From: fhd@panix.com (Frank Deutschmann)
Newsgroups: rec.scuba
Subject: Re: Sawtooth Profiles - Why not ?
Date: 23 Nov 92 20:15:49 GMT
Organization: PANIX Public Access Unix, NYC

In <1992Nov23.124617.18245@csd.uwe.ac.uk> rj_sande@kiwi.uwe.ac.uk (Rob Sanders) writes:

>I am still a bit puzzled about the physiological reason against
>sawtooth profiles. I know that they encourage bubble formation, but
>could some enlightened person out there give a clear summary of how
>this occurs.

I'm no expert on hyperbaric medicine, but I have read and discussed
some of the issues, so here goes:

Essentially, when you ascend, small "micro-bubbles" are formed
(current thoughts are that bubble nuclei are always present, and they
grow bubbles as the gas comes out of solution, but this whole business
is complicated by lack of understanding about bubble formation,
turbulence, and gas saturation at specific points in the bloodstream),
no matter how slowly or carefully you do it.  (DCI - Decompression
Illness, as DAN likes to call it these days - is a result of the
bubbles growing too big too fast, as is AGE - Arterial Gas Embolism;
my understanding is that DCI is primarily venous/tissue related, while
AGE is exclusively arterial [anyone for corrections?].)  When you
descend on the other side of your sawtooth, the gas in the bubbles is
compressed, but does not cross into solution as readily as new gas
(current theory is that the surface tension of the gas/blood interface
is greater than the blood/aveloi surface tension, and therefore
prevents gas already in bubbles from going into solution as readily as
gas from the lungs).  This leaves you with bubbles which are larger
than they were before; when you again ascend, the bubbles start
growing from a larger starting point, leading to DCI and/or AGE
problems.

From the theory, it can be surmised that if a saw tooth profile has
the deep portion (folowing an ascent) long enough, no harm will be
done (as the gas will eventually diffuse out through the bubbles).  Some of
the newer decom models are taking this into account; notable is the
Reduced Bubble Gradient Model (Suunto was supposed to build a DC using
this model -- anyone know anything more?).  However, it is important
to note that this is mostly theory at this stage, where the theory is
attempting to explain things which are observed in real situations;
little is truly "known" about what is really going on, especially
given the difficult hydro-dynamics of the human bloodstream.

>Also, can somebody explain _why_ nitrogen becomes narcotic at depth ?
>(I am not a biologist/chemist, but like to think I have reasonable
>mental faculties !)

As far as I know, this is a mystery.  According the an
anesthesiologist friend of mine, little to none is known about the
underlying causes of both narcosis and O2 toxicity.  It is known that
CO2 accumulation affects both (primarily through increasing acidosis
of the blood), but it is not known why that has any more severe effect
that experienced in (other) athletes (runners usually don't
halucinate/convulse after running a 10K :)).  In the case of nitrogen,
it is known that narcosis is not (substantially) related to the
effects of Nitrous Oxide (whose effects seem similar).  It is
interesting to note that while modern medicine makes extensive use of
various breathing mediums for anesthesia, especially the Noble gasses,
little is understood of exactly how and why the gasses havve the
effect that they do on the CNS.

Feel free to correct the above if you have better info...

>Thanks
>Rob
>rj_sande@csd.uwe.ac.uk

-- 
-frank
(fhd@panix.com)
Newsgroups: rec.scuba