the cytosol of the blood cells but I have no idea of the dynamics of this (i.e. the half times) which I why I asked the original question.

An increase in pp O2 from surface equilibrium at 0.2 bar to the 1.3 bar used at the bottom, results in a pressure differential of 1.1 bar which in theory would result in the removal of about a litre of oxygen from a 10 litre loop (0.1 bar) but it now seems only after many, many hours.

Like Dr Deco, I remain puzzled, unless of course the low pp O2 measurements reported to me are not accurate readings. Indeed the loop O2 sensors take finite time to stabilise. I know my own oxygen meter takes at least 30 seconds to give me a steady reading when I check my Nitrox cylinders.

Yes DevJ, call me a rascal if you like, but I do not like being unable to understand practical findings that do not comply with the laws of nature (the gas laws) and if I am ever to consider using a rebreather I, for one, would like fully to understand the physiology of how they work.

As I said, I have received a considerbal amount of flack for daring to ask these questions. For example the majority of replies I have had from British rebreather divers completely dismiss my theory of "diluent enrichment";-

For air diluent this is 0.21 bar per 10 metres of descent

For Heliox 12 it is 0.12 bar andf or helium alone it is of course zero (not that I would ever recommend its use as a diluent for sports divers as it cannot be employed as a bailout gas.)

Does this make sense, or am I as mad as some suggest?

Regards,

Paul
 
Deleted due to computer glitch.
 
Dr Thomas, this suggestion may be nothing to get excited about but if you are looking for "out of the box" ideas, I have one to offer. Don't ask me for details just yet, I'll work on some examples if this has merit.

You may need to stop thinking of the counterlung(or loop or whatever it's called) as a balloon. Instead, consider that it is a rigid body that is being pressurized, much like a Scuba tank which is being filled. This seems to be a good analogy since the shape of the counterlung approximates a rigid body as long as the ambient pressure is matched by injected air. In other words, the wall strength of this "tank" is provided by external pressure, and balanced by internal pressure.

Now, think of a Scuba tank that is being partial pressure filled with oxygen and air to make Nitrox. If you've calculated the proportions you know that you cannot simply subtract the oxygen percentage in air from the Nitrox percentage and add the resultant percentage of oxygen to make up the difference. This is because the straight O2 one puts into the tank displaces air that would otherwise be in the tank along with the O2 that would be in that air, so the final mix would have less O2 than calculated.

This is the equation that mixers use:

FO2 mix-FO2 air/FN2 air = FO2

FO2 (mix) is the fraction of O2 desired in the mix
FO2 air is 21%
FN2 is 79%
FO2 is the percentage of O2 which must be added. (This is multiplied by final tank pressure to figure the Pressure of O2 to be added to the tank).

For example, common sense says that a 32% mix requires that FO2 to be added should be 11%; however, this is not so, it is actually 14%, NOT 32-21 = 11%. See the equation.

I believe the rigid body displacement model is at work in your rebreather calculations. If it is, it means that injection of air will not raise the bag's O2 partial pressure as much as you have calculated.

For some this may be difficult to picture. Home mixers may be tweaked by this explanation. I have no idea what the rebreather makers would make of this in particular, but I doubt that they designed their equipment on trial and error. I'll play with some calcs later. Comments welcome.

Dennis, the other rascal.
 
https://www.shearwater.com/products/swift/

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