... First: DCS prevention is questionable either way but perhaps one should think of DCS risk reduction. Since we don't know what causes DCS definitively, we cannot talk about pure DCS prevention. Bubbles alone do NOT cause DCS and there are multiple scientific studies that indicate that...
Question: Are you aware of any documented cases of a diver with DCS symptoms and undetectable bubbles using Doppler instruments? (Sincere question, not intended to be confrontational or snarky)
To reinforce your statement, there are also many identified and unidentified human variables. The only reliable and absolute DCS prevention is stay at sea level (people can also be bent in unpressurized aircraft).
Maybe some of this will help the OP and some other readers: It is difficult to believe that bubbles never play any role in DCS, at least in severe DCS cases. Doppler studies actually show blocked vessels and autopsies show dead tissue. Like everything in medicine though, I also don't believe that the simple physics of bubble formation is the only bad actor. DCS may not always be the result of blocked blood flow due to bubbles, but it
is caused by gas being released from tissues more rapidly than the body can accommodate. That in turn
may cause physiological responses that produce symptoms long before compromised circulation has an impact. Here is an interesting and related article written for divers.
Alert Diver | The Quest for DCS Biomarkers
As complex as poorly understood as DCS is, there is a vast body of evidence that hyperbaric treatment administered in a timely manner is very effective. On a functional level, treatment is pretty simple. Maximize PPO
2, which necessitates being under pressure, even breathing pure O
2. Increasing the PPO
2 from 0.21 to 1.0 ATA by breathing Oxygen on deck has demonstrated benefits, but a much lower efficacy than 2-3 ATA. There's not much data above 3.0 ATA due to complications of Oxygen Toxicity.
The effect of pressurizing not only increases the PPO
2, it reduces the rate that absorbed biologically inert gas comes out of tissues (typically Nitrogen and/or Helium). I chose this wording because Nitrogen is not one of the inert gases in the Periodic Table. In severe cases, pressurizing also compresses physical bubbles that are compromising blood flow.
Typical treatments for the vast majority of DCS incidents involves breathing pure O
2 at 60' in a chamber (2.8 PPO
2). "Most" of the time, 60' is deep enough to achieve symptom relief when administered within short time after surfacing (within an hour or two). There are treatment tables that take the diver deeper, but most are limited to breathing air. The problem there is that the diver can actually start to take on Nitrogen instead of giving it off, at least in the faster tissues.
More sophisticated treatment chambers can administer high PPO
2 (like 2.5 to 3 ATA) treatment gasses at any depth that provides symptom relief, but that depth is almost always significantly shallower than the max depth of the dive.
Reinforcing that DCS is a risk management game rather than one of prevention, this article may be helpful to understand the concepts. It is also written for divers rather than hyperbaric medical professionals.
Alert Diver | Gradient Factors
The principals used in DCS treatment also apply to DCS risk reduction. The body absorbs less inert gas on a richer mix, say 32% Nitrox compared to air. Therefore there is less insert gas for tissues to release. Optimizing decompression starts to get really complex when you consider how different tissues absorb and release gas at different rates. Depending of the dive profile, you can have some tissues still absorbing gas while others are releasing. Further, different diluent gases absorb and release at different rates.
