Thank you - Great thread and probably need to choose my words more carefully. Here is two stories for you and I will find more for you this evening...
From rebreather world -
I normally run a PPO2 setpoint around 1.0 for deep dives, and increase setpoint on decompression. However recently during some equipment tests, on one of the dives to 75m (testing a leak that only appeared at depth and according water capability test), to keep the deco time down, I bumped PPO2 up to 1.4 on the bottom, and planned 1.6 on deco.
For context, the dive became fairly high work rate on the deco, as I was swimming against increasing current, just to maintain position. Also, before jumping in, I had been waiting on the deck of the boat fully kitted for some time with a rebreather, 2 x 6l inboards and 2 x 12l bailout tanks so there was a fair bit of exertion overall. I was interested to see for which duration/effectiveness, the loop would stay breathable with water ingressing during the dive, hence a lot of bail out.
After 30mins at 75msw, and with slow water ingress, WOB was noticeably bad even though I was on mix. During deco I felt the WOB slowly increasing all the time, particularly exhalation resistance, despite repeatedly draining the loop, but elected to stay on the loop to further test the scale of the leak and water trap capability of this particular unit, i.e. at what point would the loop become too flooded to breathe from.
At 23 metres I felt some heavy involuntary leg spasms over which I had no control. I already had been considering that the high work rate, increased setpoint and greatly increased WOB was probably not the best combination to be testing a rebreather but life isn't always ideal.
I was instantly aware that the combination of high work rate/increased PPO2/high resistance WOB was probably responsible for the leg spasms. As always, with any unexplained physiological symptoms it is common sense to bailout so at 23 metres, I had the choice of bailing onto 10/50 mix or 60% Nx. As the nitrox would result in too high a PPO2, I switched to my 10/50. I was not impressed to see the extra deco time for full OC.
After some time I switched back onto closed circuit (on greatly decreased PPO2) to check the loop breathability this time. Again, after a few minutes of very high WOB I felt the same involuntary strong leg kicks and once again bailed out. If these spasms had been in my arms I would have been physically unable to bail out so there was no point making any further attempts at going back on the loop and I completed the dive on OC while cursing over the impending gas bill.
It is important to note that there are studies already supporting the proposition that increased WOB can exacerbate the effects of CO2 and potential of CNS O2 toxicity (even at lower setpoints). There are also studies referencing the potential for CNS O2 Toxicity when one changes from high PPO2 mixture to low PPO2 mixture.
Essentially, using higher setpoints on deeper dives is a hazardous practice, especially when reasonably high work rates are involved and *particularly* where any factor results in less than acceptable WOB. In combination, high PPO2/high workrate/increased WOB is likely to result in either severe CO2 impairment or CNS oxygen toxicity. The increased WOB is the precipitator. But the hypothesis exists that increased setpoint with increased work rate and "acceptable" WOB (within established limits) will not in fact be sufficient to potentiate increased CO2/O2 toxicity risks. The increased WOB appears to be the KEY factor. Of course, if one runs the CNS clock beyond recommended limits, that's a different matter but my point here is that even with CNS within normal limits, any increase to WOB (or unacceptable WOB to begin with) will increase the risks of CNS toxicity.
Therefore the proposition exists that even at "normal" and "accepted" PPO2 setpoints and "normal" work rate, severe CO2 and/or CNS O2 toxicity can manifest themselves IF WOB is compromised. Testing this hypothesis would require undertaking further dives with conditions where WOB is not compromised but the same profile, increased PPO2 and increased work rate
conditions are present.
From rebreather world -
Here is a brief description of my accident from last July. The text is the same that I sent to DAN.
I was diving an Inspiration rebreather in Baltic Sea. The dive was trimix decompression dive with max depth of 74 meters. The dive went fine until the last minute of my 12 meters decompression stop. At the last minute of my 5minutes stop I noticed that something was going wrong. The symptom that I reacted to was contractions of my diaphgram muscle. At first I thought it was normal cold shivers, but it got stronger quite fast. Maybe the time frame from first small contraction to convulsion was about 30 60 seconds. I had enough time to close the mouthpiece and go off the rebreather loop. I had a EAN50 stage with me, but the valve was closed. I also got the valve opened and the regulator hose behind my neck. I lost consciousness the same time I was trying to put the reg in my mouth.
My dive partner was close to me all the time and he noticed immediately that something was wrong when I came off the rebreather loop. After I convulsed and lost consciousness he waited for the convulsion to stop and then started to bring me to surface. He insured that my airways were nicely open and monitored that gas came out from my lungs. He also kept the reg against my mouth to prevent water entering my lungs. He got me to the surface in about 6 minutes.
On the boat we had good organization and my gear was removed quicly and given mouth-to-mouth because I was not breathing. After two blows I started to breathe. After that I was unconsciouss for about ten minutes. Then I woke up and was feeling quite good considering what had happened. By the time I woke up the sea rescue helicopter was on its way. I brethed oxygen on the surface from a scuba regulator. I also took one pill of aspirin and little bit of water. My lungs were basically clean off water. I never had to cough at all.
I and my dive buddy were flown to Turku for further treatment. There was a doctor in the helicopter and I was given some fluids to the vain. In Turku my lungs were x-rayd and some other basic tests. I never felt any DCI symptoms but I was put in to the chamber for safety. The treatment lasted 6-7 hours and I almoust convulsed again 6-7 times in the chamber. I noticed the same symptom in the chamber as in the water and took the O2 mask off before the convulsion. I was not able to breathe O2 at any depth (18m, 9m, 6m) for longer than 10-15 minutes at a time.
I was released from the hospital on the night of 5th of July. The doctor ordered me not to dive for the following three weeks.
When the convulsion came my CNS% was below 50% according to the calculations used today. The Rebreather was tested before and after the dive and it was working perfectly. The day before I had done a dive which lead to near 100% CNS%. The surface interval between the two dives was over 28 hours.
