Why are long-delayed or followup chamber treatments effective at all?

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OTF

Coney Island Whitefish Biologist
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My understanding is that hyperbaric treatment of DCS works by (re)compressing bubbles then allowing the dissolved gas to slowly come out of solution on controlled decompression. As I understand it, this should only be effective within hours-days after a DCS incident while acute bubbles exist. According to my mental model of this, at some number of hours after a bent diver surfaces their bubbles would peak then eventually dissolve naturally, any lasting damage being done, and chamber rides would be pointless.

HOWEVER the literature is full of cases where people receive chamber rides days, weeks, or even months after their hits with varying degrees of symptom resolution but often positive results. Sometimes these are delayed treatments, sometimes these are repeated followup treatments over time. Why does any of that work? Do bubbles actually persist in tissues much longer than I assume? Or is there something else going on?

Of course getting in a chamber sooner is better. But why isn't there a point after which chamber rides are considered useless?
 
As soon as the bubble forms, it expands to ambient pressure while all the inert dissolved gas at higher partial pressures in the region quickly diffuses into it. If the bubble is in a low perfusion area (possibly because it is blocking blood flow), its half life is very long. Since it is at ambient the pressure differential to ambient inert gas pressure is very low. Diffusion only occurs at the surface of the bubble. So the bubble collapses very slowly as the gas diffused out of it. Once bubbles of significant size occur in low perfusion regions, they can persist for a very long time.

Re-compression instantly increases the partial pressure, combined with 100% O2, maximizing the gradient and therefore the removal rate. Reducing the bubble size increases the surface to volume ratio, further accelerating things, and possibly unblocking circulation and increasing perfusion. There are many advantages to re-compression and 100% O2.

In general, particularly for bubbles not well mixed with blood flow, gas in bubbles persists much longer than dissolved gas.

In deco, you are trying to get the dissolved gas to aggregate with the "bubble" in the lungs, rather than with bubbles in tissue.
 
Why does any of that work? Do bubbles actually persist in tissues much longer than I assume? Or is there something else going on?
The bubbles are gone but injured tissue forms scars which are poorly perfused. Hyperbaric O2 pushes oxygen into that scar tissue (via diffusion even if blood flow is poor). Better oxygenation effectively speeds the healing of those damaged tissues.
 
The bubbles are gone but injured tissue forms scars which are poorly perfused. Hyperbaric O2 pushes oxygen into that scar tissue (via diffusion even if blood flow is poor). Better oxygenation effectively speeds the healing of those damaged tissues.
I do have hyperbaric training, both statements have evidence, this quoted has a paradigm in wound or healing non diving related hyperbaric treatment: to turn venous blood and serum in oxigenated medium (Henry's law) and playing a great role at recovering from tissues level, maybe not so obvious at a glance
Are both the physics and cellular process taking place
 
My understanding is that hyperbaric treatment of DCS works by (re)compressing bubbles then allowing the dissolved gas to slowly come out of solution on controlled decompression. As I understand it, this should only be effective within hours-days after a DCS incident while acute bubbles exist. According to my mental model of this, at some number of hours after a bent diver surfaces their bubbles would peak then eventually dissolve naturally, any lasting damage being done, and chamber rides would be pointless.

HOWEVER the literature is full of cases where people receive chamber rides days, weeks, or even months after their hits with varying degrees of symptom resolution but often positive results. Sometimes these are delayed treatments, sometimes these are repeated followup treatments over time. Why does any of that work? Do bubbles actually persist in tissues much longer than I assume? Or is there something else going on?

Of course getting in a chamber sooner is better. But why isn't there a point after which chamber rides are considered useless?
There is some evidence to suggest that hyperbaric oxygen can be of some benefit in treating DCS even if delayed. There are two phases of injury in DCS: the initial bubble injury and the mechanical effects of impeding blood circulation and physically impinging on tissue, and the inflammatory effects that follow those. That inflammation can take a while to resolve, and hyperbaric oxygen has demonstrated anti-inflammatory effects.

Best regards,
DDM
 

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