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Jody Svendsen writes:
> 
> My personal theory is two fold.  First, the SEA second stage has a
> particularly large air space, leaving lots of exhaled gas inside the
> regulator.  Second, the SEA has a little hole through which fresh air is
> blown directly towards the diaphragm.  I believe this is probably to act
> as some kind of negative feedback to reduce flutter in the regulator, but
> I don't know for sure.  Anyway, this air flow towards in the inside of the
> regulator certainly stirs up the gas inside the regulator sufficiently
> that you re-inhale almost an entire "second stage full" of the gas that
> you exhaled. 

All of this is interesting, but I have a strong feeling that anyone
with a background in fluid flow would discard any such arguments.  You
are inhaling several litres of air, with inevitable turbulent mixing,
through a potential deadspace of only tens of CCs.  The ratio simply
doesn't support this theory.

In addition, there are physiological constraints on the problem.

First, one's respiratory system simply isn't efficient enough to cause
an extra 100cc of exhaled air to noticably affect respiration -- you
don't exhale a high enough concentration of CO2 to make a difference
in 100cc out of 4000cc.  (Don't forget that your trachea and bronchi
are additional, nonexchanging "dead space" in your breathing apparatus.)

Second, there are **so** many other physiologic factors contributing
to the symptoms mentioned so far (headache, etc) that "CO2 retention"
as a diagnosis is in serious question.  Even if "CO2 retention" is the
right diagnosis, who is to say that rebreathing some extra quantity of
dead air caused the problem?  Why not some other cause, or combination thereof?

This discussion is fun, but none of this is provable.  I don't think
we can reasonably point the finger at dead air space in second stages.

Cheers,

David Story                        	        Silicon Graphics, Inc.
story@sg*.co*					Mountain View, California

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