 Editor’s
note: We received several questions regarding
last month’s article on DAN Day, and
particularly Dr. Peter Bennett’s comments on
decompression illness. Many expressed surprise
at how little science truly knows about the
phenomenon. Others were flabbergasted by the
theories and ideas expressed. This is easy to
understand, given the simplistic explanation of
decompression that most students are exposed to
in their training. In response to reader
queries, instead of our scheduled feature, this
month we present a special in-depth look at
decompression illness.
Like most divers, I have vivid memories of my
basic scuba training. Perhaps the most memorable is
the evening my instructor showed up for class with a
large bottle of Coke.® He proceeded to explain that,
like the bottle of soda he held in his hands, our
bodies are under pressure when diving. He made his
point while vigorously shaking the familiar
hourglass-shaped bottle. Then he placed it before me
and asked if I would open it. I resisted, but he
insisted. So cautiously and reluctantly, I removed
the top, expecting a vigorous eruption to spew
forth. Much to my surprise, however, nothing
happened. As it turned out, the bottle didn’t
contain soda after all, but food-colored water.
“What did you expect?” my instructor asked,
laughing.
“A big mess,” I replied, somewhat embarrassed.
The point of the lesson, as my instructor
explained, was that while at that point we may not
have known about the bends, we nonetheless
understood full well the phenomenon of gas
absorption and elimination in liquids — the
essential concept of decompression illness. An hour
later, after an informative discussion, we left the
room confident of our in-depth and thorough
understanding of the bends.
For most divers, the ubiquitous example of
bubbling soda is about as far as it goes when it
comes to insight into decompression illness. But the
phenomenon is far more complex and infinitely more
interesting than can be conveyed by any bottle of
soda, diet or regular.
Your Body Ain’t No Bottle of Soda
The first thing we should understand about
decompression illness is that our body, and the way
gases behave when dissolved within its tissues, is
far more involved than your instructor may have
implied. That’s not a criticism of your training;
it’s just that given all the other vital information
that must be covered, a cursory overview of
decompression — the bare essentials — is all that’s
possible. Besides, it’s all most divers need to
know, and about as much science as most students
will tolerate anyway. But for the true aficionados,
there’s a whole lot more.
Even the phenomenon of gas bubble formation in
water is a good deal more involved than you might
imagine. Because of special bonding characteristics,
water molecules are very hard to separate. (For a
quick explanation of this, take a look at
“Reinventing the Gas Laws” in the December 1999
issue of Dive Training.) This gives water a high
tensile strength, which is a measure of how
resistant a substance is to being torn apart or
separated. This characteristic makes spontaneous
bubble formation in water very difficult. For
example, you could theoretically compress a glass of
pure water to over 200 atmospheres and immediately
decompress it without forming a single bubble!
The trick to avoiding bubbles is not to shake
the glass as it’s decompressing. This incredible
resistance to bubble formation tells us that there
must be something besides supersaturation of gas
that produces bubbles. The other vital point is that
the water in question must be pure — free of all
impurities. This point goes to the heart of one
theory of bubble formation in divers.
To understand what’s happening, let’s look at
something that has absolutely nothing to do with
diving — how raindrops form. We’ve all known since
elementary school that rain comes from clouds, which
are made up of water vapor. But exactly how we go
from water vapor to rain is similar to how bubbles
form in us. At the core of every raindrop is a
particle of dust. This dust particle acts as a
“seed” — a point around which the water vapor can
coalesce and grow into a drop.
Now, if we tried the previous experiment with a
glass of water containing lots of impurities — even
if we didn’t shake it — the results would be
significantly different, too. Like raindrops,
foreign particles in the water would seed the
production of gas bubbles. Exactly how many bubbles
would form depends on the number of particles in the
liquid, the pressure differential and other factors.
The point is, the seeds make all the difference.
But what does this have to do with the bends?
More to the point, what are the “seeds” in our
bodies that form bubbles? It may surprise you to
learn that animals, including humans, have a
proclivity for creating gas “seeds,” or what are
more accurately termed gas micronuclei. These are
microscopic pockets of gas caused by various
factors, including movement. Just as in the shaken
glass, the turbulence of blood flow itself and the
natural movement of the body cause the formation of
micronuclei. These seeds, like the impurities
discussed previously, are the precursors to bubble
formation. During an ascent from depth, nitrogen
diffuses into these seeds (which are actually areas
of low pressure), forming tiny microbubbles.
 This
phenomenon tends to occur in the capillaries — the
smallest structures of the circulatory system. From
there, many of the bubbles enter the venous
circulation and flow back to the heart. Since
they’re very tiny bubbles, they normally don’t cause
any blockage in the vessels during their transit.
From the heart, blood travels to the lungs. When the
bubbles reach the extremely fine capillary bed of
the alveoli, they’re trapped. The bubbles diffuse
back into the alveoli, and nitrogen gas is expired
in the normal respiratory process. Since these
bubbles have no effect on us, they’re called
subclinical, or asymptomatic. We also know them as
“silent bubbles.”
So if the lungs filter out all the bubbles, why
do we still get decompression illness? There are
actually two answers. First, not all the bubbles are
filtered out. Exactly how this happens is still
debated by researchers, although several mechanisms
have been proposed. One may involve the anatomy of
the lungs. This theory holds that when bubbles in
the capillary beds build to excessive levels,
vessels can open up, allowing some blood to bypass
the lungs altogether. This bypass mechanism is
called shunting and allows bubbles present in the
blood to migrate around the alveoli and into
arterial circulation. This is a very big problem,
because the path is now clear all the way to the
brain.
Another bubble bypass theory has great
implications for repetitive diving. The theory goes
like this: On an initial dive, significant silent
bubbles develop, but then, as described before,
migrate to the tiny vasculature of the lungs. But if
you make a repetitive dive, the bubbles may not be
filtered and diffuse back into the alveoli. During a
subsequent dive, the remaining bubbles are
recompressed — possibly to the size where they can
get through the capillaries and into the arterial
circulation. This is one reason some researchers
have cautioned against making deep, short-duration
repetitive dives, sometimes called “bounce dives.”
Another explanation, which has elicited renewed
interest of late, is the “hole in the heart” theory.
This mechanism involves what’s called a patent
foramen ovale, or PFO. To understand what a PFO is,
and how it affects divers, we must review some basic
anatomy and human development. While in the womb, a
fetus has no use for its lungs. It receives oxygen
directly from the mother’s blood supply. Thus, in
fetal circulation, blood bypasses the lungs. One way
this bypass occurs is by shunting the blood entering
the right atrium directly into the left atrium
through an opening called the foramen ovale. The
foramen ovale is similar to a one-way “flapper
valve.”
At birth, when the newborn takes its first
breath, the pressure in the left atrium increases
and causes the flapper valve to close. Over time the
valve normally seals shut. However, in perhaps as
many as 25 to 30 percent of the population, the
valve remains partially open. (The medical term is
“patent.”) This allows small amounts of blood from
the right atrium to seep into the left atrium. Under
normal circumstances, this condition is of no
consequence, because the pressure in the left atrium
is higher than the right and tends to keep the valve
closed.
The implications are pretty obvious. Silent
bubbles that develop in the venous circulation
eventually make their way back to the heart. Under
normal conditions, these bubbles are trapped by
minute blood vessels as the blood makes its way from
the heart to be reoxygenated by the lungs. As
described earlier, the trapped bubbles then diffuse
into the lungs, and the gas is expired in the normal
respiratory process.
But all is not necessarily well if you have a
PFO. Under some circumstances — like when you
equalize your ears — the pressure in the right
atrium can increase slightly over the left atrium.
It’s then possible and likely that blood will shunt
from the right to left heart. This provides a
pathway not only for small amounts of venous blood
to bypass the lungs, but the silent bubbles
contained in that blood as well.
Once in the left atrium, these micro-bubbles go
directly into arterial circulation. Several studies
have documented this phenomenon. Yet, as research is
still limited on this subject, it’s impossible to
draw any solid conclusions about the implications of
PFO. Nonetheless, while the PFO does not cause
decompression illness, additional bubbles entering
the arterial blood flow in this manner may hasten
the onset of symptoms or cause more severe forms of
DCI. It could perhaps even cause arterial gas
embolism.
One intriguing study comes from England, where a
researcher examined over 100 cases of DCI. Of the
test subjects who experienced symptoms of DCI within
30 minutes of surfacing, 66 percent had a PFO. In
subjects experiencing symptoms after 30 minutes,
only 26 percent had a PFO. This data suggests that a
PFO may contribute to the early onset and severity
of DCI.
Understand, however, that researchers caution
against drawing any definitive conclusions about the
ramifications of PFOs in divers, as the phenomenon
requires far more study. While certainly
inconclusive, the PFO issue provides yet another
reason why we should dive conservatively. The PFO
issue also offers one more example of how much
science has yet to learn about the mechanism of DCI.
Bubbles That Stay Put
How bubbles bypass the lungs may be interesting,
but that’s probably not what causes the vast
majority of bends. The real culprits are the bubbles
that don’t circulate, and with present technology,
can’t even be detected. But the question remains,
exactly how do they form?
One mechanism used to explain the phenomenon has
to do with the nature of the blood vessels
themselves. We know that bubbles form much more
easily on surfaces that are termed nonwettable, or
hydrophobic (like candle wax). This happens because
less energy is required to form on them than on a
wettable surface.
But you have to be wondering what in the world
bubbles on candles have to do with bubbles in our
bloodstream. Well, besides wax, another nonwettable
substance is the interior surface of our blood
vessels. These walls aren’t smooth, as you might
have imagined, but highly irregular. They’re also
made up of tissues that are primarily lipid (fat).
Like a candle, this makes the interior walls of our
blood vessels nonwettable surfaces. So it’s not a
huge leap of the imagination to conclude that
bubbles — or micronuclei — may form here as easily
as on a candle.
As the diver ascends and continues offgasing,
the bubbles or gas seeds grow. But unlike what you
might imagine from day-to-day experience, these
bubbles tend not to form the familiar spherical
shape. Experiments in animals have shown that they
instead become elongated — a shape that increases
their surface area and resistance to movement.
Bubbles in blood vessels can stop or interfere with
normal blood flow. This further compounds the
decompression process, because it’s now more
difficult for dissolved nitrogen to escape from the
tissues.
Some have termed this phenomenon the “bottleneck
effect.” The dissolved nitrogen tries to escape or
wash out, but the localized bubble formation impedes
the flow of blood that would otherwise carry away
the dissolved nitrogen. The nitrogen has to go
somewhere, so it diffuses into the newly formed
bubbles, causing them to grow even larger. It’s
believed that this mechanism is a primary cause of
neurologic DCI, the more serious and common form of
the disorder in recreational divers.
But the story doesn’t end with blood vessels.
Nitrogen can diffuse into seeds between tissues. In
this case, the bubbles can distort and permanently
damage the tissue. As they grow, the bubbles also
put pressure on nerves. This type of bubble
formation is called extravascular, meaning “outside
the vessel.” Aqueous (watery) tissues — the type
that make up ligaments and joints — are especially
prone to developing these types of bubbles. That’s
one reason for the widely held theory that
extravascular bubbling is the primary mechanism for
joint pain, one of the classic symptoms of DCI.
It Ain’t Just the Bubbles
Another misconception that many divers have
about decompression illness is that it’s all about
bubbles. Indeed, bubbles are the cause, but how our
body reacts to this insult is a major factor in the
eventual outcome. The mechanism of DCI involves a
highly complex interplay of both bubble mechanics
and biochemistry. During the treatment process, in
fact, dealing with the biochemical complications of
DCI is as important as recompression.
Research has shown that a substance in the blood
called smooth muscle activating factor causes
inflammation and could induce bends in decompressed
animals. Conversely, a substance called anti-smooth
muscle activating factor has just the opposite
effect. This insight led to experiments where
researchers were unable to induce DCI in animals
given the smooth muscle activating factor, and the
symptoms resolved once the animals were given
anti-smooth muscle activating factor. These findings
led to other exciting studies into the immunological
involvement in DCI.
Other researchers have shown that gas bubble
formation brings about important changes in blood
chemistry. First, the presence of bubbles in the
blood activates the clotting process. Platelets —
blood components responsible for clotting — become
sticky, attaching themselves to each other and to
the newly formed bubbles. This was the genesis of
the once popular practice of taking aspirin as a
preventative to DCI — a practice that is now
discouraged by most diving medical experts.
Bubbles also cause inflammation of the capillary
walls, inducing leakage of fluid into the tissues,
which contributes to dehydration. Eventually, the
blood vessels themselves begin losing their
integrity and start to break down. This causes the
vessels to narrow and dislodges fat particles into
the blood. These particles are yet another possible
origin of gas seeds.
Other studies have shown that bubble formation
activates antibodies called complement proteins.
These substances cause the release of histamines and
other chemicals that cause still further fluid
leakage from the capillaries into the surrounding
tissues (edema). This process, incidentally, is
similar to the way our bodies react when we go into
shock.
Amazingly, animal experiments have shown that if
the release of these antibodies is stopped, the
severity of decompression illness lessens. From this
evidence, researchers hypothesize that a person’s
susceptibility to DCI may depend on how easily his
or her body releases these complement proteins. The
implication of this is very exciting. Perhaps one
day we may be able to develop a blood test that can
identify divers who are prone to DCI. More recent
studies have demonstrated that when DCI bubbles come
into contact with white blood cells, the cells
release toxic oxygen radicals. Their release also
causes inflammation, which further slows the blood.
The overall effect of all this biochemical
activity is like a snowball rolling downhill. The
blood thickens, becomes sticky and cannot move as
efficiently through the vessels. Red blood cells now
clump or “sludge” together. This, in turn, decreases
circulatory efficiency and nitrogen wash-out. More
bubbles form, and bubbles that already exist grow.
The blood flow slows even further, and the condition
gets worse.
So while the decompression problem starts with
the formation of bubbles, exactly how and why they
form is more complex than you probably thought.
Additionally, what happens after they form is almost
incomprehensibly complex from a biochemical
perspective. To add even more uncertainty to the
recipe, very little of what you’ve just read has
been definitively proven. It’s mostly informed
speculation based on some preliminary
experimentation and a lot of inferences based on how
the body works under similar circumstances. But I,
for one, am not about to buck the tide of medical
opinion or speculation. If you’re smart, you won’t
either. Dive conservatively, maintain good physical
fitness and follow the advice of experts, and you’ll
reduce your chances of experiencing a ride in a
recompression chamber.
Ain’t science great?
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