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O2 window refers to the difference b/ the sum of the tissue pp of dissolved
gases & the ambient P or:

Pd = Pamb - (ppN2 + ppO2 + ppCO2 + ppH20 + ppX)

Where Pd = O2 window
Pb = ambient P
ppN2, ppO2, ppCO2 & ppH2O refer to the tissue part press of the gases indicated
& ppX is the tissue part P of any other gases that may B present in the
breathing mix.
Numeric solution of this equation requires certain assumptions, the most common
one is to set ppN2 = ppN2 alveolar, wh/ is not truly applicable to a system
that is undergoing a pressure change - diving.

This is due to O2 xtraction @ tissues wh/ lowers tissue ppO2 below that of
arterial ppO2 & the binding of O2 to Hb.  Though mole by mole the depletion of
O2 & production of CO2 R comparable, ppCO2 does not rise appreciabl
y due to its high dissolution.
From the stndpt of DCI, the O2 window is significant because it allows for the
bubbles to B absorbed.

Though theoratical basis for such a putative disequilibrium is adequately
understood, actual measure,emt of it has been elusive as it requires accurate
determination of tissue ppO2 & tissue CO2 wh/ R not considered to B c
onstant over time; they also vary from tissue to tiss.  They R difficult
parameters to measure.  Furthermore both influence tiss blood flow, thus inert
gas loading & off gassing.

Again through a cascade of simplifications of the above relationship, it is
possible to conclude:

Pd = ppNb - ppNa

where ppNb & ppNa refer to the pp of N2 in a bubble and in the alveoli,
respectively.  In essence the O2 window is now defined in terms of the pp
difference that drives diffusion.

Based on that concept, when breathing air the magnitude of Pd should increase
as Pamb increases.  The O2 window is higher @ any given P when pure O2 is being
breathed.  However the actual magnitude of the increase in the 
O2 window may not B as great when switching from air to 100 O2 due to the O2
mediated local perfusion changes.


Esat Atikkan

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