Oxygen Window Revisited

[boulderjohn]

One of the threads in this forum is evolving into a topic I find interesting, but I fear that it is being buried at the end of an old thread and will not get proper treatment. I am therefore starting a new thread.

Nearly two years ago this forum hosted a very interesting and informative thread on the topic of the oxygen window. It ended with what I thought was a consensus that the oxygen window (as I am about to define it) was not an important factor in decompression.

Since then, I have encountered some opposing viewpoints that were not represented in that debate. I myself do not have the expertise to have a firm position, and I am very interested to hear what those more knowledgeable than I have to think.

First of all, I want to be clear on the terms. I have witnessed and been a part of debates in which it was clear to me that the two parties were not talking about the same thing. In Deco for Divers, Mark Powell identifies three different definitions for the term oxygen window. One of them is simply the fact that having a higher percentage of oxygen in the mix lowers the percentage of nitrogen and thus creates a larger gradient between tissue N2 and inspired N2. I am not talking about that definition.

I am talking about the belief that high PPO2s (1.6) create an oxygen vacancy, a differential between the amount of oxygen in the arterial side and the venous side. According to this theory, the loss of oxygen makes more room for nitrogen to leave the tissues and thus speeds up off gassing. It is on this theory that UTD, for one, advocates prolonging decompression stops at the time of a gas switch to take advantage of the O2 window when the PPO2 is at its highest.

Others disagree. Mark Powell says that this will have no effect whatsoever, since N2 does not care what the levels of O2 may be. This also seemed to be the consensus of the 2008 SB thread. Ross Hemingway (creator of V-Planner) told me that prolonging the stops at 70 and 60 feet after a switch to EANx 50 essentially adds to the bottom time. The feeling is, in general, that the amount of O2 in the blood does not impact N2.

In support of its position, UTD cites a chapter in book The Physiology and Medicine of Diving, by Bennett and Elliott. I do not have access to this book. Because of Dr. Bennett's relationship to DAN, I asked DAN for an opinion. To my surprise, DAN supported this position. In the next couple of posts I will give their reasoning.

As I said earlier, I am myself not advocating anything--I am just looking for some expert thinking.

 

[boulderjohn]

The first reply from DAN misunderstood my question and assumed I was simply talking about the pressure gradient. When I clarified, I got this reply from Petar Denoble:

In chemistry and physics, Dalton's law (also called Dalton's law of partial pressures) states that the total pressure exerted by a gaseous mixture is equal to the sum of the partial pressures of each individual component in a gas mixture. This empirical law was observed by John Dalton in 1801 and is related to the ideal gas laws.

Since the total pressure of dissolved gases in liquids is proportional to the surrounding pressure, the capacity for combined dissolved nitrogen and oxygen is limited. The more oxygen, less of the other may be dissolved. This is not the same as with the tissues which act as a practical black hole. The amount of liquid blood (plasma) for which nitrogen competes with oxygen is very limited. The more oxygen is removed from the plasma, more nitrogen can dissolve.

I have to add that you are right regarding the force that drives nitrogen out from solution in tissues. That is the pressure gradient. But gas that comes out of tissues may or may not all be transported in dissolved state in plasma. The larger the capacity for dissolved nitrogen (“Oxygen Window”) more of it will be transported in a harmless dissolved state and less will be available to form the free gas phase that can harm body.

 

[boulderjohn]

I then received the following message from DAN's Richard Vann, who sent along a chapter he wrote "Inert gas exchange and bubbles." In Bove and Davis’ Diving Medicine, 4th edition. Chapter 4, Bove AA, ed, WB Saunders, Philadelphia. 53-76, 2004.

Here is some additional information about the O2 window. (If the attachment is too big, we’ll find another way to send it.) The O2 window is real (it has been measured), but it’s a tricky concept and can be difficult to understand. It applies particularly to the elimination of bubbles. In fact, decompression would be impossible (due to bubbles) without the O2 window.

The PDF he sent is too large for me to attach here. I will see what I can do about it. I am myself still in the process of digesting it.

 

[Mr Carcharodon]

John,

This is a good explanation:
"Gas Exchange Partial Pressure Gradients and the Oxygen Window", Johnny E. Brian, MD.


Dr. Brian suggests that increasing the oxygen window by breathing a higher fraction of O2 or by maintaining higher ambient pressure causes a greater pressure drop between arterial and venous blood. The lower pressures on the venous side may reduce bubble formation.

 

[adm3745]

IS this what your talking about?

"Oxygen can be pushed to above its partial pressure effectiveness as a result of this imbalance for a "window" that then exceeds what would be the net effect of the partial pressures of the gases, and this is especially important in diminishing bubbles of inert gas as the pressure of the bubble can always be faced with a negative gradient or "tension" on the outside due to the fact that metabolized oxygen is creating a "vacuum" in the total sum of the partial pressures of the gases, leaving a consistent imbalance between bubble pressure and surrounding tension of any given inert.

This is why oxygen (pure, not 80/20) works so well in DCS cases after the fact to reduce bubbles, as well as the fact that saturation with oxygen tends to move that gas to where it is needed even if the vessels are blocked by damage. "



Thats from Mr. Irvine

 

[gcbryan]

It seems to me that, so far anyway, everything is the same as in the discussion cited from two years ago. In other words, nitrogen doesn't come out of solution any faster due to the oxygen vacancy which was the claim.

I believe the conclusion then as now was that due to the total pressure being reduced that any nitrogen that did come out of solution would be less likely to result in bubbles or or bubbles that existed would likely reduce in size.

So the oxygen window was always acknowledged as something that existed but it just wasn't being defined correctly when it was being promoted as something that would speed up the offgassing of nitrogen.

Is anyone from DAN arguing otherwise?

 

[boulderjohn]

It seems to me that, so far anyway, everything is the same as in the discussion cited from two years ago. In other words, nitrogen doesn't come out of solution any faster due to the oxygen vacancy which was the claim.

...

Is anyone from DAN arguing otherwise?

THis is what they said:

The amount of liquid blood (plasma) for which nitrogen competes with oxygen is very limited. The more oxygen is removed from the plasma, more nitrogen can dissolve.

 

[gcbryan]

Yeah, it's interesting wording for sure. In the next sentence (and paragraph) they say:

I have to add that you are right regarding the force that drives nitrogen out from solution in tissues. That is the pressure gradient. But gas that comes out of tissues may or may not all be transported in dissolved state in plasma. The larger the capacity for dissolved nitrogen (“Oxygen Window&#8221 more of it will be transported in a harmless dissolved state and less will be available to form the free gas phase that can harm body.

So, they're still not talking about the rate of off gassing increasing and as far as I can tell are still talking about factors that would reduce bubbles.

 

[Gene_Hobbs]

I tried to start aggregating the history and references here a while back.

 

[boulderjohn]

John,

This is a good explanation:
"Gas Exchange Partial Pressure Gradients and the Oxygen Window", Johnny E. Brian, MD.


Dr. Brian suggests that increasing the oxygen window by breathing a higher fraction of O2 or by maintaining higher ambient pressure causes a greater pressure drop between arterial and venous blood. The lower pressures on the venous side may reduce bubble formation.

OK, I read it carefully, and I am not sure I am seeing what I am looking for in there.

Here is the conclusions section in its entirety:

CONCLUSIONS
It should be obvious from the above discussion that much decompression physiology is poorly understood, and models used at best approximate in vivo physiology. Clearly, not all decompression illness can be predicted to prevented. However, thoughtful application of available models coupled with careful diving technique can minimize risk of decompression illness. By reducing non-metabolic gas to a minimum and reducing tissue on-gassing, the oxygen window can be utilized to increase tissue off-gassing during decompression. Real life experience indicates that use of O2-enriched deco mixes can function to limit decompression time and possible the incidence of decompression illness. Use of high O2-mixes requires careful attention to dive planning and execution. As always, the careful, thoughtful diver will be the safer diver.

As I read it (and again, this is not my area of expertise), he is talking in this paper primarily about the fact that breathing high PPO2s will reduce the deco time by limiting the amount of inspired N2. As I said earlier, that is not the effect I want to talk about in this thread.

Here is what he says just before the conclusions paragraph (I added color to parts I found interesting):

IS THE OXYGEN WINDOW IMPORTANT?
It should be intrinsically obvious that removal of a gas from tissue can be speeded by elimination of the gas from the inspired mixture. If the arterial partial pressure of a gas is zero, then no gas will diffuse into tissue while the gas is diffusing out of the tissue. As discussed above, diffusion of one gas in solution is not affected by the presence of other gases. Despite all of the above discussion of gas diffusion, most decompression models in common use, including Bühlmann’s models, are perfusion-limited models. In a perfusion-limited model, diffusion is assumed to be infinite and thus cannot limit tissue gas uptake or removal. Tissue half-times for He and N2 are independent of each other, so the presence or absence of N2 does not change the rate of He on- or off-gassing and visa versa. In theory, He off-gassing should not altered by breathing air, 50% nitrox or 100% O2 during decompression from a He dive. He elimination during air or O2 decompression from a He-based dive has been measured, and the decompression gas did not affect the rate or volume of expired He (4). In another study at 1 ATA, tissue N2 washout is not different during O2 or heliox breathing (3). Both studies are consistent with the physics of gas diffusion in solution, where the presence of a second non-metabolic gas does not slow diffusion of the first nonmetabolic gas. The reality is that at any given ambient pressure, regardless of the size of the oxygen window, as long as there is no inspired He, the rate of He off-gassing will be unchanged.

Decompression from an N2-based dive is longer with N2 containing deco mixes because some N2 is continuously diffusing into tissue during deco. Decompression from a He-based dive can be longer with N2 containing deco mixes because N2 is diffusing into tissue as He is diffusing out of tissue. The decompression obligation of a tissue compartment is based on the sum of gas partial pressures in the compartment. This means that if a tissue is loaded with N2 as He is being removed, it tissue has a greater decompression obligation than when no N2 is added to tissue during He off-gassing. Enlarging the oxygen window can only occur when PaO2 is increased to a maximum tolerated value, either by increasing depth or increasing FiO2 of the gas mix, or both. Although enlarging the oxygen window may not directly affect tissue gas removal, it does directly affect tissue on-gassing during decompression, which affects the amount of time required to decompress the tissue.

As for the bubble reduction, he only mentions that in one paragraph, just after the last quote above. Notice the degree to which he is committed to the concept:

Enlarging the oxygen window may have another effect, which is more subtle than tissue on or off-gassing. The following discussion is conjecture based on data available in the literature, and has not been directly studied. During decompression of animals from air dives, venous blood becomes supersaturated with N2 during the early stages of decompression, and venous blood super saturation appeared related to venous bubble formation (2). Venous blood N2 supersaturation occurred following a relatively mild decompression stress of ascent from 33 FSW to surface. Once bubble formation had occurred, gas removal was slowed, possibly by bubbles in the venous circulation (2). By limiting the speed with which ambient pressure is changed, deep stops may function to limit venous blood supersaturation and limit bubble formation related to the supersaturation. Increasing the oxygen window during decompression will also limit venous blood supersaturation by limiting the amount of non-metabolic gas in blood. In essence, the presence or absence of a second non-metabolic gas will not alter the amount of gas evolved from tissue. However, the presence of an inspired non-metabolic gas could increase the severity of venous blood supersaturation. Figure 12 demonstrates hypothetical venous partial pressures during decompression from a He dive with either O2 or air at 20 FSW. In this example, the partial pressure of He in venous blood is assumed to be 1000 mmHg in both conditions. During air breathing at 20 FSW, PaN2 would be approximately 1140 mmHg, so an assumed PvN2 value of 800 mmHg allows some tissue N2 uptake. Ambient pressure at 20 FSW is 1216 mmHg. Due to the oxygen window, the total partial pressure in venous blood during O2 breathing would be 1150 mmHg, less than ambient. Total venous partial pressure during air breathing at 20 FSW would be 1937 mmHg, above ambient pressure Although no direct experimental data exists on this topic, oxygen breathing may limit venous blood supersaturation, prevent venous bubble formation, and thus speed tissue gas removal.

Once again, the theorized bubble reduction benefit is due to a lowering of the percentage of nonmetabolic inspired gas, not by increasing the amount of room available for nonmetabolic gases in the venous blood by the oxygen vacancy.

Once again, I feel like I must be missing something here, and I invite those with greater expertise to show me where I am missing it.