Closed-circuit oxygen divers are subject to many of the same medical problems as
other divers. Volume 5 provides in-depth coverage of all medical considerations.
Only the diving disorders that merit special attention for closed-circuit oxygen
divers are addressed in this chapter.
Breathing oxygen at high partial pressures may have toxic
effects in the body. Relatively brief exposure to elevated oxygen partial pressure,
when it occurs at depth or in a pressurized chamber, can result in CNS oxygen
toxicity causing CNS-related symptoms. High partial pressures of oxygen are
associated with many biochemical changes in the brain, but which of the changes
are responsible for the signs and symptoms of CNS oxygen toxicity is presently
unknown.
The off-effect, a hazard associated with CNS oxygen toxicity, may
occur several minutes after the diver comes off gas or experiences a reduction of
oxygen partial pressure. The off-effect is manifested by the onset or worsening of
CNS oxygen toxicity symptoms. Whether this paradoxical effect is truly caused by
the reduction in partial pressure or whether the association is coincidental is
unknown.
Pulmonary oxygen toxicity, causing lung irritation
with coughing and painful breathing, can result from prolonged exposure to
elevated oxygen partial pressure. This form of oxygen toxicity produces symptoms
of chest pain, cough, and pain on inspiration that develop slowly and become
increasingly worse as long as the elevated level of oxygen is breathed. Although
hyperbaric oxygen may cause serious lung damage, if the oxygen exposure is
discontinued before the symptoms become too severe, the symptoms will slowly
abate. This form of oxygen toxicity is generally seen during oxygen recompression
treatment and saturation diving, and on long, shallow, in-water oxygen
exposures
In diving, the most serious effects of oxygen
toxicity are CNS symptoms. The most hazardous is a sudden convulsion which
can result in drowning or arterial gas embolism. The symptoms of CNS oxygen
toxicity may occur suddenly and dramatically, or they may have a gradual, almost
imperceptible onset. The mnemonic device VENTIDC is a helpful reminder of
these common symptoms.
The most serious symptom of CNS oxygen toxicity is convulsion. Refer to
Chapter 3 for a complete description of a convulsive episode. The following
factors should be noted regarding an oxygen convulsion:
-
The diver is unable to carry on any effective breathing during the convulsion.
-
After the diver is brought to the surface, there will be a period of unconsciousness
or neurologic impairment following the convulsion; these symptoms are
indistinguishable from those of arterial gas embolism.
-
No attempt should be made to insert any object between the clenched teeth of
a convulsing diver. Although a convulsive diver may suffer a lacerated tongue,
this trauma is preferable to the trauma that may be caused during the insertion
of a foreign object. In addition, the person providing first aid may incur significant
hand injury if bitten by the convulsing diver.
-
There may be no warning of an impending convulsion to provide the diver the
opportunity to return to the surface. Therefore, buddy lines are essential to safe
closed-circuit oxygen diving.
Factors that increase the likelihood of CNS
oxygen toxicity are
-
Increased partial pressure of oxygen. At depths less than 25 fsw, a change in
depth of five fsw increases the risk of oxygen toxicity only slightly, but a similar
depth increase in the 30-fsw to 50-fsw range may significantly increase the
likelihood of a toxicity episode.
-
Increased time of exposure
-
Prolonged immersion
-
Stress from strenuous physical exercise
-
Carbon dioxide buildup. The increased tendency toward CNS oxygen toxicity
may occur before the diver is aware of any symptoms of carbon dioxide
buildup.
-
Cold stress resulting from shivering or an increased exercise rate as the diver
attempts to keep warm.
-
Systemic diseases that increase oxygen consumption. Conditions associated
with increased metabolic rates (such as certain thyroid or adrenal disorders)
tend to cause an increase in oxygen sensitivity. Divers with these diseases
should be excluded from oxygen diving.
The stricken diver should alert his dive
buddy and make a controlled ascent to the surface. The victim’s life preserver
should be inflated (if necessary) with the dive buddy watching him closely for
progression of symptoms
The following steps should be taken when
treating a convulsing diver:
1. Assume a position behind the convulsing diver. Release the victim’s weight
belt unless he is wearing a dry suit, in which case the weight belt should be left
in place to prevent the diver from assuming a face-down position on the
surface.
2. Leave the victim’s mouthpiece in his mouth. If it is not in his mouth, do not
attempt to replace it; however, if time permits, ensure that the mouthpiece is
switched to the SURFACE position.
3. Grasp the victim around his chest above the UBA or between the UBA and his
body. If difficulty is encountered in gaining control of the victim in this
manner, the rescuer should use the best method possible to obtain control. The
UBA waist or neck strap may be grasped if necessary.
4. Make a controlled ascent to the surface, maintaining a slight pressure on the
diver’s chest to assist exhalation.
5. If additional buoyancy is required, activate the victim’s life jacket. The rescuer
should not release his own weight belt or inflate his own life jacket.
6. Upon reaching the surface, inflate the victim’s life jacket if not previously
done.
7. Remove the victim’s mouthpiece and switch the valve to SURFACE to
prevent the possibility of the rig flooding and weighing down the victim.
8. Signal for emergency pickup.
9. Once the convulsion has subsided, open the victim’s airway by tilting his head
back slightly.
10. Ensure the victim is breathing. Mouth-to-mouth breathing may be initiated if
necessary.
11. If an upward excursion occurred during the actual convulsion, transport to the
nearest chamber and have the victim evaluated by an individual trained to
recognize and treat diving-related illness.
Oxygen deficiency, or hypoxia, is the condition in
which the partial pressure of oxygen is too low to meet the metabolic needs of the
body. Chapter 3 contains an in-depth description of this disorder. In the context of closed-circuit oxygen diving, the cause of hypoxia may be considered to be the
result of too much inert gas (nitrogen) in the breathing loop. Although all cells in
the body need oxygen, the initial symptoms of hypoxia are a manifestation of
central nervous system dysfunction.
If a diver begins breathing from a MK
25 UBA with too low an oxygen fraction in the breathing loop, hypoxia may
develop. A diver can become hypoxic in a rig that uses pure oxygen. Oxygen is
added to the UBA only on a demand basis as the breathing bag is emptied on inhalation.
If, as the diver consumes the oxygen in the UBA, there is sufficient
nitrogen in the breathing loop to prevent the breathing bag from being emptied, no
oxygen will be added and the diver may become hypoxic even though he has sufficient
gas volume in the breathing bag for normal inhalation. If a diver waiting to
begin a dive finishes his purge with a low level of oxygen (e.g., 25 percent) in the
breathing loop and the oxygen fraction remains at 25 percent, there will be no
problem. As the diver consumes oxygen, the oxygen fraction in the breathing loop
will begin to decrease, as will the gas volume in the breathing bag. If the breathing
bag is emptied and the UBA begins to add oxygen before a dangerously low fraction
of oxygen is obtained, hypoxia may be avoided. If the diver begins with a
very full breathing bag, however, the gas volume in the bag may decrease two or
three liters without adding any oxygen. In this case, the oxygen fraction may drop
to ten percent or lower and hypoxia may result. The risk of this happening is
greatest when the diver is on the surface before the dive starts because as the diver
descends to the transit depth of 15-25 fsw, two things happen: (1) pure oxygen is
added to the rig to maintain volume as the diver descends and the oxygen fraction
in the rig increases and (2) the pressure increase causes a rise in the partial pressure
of the oxygen.
If the diver conducts an underwater purge or purge under
pressure at depth, no descent may be required following the purge procedure and
the pressure-related increase in oxygen fraction as described above would not
occur. Therefore, in the under-pressure purge procedure strict adherence to
prescribed procedures is extremely important to ensure an adequate oxygen fraction
in the rig.
The possibility of hypoxia developing in the situation
described above led to the development of a detailed purge procedure for the
MK 25 UBA to ensure that the oxygen fraction in the breathing loop is sufficiently
high to prevent such an occurrence. This is accomplished by using the purging
procedures described in the appropriate MK 25 Operation and Maintenance
Manual.
Hypoxia due to a low oxygen content in the breathing gas
may have no warning symptoms prior to loss of consciousness. Other symptoms
that may appear include confusion, incoordination, dizziness, and convulsion. It is
important to note that if symptoms of unconsciousness or convulsion occur at the
beginning of a closed-circuit oxygen dive, hypoxia, not oxygen toxicity, is the
most likely cause.
Treatment for a suspected case of hypoxia consists of the
following
-
If the diver becomes unconscious or incoherent at depth, the dive buddy
should add oxygen to the stricken diver’s UBA.
-
The diver must be brought to the surface. Remove the mouthpiece and allow
the diver to breathe fresh air. If unconscious, check breathing and circulation,
maintain an open airway and administer 100-percent oxygen.
-
If the diver surfaces in an unconscious state, transport to the nearest chamber
and have the victim evaluated by an individual trained to recognize and treat
diving-related illness. If the diver recovers fully with normal neurological
function, he does not require immediate treatment for arterial gas embolism.
Carbon dioxide toxicity, or hypercapnia,
is an abnormally high level of carbon dioxide in the body tissues.
Hypercapnia is generally the result of a buildup of carbon dioxide in the breathing
supply or in the body. Inadequate ventilation (breathing volume) by the diver or
failure of the carbon dioxide-absorbent canister to remove carbon dioxide from the
exhaled gas will cause a buildup to occur.
Symptoms of hypercapnia are:
-
Increased rate and depth of breathing
-
Labored breathing (similar to that seen with heavy exercise)
-
Headache
-
Confusion
-
Unconsciousness
NOTE Symptoms are dependent on the partial pressure of carbon dioxide,
which is a factor of both the fraction of carbon dioxide and the absolute
pressure. Thus, symptoms would be expected to increase as depth
increases.
It is important to note that the presence of a high partial pressure of oxygen may
reduce the early symptoms of hypercapnia. As previously mentioned, elevated
levels of carbon dioxide may result in an episode of CNS oxygen toxicity on a
normally safe dive profile.
To treat hypercapnia:
-
Increase ventilation if skip-breathing is a possible cause.
-
Decrease exertion level.
-
Abort the dive. Return to the surface and breathe air.
-
During ascent, while maintaining a vertical position, the diver should activate
his bypass valve, adding fresh gas to his UBA. If the symptoms are a result of
canister floodout, an upright position decreases the likelihood that the diver
will sustain chemical injury (paragraph 18-2.4).
-
If unconsciousness occurs at depth, the same principles of management for
underwater convulsion as described in paragraph 18-2.1.6 apply.
NOTE If carbon dioxide toxicity is suspected, the dive should be aborted even
if symptoms dissipate upon surfacing. The decrease in symptoms may
be a result of the reduction in partial pressure, in which case the
symptoms will reappear if the diver returns to depth.
To minimize the risk of hypercapnia:
-
Use only an approved carbon dioxide absorbent in the UBA canister.
-
Follow the prescribed canister-filling procedure to ensure that the canister is
correctly packed with carbon dioxide absorbent.
-
Dip test the UBA carefully before the dive. Watch for leaks that may result in
canister floodout.
-
Do not exceed canister duration limits for the water temperature.
-
Ensure that the one-way valves in the supply and exhaust hoses are installed
and working properly.
-
Swim at a relaxed, comfortable pace.
-
Avoid skip-breathing. There is no advantage to this type of breathing in a
closed-circuit rig and it may cause elevated blood carbon dioxide levels even
with a properly functioning canister.
The term “chemical injury” refers to the introduction of a caustic
solution from the carbon dioxide scrubber of the UBA into the upper airway of a
diver.
The caustic alkaline solution results from water
leaking into the canister and coming in contact with the carbon dioxide absorbent.
When the diver is in a horizontal or head-down position, this solution may travel
through the inhalation hose and irritate or injure his upper airway.
The diver may experience rapid breathing or
headache, which are symptoms of carbon dioxide buildup in the breathing gas.
This occurs because an accumulation of the caustic solution in the canister may be
impairing carbon dioxide absorption. If the problem is not corrected promptly, the
alkaline solution may travel into the breathing hoses and consequently be inhaled
or swallowed. Choking, gagging, foul taste, and burning of the mouth and throat may begin immediately. This condition is sometimes referred to as a “caustic
cocktail.” The extent of the injury depends on the amount and distribution of the
solution.
If the caustic solution enters the mouth,
nose, or face mask, the diver must take the following steps:
1. Immediately assume an upright position in the water.
2. Depress the manual bypass valve continuously and make a controlled ascent to
the surface, exhaling through the nose to prevent overpre
3. Should signs of system flooding occur during underwater purging, abort the
dive and return to open-circuit or mixed-gas UBA if possible.
Using fresh water, rinse the mouth several times. Several mouthfuls should then
be swallowed. If only sea water is available, rinse the mouth, but do not swallow.
Other fluids may be substituted if available, but the use of weak acid solutions
(vinegar or lemon juice) is not recommended. Do not attempt to induce vomiting.
As a result of the chemical injury, the diver may have difficulty breathing properly
on ascent. He should be observed for signs of an arterial gas embolism and treated
if necessary. A victim of a chemical injury should be evaluated by a Diving
Medical Officer or a Diving Medical Technician/Special Operations Technician as
soon as possible. Respiratory distress which may result from the chemical trauma
to the air passages requires immediate hospitalization.
NOTE Performance of a careful dip test during predive set up is essential to
detect system leaks. Additionally, dive buddies should check each other
carefully before leaving the surface at the start of a dive.
Middle ear oxygen absorption syndrome
refers to the negative pressure that may develop in the middle ear following
a long oxygen dive. Gas with a very high percentage of oxygen enters the middle
ear cavity during the course of an oxygen dive. Following the dive, the oxygen is
slowly absorbed by the tissues of the middle ear. If the Eustachian tube does not
open spontaneously, a negative pressure relative to ambient may result in the
middle ear cavity. Symptoms are often noted the morning after a long oxygen
dive. Middle ear oxygen absorption syndrome is difficult to avoid but usually does
not pose a significant problem because symptoms are generally minor and easily
eliminated. There may also be fluid (serous otitis media) present in the middle ear
as a result of the differential pressure.
Symptoms of middle
ear oxygen absorption syndrome are:
-
The diver may notice mild discomfort and hearing loss in one or both ears.
-
There may also be a sense of pressure and a moist, cracking sensation as a
result of fluid in the middle ear.
Equalizing the pressure in
the middle ear using a normal Valsalva maneuver (paragraph 3-8.3.1) or the
diver’s procedure of choice (e.g., swallowing, yawning) will usually relieve the
symptoms. Discomfort and hearing loss resolve quickly, but the middle ear fluid is
absorbed more slowly. If symptoms persist, a Diving Medical Technician or
Diving Medical Officer shall be consulted.
