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- Divers face an array of unique health hazards. The first
two effects below are associated with hyperbaric conditions;
the latter three occur due to changing pressures:
- Gas narcosis caused by
nitrogen in normal air dissolving into nervous tissue
during dives of more than 120 feet [35 m]. Helium,
substituted for nitrogen in "mixed-gas diving,"
can cause an effect called High Pressure Nervous Syndrome
beyond 500 feet of salt water (fsw). [more...]
- Gas toxicities caused by
oxygen and carbon dioxide. The damage of oxygen to the
lung and brain will vary with partial pressure above one
atmosphere and time of exposure and is a concern when the
molar fraction of oxygen is increased, as in NITROX
diving. The effect of carbon dioxide changes from a
respiration stimulant at normal partial pressures of 15-40
mm Hg to a respiration suppressor above 80 mm Hg. [more...]
- Pain due to expanding or
contracting trapped gases, potentially leading to Barotrauma.
This acute symptom and potential damage can occur either
during ascent or descent, but are potentially most severe
when gases are expanding.
- Decompression sickness [DCS]
due to the evolution of inert gas bubbles, in vivo. Acute
symptoms of DCS can occur during a decrease in pressure,
but they occur most commonly soon after the ascent has
been completed.
- Dysbaric Osteonecrosis is
detectable bone lesions most commonly on the body's long
bones. Although its etiology is unknown, this chronic
disease may be related to the evolution of gas bubbles
that may or may not be diagnosed as a decompression
sickness. [more...]
- Other hazards presented to divers include microbes and
parasites (3,
7-9),
noise (3,
7,10,11),
fire (3,12)
and chemicals during underwater cleanup operations.(3)
- Most dysbarisms are predictable using some combination of
Boyle's Law, Dalton's Law, and/or Henry's Law. Boyle's
Law applies to the expansion and contraction of
gases within the body because of external pressure changes
due to depth. Dalton's
Law states that in a mixture of n gases the
partial pressure of each gas [Pi] is proportional
to the molar fraction of each gas [Yi] that makes
up the total, and can be used to determine how much
nitrogen, oxygen, or carbon dioxide is in the ambient air at
any hyperbaric pressure underwater. Henry's
Law states a gas will dissolve into a liquid in
proportion to its partial pressure in the air and its
solubility in the liquid, and can predict the body's
absorption of inert gases into and back from the body at any
pressure or depth.
- Pain and barotrauma from expanding or contracting gases
while transiting between pressure zones are the most direct
effects predictable from Boyle's Law. The most common sites
of pain from trapped gases are the digestive tract, sinuses,
teeth, middle ear, and lungs (the latter particularly during
ascent).(1,3,7,16)
Good dental care should avoid trapped gas in teeth. Divers
and flyers should anticipate these effects and not attempt
to suppress the release of natural digestive gases that will
expand during ascent. Blockage of sinus passages due to
nasal congestion or a head cold can cause pain during either
ascent or descent. Sinus pain during descent is called
"sinus squeeze." Divers should be trained to
detect blocked sinuses and not dive with a cold or an
allergic inflammation. The most common source of pain on
descent is from the contraction of air in the middle ear if
the eustachian tubes are inflamed or blocked. Divers should
be trained to clear their ears every two feet, and to stop
and rise back up a few feet before attempting to clear a
blockage.(1,13)
The most severe outcome of expanding gases is pulmonary
barotrauma. An increase in gas volume of 20 to 30 percent
can cause an initially full lung to rupture. It is important
to realize that the proportionate change in pressure and
trapped gas volume (predictable by Boyle's Law) occurs over
smaller distances at shallow depths than when starting from
deeper depths.
- Decompression sickness (DCS) is the most commonly known of
the many dysbarisms. It is sometimes referred to as
"evolved gas dysbarism," "compressed air
sickness," "caisson worker's syndrome," or
various common names listed in Table
2. DCS is completely different from the preceding direct
effects. DCS is caused indirectly by the formation of inert
gas bubbles (nitrogen or helium if used) at one or more
locations within the body, corresponding to the symptoms.
The gas is absorbed slowly at depth from the blood to the
tissues. The amount of gas absorbed depends upon depth and
"bottom time."(1,3)
During ascent, divers can easily decompress to lower
pressures at rates much faster than the stored gases can be
reabsorbed back into the blood and exhaled out of the body.
If the pressure ratio is too large, bubbles form and
symptoms of DCS occur, ranging from mildly irritating to
severe. A simple medical classification of DCS has evolved.
Type I DCS consists of only skin, lymphatic, or joint pain.
DCS Type II involves respiratory symptoms, neurologic or
auditory-vestibular symptoms, and shock or barotrauma
symptoms. Type II DCS is potentially life-threatening. The
incidence of DCS is largely unknown.(13,17,18)
- Dysbaric Osteonecrosis (sometimes also called Aseptic Bone
Necrosis) manifests itself as regions of bone and marrow
necrosis, especially of the humerus, femur, or tibia.(13,17,19)
The condition is generally asymptomatic, with detection
relying on differential diagnosis of high-quality
radiographs and by excluding other causes.(15,18,20)
The prevalence of detectable bone lesions was reported as
6.2 percent among British divers.(17)
Most lesions were in parts of the bone unlikely to cause
symptoms; however, lesions at joints were found in 1.2
percent of divers. There are strong positive associations
between lesions and length of diving experience (but not
age), the maximum depth dived (in fact, none were found in
those who had never dived below 30 m [100 feet]), and a
history of at least one prior DCS (although it can also
occur without any known prior acute DCS symptoms).(17)
There is a tendency to assume that bone necrosis is caused
by evolved gas bubbles that did not necessarily cause acute
symptoms, but there is no direct evidence for any clear
etiology. It is probably important to understand that
existing decompression schedules have been defined and
refined experimentally based on symptoms, rather than on
preventing bubbles per se or by
maintaining and applying good epidemiological health
surveillance.(7)
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- The severity of nitrogen narcosis symptoms listed in Table
1 depends primarily on depth; however, severity also
depends strongly on personal susceptibility, experience,
training, rate of descent, and level of exertion.(1,3,4,7)
- Administratively limiting depth has been the most common
control for nitrogen narcosis. Reducing nitrogen as the
source by using enriched oxygen mixtures (called NITROX) can
be a cost-effective control by speeding the ascent rate,
thus decreasing the total diving time. However, it is
limited to a shallower depth than air diving because of
oxygen's own toxicity at pressures of more than one
atmosphere.(3)
- Substituting helium for all or most of the nitrogen
(called "mixed gas diving") is a cost-effective
control for surface supplied He/O2 dives down to
380 feet of salt water (fsw). Dives beyond that are only
practical by keeping the diver under pressure for several
days (called "saturation diving"). The rate of
compression must be kept slow to avoid symptoms of High
Pressure Nervous Syndrome, such as nausea, fine tremors, and
incoordination that can begin to appear at about 500 fsw.(1,2,13)
Dives deeper than 1000 fsw have been made using a tri-mix of
nitrogen, helium, and oxygen.(2)
- The risk of DCS is controlled by administratively limiting
the pressure ratio during ascent through the use of
decompression schedules, such as those published in the US
Navy Diving Manual(1,2)
or the NOAA Diving Manual.(3)
These manuals also define short dives that may be made with
no decompression time. The substitution of helium for
nitrogen changes the rates of gas exchange and the
decompression schedule, but does not remove the bubble
hazard. Motivational training and close supervision of
decompression schedules are essential components of a
successful diving program. The use of one atmosphere suits
is a recent development that has some promise if issues of
functional flexibility can be overcome.(15)
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- Most symptoms of oxygen toxicity can be categorized into
either pulmonary (coughing, substernal soreness, and
pulmonary edema) or central nervous system (including body
soreness, nausea, muscular twitching, and convulsions). (4,5,7,14)
Oxygen toxicity effects to the central nervous system are
more common in the time-frame of a working day, while
pulmonary effects are more of a concern during saturation
diving.(7)The
preferred control is to maintain the oxygen partial
pressure close to 0.21 absolute pressure at sea level
(ATA), and administratively limiting the time of exposure
above one atmosphere.(2,13)
- Carbon dioxide becomes toxic when it suppresses
respiration. Normally an increase in PCO2
decreases blood pH, which acts to increase the respiratory
rate. However, at PCO2 >80 mm Hg (about
twice the IDLH), the respiratory control center becomes
depressed and will soon cease to function.(15)
Such partial pressures only occur from the accumulation of
exhaled carbon dioxide at increased pressure (either in
the breathing system's dead space or due to a system
malfunction). OSHA regulations for commercial diving
(1910.430 and 1926.1090) limit CO2 to 1000 ppm
in supply air and to "0.02 ATA" within the mask,
usually by assuring that the flow of surface supplied air
to masks and helmets is at least 4.5 actual cubic feet per
minute (acfm) at any depth.
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