Hyperbaric without extra oxygen

[Hip]

@aaron_c, the increase in dissolved oxygen in the blood during HBOT is not tiny, but very substantial.

I found some actual figures in this paper:

At sea level the blood oxygen concentration is 0.3 ml/dl.

Administering 100% oxygen at normobaric pressure increases the amount of oxygen dissolved in the blood to 1.5 ml/dl (five folds) and at 3 ATA the dissolved oxygen content is approximately 6 ml/dl

So the normal amount of oxygen dissolved in the blood is 0.3 ml/dl.

Then if you breath pure 100% oxygen at normal atmospheric pressure, you get 1.5 ml/dl of dissolved oxygen in the blood, which is a 5-fold increase.

And when you breath 100% oxygen and while doing HBOT at 3 atmospheres pressure, your dissolved oxygen goes up to 6 ml/dl, which is a 20-fold increase over normal.


The maximum amount of oxygen dissolved in the blood is always limited by the partial pressure of oxygen in the air you breath. This is Henry's law. When breathing normal air at normal pressures, it is impossible to get any higher than 0.3 ml/dl of dissolved oxygen in the blood (at equilibrium conditions). To get higher amounts of oxygen dissolved, the only way is to increase the partial pressure of oxygen, which is what breathing pure oxygen achieves, and what doing HBOT achieves.

 

[aaron_c]

The maximum amount of oxygen dissolved in the blood is always limited by the partial pressure of oxygen in the air you breath. This is Henry's law. When breathing normal air at normal pressures, it is impossible to get any higher than 0.3 ml/dl of dissolved oxygen in the blood (at equilibrium conditions).

Thanks for helping walk me through this. You may have indirectly answered my question: 0.3 ml/dl is generally what the body aims for as far as dissolved oxygen in the serum. And it would follow (I think) that this is why we produce more red blood cells and more hemoglobin when we travel to higher altitudes, because all else being equal more hemoglobin equals more oxygen dissolved in the serum.

On another note I decided to see just how much almost quadrupling the dissolved oxygen would actually increase oxygen available to the tissues. It turns out it would do a decent bit, and that my earlier assumption that dissolved oxygen was an inconsequential portion of total blood oxygen overlooked the fact that much of total blood oxygen is basically wed to hemoglobin--it never leaves, or only leaves come catastrophic conditions. Here's how I came to that conclusion:

Breathing pure oxygen pretty much only increases the amount of dissolved oxygen, not the amount of oxygen attached to hemoglobin at the lungs, as we assume that almost all hemoglobin becomes saturated with oxygen there anyways. According to this paper the oxygen dissolved in plasma makes up about 2% of total blood oxygen, the rest being reversibly bound to hemoglobin. I couldn't find much information on the O2 saturation of venous blood, just this one website that claims that dark venous blood can have an O2 saturation of 75% (correct me if I've got this wrong). But if we assume that the normal range of O2 saturation for blood as it circulates is 100%-75% then we can say that about 24.5%* of all oxygen in the blood is oxygen that is bound to hemoglobin in the lungs but then dissolves in the the serum before the blood returns to the lungs.

If we do the math, we can see that if we breathe 100% oxygen and thus almost quintuple the 2% of dissolved oxygen in the blood we more than double** the pool of oxygen that is easily available to the body.


*Out of all oxygen in the body we are looking for the 98% that is reversibly bound to hemoglobin. And now we assume that one quarter of hemoglobin will be unsaturated upon return to the lungs. 0.98 * 0.25 = 0.245 or 24.5%

**Normal oxygen concentration of air is 21%. So air with 100% oxygen would increase the oxygen by 100 / 21= 4.76 times. 2% of the total blood oxygen is normally not associated with hemoglobin, so 2% * 4.76 = 9.52%. We can then calculate the amount that we just gained: 9.52% - 2% = 7.52%. We can then compare this to 24.5% (I assume that there is still something like 2% oxygen dissolved in the serum in venous return blood?), and we find that breathing 100% oxygen would increase available oxygen by about 7.52 / 24.5 = .307 or 30.7%.

[This post edited 9/24. I originally misunderstood SO2 to indicate what % of hemoglobin is missing at least one oxygen rather than that SO2 just indicates the % of bindings sites on hemoglobin filled with oxygen.]

 

[Hip]

I decided to see just how much almost quadrupling the dissolved oxygen would actually increase oxygen available to the tissues.

I am not sure if your approach to this is along the right lines, although I am not 100% clear on this myself.

I think this sort of calculation (on how much HBOT increases oxygen availability to the tissues) would be a bit complex to perform, and I would not be sure how to do it, because I don't fully understand the dynamics. But I think we can assume that there will be a huge increase in oxygen availability to the tissues under HBOT, as the following explains.

To start with, note that the reason we need hemoglobin is because the 0.3 ml/dl of oxygen that gets dissolved in the blood under normal conditions in the lungs is insufficient to meet the tissue requirements for oxygen. With speed at which blood flows though the blood vessels, that 0.3 ml/dl of dissolved oxygen it carries just cannot meet the constant oxygen demands of the tissues.

So that's where hemoglobin comes in, because it can carry a lot more oxygen, and acts a sort of "oxygen buffer" of the blood. So when blood carrying the normal 0.3 ml/dl of dissolved oxygen flows into the tissues, and those tissues extract this dissolved oxygen from the blood to meet their oxygen needs, the blood is not left without any dissolved oxygen, because the hemoglobin replaces the lost dissolved oxygen that the tissues have taken.

Thus there is constant exchange between the reservoir of dissolved oxygen in the blood, and the (larger) reservoir of oxygen carried by the hemoglobin, with the latter constantly replenishing the former each time the tissues take some of the dissolved oxygen out from the blood.


Now when you increase the partial pressure of oxygen (via HBOT and/or breathing pure oxygen), this increases the amount of oxygen that can be dissolved in the blood, as we saw earlier, from 0.3 ml/dl to typically around 6 ml/dl. This then increases the dissolved oxygen storage capacity of the blood, since now a lot more dissolved oxygen can be stored in each dl (deciliter) of blood.

So this means that as the blood leaves the lungs and flows into the tissues, because it carries so much more dissolved oxygen in HBOT (20 times more than normal), it is less reliant on the hemoglobin reservoir to replenish the dissolved oxygen that is snatched up by the tissues. But I am guessing (but am not sure) that even at these much higher levels of dissolved oxygen, when this dissolved oxygen is snatched up by the tissues, the hemoglobin will immediately replace the oxygen that the tissues have taken out of the blood as per usual, in order to maintain the dissolved oxygen level.

So the actual levels of dissolved oxygen in the blood during HBOT would be a complex interplay between the starting level of 6 ml/dl as the blood leaves the lungs, the amount of dissolved oxygen snatched up by the tissues that the blood flows through, and the speed at which the hemoglobin reservoir can replace this snatched dissolved oxygen. I am not sure how you would calculate that.

But what we need to remember is that increasing the ambient partial pressure of oxygen via HBOT allows each dl of blood to hold up to 20 times more dissolved oxygen. This comes from Henry's law. So under HBOT conditions, assuming that the hemoglobin continues to efficiently do its job of replenishing the dissolved oxygen that is snatched up by the tissues, we might assume that the levels of dissolved oxygen in the blood will remain close to this very elevated level of 20 times higher than normal.

Some of the complex dynamics of how hemoglobin binds to and later releases oxygen in the blood is detailed in this article; see: "Chapter 2 – Bound Oxygen in the Blood". I don't really understand the intricacies.

What I have read is that with pure oxygen HBOT at 3 atmospheres, the oxygen dissolved in the blood in the lungs is alone capable of supplying all the body's resting oxygen needs, without needing any help from the hemoglobin. †

Thus during HBOT, I would guess that the tissues of the body will "see" up to around 20 times the amount of dissolved oxygen in the blood, which is a huge increase in oxygen availability to the tissues.

But the actual dissolved oxygen figure I think would depend on how easily the hemoglobin can, under hyperbaric conditions, replenish the lost dissolved oxygen snatched up by the tissues, in order to maintain this elevated dissolved oxygen level. I could not find any info on that, and maybe hemoglobin works differently under hyperbaric conditions.




† Note that the body's resting requirements for oxygen are 250 ml of oxygen per minute. In HBOT, when the dissolved oxygen in the blood is 6 ml/dl (= 60 ml per liter), since the heart in the resting state pumps 5 liters of blood every minute, you can see that the dissolved oxygen alone delivered to the body will be 5 x 60 = 300 ml of oxygen per minute, which is more than enough to meet the body's resting needs of 250 ml.

 

[Hip]

By the way, there is a discrepancy between my earlier calculation (based on Henry's law) that that pure oxygen HBOT at 3 ATM would increase the amount of oxygen dissolved in the blood by 14.3 times, and the figure provided in the paper I mentioned above, which indicates this increase would in fact be 20 times, not the 14.3 times I calculated.

I think we can assume the paper's figure of 20 times is correct, and that my figure of 14.3 times is wrong, which then raises the question of why my Henry's law calculation got it wrong. I believe the shortcoming of my Henry's law calculation is that I did not account for the intriguing fact that the oxygen partial pressure inside the lungs (called the alveolar partial pressure) is not actually the same as the oxygen partial pressure in the surrounding air.

The oxygen partial pressure inside the lungs is approximately one third less than the oxygen partial pressure in the surrounding air, and there are several reasons for this. So since it is this oxygen partial pressure in the lungs that determines (via Henry's law) how much oxygen gets dissolved into the blood, to be correct in your calculations, you need to use the lung oxygen partial pressure value, rather than the value in air that I used.

See this Wikipedia article for the reasons why the partial pressure in the lungs is lower than the partial pressure in the ambient air.



However, according to that same paper, my earlier calculation that breathing 100% oxygen alone (without using HBOT) will increase the dissolved oxygen in the blood by around 5 time appears to be correct, because the paper provides the same figure of a 5-fold increase.

 

[aaron_c]

OK, I see where I may have gone wrong. I was confused by how SO2 is defined: Many websites, including for example wikipedia, say that oxygen saturation is "a term referring to the fraction of oxygen-saturated hemoglobin relative to total hemoglobin (unsaturated + saturated) in the blood." Since "saturated" hemoglobin has four oxygens attached to it non-saturated hemoglobin could have 0-3 oxygens attached. Under this definition 0% SO2 could contain anywhere from 0-75% of the oxygen that can potentially be bound to it.

On the other hand SO2 is also defined as "the percentage of hemoglobin binding sites in the bloodstream occupied by oxygen," sometimes by the same website (see wikipeida).

Since it is the second definition that I've seen illustrated with examples I will assume the second definition is the accurate one. I've edited my above post to reflect this.

I think that now our math agrees; In my example I used 100% oxygen at normal atmospheric pressure, so increasing the pressure to 3 ATM would increase the dissolved oxygen 3-fold. I now estimate that 100% oxygen at normal pressure would yield 30.7% increase in usable oxygen. Times three that's 92.1%, and I think the extra can be explained by people being approximate and in particular the fuzziness in the SO2% of venous return.

So the actual levels of dissolved oxygen in the blood during HBOT would be a complex interplay between the starting level of 6 ml/dl as the blood leaves the lungs, the amount of dissolved oxygen snatched up by the tissues that the blood flows through, and the speed at which the hemoglobin reservoir can replace this snatched dissolved oxygen. I am not sure how you would calculate that.

Agreed.

So under HBOT conditions, assuming that the hemoglobin continues to efficiently do its job of replenishing the dissolved oxygen that is snatched up by the tissues, we might assume that the levels of dissolved oxygen in the blood will remain close to this very elevated level of 20 times higher than normal.

This is something I've been wondering about too. But why would hemoglobin continue to replenish the dissolved oxygen at a steady rate that keeps the (radically increased) dissolved oxygen at almost the same level throughout the body? I still don't understand how this could be the case. As far as I can tell the partial pressure of dissolved oxygen in the blood needs to drop below a certain threshold (about 10 kPa or 75 mm Hg according to wikipedia) for this to occur.

Here is one chart illustrating this relationship (thank you ventworld.com).

So a change in SO2 from 50 mm Hg to 40 mm Hg would result in much more oxygen being released than a change in SO2 from 150 to 140.

Do you have a handle on how to use ideal gas laws to figure out the partial pressure of a given amount of dissolved oxygen in the blood? My brain is too crashy right now to do it.

I could not find any info on that, and maybe hemoglobin works differently under hyperbaric conditions.

I've also wondered if the hyperbaric conditions might increase the oxygen dissolved in the plasma quite aside from what we've talked about with increasing the oxygen that gets into the blood at the lungs...but I can't see how that would work either unless our bodies are detecting and reacting to air pressure in ways we don't yet understand.

I'm going to talk to my doctor about using a non-rebreather oxygen mask for an hour a day for a few days. I've done mHBOT once or possibly twice before and I had a mild but noticeable reaction to it so hopefully I'll be able to report back on whether the oxygen mask does anything similar.

 

[Hip]

I think you will find that the two definitions of oxygen saturation you quoted basically mean the same thing. Out of all the hemoglobin binding sites in all the red blood cells in the blood, the oxygen saturation is simply the percentage of these sites that are currently carrying oxygen.

Oxygen saturation does not really come into HBOT considerations at all, since oxygen saturation is always nearly 100% in everyone (with healthy lung function), even when breathing normal air. If you have ever used one of the those pulse oximeters that you put on your finger to measure your blood oxygen saturation, you will know that it is close to 100% all the time. So nothing changes with HBOT regarding oxygen saturation.

Do you have a handle on how to use ideal gas laws to figure out the partial pressure of a given amount of dissolved oxygen in the blood? My brain is too crashy right now to do it.

Yes, this document (on page 10) gives Henry's law in a form for determining how much oxygen dissolves in blood at a given partial pressure of oxygen; the equation is:

Dissolved oxygen in blood (expressed in ml oxygen per deciliter of blood) = 0.003 x P

where P is the oxygen partial pressure in the lungs, measured in mmHg (millimeters of mercury). Note that 1 atmosphere = 760 mmHg. You can see in this Wikipedia article that under normal conditions, the oxygen partial pressure in the lungs is 104 mmHg.

 

[aaron_c]

I think you will find that the two definitions of oxygen saturation you quoted basically mean the same thing. Out of all the hemoglobin binding sites in all the red blood cells in the blood, the oxygen saturation is simply the percentage of these sites that are currently carrying oxygen.

With the brainfog from this illness I'm always afraid that there's something obvious that I'm not seeing. That said, I'm not seeing it. Since unsaturated hemoglobin could have anything from 0-3 oxygens attached, the definition of SO2 as "the fraction of oxygen-saturated hemoglobin relative to total hemoglobin (unsaturated + saturated) in the blood" doesn't come out to the same thing as just "the percentage of these sites that are currently carrying oxygen." Or I suppose you could define unsatured hemoglobin as hemoglobin with zero oxygen attached, but that would just cause the the inverse of the same problem.

Minor point though. In a sense they could define SO2 as the percent of blood currently playing a kazoo--in most cases how it works is basically academic once we have experimented enough to know that SO2 of 60% (or whatever) is dangerous and requires supplemental oxygen.

Brain still isn't up to parsing the second part, but thanks for the links.

 

[aaron_c]

I just got back from a clinic specializing in "Exercise with Oxygen Therapy." The ND I saw was knowledgeable about HBOT and he took great pains to point out that the benefits of HBOT for ME/CFS were only anecdotal and that potential benefits from a simple face-mask were only theoretical. He didn't do this in an attempt to sell me anything--he doesn't provide HBOT services there, his bread and butter is providing the oxygen exercise therapy to people who have had heart attacks, and insurance pays for that.

So we talked for a while comparing HBOT to exercise with oxygen therapy. He said that when HBOT works on burns it works because oxygen comes into the tissue not just through the lungs but also through the wound. Normally, of course, oxygen doesn't enter or leave the skin in appreciable amounts. So while he thought HBOT worked for some people with a number of conditions like fibro and potentially ME/CFS, he had to admit that much of the benefit had to be through some means other than increasing the oxygen entering through the lungs. He didn't know what that would be.

He told me how to go about experimenting with a facial mask should I so desire:

-Use a partial rebreather mask: He was concerned about the dangers of using a non-rebreather mask because, as we've mentioned, the oxygen can damage corneas and other tissue.
-Use the highest flow rate your regulator will permit, at least 15 L/min
-Wear swim goggles as eye protection and tape the upper portion of the mask to your face to prevent oxygen escaping and touching your eyes. (I think this was mentioned elsewhere? But I forgot it so I'm mentioning it again)

He also suggested the use of antioxidants like co-q10 and vitamin E, plus some others that were less situation-specific.

 

[Hip]

-Use a partial rebreather mask: He was concerned about the dangers of using a non-rebreather mask because, as we've mentioned, the oxygen can damage corneas and other tissue.
-Use the highest flow rate your regulator will permit, at least 15 L/min
-Wear swim goggles as eye protection and tape the upper portion of the mask to your face to prevent oxygen escaping and touching your eyes. (I think this was mentioned elsewhere? But I forgot it so I'm mentioning it again)

He also suggested the use of antioxidants like co-q10 and vitamin E, plus some others that were less situation-specific.

That's useful to know, thanks.

With a Google image search on "non-rebreather mask", all of the masks pictured exclude the eyes, and just cover the mouth and nose, so oxygen would get to the corneas unless the gas leaks from the upper portion of the mask, if the mask does not fit snugly to the face.

But most of them look like cheap plastic disposable masks, which might be more prone to leaking. So this might be an issue.

Perhaps one can obtain a higher quality non-disposable rubber or neoprene mask one that will have a closer and more leak-proof fit on the face.

 

[Hip]

benefits of HBOT for ME/CFS were only anecdotal

My feeling is that HBOT will never be curative for ME/CFS, as it appeared to be for that Lyme patient in the other thread (oxygen may be toxic to Borrelia, but not to viruses). However, it's possible that HBOT might bring some mild benefits to ME/CFS, such as temporarily reduced brain fog.

 

[cigana]

My feeling is that HBOT will never be curative for ME/CFS, as it appeared to be for that Lyme patient in the other thread (oxygen may be toxic to Borrelia, but not to viruses). However, it's possible that HBOT might bring some mild benefits to ME/CFS, such as temporarily reduced brain fog.

Hip, just wondering why you think HBOT might only bring some mild benefits, when there are patients in the other thread reporting life-changing improvements?

 

[Hip]

Hip, just wondering why you think HBOT might only bring some mild benefits, when there are patients in the other thread reporting life-changing improvements?

Aren't those people in the other thread Lyme patients though?

 

[Jesse2233]

Aren't those people in the other thread Lyme patients though?

Some of them have dual diagnoses of CFS and POTS, it's hard to tease out. Also in the FB group there some pure ME patients reporting significant improvements. But it's not everyone, and some have adverse results

 

[cigana]

Aren't those people in the other thread Lyme patients though?

Looks like a few PWC's in there, e.g. this one

I was 90% housebound and 50% bedbound. After about 4 - 6 months, I was virtually like my old pre M.E self. I can't describe the joy that I felt.

And there is junkcrap50's experience:

I've had full remission from HBOT.

as well as a couple of other forum members.

BTW Jamie Deckoff-Jones' blog on HBOT is well worth reading, it seems she recommends its use for MECFS. There is also a little discussion of partial pressures and normobaric oxygen.

Some interesting ideas on how it might work, including a study reportedly showing HBOT inhibits endoneuronal TNF-alpha production, and an increase in concentration gradients helping to get oxygen across mitochondrial cell membranes.

 

[Hip]

And there is junkcrap50's experience:

Just looking at @junkcrap50's two HBOT posts here and here, he says that the remission lasted for a month, but then disappeared, even though he continued with the HBOT (and he speculates that the continued sessions he did after remission appeared may have reversed the benefits).

So that's intriguing, but not really a long term success.



But in terms of trying out HBOT, I still cannot see why there is a need to use a hyperbaric chamber, when the paper I mentioned earlier quite clearly states that breathing 100% oxygen at normal pressure increases the dissolved oxygen in the blood by 5 times, which is a substantial amount.

That's probably more dissolved oxygen than you get from a mild HBOT chamber, even if you breathe oxygen through a simple face mask in the chamber.

 

[cigana]

Just looking at @junkcrap50's two HBOT posts here and here, he says that the remission lasted for a month, but then disappeared, even though he continued with the HBOT (and he speculates that the continued sessions he did after remission appeared may have reversed the benefits).

So that's intriguing, but not really a long term success.

But in terms of trying out HBOT, I still cannot see why there is a need to use a hyperbaric chamber, when the paper I mentioned earlier quite clearly states that breathing 100% oxygen at normal pressure increases the dissolved oxygen in the blood by 5 times, which is a substantial amount.

That's probably more dissolved oxygen than you get from a mild HBOT chamber, even if you breathe oxygen through a simple face mask in the chamber.

It seems to me from reading those posts that junkcrap50's remission stopped when he/she stopped treatment (due to the cost), although it's not entirely clear. EDIT: perhaps this means it's not classified as "remission".

I think your ideas re normobaric are good, but wonder if there is some effect that pressure provides which we're not aware of. This is discussed in the blog I posted, where there are some references from a researcher "Dr. Rossignol" who apparently believes there is an independent effect from the pressure.

 

[Hip]

but wonder if there is some effect that pressure provides which we're not aware of.

I guess that's possible, although I've never read anything along those lines in HBOT literature. Shame the four HBOT experts I wrote to on this matter all failed to reply to my email.

I guess I could write to some manufacturer's of mild HBOT chambers and ask them, but they are hardly going to say "sure, breathing 100% oxygen from a $300 oxygen concentrator is just as effective as using one of our $6000 chambers".

 

[cigana]

I guess that's possible, although I've never read anything along those lines in HBOT literature. Shame the four HBOT experts I wrote to on this matter all failed to reply to my email.

I guess I could write to some manufacturer's of mild HBOT chambers and ask them, but they are hardly going to say "sure, breathing 100% oxygen from a $300 oxygen concentrator is just as effective as using one of our $6000 chambers".

I suspect the experts haven't answered because they can't answer...

Glancing at this study, it seems to suggest 1.5ATA HBOT is superior to 100% normobaric oxygen (although both are helpful).

 

[Hip]

Glancing at this study, it seems to suggest 1.5ATA HBOT is superior to 100% normobaric oxygen (although both are helpful).

That's a good find. Although in the case of treating TBI, which involves increased intracranial pressure due to the brain injury and brain inflammation, maybe the application of increased hyperbaric pressure may have advantages just on its own in combating this dangerous increase in pressure in the head.

In the full paper, it concludes:

Hyperbaric O2 had a significantly greater positive posttreatment effect than NBH on oxidative cerebral metabolism and ICP.

NBH = normobaric hyperoxia = breathing 100% oxygen at normal pressures
ICP = intracranial pressure

However, I did not understand quantitatively how much HBOT was better at treating TBI compared to breathing 100% oxygen at normal pressures (I think the quantitative results are in table 3, but I don't understand it).

 

[cigana]

Looking at Fig. 2, it seems the enhanced oxygen concentration in the HBOT group is maintained for a long time after the treatment session, but in the NBOT group the concentration falls soon after the treatment.