Repetitive dives

[Deeply Safe Labs]

Hello Wallowa,
We are in complete agreement. Inflammatory stress is an important concept but I'm not competent in this field. I simply assumes that to provoke this stress, you need a bubble.
I'm definitely in favour of the use of dive computers. The equipment has evolved since the mid-1990s, even if the algorithms are virtually the same.
Thanks for this article, I wasn't familiar with it but it analyses the debates at the 1995 workshop, which is well known in the decompression community. I'm going to read it carefully, but you know that English isn't my mother tongue (Unfortunatelly, I'm French...), so I'll take my time.
On first reading, it seems to me that Edmonds is talking about his experience with computers in the early 80s and some of his points are no longer relevant. The fact that computers don't take descent into account seems wrong to me, even in the days of EDGE, Guide and SME.
Edmonds (and Bennet) denounced the break with tested and validated procedures. The rounding off of depth and time is an old debate that no longer applies, but I thought that no manufacturer would ever forget to add a Residual Nitrogen Time (whatever the method used) for repetitive dives... I was wrong.

 

[Wallowa]

Hello Wallowa,
We are in complete agreement. Inflammatory stress is an important concept but I'm not competent in this field. I simply assumes that to provoke this stress, you need a bubble.
I'm definitely in favour of the use of dive computers. The equipment has evolved since the mid-1990s, even if the algorithms are virtually the same.
Thanks for this article, I wasn't familiar with it but it analyses the debates at the 1995 workshop, which is well known in the decompression community. I'm going to read it carefully, but you know that English isn't my mother tongue (Unfortunatelly, I'm French...), so I'll take my time.
On first reading, it seems to me that Edmonds is talking about his experience with computers in the early 80s and some of his points are no longer relevant. The fact that computers don't take descent into account seems wrong to me, even in the days of EDGE, Guide and SME.
Edmonds (and Bennet) denounced the break with tested and validated procedures. The rounding off of depth and time is an old debate that no longer applies, but I thought that no manufacturer would ever forget to add a Residual Nitrogen Time (whatever the method used) for repetitive dives... I was wrong.

Never have to apologize for being French! Or for any nationality. The micro nuclei and subsequent pitting of vascular walls has been established and can promulgate several issues long after the dive. DCI is not just about bubbles. Your observations about descent times, rounding errors are all in the mix. Computers are not intuitive and simply record pressure and time as they change, that is it. Then of course these changes are compared to an algorithm/model to adjust the profile during the dive.

Testing to validate these models after open water dives must have defined measurable physiological parameters that describe any signs of tissue level damage. This field data must be repeated and then produce the same results for the data set to be considered valid. Alas for a variety of reasons these data sets must contend with a wide variety of variables, many undefined, that differ for each diver on each dive.

Unfortunately, the wild card in all this is the variability in the physiology of the individual diver on the dive day and on that dive. Every day each diver will react differently to the pressure and time changes. That is why in my layman’s opinion the "stress" of diving should be the fundamental basis for all DCI research. Heck, even diagnosis of full-blown DCI is often misdiagnosed mainly due to the wide range of signs and expressed symptoms without verified definitive diagnostic tests being available. Dopplers are neat, but not definitive. Asymptomatic injury is a given considering the paucity of diagnostic testing or clinical standards for determining the level of or even if DCI occurred.

Diving is and always has been about assumption of risk along with the privilege of diving. Has diving been worth the potential and realized injuries from my decades of diving? You bet.

My opinions are just that, opinions and I always consider that I could be wrong.



Thanks for the dialogue.

 

[dmaziuk]

.... So called "Diving Stress" rather than "DCS" may be the overlooked form of DCI that ultimately will injury more if not all divers.

Last I heard there was no way to quantify that. Inflammatory markers may look promising, but until they collect a lot of those, preferably correlated to doppler scans, we won't really know.

 

[Wallowa]

Absence of proof is not proof of absence....your statement is correct; but not an answer to the question of potential injury to every diver on every dive... asymptomatic DCI has been shown to create damage to vessel linings...quantification would require the diving medical community's focus on exactly what level of tissue damage is occurring and like stated above given the many variables; that at best would be an expensive and resource consuming undertaking...my issue with all this is that it is easier for everyone to look the other way and only focus on the 'known' DCS and AGE events and presented overt damage ...doppler is a crude tool to determine micro tissue events or possible damage and systematic histological examinations are not forthcoming....in the end, the diving community, including the 'business of diving', prefers to believe that it is better to know the injury that they know, than the injury that they don't know...that axiom fits the current state of diving medicine's approach...pragmatic but at what long term determent to divers?

My advice is to expend diving medical research on the actual level of tissue damage and then work from there on prevention or treatment. Gross aspects, and most are subjective diagnoses, are the low hanging fruit, but the cellular level is what ultimately counts. Inflammatory markers may or may not point the way, but what is the definitive source of the inflammation? Again, I think all diving DCI research should first determine exactly what and when cellular damage is incurred and then work out from there. Bottom up not top down.

Not trying or wanting to start a debate, but only offer my insights and opinions. I could be wrong and hope I am about the potential extent of tissue damage to all divers.

 

[Deeply Safe Labs]

Absence of proof is not proof of absence....your statement is correct; but not an answer to the question of potential injury to every diver on every dive... asymptomatic DCI has been shown to create damage to vessel linings...quantification would require the diving medical community's focus on exactly what level of tissue damage is occurring and like stated above given the many variables; that at best would be an expensive and resource consuming undertaking...my issue with all this is that it is easier for everyone to look the other way and only focus on the 'known' DCS and AGE events and presented overt damage ...doppler is a crude tool to determine micro tissue events or possible damage and systematic histological examinations are not forthcoming....in the end, the diving community, including the 'business of diving', prefers to believe that it is better to know the injury that they know, than the injury that they don't know...that axiom fits the current state of diving medicine's approach...pragmatic but at what long term determent to divers?

My advice is to expend diving medical research on the actual level of tissue damage and then work from there on prevention or treatment. Gross aspects, and most are subjective diagnoses, are the low hanging fruit, but the cellular level is what ultimately counts. Inflammatory markers may or may not point the way, but what is the definitive source of the inflammation? Again, I think all diving DCI research should first determine exactly what and when cellular damage is incurred and then work out from there. Bottom up not top down.

Not trying or wanting to start a debate, but only offer my insights and opinions. I could be wrong and hope I am about the potential extent of tissue damage to all divers.

I'm neither a doctor nor a physiologist and I'm not competent to answer the question of silent damages. Perhaps you should address your advice to a medical society like UHMS, SPUMS or EUBS, to finance and conduct a study.

Avoiding this kind of damage would be a good thing, but the questions raised by the series of videos on repetitive diving are very simple:
- Is it possible, serious and safe to manage a repetitive dive without applying a safety procedure that has been used since the end of the Second World War?
- Knowing that the first decompression meters were the cause of many bends because they didn't include a procedure of this type, aren't the ZHL16C GF computers also likely to cause a few bends?

Take care,

 

[Deeply Safe Labs]

A new video is online : Paul Bert's work is not as well known as others...

 

[Wallowa]

DS,

Bert's work in 1865 [?] was correct in demonstrating that decompression [hypobaric] was the event/time when bubbles were produced, This does not address the issue of asymptomatic DCI; but merely restates when the bubbles are generated, on ascents. Old news.

I am definitely not proffering "advice" with my observations and opinions. Only posing questions. Yes, I am a member of UHMS, DAN and AAUS but know what I don't know and that is a lot!

The diving medical community has known for sometime that micro events occur without signs or symptoms of DCI and inflict tissue damage. In my view they have not dedicated the research needed to determine the extent and severity of tissue damage caused by micro nuclei or vascular pitting. Does the identified tissue damage repair or is it permanent and accumulative and a precursor for more damage on subsequent dives?

Do current or past computers provide vouchsafe for divers from DCI on repetitive or single dives? Arguable considering so-called "silent [unexplained] hits". Same question concerning tables and modeling. Again, all the computers and tables strive to reduce or eliminate [good luck with that] symptomatic DCI; not damage from so called "silent bubbles" and micro nuclei. Considering the multitude of variables involved with the physiological state of the diver on that day on that dive, the exact profile parameters, activity during dive, equipment/gases used and environmental factors it is no wonder investigators may be reluctant or even unable to determine how to prevent all injury to divers on all dives. Let alone describe asymptomatic cellular injuries.

Anyway, not wanting to stir the pot, just present my views and opinions. All my ruminations could be wrong.....

 

[scubadada]

Hi @Wallowa

I asked @Dr Simon Mitchell about biomarkers for decompression stress 5 years ago and this was his response. I am unaware of biomarkers being validated since, but it would be interesting to have an update.

Post in thread 'Bubble model vs. Gradient Factors redux'

May 2, 2020

Thanks for your response in this thread. Given no comparitive human study has demonstrated benefit in deep stops, I'm curious why you believe the ideal strategy "is almost certainly not as far as raw Buhlmann". Buhlmann's work was based on real dives, and had some rational method to determine the parameters he did. Why do you suspect he could have been neglecting the importance of protecting the fast tissues.

I ask that because I'm interested, not stating I disagree with your suspicion. When I can dive again I can assure you mu gf lo will be lower than my gf hi.

Hi Elmo,

Good...

• Dr Simon Mitchell

• 

 

[Wallowa]

Concur, that in relationship to asymptomatic injuries, 'stress', Simon's statement still stands: "Unfortunately there is no well validated biomarker for decompression stress. "......also even if 'markers' are correlated with the ill defined 'stress' event that does not determine the level and extent of injury.

My issue with all this verbiage is that it does not details exactly the type, location, extent and persistence of micro tissue injuries. Which possibly may occur on ALL hyperbaric/hypobaric exposures. Researchers are still trying to identify higher order of DCI events and not getting down to the LCDs which I believe occur at the tissue levels in perhaps numerous tissue types and locations. I understand that all these investigations are a work in progress, but so far have not heard what the "end game" is; histological examinations are needed and even then I am guessing that the what, when, where and why will change day to day and diver to diver.

Beyond that, how can all levels of tissue damage on dives be prevented? Not just treated, but prevented.

 

[Capt Jim Wyatt]

it does not details exactly the type, location, extent and persistence of micro tissue injuries. Which possibly may occur on ALL hyperbaric/hypobaric exposures.

I don't believe there are any significant/measurable tissue injuries due to micro-bubbles.

Anecdotal evidence from me with over 50 years of mostly continuous diving does tell me that sometimes there is a noticeable physiological remnant after longer/deeper dives that manifests itself as feeling very tired.

Same dive, different day with better hydration, better overall physical shape than the previous dive I have not felt tired at all.

I don't think it's a tissue injury that caused this or I probably would not have any healthy tissue remaining.

Maybe Richard Pyle and I have something in common.... erroneous anecdotal data.