Randy, I axed the white rabbits years ago, but I did get to hang out with
Grace Slick at Duke University - not at the hyperbaric center, but when I
was in college. Jefferson "Airplane" at the time was playing a concert and
she came down to the football field where we were playing a pickup game and
waiting for the concert which was later.

Unfortunately, most people in diving still believe in white rabbits, and
most of the information that the strokes attempt to apply to what we do
comes quite clearly from The White Rabbit, including any argument not to use
helium to its fullest extent, which is the genesis of this conversation.

In my experience calling the plays at WKPP over a vast amount of time,
number of extreme dives, and number of divers, I have discovered that you
are either physically suited for this or you are not, and there are so many
"moving parts" to the equation as to "why" that my policy is simply to
screen for the fit and then use our programs to decompress them. We have no
problems , and we do not attempt to explain them away otherwise.

I consider a successful deco to be if I get out of the water ready to rock.
If I feel otherwise, I consider myself bent. If I were to get any of the
effects that are discussed in these studies you cite below, you would never
see me in the water again. So far, that has not happened.

As far as effects cited here, anything that alters blood chemistry will
produce them, and in fact anything that mimics anesthetic will produce
itching in the skin. argon and nitrogen mimic anesthetics. Any creature with
a capillary bed under the skin will experience bubbles if the skin is too
thick and not perfused while the underlying perithelium is, and that is a
fact of life. You could not bend me in that fashion with any gas, and one
look at me answers that question, so now we are back to screening again. If
you can cause the blood to shunt away from the skin, which is the body's
first reaction to insult, whether it be cold or any perceived trauma, they
will get skinbent.

There are too may moving parts here for any of this to be taken seriously.
In real life, it does not happen to screened divers. Unscreened divers need
to get tested, and those who do not belong here need to stop doing it.

----- Original Message -----
From: "Randy F. Milak" <milak@di*.zz*.co*>
To: "Techlist" <techdiver@aquanaut.com>
Cc: <scottk@nw*.co*>
Sent: Saturday, April 21, 2001 9:47 AM
Subject: Re: Counter diffusion


> Just some comments and background info on mixed gas diving and isobaric
> inert gas counter-diffusion.  It's been hypothesized that helium
> surrounding the body in a dry suit may contribute to a supersaturated
> condition in skin tissue, caused by isobaric inert gas
> counter-diffusion, while a diver is on decompression.  Therefore,
> hypothetically one could never use their bottom mix for dry suit
> inflation, nor, should the gas that surrounds the eyes and face be that
> of a helium based mix.  Whilst one would not wish the latter in their
> drysuit anyways, the reasoning is one of heat retention, not fear of
> isobaric inert gas counter-diffusion.  It's also realized that certain
> circles are strongly advocating such a premise. This premise however, is
> an academic concern more so than a real concern to the trimix diver.  A
> little background info:
>
> In 1975 it was discovered that some men had been found to develop
> pruritus (itching) and gas bubble lesions in the skin and, disruption of
> vestibular function (the sense of balance), when breathing nitrogen or
> neon with oxygen while surrounded by helium at increased ambient
> pressure (1). This phenomenon, which occurs at stable ambient pressures,
> at one or many ATA, had been designated the Isobaric Gas
> Counter-diffusion Syndrome.  In a series of analyses and experiments in
> vivo (occurring in living organisms) and in vitro (occurring in
> laboratory apparatus) the cause of the syndrome had been established as
> due to gas accumulation and development of gas bubbles in tissues as a
> result of differences in selective diffusivities, for various respired
> and ambient gases, in the tissue substances between capillary blood and
> the surrounding atmosphere. The phenomenon here described in man is an
> initial stage of a process shown later in animals to progress to
> continuous, massive, lethal, intravascular gas embolization.
>
> Then there's the study that Trey eluded to previously.  Later in 1979,
> one study measured the changes in subcutaneous tissue pressure caused by
> nitrous oxide (N2O), helium (He) and 1 ATA isobaric counter-diffusion
> gas phase development (2).  Only the ears of New Zealand white rabbits
> were subjected to counter-diffusion. The rabbits breathed a mixture of
> 80% N2O - 20% O2 while their ears alone were surrounded by helium and
> the rest of their bodies continued to be surrounded by air.
> Subcutaneous pressure changes were transmitted to a transducer recorded
> system via a fluid-filled subcutaneous needle. When the gas phase
> developed in subcutaneous tissue, pressure rose and a maximum pressure
> (Pmax) was reached. Pmax in the counter diffused ear was 48 +/- 10
> standard deviation (SD) Torr, and mean time to reach Pmax was 75 +/- 10
> (SD) min. The findings are in relation to the pathological processes of
> isobaric inert gas counter-diffusion.
>
> Studies such as these, are what gives rise to the 'helium in the dry
> suit supersaturation condition' theories and the like.  The problem
> however, is that studies such as these do not account for the realities
> of an actual open circuit trimix dive; nor should they -- it was never
> the objective.  Time and gas diffusivity differences are the greatest
> factors influencing isobaric inert gas counter-diffusion.  For example,
> nitrous oxide is some 20 times more soluble than nitrogen, and
> substantially more soluble than helium.  Even with such a high
> solubility coefficient (as N2O), it took nearly 75 minutes to reach
> maximum subcutaneous pressure. Assuming that counter-diffusion could be
> demonstrated by breathing nitrogen (air/EAN such as on decompression);
> and, considering the difference in solubility coefficients; that would
> translate into a subcutaneous maxing pressure somewhere around the 1500
> minute mark (if the pressure was to increase by even 48 Torr.).  An open
> circuit trimix diver would never have the extreme difference of
> diffusivity such as nitrous oxide to helium, nor would the diver ever be
> subjected to 1500 minutes of 100% helium, surrounding their body.  Most
> trimixes for dives to 300 ft contain a FHe around 0.5 and decompression
> times are usually less than 240 minutes.  It should be noted that
> Isobaric Gas Counter-diffusion Syndrome was observed only on rare
> occasions and only after a very long period of time (i.e.. the afflicted
> were saturation divers).
>
> Diffusion of an inert gas by respiration will play the most significant
> role in counter-diffusion (3,4). Simply, the gas a diver breathes will
> saturate tissue much faster and more thoroughly throughout the body than
> the gas that surrounds the diver's skin (5). Skin is a unique boundary
> condition, and physical properties of skin as a diffusion barrier for
> helium render such arguments void. The eyes are surrounded by the bottom
> mix helium based gas within the mask space, however the structures of
> the eye appears to be relatively insensitive to the counterdiffusion
> process (6).
>
> While it is true that the skin may absorb or give off gas (termed
> transcutaneous diffusion), counterdiffusion has a rather insignificant
> influence (3). A heavier gas (e.g. nitrogen) saturated into a certain
> tissue will not suddenly pop out of solution because a lighter gas
> surrounds the outer skin. Reversely, a lighter gas (e.g. helium)
> saturated into a certain tissue will not be held in solution because a
> heavier gas such as argon, surrounds the outer skin. The outer skin is
> an isolated, unique boundary condition unlike other lipid tissue. The
> rate of inert gas diffusion in a hyperbaric environment through human
> skin, expressed as conductance (G, in ml STPD x h-1 x m-2 x atm-1),
> increases exponentially as a function of blood flow, not
> counterdiffusion and is indistinguishable between helium and nitrogen (G
> = 21.19 x 100.0124Q) (7). The permeability (cutaneous), diffusion
> coefficient per unit of diffusion distance (D/h, in cm/h), also rises
> exponentially as a function of blood flow (7).  Therefore, it could be
> said that, the gas that surrounds the body in a dry suit is of ambient
> pressure and its diffusivity is somewhat insignificant. Time is also a
> factor in counterdiffusion, and where time is short, as in all
> open-circuit diving, absorption of gas into the skin is irrelevant. Skin
> is a well perfused tissue and any diffused inert gas will be
> transported by capillaries. Gas tension is far more complex than simply
> the solubility of an inert gas.
>
> We must also scrutinize the amount of supersaturation occurrence as
> well. We know that well perfused tissue can tolerate a substantial
> over-pressurization ratio; some as much as 3.26:1 (e.g. a hypothetical
> tissue with a 5 minute compartmental halftime). The standing pressure in
> 1 ATA at sea level is approximately 760 torr. An increase of 48 torr in
> well perfused tissue such as skin is meaningless as far as a critical
> supersaturation point is concerned. Therefore, even if the cutaneous
> tissue pressure is increased by a counterdiffusion process, the amount
> of demonstrated supersaturation is of no concern to the diver. This is
> not to say that the counterdiffusion process will not occur; simply that
> the amount of occurrence is not sufficient to jeopardize a diver's
> decompression under typical trimix diving situations.
>
> The notion that a FHe within a divers dry suit contributes to a
> supersaturated condition, caused by isobaric inert gas counterdiffusion
> is an unproven hypothesis; and, it would appear to be more of an
> academic, rather than a real concern. There exists several reasons for
> not using a helium based mixture in a dry suit; however, isobaric inert
> gas counter-diffusion plays an insignificant role. There has not been a
> reported incidence of an open circuit trimix diver ever suffering the
> effects of Isobaric Gas Counterdiffusion Syndrome. This is the basis of
> lengthy and often misguided discussions on isobaric inert gas
> counter-diffusion.
>
> Many trimix divers have observed that, on occasion when they switch
> from there bottom mix (usually an FHe greater than 40%) to an EAN mix,
> it feels as if theirs eyes, specifically the outer tissue are being
> pushed from the inside of the eyeball out. Mask fogging may occur and a
> slight blur to vision may be present. This occurs at a stable ambient
> pressure and usually only lasts for one to two minutes.  This may be the
> occurrence of an extremely rapid offgassing situation, possibly
> compounded by counter-diffusion (meaning that the diver can "feel" the
> offgassing of helium through the well perfused nerve tissue), although
> this suggestion is speculative.  The temporary myopia could be related
> to subjective hyperoxia immediately following gas switch to a high PO2
> gas, but as well, this suggestion is speculative. Whether intravascular
> retinal bubbles contribute to the etiology of this phenomenon remains
> and interesting question as well.  I'll leave comment of such to our
> esteemed colleague, Mikey J. Black.
>
> Optimum PO2 is a major factor in decompression. Oxygen provides for an
> ideal offgassing gradient of high to low inert gas partial pressures.
> Since 100% oxygen cannot be utilized throughout decompression due to
> cytotoxic concerns, an inert gas must be used (nitrogen most notably)
> (8). It is the sequencing of these gases bound by counterdiffusion that
> stages the decompression regime. Special consideration must be given to
> the sequencing of gases throughout the decompression to allow for
> optimum PO2 and inert gas counterdiffusion to be used as an advantage,
> not a liability (9-14).
>
> --
> Randy F. Milak
> ~~
>
> (1) Kang JF, 1992 Delayed occurrence of dysbaric osteonecrosis: 17 cases
> Undersea Biomed Res 19(2), 143-145 (1992)
> (2) Cowley JR, Allegra C, Lambertsen CJ. Subcutaneous tissue gas space
> pressure during superficial isobaric counter-diffusion. J Appl Physiol.
> 1979 Jul;47(1):224-7.
> (3) Briantseva LA, et al. Respiration and gas exchange in a hyperbaric
> environment. Kosm Biol Aviakosm Med. 1980 Mar-Apr;14(2):3-10. Review.
> (4) Dueker CW, Lambertsen CJ, Rosowski JJ, Saunders JC. Middle ear gas
> exchange in isobaric counter-diffusion. J Appl Physiol. 1979
> Dec;47(6):1239-44.
> (5) Semko VV, et al. Conditions for the development of isobaric
> counter-diffusion of inert gases and the criteria of its evaluation.
> Fiziol Zh. 1991 Jul-Aug; 37(4):46-52.
> (6) Cowley JR, et al. Isobaric gas counter-diffusion in rabbit eye J
> Appl Physiol. 1979 Jul; 47(1):220-3.
> (7) Lin YC, Kakitsuba N, Watanabe DK, Mack GW. Influence of blood flow
> on cutaneous permeability to inert gas. J Appl Physiol. 1984
> Oct;57(4):1167-72.
> (8) Butler and Thalmann. Oxygen exposure limit table - 1986. Adapted
> from data in the international diving and aerospace data system,
> Institute for Environmental Medicine, University of Pennsylvania by CJ
> Lambertsen and R Peterson.
> (9) Dueker CW, et al. Middle ear gas exchange in isobaric
> counter-diffusion. J Appl Physiol. 1979 Dec;47(6):1239-44.
> (10) Cowley JR, et al. Subcutaneous tissue gas space pressure during
> superficial isobaric counter-diffusion. J Appl Physiol. 1979
> Jul;47(1):224-7.
> (11) Cowley JR, et al. Isobaric gas counter-diffusion in rabbit eye. J
> Appl Physiol. 1979 Jul;47(1):220-3.
> (12) Collins JM. Isobaric inert gas supersaturation: observations,
> theory, and predictions. J Appl Physiol. 1978 Jun;44(6):914-7.
> (13) D'Aoust BG, et al. Venous gas bubbles: production by transient,
> deep isobaric counter-diffusion of helium against nitrogen. Science.
> 1977 Aug7(4306):889-91.
> (14) Karreman G, Kinetics of isobaric counter-diffusion. Bull Math Biol.
> 1977;39(5):587-95..
> --
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