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ISOBARIC COUNTER GAS
TRANSPORT
(When we learned of Rob
Parker’s death, Fred Winstanley – the Cave Diving Group’s
Technical Officer wrote the following:)
It was with great sadness
that I learned of Rob’s Parker’s untimely demise. Although I only
met him a couple of times I gained the impression of a modest, pleasant,
genuine person full of the thrill of exploration.
Over a period of time more
facts have come to light regarding the details of his dive profile and
this may give some clues as to the cause of death. As I understand it
Rob was completing a trimix dive and was on his way up when his accident
occurred. He became distressed after a switch to air at 60m depth. The
symptoms displayed were classical symptoms of those of someone suffering
what is incorrectly known as a vestibular bend.
In the early to mid
sixties commercial diving in the North Sea depended upon a lot of heliox
bounce diving as opposed to saturation. The tables devised for this
procedure called for a switch from heliox to air at eighty feet. At this
switch some divers would show signs of loss of balance and extreme
vertigo and vomiting. The symptoms where identical to those of someone
suffering from an infection in the inner ear, specifically the
semi‑circular canals which are involved in control of balance. For
many years it was thought that the bubbles causing the damage occurred
in the vestibule part of the ear, hence the name given to that specific
type of decompression sickness. It is now thought that the bubbles do
not form in this region but in the cerebellum of the brain. This part of
the brain controls muscles and receives the impulses from the
semi‑circular canals of the ear, hence the symptoms displayed.
Wherever the bubbles occur the result is the same, severe disability
which can leave survivors quadriplegic. It is also thought that the
symptoms shown are only the most noticeable and in fact the brain is
suffering massive trauma with huge bubble formation. The divers in the
North Sea where decompressing in a chamber and so did survive, anyone
suffering such an occurrence in the water, especially on SCUBA, would
stand little chance of survival. So what causes these bubbles to form?
The answer seems to lie in an occurrence known as Isobaric Counter Gas
Transport. To understand the mechanics of this phenomenon it is
essential to understand gas solubility in the body’s tissues. In fatty
tissues helium is twice as soluble as oxygen but nitrogen is twice as
soluble as helium. This means that the body’s tissues become saturated
to different levels dependent upon the inert gas breathed. Henry’s law
states that the solubility of a gas in a liquid is directly proportional
to the pressure exerted on that liquid. In other words the deeper you
are the more inert gas you have in your body, but remember that gases
are soluble at different rates. So where does this leave us in Rob’s
case?
As you ascend, gas comes
out of saturation and is removed from the blood by the lungs. If,
however, you switch to a different gas, specifically a nitrogen rich gas
like air, the nitrogen dissolves into the tissues quicker than the
helium can come out, creating a super saturation situation - hence
bubbles of helium are formed in the blood. This bubble formation can
occur with no change in depth, hence the name Isobaric, meaning “same
pressure”.
How do we prevent this
situation arising? The answer is quite simple, during decompression
never let your partial pressure of nitrogen rise. Come as shallow as is
safely possible on your bottom-mix, and avoid switching to air at any
stage of the decompression, using nitrox or pure oxygen instead. This
procedure will result in a slightly longer decompression profile but,
remember, ‑ you’re an awful long time dead.
Fred
Winstanley
Technical
Officer – Cave Diving Group
(In reply, Rupert
Skorupka, a Qualified Diver with the Cave Diving Group (Northern
Section) wrote:)
Fred Winstanley’s
article (copied above) on the subject of Isobaric Counter Gas Transport,
whilst being generally correct and informative, was rather brief to deal
with such a complex subject. I have therefore attempted to produce a
more in depth explanation of the principles involved in this phenomenon.
(Those divers not interested in the details of diving physiology should
move on to prevent an attack of acute boredom.) My main contention with
Fred’s article is that we are discussing a phenomenon governed by the
principles of diffusion rather than solubility, and that the biological
site at which this occurs is the cell membrane, rather than fatty
tissues in general.
Let us specifically follow
the course of events after a gas switch from a high percentage helium
mix to a high percentage nitrogen mix during ascent (partial pressures
being irrelevant as we are observing at isobaric conditions), from the
point of view of an interneuron (i.e. nerve cell), from which a large
proportion of the cerebellum is composed. A high concentration of
nitrogen is carried in solution, by bulk flow in the bloodstream. Rapid
diffusion occurs via the aqueous medium into the extra cellular fluid
surrounding the interneuron. A situation then exists whereby two aqueous
compartments are separated by the cell membrane, one containing a high
nitrogen concentration (extracellular), and one containing a high helium
concentration (intracellular). The mechanism by which equilibrium is
reached is by passive diffusion through the membrane. (i.e. generated
only by the concentration gradient) until the concentrations in both
compartments equalise. The rate at which any molecule can pass through
the cell membrane is given by its permeability constant. This will
depend on factors such as the size of the molecule, its diffusion
coefficient and its partition coefficient between the lipid and aqueous
phases of the cell. So even though the helium atom moves three times as
fast as the nitrogen molecule in terms of its diffusion rate, the
nitrogen molecule can cross the cell membrane more rapidly as it has a
higher permeability constant.
The flux of molecules
across the cell membrane therefore results in more nitrogen molecules
entering the cell cytoplasm than helium atoms leaving. Since the partial
pressure of any component in a mixture of gases above a solution is
directly proportional to the number of molecules of that gas dissolved
in the solution, it follows that as the number of molecules of nitrogen
in the cytoplasm increases, then the partial pressure required to
prevent them coming out of solution also increases.
Consider the simplified
situation of a diver decompressing at 20 metres i.e. 3atms. Supposing he
arrived at the stop with tissue partial pressures of 2.5atm helium,
0.5atm nitrogen. 10 minutes after switching to air, these have changed
due to isobaric counter diffusion, to 2.3atm helium, 1.0atrn nitrogen.
Thus he is still not supersaturated for either gas (i.e. neither exceeds
3atm). But, the crucial principle is that these partial pressures are
additive with respect to the tendency to form a gas phase. Thus bubble
formation will now occur, whether for helium, nitrogen or a mixture (a
difficult question). The site of bubble formation will be the
cellular cytoplasm, not the bloodstream as Fred states. This simply
means that damage to our interneuron is not indirectly caused by it
being starved of oxygen and nutrients due to bubble occlusion of the
capillaries but by physical disruption of the cellular mechanisms from
within. If the damage was to effect the cerebellum alone, the
diver would display very distinctive symptoms of DCS. The cerebellum
does not initiate movement, but acts by influencing other regions of the
brain responsible for motor activity. Destruction of the
cerebellum does not cause the loss of any specific movement, rather it
is associated with general inadequacy of that movement.
Damage to the cerebellum
would cause our diver symptoms as follows:
1 . He cannot perform
movements smoothly. These are accompanied by oscillating tremors.
2. His walk is
awkward and drunken, with difficulty maintaining balance.
3. He cannot start
or stop movements quickly or easily.
4. He may not be
able to combine the movement of several Joints into a smoothly co-ordinated
motion.
The most important factor
from the point of view of the cave diver decompressing in water is the
rapid time scale over which these events occur. The symptoms are likely
to be so severe that they result in death by drowning within minutes of
the gas switch having taken place.
Now to the question of how
we prevent the situation arising in the first place. Obviously, using
trimix will have an advantage over heliox as the cells will have an
inherent partial pressure of nitrogen, thereby decreasing the
concentration gradient over the cell membrane after the gas switch. Fred
advocates never allowing the partial pressure of nitrogen to rise during
the decompression. If breathing heliox, this would entail carrying out
all decompression on pure oxygen, no nitrogen would be permitted
whatsoever. Consider the case of a diver using a 50% helium trimix (i.e.
40% nitrogen 10% oxygen). In order to maintain an equal nitrogen partial
pressure during decompression he would have to switch to a 60% oxygen
nitrox. In order to avoid acute oxygen toxicity for any significant
period of decompression, it is necessary to keep the PP02 below 1.6atm.
Thus for an f02 of 0.6, it would be inadvisable to switch to this mix
below 17 metres. Our diver therefore would not be able to switch from
his bottom mix until this depth was reached, resulting in a massive (if
not unsustainable) time increase to the deeper stops.
The present consensus of
opinion recommends a switch to nitrox at or around 30 metres. This depth
lies at an optimal point where the f02 that can be safely tolerated is
sufficiently high to reduce the fN2 in our mix to a level that more
closely approximates to the fN2 in our trimix (i.e. an fN2 of 0.4 as
opposed to approximately 0.8 for air). Also, by maximising the f02, we
take advantage of the phenomenon known as the oxygen window. Simply put,
this is the mechanism whereby oxygen dissolved in the blood is absorbed
and metabolised by our cells in preference to that combined with
haemoglobin, which does not contribute to the PP02. At high partial
pressures this is the predominant fraction of the inspired oxygen.
As this oxygen is
metabolised, it leaves a partial pressure “window” in the tissues,
which enables the other inert gases to increase their partial pressures
without bubble formation. Reading accounts of past deep diving exploits
it becomes apparent that some frightening practices were used during
decompression, seemingly accepting vestibular bends as a necessary
occupational hazard. The problem was, predictably, evaluated by Jochen
Hasenmayer during his Fontaine de Vaucluse dives.
Unfortunately, the details
of his decompression procedures were kept a secret. It is probable that
the vestibular bend strikes with the same random pattern of distribution
as DCS in general, being more common in extreme exposures but by no
means limited to these cases, and not an inevitable consequence of deep
gas switches. What is probable is that in the past due to an overall
ignorance of the facts concerning isobaric gas diffusion, and even its
existence at all, several deaths have been wrongly attributed to other
factors such as severe nitrogen narcosis during decompression. For
example refer to the American publication “Mixed Gas Diving” by
Mount and Gilliam. I could not find one reference to vestibular bends or
isobaric counter diffusion in the entire book.
Hopefully, we can continue
to avoid accidents in the future by learning from the mistakes of our
predecessors. We owe it to them to improve our techniques and thereby
prevent the pointless repetition of past tragedies.
Rupert Skorupka
Cave Diving Group
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