Oxygen Window: Explanation and Purpose?

[gcbryan]

I've read several papers on the Oxygen Window as well as several posts on this board.

If Charlie reads this post perhaps he has a simple explanation as his posts seem to be the clearest on all topics regarding decompression.

I understand that oxygen is metabolised and replaced in part by CO2 and that more O2 is used and less CO2 is exchanged thereby resulting in a "partial pressure vaccum".

What is the main benefit of this to diving? Since N2 offgassing is only affected by N2 ongassing and not other gasses how does reducing O2 levels in the blood result in faster N2 offgassing? Perhaps it doesn't and this is not the point?

I also understand that with 100% O2 you aren't taking in any more N2 so of course N2 offgassing will take less time but this is not the Oxygen Window.

Is the whole point of the Oxygen Window not that N2 will offgass faster but rather that total partial pressures will be reduced and therefore there will be less bubble formation. Is reduced bubble formation really the whole point of the Oxygen Window? Is there a point?

 

[Bismark]

Hi,

Read the posts in the technical diving section here on SB about deco. We are discussing this right now and I promised to get back by Monday with more information.

Oops, forgot to mention: the thread is called "calculating deco"

 

[do it easy]

Oops, forgot to mention: the thread is called "calculating deco"

Clink the link!

http://www.scubaboard.com/forums/technical-diving-specialties/224715-calculating-deco-mix.html

 

[Charlie99]

Decompression is the balance between staying deep to avoid bubble formation versus going shallow to speed up offgassing.

The subtle thing is that total ambient pressure is the key to avoiding bubbles, while offgassing is independently controlled by the individual partial pressures of each of the inert gases.

High oxygen content mixes (and of course 100% O2) allow you to have a higher ambient pressure (i.e. stay deeper) for any given set of inert gas pressures. The higher partial pressure of O2 doesn't have any bad effects on decompression (other than 2nd order stuff like vasoconstriction) because any excess O2 in the tissues is simply metabolized away.

If you are breathing 100% O2 at any depth, the partial pressures of N2 and He are ZERO. Or as the article below puts it, the equivalent-air-depth is -33'. But you can be as deep as 20' on 100% O2 and not exceed the 1.6atsa ppO2 that most divers observe to reduce the risk of oxtox seizures.

2000-11 Out The Oxygen Window is a pretty good explanation.

IMO, the oxygen window is just term that was used to help explain what is going on, and somehow that explanatory term has taken on a life of its own, as if there is some magic factor in play.

I'm open to correction, but I'm relatively certain that there is nothing more complicated going on than a high FO2 mix allowing you to maintain high ambient pressure (ie. stay deep) to avoid bubbles, while reducing the partial pressures of inert gases to speed up offgassing. At the tissue level there is some other stuff going on where the local ppO2 is reduced a bit through the bodies metabolizing O2, but that is very small compared to the more basic effect discussed above.

 

[MookieMoose]

The idea of the Oxygen Window, as I understand it, is that as oxygen is consumed from arterial blood and CO2 is produced, less CO2 is added to the blood than O2 was removed, leaving the partial pressure vacuum you referred to. This partial pressure vacuum can then be filed with nitrogen disolving out of tissue into the venous blood.

Cam

 

[Charlie99]

The only numbers I've seen thrown around for the reduction in ppO2 in venous blood have been around 0.04ata/1.3fsw. And if the reduction ppO2 merely results in lower total pressure in the venous system as compared to arterial or capillary (which is much be if you want blood to flow in the right direction), then this reduction in ppO2 doesn't have any affect on N2 offgassing at all. Of course, this is consistent with only the relative partial pressures of N2 being what matters in N2 offgassing.

Even if that 1.3fsw difference in ppO2 does have an effect, it is much smaller than the more basic effect of being able to stay deep with higher total ambient pressure with lower ppN2 due to it's lower % in the breathing mix. For comparison, ppN2 on air at 20' is 1.27ata, on 100% O2 is is 0ata, for a difference of 1.2ata or 42fsw. Obviously much bigger than 1.3fsw.

As an aside, the water vapor pressure in the lungs of about 1.6fsw is also at play here, as it reduces the total pressure of other gases in the lungs. But often we just ignore this 1.6fsw correction.

Dr Deco has addressed the oxygen window before, in http://www.scubaboard.com/forums/ask-dr-decompression/66900-oxygen-window.html . Rather confusing, to me at least.

 

[Gene_Hobbs]

Well, took a couple of hours to pull these together but I think it will help a few of you on your quest...

The first use of the term 'oxygen window' is by Albert Behnke [1]. Behnke also refers to early work by Momsen on 'partial pressure vacancy' (PPV) [2] where he used partial pressures of O2 and He as high as 2-3 ATA to create a maximal PPV [3]. Behnke then goes on to describe 'Isobaric inert gas transport' or 'inherent unsaturation' as termed by LeMessurier and Hills [4] and Hills [5, 6] who made independent observations at the same time. Van Liew et. al. also made a similar observation that they did not name at the time [7]. The clinical significance of their work was later shown by Sass [8]

The 'oxygen window' effect in decompression has been described by many authors and the limits reviewed by Van Liew et. al. in 1993 [9]. The following passage is quoted from their Technical Note [9]:

When living animals are in steady state, the sum of the partial pressures of dissolved gases in the tissues is usually less than atmospheric pressure, a phenomenon known as the "oxygen window", "partial pressure vacancy" or "inherent unsaturation" [1, 7, 10, 11]. This is because metabolism lowers partial pressure of O2 in tissue below the value in arterial blood and the binding of O2 by hemoglobin causes a relatively large PO2 difference between tissues and arterial blood. Production of CO2 is usually about the same as consumption of O2 on a mole-for-mole basis, but there is little rise of PCO2 because of its high effective solubility. Levels of O2 and CO2 in tissue can influence blood flow and thereby influence washout of dissolved inert gas, but the magnitude of the oxygen window has no direct effect on inert-gas washout. The oxygen window provides a tendency for absorption of the gas quantities in the body such as pneumothoraces or decompression sickness (DCS) bubbles [7]. With DCS bubbles, the window is a major factor in the rate of bubble shrinkage when the subject is in a steady state, modifies bubble dynamics when inert gas is being taken up or given off by the tissues, and may sometimes prevent the transformation of bubble nuclei into stable bubbles [12].

This paper then goes on to describe the measurements important to evaluating the oxygen window as well as simplify the "assumptions available for the existing complex anatomical and physiological situation to provide calculations, over a wide range of exposures, of the oxygen window" [9]. (abstract summarizes the results)

1. Behnke. (1967) The isobaric (oxygen window) principle of decompression. In: The New Thrust Seaward. Trans. Third Marine Tech. Soc. Conf. 5-7 June, San Diego. Washington, DC: Marine Tech. Soc. RRR ID: 4029
2. Momsen. (1942) Report on Use of Helium Oxygen Mixtures for Diving. US Naval Experimental Diving Unit Washington, DC Technical Report 42-02. RRR ID: 3312
3. Behnke. (1969) Early Decompression Studies. In: The Physiology and Medicine of Diving and Compressed Air Work, Bennett and Elliott. First Edition. p234
4. Hills. (1965) Decompression Sickness. A thermodynamic approach arising from a study on Torres Strait diving techniques. Hvalradets Skrifter, Nr. 48, 54-84.
5. Hills. (1966) A thermodynamic and kinetic approach to decompression sickness. Thesis
6. Hills. (1978) A fundamental approach to the prevention of decompression sickness. South Pacific Underwater Medicine Society Volume 8 Number 2. RRR ID: 6176
7. Van Liew HD, Bishop B, Walder P, Rahn H. (1965) Effects of compression on composition and absorption of tissue gas pockets. J Appl Physiol. 1965 Sep;20(5):927-33. PMID: 5837620
8. Sass (1976) Minimum <delta>P for bubble formation in pulmonary vasculature. Abstract of the Undersea and Hyperbaric Medical Society, Inc. Annual Scientific Meeting held May 12-13, 1976. Carillon Hotel, Miami Beach, FL. RRR ID: 5257
9. Van Liew HD, Conkin J, Burkard ME. (1993) The oxygen window and decompression bubbles: estimates and significance. Aviat Space Environ Med. 1993 Sep;64(9 Pt 1):859-65. PMID: 8216150
10. Hills. (1977) Decompression Sickness. The biophysical basis of prevention and treatment. New York: John Wiley, 1977:239-43.
11. Vann. (1982) Decompression theory and applications. In: Bennett PB, Elliott DH eds. The physiology and medicine of diving. 3rd ed. London: Bailliere Tindall, 1982; 352-82.
12. Van Liew. (1991) Simulation of the dynamics of decompression sickness bubbles and the generation of new bubbles. Undersea Biomed Res. 1991 Jul;18(4):333-45. RRR ID: 2592

Other articles of interest:

-- Hills and LeMessurier. Unsaturation in living tissue relative to the pressure and composition of inhaled gas and its significance in decompression theory. Clin Sci. 1969 Apr;36(2):185-95.
-- Yount and Lally. On the use of oxygen to facilitate decompression. Aviat Space Environ Med. 1980; 51:544-50.
-- Reinertsen, R. E., V. Flook, S. Koteng, and A. O. Brubakk. Effect of oxygen tension and rate of pressure reduction during decompression on central gas bubbles. J. Appl. Physiol. 84(1): 351-356, 1998.

*and third Conkin ref in 24 hours so I am done for a while... :14:

 

[gcbryan]

So what I've learned (here and elsewhere) is that the Oxygen Window is the result of oxygen in the breathing gas being metabolized (used up) by the body resulting in lower total gas pressure in the blood which has the results of reducing potential DCS bubbles. Nothing more, nothing less.

Why can so few people answer the question "What is the Oxygen Window" without writing 15 page papers and still not clearly answering the question. Others who don't really know the answer seem to just keep repeating portions of articles that they don't understand.

For all those who helped...thanks!

I've put my thoughts in this last post in case someone in the future with similar questions to those I had will use the search feature and find this post.

 

[Dr Deco]

Hello gcbryan:

Old Term

The “oxygen window” is a term coined many decades ago, along with synonyms such as “inherent unsaturation” and “partial pressure vacancy.” To some extent, I am surprised to see the term being used.

Decades ago, it referred to the fact the oxygen consumption (by metabolism) and carbon dioxide production (by metabolism) did not add up to zero. There was a lower CO2 partial pressure (because of its very high solubility). As originally envisage decades ago, the “oxygen window” dealt with:

[1] The dissolving of microbubbles, and
[2] A method to decompress whereby a supersaturated condition was never achieved.

[/B] Dissolving of Tissue Microbubbles

Early barophysiologists (1940s and 50s) were not so much concerned with decompression but rather more with the question of microbubble stability. Bubbles that caused DCS must redissolve or decompression pain would remain forever. Bubbles were unstable in the body because the partial pressures of all free gases [i.e., non-dissolved gases] in a bubble (nitrogen, oxygen, carbon dioxide, and water vapor) were actually greater than the sum of the dissolved gases; this is because of surface tension of the bubble surface (the Laplace pressure).

There was also the connected question of bubble micronuclei generation in the body. E. Newton Harvey (in the 1940s) was well aware that supersaturations during ascent were much, much smaller than needed to generate bubbles (de novo generation). He believed from his experimental studies that muscle activity generated microbubbles. Again, because of surface tension – and inherent unsaturation - microbubbles would shrink.

EN Harvey proposed an answer to this by suggesting bubbles resided in non-wettable pores (hydrophobic cavities); these came to be called “Harvey pores.” These microbubbles would have lifetimes of days or weeks.

Decompression

Brian Hills, PhD, proposed that any saturation greater than ambient would cause microbubbles to form. He proposed that a diver be brought up slowly enough that the partial pressure of gases in the critical tissue never exceeded the ambient pressure. He achieved this by keeping tissue partial pressures below the maximum allowed by this “partial pressure vacancy.”
Today we know that tissue fluids already contain micronuclei; low supersaturations are not needed. [His idea of keeping divers deeper persists but for different reasons.]

Current Thought

Ideas of very high oxygen partial pressure would fall under the umbrella of the “oxygen window” although this is a contemporary usage of the term.

Dr Deco :doctor:

 

[Charlie99]

Brian Hills, PhD, proposed that any saturation greater than ambient would cause microbubbles to form. He proposed that a diver be brought up slowly enough that the partial pressure of gases in the critical tissue never exceeded the ambient pressure. He achieved this by keeping tissue partial pressures below the maximum allowed by this &#8220;partial pressure vacancy.&#8221;

How much of this "partial pressure vacancy" is present in the tissues as compared that in the venous system?

If for example when breathing 100% O2 at 20' there is a difference of 1066 Torr between arterial and venous for the total sum of partial pressures -- i.e. there is a "partial pressure vacancy" of 1066 Torr in the venous system, mostly due to lower ppO2 (using J E Brian's number). Is the ppO2 in tissues closer to arterial or to venous? Or varies over the whole range?

Does the oxygen window (the partial pressure vacancy -- not simply the reduction of inert gas in the breathing mixture) have any affect on bubble formation within body tissue in addition to the postulated (ever proven??) effect of lower venous bubbling?



Still trying to figure out the implications of Oxygen Window.....

Charlie Allen