OP
isobaric decompression on CCR
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The few (3?) inner ear hits I can recall all had a PFO in common. And they all occurred quite shallow, 2 on O2 at 20ft. Not a big dataset, but I have never thought of IBCD and inner ear hits as related.
Would like to see some data on inner ear hits too, I'll draw my own conclusions on their relevance to IBCD thank you
The IBCD warnings in V-Planner trip at 0.5 pp inert gas difference for a mix swap in the deco phase. Its a level that was fitted into the incident reports and common dive practices that I looked at. You can change that limit, or turn it off in V-Planner. Don't be fooled by the misfortune of others :shocked2:
The counter diffusion exists in small amounts at every gas swap point. That is a basic part of every deco ascent and I don't think anyone would dispute that.
The chances of injury increases when that gas swap causes significant tissue pp reversal, coupled with a large (long) deco obligation. Your body is expected to do an accelerated off gassing while also on gassing at the same time. The body doesn't seem to easily do this reversal and exchange of inert gas in mid water, under hi ambient pressure. Hence the diver has planned for, but not achieved this significant exchange, and instead has created a large off gas deficiency in the middle of his deco, which is carried to the surface and can lead to injury.
Hence the diver doing deep dives with long deco obligations is more at risk. They also tend to use the biggest N2/He reversals to accelerate deco. The regular diver can tolerate the same N2/He exchange, because they ascend more quickly through stops, reducing ambient pressure which will null out the reversal problem.
I'm certain the diagrams show the problem and its cause, but it is a difficult situation to grasp. I could add pressure numbers to the examples, but its all meaningless without a full understanding of the entire ascent process, viewed from within a model.
You can think of this problem another way - the best and easiest deco is when the ratio of inspired N2/He is kept uniform through the dive. The off gas process starts with a smooth reversal of pressure gradients, and continues this way through the ascent. It can be accelerated easily by reducing the inert component by the same proportions. But a reversed gas swap with its big re-arrangement of stored inert gas in the body, interferes with the off gas process.
Its like the tide - it comes up, slowly reverses and leaves. But the reversed gas swap IBCD event is like a rouge wave or tsunami in the middle.
Regards
The counter diffusion exists in small amounts at every gas swap point. That is a basic part of every deco ascent and I don't think anyone would dispute that.
The chances of injury increases when that gas swap causes significant tissue pp reversal, coupled with a large (long) deco obligation. Your body is expected to do an accelerated off gassing while also on gassing at the same time. The body doesn't seem to easily do this reversal and exchange of inert gas in mid water, under hi ambient pressure. Hence the diver has planned for, but not achieved this significant exchange, and instead has created a large off gas deficiency in the middle of his deco, which is carried to the surface and can lead to injury.
Hence the diver doing deep dives with long deco obligations is more at risk. They also tend to use the biggest N2/He reversals to accelerate deco. The regular diver can tolerate the same N2/He exchange, because they ascend more quickly through stops, reducing ambient pressure which will null out the reversal problem.
I'm certain the diagrams show the problem and its cause, but it is a difficult situation to grasp. I could add pressure numbers to the examples, but its all meaningless without a full understanding of the entire ascent process, viewed from within a model.
You can think of this problem another way - the best and easiest deco is when the ratio of inspired N2/He is kept uniform through the dive. The off gas process starts with a smooth reversal of pressure gradients, and continues this way through the ascent. It can be accelerated easily by reducing the inert component by the same proportions. But a reversed gas swap with its big re-arrangement of stored inert gas in the body, interferes with the off gas process.
Its like the tide - it comes up, slowly reverses and leaves. But the reversed gas swap IBCD event is like a rouge wave or tsunami in the middle.
Regards
Last edited:
No offense, but it sounds to me like above statements are deduced from the way numbers in model happen to work, not from actual empirical data. AFAIK Physiology and Medicine of Diving pretty much dismisses IBCD when going from faster inert gas to slower.
I looked at all the dive profiles I could at the time. Yes, this is deduced from theory models and physics and pressures and the internal operations thereof. Co-incidently, humans also seems to suffer from the effects of excess off gassing and ignoring the problems of significant reversed inert gas exchanges. There might just be a correlation?
This problem affect only a small cross section, and its not something any researcher is going to spend time on. Its just an observation by me into the plain and obvious, right there in front of you. Most divers, instructor and researchers will never appreciate the causes, because you need to work with model internal calculations and design to see how it functions.
Just 6 short years ago, the deep diver (100m+) and the dive practice would typically make big inert gas reversals by choice - to speed up deco, and to accelerate removal of that nasty helium from the system. Then they would tend to get injured. Some of those divers would spend the afternoon vomiting into the ocean at 30m deep.
In the last 10 years, GUE (and similar) has pioneered the use of increased He in the deco mix in the rec/tech diver, and helped change the way all divers approach the selection of deco mixes. I presume UTD also promotes this approach, and therefore helped divers avoid IBCD problems by default.
In 2004, my V-Planner added the ppInert graphs, and then the IBCD warnings. Divers now had the tools to look at profiles from an inert gas perspective, and were forced to think about ascents and deco in terms of complimentary deco mixes. These decisions are now taking precedence over the older 'fastest set' of deco mixes.
Today, divers are going deeper and longer and tech diving continues to grow rapidly. The injury rate is reducing in real terms. An anecdotal observation would suggest we are all collectively doing diving better, and avoiding the trouble spots.
Regards
For a blast from the past (the Techidver archives) which as far as I know are not copyrighted. This is from Randy Milak who was a very well read poster on rec.scuba and elsewhere -
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..
--
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..
--
GIII's response-
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.
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.
I agree with G3. Also now I understand why the DIR trained always seem to associate IBCD with skin transfers. That is NOT how I view IBCD!
IBCD takes place in tissues as part of the normal on-gas / off-gas diffusion processes of compression and decompression. The IBCD comes from your inspired mix and tissue state, and the changes made in inert gas ratios in deco mix swaps.
Regards
IBCD takes place in tissues as part of the normal on-gas / off-gas diffusion processes of compression and decompression. The IBCD comes from your inspired mix and tissue state, and the changes made in inert gas ratios in deco mix swaps.
Regards
Again - I agree - he is right. I can't imagine enough transfer exists across the skin for any effect on deco. This is NOT the medium I'm concerned about.
Tissues and blood and circulation and diffusion and inspired mix - where the problem actually occurs. You can't possibly deny this - its the same medium that transports all inert on and off gassing in the body.
Regards
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