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All,

I was approached by one of my club's dive leaders last night with a question about saw tooth dive profiles. He was trying to explain to a trainee dive leader why a dive in Capernwray which went to 18m, then to 6, then to 18 again and then up to 10 (and could have gone back to 14 if the DL had not have stopped him), was a bad idea.

The reply to the inevitable chat afterwards was "O.K, that's fine, but why"? The DL concerned was therefore asking me.

I tried to explain it in terms of constantly changing pressure gradients and tissue supersaturation. I had to conceive in the end that I was unsure and would find out.

I know there are some pretty clued up people who post in this section. Is there any medical evidence that saw tooth dive profiles are provocative? What is the physiology behind this?

I would be very interested to know, as would one of our DLs and he will gladly pass it on to the trainee concerned!

Paul
 

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Just not enough dive time.
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Paul
dont know what the physiology is BUT Whipps Cross Hyperbaric told me it was BAD and found in lots of bent divers, so for me that was good enough. Probably on gassing/off gassing etc bubble formation allowing the micro bubbles to grow, get in the blood or elsewhere and then get too big when ascending/descending/ascending on a saw-tooth profile

Matt
 

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I can't say I know for sure , but with DCI being prone to so many different factors and variance between individuals, I suspect that in the early days of diving they simply collated all the factors about the dives which led to problems and put two and two together. But no doubt Haldane et al saw-toothed a whole bunch of hapless goats and showed it was a bad idea.

BTW once, during scientific diving, we did a couple of STP dives in one day, near the end of four weeks repetetive diving (ie diving every day). We were collecting equipment from the sea bed at around 25m and carting it back up to the waiting boat. Neither of us experienced any problems, but by the end of the four weeks I had the most weird fatigue I've ever known, felt totally spaced out
 

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Herewith a (much) shortened explanation. Slow tissues, fast tissues.
Descend, both gas in.
Ascend, both gas out - to different percentages (slow in = slow out etc).
Re-descend, both gas in BUT faster tissues accept gas from both the re-descent pressure and the slower tissues (cos they're still gassing out to the faster tissues, but also back in to themselves).
Saturation of faster tissues faster, off tables, customer.
I'll let you follow the graphs of gas in/out times for 12+ tissue groups on multiple ascents yourself.
OK?
 

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Phill, I'm going to print that out and stick it in my logbook or somewhere for reference. Thanks.
 

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It is the same reason that reverse profile dives (either deepest second, or deepest of first last) causes many chamber visits. (I really don't know why I tell you this - I'm still £300,000 down on the new pot !
)
 

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Phill gives an answer in terms of dissolved nitrogen exchange between tissues which may be part of the picture. Decompression illness is complicated and not fully understood, so categorical answers are not possible. Modern thinking is that microbubbles form on most ascents. Once formed on the first ascent, they will be squeezed by a subsequent descent, but may not be completely dissolved. Microbubbles are thought to affect nitrogen absorption and release and to act as seeds for larger bubbles on a subsequent ascent. In addition, the capillaries in the lungs are thought to trap and filter out microbubbles from the blood. A further danger is therefore that microbubbles trapped in the lung capillaries may be compressed by a subsequent descent to allow them to pass through the lungs to the heart to be pumped into the arterial circulation direct to the tissues, particularly the brain, possibly clumping together on the way.

Ian W
 

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[b said:
Quote[/b] (Ian W @ Feb. 08 2004,22:31)]microbubbles form on most ascents. Once formed on the first ascent, they will be squeezed by a subsequent descent, but may not be completely dissolved. Microbubbles are thought to affect nitrogen absorption and release and to act as seeds for larger bubbles on a subsequent ascent.

In addition, the capillaries in the lungs are thought to trap and filter out microbubbles from the blood.

A further danger is therefore that microbubbles trapped in the lung capillaries may be compressed by a subsequent descent to allow them to pass through the lungs to the heart to be pumped into the arterial circulation direct to the tissues, particularly the brain, possibly clumping together on the way.

Ian W
Microbubbles form on all ascents.

All bubbles (although "trap" isn't a word I've seen used, in this respect before).

Any cessation of blood flow causes damage to all the blood starved areas "down current". I sincerely hope you do not suffer from blocked pulmonary blood vessels - of any size - post dive.
 

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You actually need several large syringes full of air in your heart to stop it (acording to my doctor friend).

The danger is as you pointed out - if blood flow is stopped "downstream".  Clots usually do this better though...

My friend, martial arts instructor, aerobics instructor, fit as fcuk, ended up in hospital with multiple clots on his lung - for no reason.  He's damaged a large part of his lung as a result, and I don't think it grows back.  Poor sod.  

I don't know if the same damage can happen from sawtooth or reverse profile, but if it could, I expect we'd all be a bit more careful...
 

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[b said:
Quote[/b] ]Microbubbles form on all ascents.
As I said, categorical answers are not possible. There have been dives with no bubbles detected. They may have been there, but with the limitations in detection technology we will never know.

[b said:
Quote[/b] ](although "trap" isn't a word I've seen used, in this respect before).
Really? That's surprising. Most explanations of the risks of PFO refer to the lungs "filtering" or "trapping" bubbles.

"The lungs can trap and excrete venous bubbles. Without this capability, compressed gas diving would be associated with a much higher arterial bubble load."

" ... it has been demonstrated in vivo that venous bubbles trapped in the pulmonary capillaries after diving may redistribute to the arterial circulation during a subsequent compression."

From: Francis and Mitchell in Bennett and Elliott 5th Ed.

HTH,
Ian W.
 

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[b said:
Quote[/b] (Ian W @ Feb. 10 2004,08:36)]
[b said:
Quote[/b] ]Microbubbles form on all ascents.
As I said, categorical answers are not possible. There have been dives with no bubbles detected. They may have been there, but with the limitations in detection technology we will never know.

[b said:
Quote[/b] ](although "trap" isn't a word I've seen used, in this respect before).
Really? That's surprising. Most explanations of the risks of PFO refer to the lungs "filtering" or "trapping" bubbles.

"The lungs can trap and excrete venous bubbles. Without this capability, compressed gas diving would be associated with a much higher arterial bubble load."

" ... it has been demonstrated in vivo that venous bubbles trapped in the pulmonary capillaries after diving may redistribute to the arterial circulation during a subsequent compression."

From: Francis and Mitchell in Bennett and Elliott 5th Ed.
Granny and Sucking Eggs spings to mind
 
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