Tissue stress associated with bubble formation; potential benefits of diving enriched air

[100days-a-year]

DON and you,jury is still out on 02 and how much of a factor it is.
http://r.search.yahoo.com/_ylt=A0LE...69/18178/RK=0/RS=9ktvVpEHv5GP.yJJ7bLcJNca3SM-

 

[tarponchik]

In my language, we have a saying: if you're standing at the bottom of a hole, it might be a good idea to stop digging.

Inert gas bubbles that form during decompression are reversible. They have to be. They will dissolve back into the tissue fluids over time. And this process can be accelerated by increasing the ambient pressure, which is one of the main reasons for hyperbaric treatment of DCS. This is high school chemistry.

Now, given that inert gas bubbles are reversible, how do you explain the chronic joint or neurological problems that some patients have after a bad DCS hit? That's not tissue damage?

I think it's time you stopped digging.

Looks like you spent half day printing your reply here? I am so sorry I hurt your ego. It would be better to ignore this thread, but for sake of all your efforts, here is my short reply.

Above, you stated that "Inert gas bubbles that form during decompression are reversible. They have to be. They will dissolve back into the tissue fluids over time." Here you only echoed what I've already said numerous times above, so I am puzzled, why would you preach me my own words with a smart face. If you go back you'll find out that I was the 1st one who used the word "reversible" here.

However, your next statement completely missed the point: "Now, given that inert gas bubbles are reversible, how do you explain the chronic joint or neurological problems that some patients have after a bad DCS hit? That's not tissue damage?" Though I do have an explanation for this (that is, bubble formation sometimes is irreversible, unless treated under certain conditions), I do not have to answer this question because I wasn't talking DCS here, and nobody else did.

The original claim I replied to was that reversible bubble formation under normal recreational diving conditions somehow causes "tissue stress" (@packrat12) or "decompression stress" (@Diver-Drex). Hence, diving NITROX is supposedly beneficial even w/o the benefit of longer bottom times because it reduces this "tissue stress". Both scientific papers mentioned here previously, that is, Souday et al (2016) referred to by @packrat12 and Marinovic et al (2012) referred to by me deal with venous bubble formation under normal recreational diving conditions; that is, reversible formation only. They had indeed demonstrated that reversible bubble formation is reduced by breathing NITROX. My point is, until someone proves that this reversible bubble formation under normal recreational diving conditions is harmful, I do not care.

You seem to imply that if irreversible bubble formation that causes DCS is indeed harmful, so is the reversible one; otherwise, I can't figure out why you keep talking about DCS. However, as I said a zillion times already, you have to prove it, not just imply.

 

[Colliam7]

I have to wonder if there is actually as much agreement here as real disagreement. I think understand the point that tarponchik is making: everybody bubbles to some extent during most dives, and that bubbling is reversible, and it is hard to identify clinically meaningful damage done by the majority of that bubbling. The bubbles recede to extinction, any vague discomfort in the shoulders and knees dissipates, and we don't see any permanent effect. At the same time, however, it has become clear over the past 5-10 years, based on actual prospective research (e.g. the Møllerløkken paper (Venous gas embolism as a predictive tool . . . ) paper cited by Storker) that bubbles can, and probably do, damage the intravascular endothelium to a certain extent. It is not entirely clear if there is a minimum bubble size beyond which this damage is significant. And, it is also not clear if this endothelial damage is cumulative - I personally suspect that it is, but I simply cannot prove it on the basis of available data. I personally think the observed osteonecrosis is probably a manifestation of a cumulative process. Others may challenge that view because it has not been proven. But, I would also define any endothelial damage as 'tissue stress'. (And, others may choose a different term.)

So, bubbles form, to some extent, in most divers, on most dives, and they are generally 'reversible', i.e. they shrink to extinction after the dive. DAN has presented data demonstrating that clinically silent, and reversible, bubble formation is quite common in recreational divers. If you look for them, you will find them, even if the divers exhibits no symptoms. There is probably some endothelial damage done by these bubbles, but the endothelium is remarkably robust, and minor damage is quickly repaired by the deposition of new endothelial cells. Therefore, in most cases, reversible bubble formation does not produce clinically significant (or even clinically evident), or sustained, 'tissue stress' even if there is transient endothelial damage.

Where I might draw a somewhat different conclusion than tarponchik - I believe there are now enough data to demonstrate tissue injury (endothelial damage) associated with bubble formation, I would describe this injury process as tissue 'stress', in the absence of a better term, and the timeline for reversal of the endothelial damage is greater / more extended than the timeline for bubble extinction. The bubbles will disappear before a new layer of endothelial cells has been laid down on the blood vessel.

 

[DevonDiver]

N2 bubbles form and dissolve later w/o any chemical reactions. Unless you get too many bubbles and develop DCS, who cares.

You overlook the fact that bubbles, even micro-emboli, trigger immune response which causes very real changes in blood/brain chemistry.

Bubbles are formed not by physiological or psychological process but by physics described by Henry's law. Thus, bubble formation by itself is not our body's reaction to something and can not be classified as stress.

Im not sure if I misunderstand you; but you quote Henry's Law... but are denying the benefit of nitrox in reducing bubble growth/accelerating bubble collapse?

As for tissue stress in particular, though the concept is still too vague to my taste, it is based entirely on tissue damage.

Since bubble formation is reversible, you need to demonstrate that it did, indeed, damage the tissue before you even start talking about "tissue stress". Until you show me the dead cells or any other evidence of such damage, this is all pseudo science.

Here's an interesting study..
Perspective on Cerebral Microemboli in Cardiac Surgery: Significant Problem or Much Ado About Nothing?
Simon J. Mitchell, FANZCA and Alan F. Merry, FANZCA

 

[dmaziuk]

... There is probably some endothelial damage done by these bubbles, but the endothelium is remarkably robust, and minor damage is quickly repaired by the deposition of new endothelial cells ...

Much quicker at 15 than at 50 I bet...

Personally I care about my lungs. I've a number of pulmonary risk factors so pumping extra O2 in my lungs is something I'd rather not do unless I really need to: it's a rather potent irritant, I'm sure that can't be good for me. YMMV of course.

 

[Diver-Drex]

Tarponchik, I'll try to summarize your points. I am actually trying to understand what you're saying. I don't agree with in the least bit, but I am curious.
1. Harmless bubbles are harmless. I can't disprove that, what's your point? You can't disprove that harmful bubbles are harmful either. Now that we cleared that up... We do not know where the line is when harmless bubbles begin to cause harm. But we do know that it is indeed the bubbles that cause tissue damage.
2. Bubbles are not stress, the body's reaction to them is stress. Ok. Collectively, inert gas bubble formation during decompression and the body's reaction to those bubbles is decompression stress.
3. Too much oxygen is bad for you. CNS and pulmonary toxicity is fairly well agreed upon. However, you grossly misinterpreted or misused the information in the Scientific American article you linked to. I think I explained that pretty clearly. The two references studies had no relevance to SCUBA.
So what am I missing?

 

[DevonDiver]

1. Harmless bubbles are harmless. I can't disprove that, what's your point? You can't disprove that harmful bubbles are harmful either. Now that we cleared that up... We do not know where the line is when harmless bubbles begin to cause harm. But we do know that it is indeed the bubbles that cause tissue damage.
2. Bubbles are not stress, the body's reaction to them is stress. Ok. Collectively, inert gas bubble formation during decompression and the body's reaction to those bubbles is decompression stress.

Some quotes and links/references that may be considered pertinent to the debate in the following articles:

Subclinical DCS, Decompression Stress and Post-Dive Fatigue

Mildly Bent - Decompression Stress and Micro-Bubbles

 

[tarponchik]

So, one antibody is crying, "Oh no! My bubble is gone! It disappeared!" But another antibody cheers her up, "Not to worry! This guy will take another dive in 10 min and we'll have plenty of bubbles again!"

Seriously, has AB formation to bubbles been demonstrated? It seems an unlikely event to me because the immune system prefers highly heterogeneous antigens. This is why, for example, Plasmodium falciparum causes poor immune response. The outer shell protein of this parasite is outlined mostly with repetitive motive of just 4 amino acids (I forgot which ones) and this makes it all but invisible to immune system. Now, in the case of a N2 bubble, its surface is just water molecules and there is no specific pattern to be recognized. Can, for example, one make ABs to small hydrophobic microspheres (for example, PTFE)?

Sorry, folks, I'm dog tired after a long trip, will get back later.

 

[KenGordon]

...is a non-issue for rec divers. There's no way you'll reach pulmonary oxtox limits if you dive normal rec profiles and do fewer than ~five dives per day. Even on EAN36.

Try imagining pulmonary oxygen toxicity as a grey line thing like deco. Contributing factors may bring it on sooner. Also consider that you may have no choice but to be breathing a ppO2 of 2.8 for extended periods.

I am a total fan of Nitrox and use it whenever possible, but it is not completely risk free even with a hard bottom above the MOD.

 

[Diver-Drex]

Try imagining pulmonary oxygen toxicity as a grey line thing like deco. Contributing factors may bring it on sooner. Also consider that you may have no choice but to be breathing a ppO2 of 2.8 for extended periods

Could you describe those circumstances? In a recreational context how is that happening? You're on 36% and drop to 220fsw? Pulmonary O2 toxicity is minor compared to your other issues if that happens. In a non recreational setting even hard to see. You run out of back gas and switch to 100% at 60fsw, risking drowning from CNS toxicity vs. drowning being out of breathing gas? Possible, but again pulmonary damage is not your primary concern.