Virginian diver dead at 190 feet - Roaring River State Park, Missouri

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KISS divers correct me if I'm wrong here but my understanding of how a kiss works is there is a constant flow or needle valve that constantly feeds oxygen into the loop. This valve is set to (hopefully) match the rate in which the diver uses the oxygen so it's being replaced and the diver breaths and the CO2 is scrubbed out. So if the diluent gas exceeds MOD for the dive it is worse because of the constant flow of gas into the loop.

So I'm wondering if the PPO2 of the diluent was 1.8 wouldn't the loop PPO2 be higher? Possibly much higher because of the constant O2 flow?
No, because the diver is metabolizing the O2 that’s being added (actually, should be metabolizing slightly more than what is leaking in if adjusted properly).
 
The official NSS report just released.

Reading the report raised q few questions for me. I am far from being an expert, so I apologise if some of these questions are dumb, and thank you in advance for anyone who takes the trouble to answer.

From reports of O2 "hits" I have read (or been told) about, I understood that it typically involved a sudden loss of consciousness. In other words, the victim maybe felt some mild unease, and then the next thing they knew was waking up with people around them asking if they were okay. In this report, the victim clearly felt something was wrong, and tried to ascend rapidly before convulsing a short time (a few minutes?) later. Does this fit the usual symptoms of a seizure caused by excess PP02?

The victim was at 190 ffw on 26% EAN. I have seen people diving on air at equivalent PPN2 depth in seawater who were narc'ed to the point of not being able to operate their equipment safely, but not really extreme impairment, and it eased immediately they ascended a little. It usually affected people who weren't used to the depth. When the victim pulled the loop out of his mouth without closing it, at ~165 ffw, would it be reasonable to say that it seems he was impaired beyond simple narcosis. Does high PP02 cause the same kind of mental impairment?

The victim pushed past Diver 3 and tried to ascend rapidly. This could be a rational response to suddenly realising his PP02 was dangerously high. But bumping into Diver 3 "hard", ascending rapidly to the ceiling, and pulling his breathing loop out without closing it, all suggest a loss of ability to think rationally. Again, is that typical of high PP02 or less-than-extreme narcosis? I have read accounts of people suffering hypercapnia who suffer similar-sounding symptoms: panic; loss of ability to think rationally; and a feeling of being unable to breathe which leads them to spit out their regulator / breathing loop in a completely irrational way. Was there a particular reason that the conclusions emphasised PP02 as the main cause and hypercapnia as only a contributory factor? If a rebreather loop is flooded for some time, is there any way of telling if the CO2 scrubbers are working properly?

It is a disturbing story and one that, from my experience in working in other safety critical areas, raises questions about the safety culture of the operation.
 
Reading the report raised q few questions for me. I am far from being an expert, so I apologise if some of these questions are dumb, and thank you in advance for anyone who takes the trouble to answer.

From reports of O2 "hits" I have read (or been told) about, I understood that it typically involved a sudden loss of consciousness. In other words, the victim maybe felt some mild unease, and then the next thing they knew was waking up with people around them asking if they were okay. In this report, the victim clearly felt something was wrong, and tried to ascend rapidly before convulsing a short time (a few minutes?) later. Does this fit the usual symptoms of a seizure caused by excess PP02?

The victim was at 190 ffw on 26% EAN. I have seen people diving on air at equivalent PPN2 depth in seawater who were narc'ed to the point of not being able to operate their equipment safely, but not really extreme impairment, and it eased immediately they ascended a little. It usually affected people who weren't used to the depth. When the victim pulled the loop out of his mouth without closing it, at ~165 ffw, would it be reasonable to say that it seems he was impaired beyond simple narcosis. Does high PP02 cause the same kind of mental impairment?

The victim pushed past Diver 3 and tried to ascend rapidly. This could be a rational response to suddenly realising his PP02 was dangerously high. But bumping into Diver 3 "hard", ascending rapidly to the ceiling, and pulling his breathing loop out without closing it, all suggest a loss of ability to think rationally. Again, is that typical of high PP02 or less-than-extreme narcosis? I have read accounts of people suffering hypercapnia who suffer similar-sounding symptoms: panic; loss of ability to think rationally; and a feeling of being unable to breathe which leads them to spit out their regulator / breathing loop in a completely irrational way. Was there a particular reason that the conclusions emphasised PP02 as the main cause and hypercapnia as only a contributory factor? If a rebreather loop is flooded for some time, is there any way of telling if the CO2 scrubbers are working properly?

It is a disturbing story and one that, from my experience in working in other safety critical areas, raises questions about the safety culture of the operation.
Anecdotally, it seems not uncommon for people to have some sort of pre-seizure action (ascend, bailout, etc), but it’s too late.

Oxygen toxicity can be exacerbated by co2, and co2 is extremely narcotic. A rebreather, dense gas, and an already hyperoxic gas is just a bad combo all around and it’s kind of a feedback loop. The gas density hinders gas exchange, which makes you work harder, which reduces dwell time in the scrubber (May or may not be a factor, the resp rate would play a role here), all of this making you more susceptible to oxygen tox and making you more and more impaired from narcosis.
 
Gareth Locke has an analysis here that is quite good: An HF perspective of the Roaring River Fatality

I pointed him to the video from Gus on Facebook too, as he seemed not to be aware of it.

I honestly hope this makes things better. And for all the grief we gave him here, I am glad Gus talked about his near miss as it is informative (staying with Just Culture)
He points out one thing that was almost as shocking to me as the accident, namely that the first "rescuer" (who was alone as his buddy had split during deco) almost ran into an ox-tox situation himself... Which goes to remind us that everyone can make really basic mistakes under pressure (so whether or not the first accident was due to lack of awareness due to a "routine job to be done" type of focus is as much of a question as whether or not the team's SOP was appropriate).
 
Does high PP02 cause the same kind of mental impairment?
O2 and N2 are approximately equivalent when it comes to narcosis. Nitrox does not help with narcosis, it's advantages are NDL and deco.

I have read accounts of people suffering hypercapnia who suffer similar-sounding symptoms: panic; loss of ability to think rationally; and a feeling of being unable to breathe which leads them to spit out their regulator / breathing loop in a completely irrational way. Was there a particular reason that the conclusions emphasised PP02 as the main cause and hypercapnia as only a contributory factor?
CO2 is much more narcotic than O2 and N2, as well as increasing susceptibility to ox-tox.

The high gas density(lack of He) causes increased WOB and increased CO2.
 
I'm still trying to think of all the possible reasons he could have died except oxtoxing.
At 165feet his ppo2 should be around 1.4-1.5 even with more o2 getting pumped in the loop, the highest reported ppo2 of 1.8 is still nowhere close to immediate oxtox symptoms (the Yugoslav navy manual claimed those are expected at 2.5 or higher ppo2, and they actually tested that in dry chambers and working dives)
I personally know a lot of divers who were under very high work loads at higher ppo2, including me.
 
(the Yugoslav navy manual claimed those are expected at 2.5 or higher ppo2, and they actually tested that in dry chambers and working dives)
I personally know a lot of divers who were under very high work loads at higher ppo2, including me.
But dry chambers do not induce oxtox like wet immersion, by all research and reports. You are missing personal variations in sensitivity -- unknown. Were you and your "lot of divers" on CCR or OC?
 
But dry chambers do not induce oxtox like wet immersion, by all research and reports. You are missing personal variations in sensitivity -- unknown. Were you and your "lot of divers" on CCR or OC?
Me, and the other people I know off were on OC, which I know solves much of the co2 problems, not all.
The divers in the study were on o2 rebreathers, both in the dry chamber and open water.


Another possibility could be panic caused by hypercapnia and narcosis, the resulting struggle to breath off a bailout and loss of buoyancy could look like oxtox seizures. The cause would still be the wrong diluent choice so I'm not sure if it even matters except to satisfy some pedantic morbidity.
 
I'm still trying to think of all the possible reasons he could have died except oxtoxing.
At 165feet his ppo2 should be around 1.4-1.5 even with more o2 getting pumped in the loop, the highest reported ppo2 of 1.8 is still nowhere close to immediate oxtox symptoms (the Yugoslav navy manual claimed those are expected at 2.5 or higher ppo2, and they actually tested that in dry chambers and working dives)
I personally know a lot of divers who were under very high work loads at higher ppo2, including me.
It is entirely possible that he was simply narced out of his mind, hypercapnic, and panicked and pulled the mouthpiece out of his mouth as so many panicked divers do. The teammate (who was also probably very stressed) may have misinterpreted the signs of drowning as a convulsion. I’ve never witnessed it myself, but have heard that someone drowning can resemble a convulsion.

Either way, it’s a pretty cut and dry case of being on the wrong gas. Whether he toxed or just panicked is almost irrelevant. Being on 26% dil and the decisions that put him in the water on that gas are what killed him.
 
But dry chambers do not induce oxtox like wet immersion, by all research and reports. You are missing personal variations in sensitivity -- unknown. Were you and your "lot of divers" on CCR or OC?
And WOB in a dry chamber is much lower (no restrictive clothing and equipment, not breathing through tubes, etc.), making CO2 elimination more effective. It seems the CO2 plays a fairly large part in O2 sensitivity.
 
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