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William,
This is the kind of stuff I like and you seem to be interested in it
as well so let me throw in some related thoughts and questions
if I may :
Pyle :
However, there are other factors associated with O2 that can
(theoretically) work against you. For example, high PO2 leads to
vasoconstriction, which means reduced perfusion. This can
theoretically lead to reduced N2/He elimination efficiency from
the tissues.
Chuck :
Could this not also lead to reduced �delivery� of N2/He to the
tissues ? Perhaps a benefit of high O2 mixes within safe tox
limits such as 100� dives on nitrox 32. Maybe not enough O2 !
Pyle :
My hunch is that the main advantage of doing the 10-foot stop time at 20
feet is that, because of the increased ambient pressure, bubble diameters
are smaller. Smaller bubble diamters lead to proportionally greater
internal bubble pressures (due to surface tension effects on the bubble).
This leads to steeper gradients across bubble membranes, which means
faster gas elimination from bubbles.
Chuck :
I've wondered if the rate of diffusion of gas across bubble membranes effected
by high surface tensions (slowed).
Is the surface tension at these interfaces caused by attraction between
molecules of the blood or of the inert gas, or both? Most likely it is a
case of the properties of adjacent surfaces interacting to create a
surface or interface with qualities specific to the combination rather than
either
substrate alone. This would mean that as the gases within the bubble
or the chemistry and physics of the blood changed so would the nature of the
interface through which these gases must pass by diffusion.
Would the surface tension of a light gas bubble such as helium be
higher or lower than that of a nitrogen bubble in the same medium ?
If oxygen is able to diffuse through tissues to parts of tissues deprived by
reduced perfusion then so should nitrogen and helium be. There are so many
avenues by which gases are being transported and redistributed and so many
variable phenomena involved that there will never be a 100% reliable or
accurate mathematical model of decompression dynamics. We will always be
stuck with "what works" with a little bit of fudge factor thrown in.
-------------------------------------------------------------------
Pyle :
I'm not sure if the unbound dissolved O2 is consumed directly, or if
metabolic use of Hb-bound O2 frees up more Hb binding sites, to which the
unbound O2 may bind. There are complicating factors (e.g., Bohr effect),
but the point is that O2 is being removed (in one way or another) by
metabolism; whereas He and N2 are not.
Chuck :
In discussions of O2 and it�s ability to cause DCS Hans Roverud
assures me that the dissolved O2 is used before the Hb bound O2 is used
as follows;
From: proverud@on*.no* (Hans Petter Roverud)
To: techdiver@aquanaut.com
In practice you do metabolize any excess of
oxygen since the body draws from dissolved
oxygen before calling upon that bonded to
hemoglobin. Oxygen becomes a deco liability
at PO2s far into the tox zone only.
Chuck :
Further input on this subject from George and others indicates that Oxygen
can and does cause mild cases of DCS that tend to resolve quickly.
------------------------------------------------------------------
It seems to me that :
Every breath you take is mixed with what tidal volume of gas you
could or did not exhale. This would keep the effective inspired mix
from ever being a result of only the gas you are breathing, rather a
resultant combination of what you inspired diluted by or mixed with
some of what you had just exhaled.
The more N2 or He you are removing from the blood at the lungs
or the faster you are removing it the higher the fraction of that gas
in the tidal volume remaining and mixing with the newly inspired mix.
So the faster you remove inert gas the greater the fraction of that
inert gas will be in your actual inspired mix.
Since the alveoli hopefully do not collapse, as long as you are
offgasing an inert gas it should be diffusing into them at all times
during the breathing cycle as the blood passes by so that in that
spanse of time between breaths they are still loading up with inert
gas to mix with the next inhalation. If this is right then it is impossible
to achieve 100% O2 in the alveoli since you are always off gassing
at least CO2 (unless, of course, you're dead and someone has you
on a DAN O2 kit).
Water vapor also exerts a partial pressure and comes into play when
considering the actual situation within the lungs during respiration.
-----------------------------------------------------
Oxidation & radicals
During normal breathing on the surface there is far far more than
enough O2 available to the body chemistry to complete any
reactions that are going to take place. O2 does not dissolve easily
in plasma and once the blood PPO2 is equalized with the ambient
PPO2 no more actually enters �into solution� at the alveoli beyond
what is needed to maintain equilibrium as some minute quantity is
used in various other reactions including those that produce
radicals. Most of the O2 and virtually all the N2 you breath simply
passes into and out of the respiratory tree having only gotten a little
wet.
So! Though more O2 is dissolved as ambient PPO2 rises, no
matter how much more O2 you breath at any time during a dive
your chemistry will not make any more radicals than it would
while watching Bevis & Butthead in your livingroom.
Every time an O2 molecule is released from the Hb it must diffuse
through the local anatomy to get to the cells and during this travel
time it is available for other reactions that might result in free O2
radicals (singlet oxygen).
Chuck Boone
--
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