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Robert Wolov wrote: > At 09:10 AM +0100 8/22/97, John Brett wrote: > >I've been told by several people now that making a rapid descent > >massively increases the effects of narcosis. Does anyone here > >have a definitive answer as to why? > > > >Best guess: > >If one is finning like &^"stlg$ to get down, the exertion increases C02 > >retention, and I can see that having an effect. Is this the case, and > >is this the only contributing factor? > > > John, > > I don't know about "massively" since narcosis onset and sensitivity to same > seems to have so many individual variants, but I too have read that rate of > decent does indeed effect the likelihood of narcosis onset. > > However, it doesn't seem to be related to CO2 retention. > > Bove & Davis's textbook on diving medicine (latest 3rd edition 1997) > specifically addresses CO2 retention as *NOT* a factor for narcosis and > cite a study by Blenkarn that showed no arterial CO2 retention on subjects > breathing either compressed air or Heliox at 190 or 286 feet. There are > other studies that also fail to support the CO2 retention theory of > narcosis, but I won't bore you with the details. > > Don't misunderstand. The effects of CO2 retention are real (and profound) > but they are ADDITIVE to not causitive of the inert gas narcosis effect (to > the best of our understanding) Hi Robb, I think the effect of rapid descents on inert gas narcosis has been confirmed in some chamber studies. Subjects had a poor performance score immediately after the initial pressurisation, then it improved despite the fact that they were (slowly) being taken deeper, then fell off again as they got seriously deep. As you say, the theory that CO2 is responsible for narcosis is long out the window, but I'm still wondering whether CO2 retention might be an important potentiating factor in narcosis immediately after a rapid descent. If the effects of inert gases and CO2 are additive (and more so if they are synergistic), could it explain the observations if rapid descents cause temporary CO2 retention? I don't know whether this actually happens, but it seems at least conceivable. Apart from the effect of exertion mentioned by John (which wouldn't apply in the chamber dives), could respiratory depression and/or reduced blood CO2 transport due to a suddenly increased PaO2, or even increased work of breathing, cause a blip in tissue CO2 before there's a respiratory response to blow it off? Cheers, Wilson PS Since writing the above I've had a chance to go home and check out Bennett & Elliott 2nd ed. 1975. In Bennett's chapter on inert gas narcosis he states that "normally rapid compression potentiates compressed air narcosis due to carbon dioxide retention" and cites several studies. I haven't seen any of the original papers and don't know which of them just address the effect of rapid compression as opposed to causal mechanisms. One of them is Bean (1950), which reportedly showed an acute rise in alveolar CO2 associated with rapid compression of dogs. As I'm sure you'll know, this was one of the studies that led to the now discredited theory that CO2 is *solely* responsible for narcosis, but it may be that the data are still relevant to the question of potentiation of N2 narcosis by CO2 in the context of rapid compression. I'll forward all the references if you're interested, but maybe there is some more recent work (i.e. post 1975) that addresses this? In your later post you make the point that hypercapnia produces different symptoms from inert gas narcosis. But would it be fair to say that, as far as some of the performance tests used to study narcosis are concerned, narcosis *plus* hypercapnia just looks like more severe narcosis? PPS Got a nice surprise last night - last minute place on a boat for the Sound of Mull wrecks tomorrow :-) Cheers again Wilson -- Send mail for the `techdiver' mailing list to `techdiver@aquanaut.com'. Send list subscription requests to `techdiver-request@aquanaut.com'.
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