Answering my own post, here's a theory that just occurred to me:

It may be the case that although 100% O2 increases the likelihood of more
bubbling, it decreases the damage caused by bubbles that already exist by
improving the oxygenation of tissues whose normal blood flow is partially
blocked.  I can see that mitigating damage that is already occurring may be
more important than preventing damage that may be caused by more bubbles
that may form due to lowering the ppN2.

That might also be a reason why in-water recompression is not recommended,
since although it will prevent formation of new bubbles, it's unlikely to
cause the existing bubbles to redissolve -- unless the bent diver is taken
deep, which poses all sorts of additional risks.  So, with the rationale
that it's more important to treat the problem that exists rather than to
prevent the possible occurrence of additional problems, the recommendation
is to stay on the surface.  (I'm ignoring all of the other risks of shallow
in-water recompression, such as loss of consciousness underwater, increased
mobility of smaller bubbles, etc.).

Does this make any sense?  Are there other reaons?

       Shawn.

The primary reason for giving the O2 post trauma as I understand it is to O2
saturate the blood so if there is any restriction/ short fall of blood
getting to some tissues, what blood does make there will hopefully carry
enough O2 to prevent those tissues from being oxygen starved and damaged,
especially nerve tissue. I may be missled.

It's a good question and I'll take a stab at it. There is some anti-ischemic effect
from high PO2 but I don't think that's the main reason.

Someone who is bent has bubbles of air (mostly nitrogen) floating in the blood and we
want to decrease the size of these bubbles as quickly as possible. To do that there
has to a concentration gradient for nitrogen.  The greater the gradient the faster
the bubbles disappear and you get the fastest gradient by breathing as little
nitrogen as possible-- ie 100% O2.

The bubbles can be shrunk even faster by placing the victim in a hyperbaric chamber,
which compresses the bubbles mechanically through pressure.

Adam

Your reasoning is incorrect. Whether the gas comes out of solution to form bubbles
does not depend on partial-pressure gradients. It depends on the solubility and how
much gas is dissolved in the blood, and the solubility depends on the hydrostatic
pressure. When the pressure drops the blood can become supersaturated like a soda
bottle and the gas can come out solution to form bubbles.

Adam

Adam is correct.  The N2 bubbles because the air pressure on the tissues
has dropped, not because there is too little N2 there.  No matter how
much N2 you have in your blood, decreasing the N2 pressure while keeping
the overall air pressure the same won't cause bubbling.

The reason O2 is given is that you want to get that N2 diffused out of
the blood as fast as possible.. and the best way to do that is to
eliminate N2 from the air you're breathing.

The bubbleing isn't the result of ppN2 to ptN2 but of ppN2 to pA ( or in
the theory, the 'M' value of a 'compartment').

how fast a gass is transported out of the body is effected by the
ppinspired to ppT. lowwering the ppN2 but keeping the pA the same speeds
up N2 offgassing. the same reason it's used for deco in water.

Adam and John gave you most of the answer, and I'll try and cover the rest. The stuff
you said above is pretty much accurate, but there's at least one thing that's
incorrect. As Adam pointed out, it's the ambient pressure that determines the
saturation point, and therefore the possibility of bubbling, and that's what affects
gases being *dissolved.*  Relative partial pressures (or tensions, as the case may
be), OTOH, determine how the gases *diffuse*.

Those gas laws you learned in high school chemistry and scuba class were figured out
by guys who where trying to figure out the *natural* sciences of physics and
chemistry, and they didn't plan on unnatural gas switches from air to tri-mix, or
100% O2. By breathing something other than air you're creating an unnatural
situation, so you can't expect laws about natural processes to properly explain the
specific workings. We had a discussion on this point perhaps 18 months ago. A bit of
detective work with Google should scare it up.

This is the part where a literal interpretation of the gas laws has mislead you into
being completely wrong. If reducung the partial tension in the bloodstream caused
bubbling, then every trauma victim who got 100% O2 from the EMT's would also be bent
as well as broken when they got to the hospital. As already pointed out, a gas switch
increases the rate of diffusion, therefore reducing the N2 (whether it's still
dissolved or already in bubbles), but the increased partial tension of the O2
supplies the necessary pressure to keep the dissolved N2 dissolved.

Hope that explains it well enough.

Yer missing several things, the most important being confusing the
offgasing of N from non blood tissues to blood, and from blood through
the lungs.

Yes

No, and it's an important point.  At saturation, the partial pressure in the
body and the air in the lungs is the same, but only at saturation.  In a
bend diver, the partial pressure in the tissue is higher than it is in the
blood, which has higher pressure than is in the air at sea level.  By
breathing pure oxygen, you increase the differential between the blood and
gas in the lungs, speeding offgassing from the blood.  This, in turn reduces
the nitrogen partial pressure in the blood, increasing the differential
between the blood and other tissues, also speeding the offgassing from them.

No.  It occurs when teh tissues have achieved a ppN2 enough higher than will
remain in solution at the present ambient pressure, allowing the gas to come
out of solution while still inside the tissue.  Note that there is no
relation to the ppN2 of the gas being aspirated.  There is a relationship to
the pressure of the mixture of gasses being aspirated, but only because the
gas being aspirated is pretty much the same pressure as ambient.

You've got something wrong.  The differential between the ppN2 in a tissue
and the PPN2 in an adjoining tissue or blood drives the movement of N2 from
one tissue to the other.  That's how it gets into the body and how it gets
out.  The amount the differential between the ppN2 in the body exceeds the
level the body can sustain in solution at the current ambient pressure is
what causes the bends.  Reducing the ppN2 in the gas breathed speeds the
normal transfer of N2 that otherwise, would be, or already has, come out of
solution while still in body tissues.

Lee

There have been a lot of good replies to this already, but I'll take a
stab at this as well

Firstly, breathing pure O2 will accelerate the rate at which you release
nitrogen.  This is a direct result of the gas laws you refer to.  
Basically the rate of N2 release through the lungs is related to the
concentration of N2 in the blood verses the concentration of N2 in the
lung.  The higher the concentration of N2 in the air (i.e. in your
lungs) the slower your body can release N2.  So by breathing 100% N2 you
maximize the rate at which your body releases N2 from the blood.  This
in turn will allow the body to release N2 faster from other tissues,
into the blood.  If bubbles have formed this therapy will also reduce
bubble size.  Bubbles of N2 cannot be released by your lungs - instead
they must be reabsorbed into the blood, and only then can the N2 form
the bubbles be released through your lungs.  This process occurs because
N2 from the bubbles will reabsorb into the blood as you reduce the
bloods N2 concentration.  Given enough time most of the N2 bubbles which
form during DCS can be reabsorbed and excreted (via the lungs) if a
patient is given 100% O2.  This is the only effective way, aside from
decompression therapy, that we know of to decrease bubble size/number.

Secondly, those N2 bubbles can do a lot of tissue damage.  Much of that
damage is due to ischemia (decreased/no blood flow to a tissue or
organ).  This occurs when bubbles either block blood flow, or induces
excessive swelling (which can also block blood flow).  Ischemia is a
serious problem (it is what causes heart attacks and strokes), and is
one of the major routs of DCS-induced damage.  Giving a patient 100% O2
will maximize the oxygen carrying capacity of the blood, thus limiting
ischemia.  This is one reason why EMS workers immediatly put most
patients on O2 - it is an excellent way of limiting tissue damage after
trama.

Bryan

The speed of offgassing is related SOLELY to the relative difference in PP
of the inert gas between the tissues and the inspired mix.

You therefore offgas most quickly if there is ZERO PPx (inert gas) in the
inspired mix.

Thus, you want to breathe 100% O2 if you are bent (or think you might become
bent), so as to maximize the amount of N2 (or He, or both) you offgas in a
given amount of time.

By reducing the total inert gas load in the body, you reduce the amount of
dissolved gas that can grow the size of bubbles.  When the tension of gas in
the blood falls below that of the gaseous bubbles, they will begin to be
reabsorbed into the blood, shrinking and alleviating the symptoms.

--

The reason that pure O2 is administered is that Research Studies and
hard experience have shown compelling evidence (though not proof) that
DCS incident severity is reduced by taking such measures.

The reasons that it cannot be "proven" are manifold but most significant
is that every DCS incident is unique. There are no "do-overs".

You have some serious misunderstandings about actual decompression as
opposed to decompression *models*.

First, and foremost, if you, or anyone you know, actually knows exactly
what DCS *is* (not it's symptoms or circumstance), as well as how to detect/
positively identify it, come forward and receive your Nobel. Otherwise
save your theories for a later date.

Secondly, you err grossly in assuming that trapped inert gas has
any preferences about the source of pressure that restrains its
expansion.

What stops gas from expanding (the *presumed* cause of DCS) is
AMBIENT PRESSURE. Once a diver has been moved to  lower pressure
environs, captured inert gas doesn't give a horses petoot what
the diver is breathing. If ambient pressure (instantly transmitted
throughout the fluid body) is too low to restrain expansion, then
it expands, and that's that.

Your assumption that inert gas transports across the blood
barrier according to the ratio of partial pressures is correct.

If captured inert gas is causing a problem, then using that fact
to remove the inert gas at the most rapid pace possible leads to
eliminating the inert gas from the inspired gas completely as the
most efficient means of eliminating the problem in the shortest time.

In your original posts you have a presumption that partial pressure
of inert gas in the mixture being breathed is somehow restraining the
expansion of the inert gas in solution. That is not the case at
all. It only restrains the speed of transport across the blood/lung
interface.

safe diving,

bullshark