Are some divers more prone to bubble formation than others?+

[danvolker]

RJP

A lot of small-scale studies are conducted primarily to justify funding for large scale studies. A statistical study of the number of diagnosed DCS cases would probably be more useful to the industry. People need a simple number of hours to avoid flying rather than an algorithm that factors in every environmental and biomedical variable.

Right...
My number of hours is about one or two. But usually it will be 4 or more before I could get on a plane after diving. More from the "art" of diving than from the "science".

 

[DocVikingo]

Was the presence/absence of a PFO collected as part of this study?

Hi JohnN,

I do not have the full text article at hand, so I don't know if the possibility of PFO in this cohort was evaluated. Since the authors make no mention of it, I suspect not.

However, the study, which focuses on bubble formation in divers and not on bubble movement around their circulatory systems, does indicate that no bubbles in the right heart were found in any diver at the 24-hr post-diving preflight control.

You may wish to consider that inert gas bubble formation takes place in the venous system (blood that flows through the right chambers of the heart), not the arterial system (blood that flows through the left chambers of the heart). As such, there seems to be little reason to expect that bubbles arising in the right heart during the subsequent return flight were the result of blood flow across a PFO or similar mechanism.

Cheers,

DocVikingo

 

[JohnN]

Hi JohnN,

I do not have the full text article at hand, so I don't know if the possibility of PFO in this cohort was evaluated. Since the authors make no mention of it, I suspect not.

However, the study, which focuses on bubble formation in divers and not on bubble movement around their circulatory systems, does indicate that no bubbles in the right heart were found in any diver at the 24-hr post-diving preflight control.

You may wish to consider that inert gas bubble formation takes place in the venous system (blood that flows through the right chambers of the heart), not the arterial system (blood that flows through the left chambers of the heart). As such, there seems to be little reason to expect that bubbles arising in the right heart during the subsequent return flight were the result of blood flow across a PFO or similar mechanism.

Cheers,

DocVikingo

I'm even more confused, sorry to badger you about this. My understanding is that dissolved gas / microbubbles are generally cleared as the blood passes through the alveoli in the lungs. A PFO allows blood to pass back into the circulatory system without going through the lungs. Doesn't it follow that a PFO would increase the number of gas bubbles measured at the right ventricle? (I'm presuming there was some non-zero time between the end of the dive and when the bubbles in the ventricle were measured)

 

[DocVikingo]

Hi JohnN,

Inert gas bubble formation takes place in the venous system (blood that flows through the right chambers of the heart, or “low pressure” side), not in the arterial system (blood that flows through the left chambers of the heart, or “high pressure” side). This is the case whether or not a PFO or other atrial septal defect exists.

With this in mind, let’s follow your line of reasoning, “A PFO allows blood to pass back into the circulatory system without going through the lungs. Doesn't it follow that a PFO would increase the number of gas bubbles measured at the right ventricle?”

Let’s assume that a diver has a PFO and that equalization of the ears via the Valsalva maneuver has, through brief changes in intrathoracic pressure, transiently altered the normal L->R intracardiac pressure gradient and allowed scuba-related inert gas bubbles to bypass the filtering mechanism of the lungs and move directly from the R->L side of the heart.

This now begs the question by what mechanism would these L-side bubbles appear on the R-side of the heart during a return plane flight subsequent to a 24-hr post-diving delay? How could a PFO be responsible for gas bubbles appearing on the R-side of the heart when they did not exist there at 24-hr pre-flight measurement?

In the absence of a continuous loop of active R->L shunting of blood containing very long lasting unabsorbed bubbles, which would be nearly impossible from several respects, after 24-hrs the entire circulating blood supply would have passed through the lungs well over a thousand times.

Regards,

DocVikingo

 

[bvanant]

Is this really surprising to anyone? In my day job we used to build infusion pumps for IV therapies. Bubble formation in the tubing was significantly impacted by the chemistry of the tubing and more importantly by the surface roughness. Lipid coatings and lipid based drugs were much more trouble than hydrophilic surfaces. Surface roughness was also important, very smooth surfaces were bad, slightly rough surfaces were better, and surfaces with significant roughness was bad again. It would be interesting to look at blood chemistry/cholesterol particles in the bubblers vs. the non-bubblers, I would expect that they would be correlated.
Bill

 

[Akimbo]

It is well known that previously injured tissue is more susceptible to bubble formation. I have observed it myself. Divers will often get hit in areas previously injured, often as a child or adolescent.

 

[Rich Keller]

This indicates a possible higher susceptibility to bubble formation in certain individuals, who may need longer PFSI before altitude exposure after scuba diving."

This has been known for a long time but exactly why some people are more susceptible and what factors those people have that makes them more susceptible then others has not been known. We know that body mass, body tissue ratios and lung capacity are all factors but there is no way to test for this on an individual basis other then trial and error in a recompression chamber. The same thing applies to oxygen poisoning, some are more susceptible but there is no way to identify them without an oxygen tolerance test in a recompression chamber.

 

[dreamdive]

Just like a lot of things in nature, things fall on a bell shaped curve. Same as with divers developing bubbles. There are some that demonstrate bubbles more and less than what falls in the middle of the curve! Mind you, there are inter- and intra-individual variation of this phenomena. What this means is that on any given day, Diver A may develop less bubbles but on another day develops more bubbles for the same dive with the same profile, same temperature...etc.

That has been documented for a while and when you read the studies, you will see this.

Factors that may vary the amount of bubble development on any given day may be related to last exercise prior to diving, and the phenomena of adaptation, as well as processes yet to be discovered. Regarding adaptation: Here it has shown that as you continue to dive the same depth, the amount of bubbles formed become less and less.

If you are interested reading the studies yourself, I have compiled a list of over 200 articles on diving related research and posted it on the AddHelium website under "Resource Library: Add Helium Resource Library | Add Helium

Another very important thing to keep in mind is: JUST BECAUSE YOU HAVE BUBBLES, DOES NOT MEAN THAT YOU ARE GOING TO BEND!

The relationship of developing DCS and bubbles is still not understood. Most of us have bubbles but very few of us develop DCS.

For those with further interests on studies regarding PFO's, the above recently updated list has few more additions in that section, as well.

Happy Reading and Safe Diving!

Claudia

 

[Akimbo]

…Another very important thing to keep in mind is: JUST BECAUSE YOU HAVE BUBBLES, DOES NOT MEAN THAT YOU ARE GOING TO BEND!...

I concur, to a point. However, extreme cases like explosive and omitted decompression can generate enough gas in the bloodstream to block flow in major systems. That will make anyone symptomatic. Divers have developed DCS symptoms without detectable bubbles and have developed detectable bubbles without symptoms. Does that mean (A) that bubbles don’t cause DCS, (B) our ability to detect bubbles is imperfect, or (C) something else is going on and bubble are not the root indicator?

The difficult part is that broad gray area where DCS is starting to develop, which represents that vast majority of cases that are treated. We don’t have the instrumentation to simultaneously monitor everything going on in the body in real time. It is possible that there a lot of “cause and effect” interactions that we have not observed yet. There may come a time when divers monitor biochemical responses rather than physical bubble formation to regulate decompression.

 

[dreamdive]

Does that mean (A) that bubbles don’t cause DCS, (B) our ability to detect bubbles is imperfect, or (C) something else is going on and bubble are not the root indicator?

The difficult part is that broad gray area where DCS is starting to develop, which represents that vast majority of cases that are treated. We don’t have the instrumentation to simultaneously monitor everything going on in the body in real time. It is possible that there a lot of “cause and effect” interactions that we have not observed yet. There may come a time when divers monitor biochemical responses rather than physical bubble formation to regulate decompression.

Perhaps all three are correct, perhaps none. The "bubble paradigm" is not as clear cut as some used to have us believe. It appears that the "bubble" plus another trigger (or triggers) are needed to develop DCS outside your example of "explosive decompression". Even the more recent literature is hinting to an acute vs delayed onset of DCS having different mechanisms. All we can due is stay tuned and watch as new data emerges.

C