When using a closed-circuit mixed-gas UBA, the diver is susceptible to the usual
diving-related illnesses (i.e., decompression sickness, arterial gas embolism,
barotrauma, etc.). Volume 5 gives in-depth coverage of all diving-related
illnesses. For closed-circuit mixed-gas UBAs there are special medical considerations
that must be addressed.
Central Nervous System (CNS) Oxygen Toxicity. Toxic effects may result from
breathing oxygen at high partial pressures. CNS oxygen toxicity is usually not
encountered unless the ppO2 exceeds 1.6 ata. Environmental factors, however,
such as cold and exercise, can make a diver more susceptible. Though the MK 16
UBA maintains a ppO2 of approximately 0.7/0.75 ata, a rapid descent may not
allow the oxygen already in the circuit to be consumed fast enough. In addition,
malfunctioning oxygen sensors or oxygen-addition valves can cause a hazardous
oxygen level.
Preventing CNS Oxygen Toxicity. All predive checks must be performed to
ensure proper functioning of the oxygen sensors and oxygen-addition valves.
Monitoring the primary and secondary displays will help ensure that the proper
ppO2 is maintained. When high levels of oxygen are displayed, the descent must be slowed. If the diver is in less than 20 fsw, little danger of oxygen toxicity exists.
If the diver is deeper than 20 fsw, the O2 bottle valve shall be secured and manually
controlled to maintain the ppO2 below 1.3 ata.
Symptoms of CNS Oxygen Toxicity. Symptoms of CNS oxygen toxicity include
convulsion (the most serious symptom) and nonconvulsive symptoms. The symptoms
may be remembered by the mnemonic device VENTIDC:
V: Visual symptoms. Tunnel vision, a decrease in the diver’s peripheral vision,
and other symptoms, such as blurred vision, may occur.
E: Ear symptoms. Tinnitus is any sound perceived by the ears but not resulting
from an external stimulus. The sound may resemble bells ringing,
roaring, or a
machinery-like pulsing sound.
N: Nausea or spasmodic vomiting. These symptoms may be intermittent.
T: Twitching and tingling symptoms. Any of the small facial muscles, lips, or
muscles of the extremities may be affected. These are the most frequent
and
clearest symptoms.
I: Irritability. Any change in the diver’s mental status including confusion,
agitation, and anxiety.
D: Dizziness. Symptoms include clumsiness, incoordination, and unusual fatigue.
C: Convulsions. The first sign of CNS oxygen toxicity may be a convulsion with
little or no warning.
Treating Nonconvulsive Symptoms of CNS Oxygen Toxicity. If a diver convulses:
-
Ascending. Boyle’s law will lower the oxygen partial pressure.
-
Adding diluent to the breathing loop.
-
Securing the oxygen cylinder if oxygen addition is uncontrolled.
Treating CNS Oxygen Toxicity Convulsions.. If nonconvulsive
symptoms of CNS oxygen toxicity occur, action must be
taken immediately to
lower the oxygen partial pressure. Such actions include:
-
Ventilate the UBA with diluent to lower the ppO2 and maintain depth until the
convulsion subsides.
-
Make a controlled ascent to the first decompression stop.
-
If the diver regains control, continue with appropriate decompression.
-
If the diver remains incapacitated, surface at a moderate rate, establish an
airway, and treat for symptomatic omitted decompression as outlined in
paragraph 17-10.6.Frequent monitoring of the primary and secondary displays (every 2-3 minutes) as
well as the oxygen- and diluent-bottle pressure gauges will keep the diver well
informed of his breathing gas and rig status.
Additional information on recognizing and treating oxygen toxicity is contained in
Chapter 3.
Oxygen Deficiency (Hypoxia). Oxygen deficiency, or hypoxia, results from
breathing a gas mixture in which the partial pressure of oxygen is too low to meet
the metabolic demands of the body.
Causes of Hypoxia. During a rapid ascent, particularly in shallow water, Boyle’s
law may cause the ppO2 to fall faster than can be compensated for by the oxygenaddition
system. If, during ascent, low levels of oxygen are displayed, slow the
ascent. Add oxygen if necessary. Depletion of the oxygen supply, or malfunctioning
oxygen sensors or oxygen-addition valves, can also lead to a hypoxic gas
mixture.
Symptoms of Hypoxia. In hypoxia, the diver may have no warning symptoms
prior to loss of consciousness. Other symptoms that may appear include incoordination,
confusion, and dizziness.
Treating Hypoxia. If symptoms of hypoxia develop, the diver must take immediate
action to raise the oxygen partial pressure. If unconsciousness occurs, the
buddy diver should add oxygen to the rig while monitoring the secondary display.
If the diver does not require decompression, the buddy diver should bring the
afflicted diver to the surface at a moderate rate, remove the mouthpiece or mask,
and have him breathe air. If the event was clearly related to hypoxia and the diver
recovers fully with normal neurological function shortly after breathing surface
air, the diver does not require treatment for arterial gas embolism.
Treatment of Hypoxic Divers Requiring Decompression. If the divers require decompression,
the buddy diver should bring the afflicted diver to the first
decompression stop.
-
If consciousness is regained, continue with normal decompression.
-
If consciousness is not regained, ascend to the surface at a moderate rate (not
to exceed 30 fpm), establish an airway, administer 100-percent oxygen, and
treat for symptomatic omitted decompression as outlined in paragraph
17-10.6. If possible, immediate assistance from the standby diver should be
obtained and the unaffected diver should continue normal decompression.
Carbon Dioxide Toxicity (Hypercapnia). Hypercapnia, an abnormally high level
of carbon dioxide in the body, may be caused by inadequate carbon dioxide
absorption resulting from channeling, flooding of the canister, or carbon dioxide
saturation of the absorbent material. Hypercapnia may also be caused by skip
breathing or controlled ventilation by the diver.
Symptoms of Hypercapnia. Symptoms of hypercapnia include labored breathing,
headache, and confusion. Unconsciousness, however, may occur with little or no
warning.
Treating Hypercapnia. If symptoms of hypercapnia develop, the diver should
immediately stop work and take several deep breaths. This will reduce the level of
carbon dioxide both in the rig and in the diver’s lungs. If symptoms do not rapidly
abate, the diver should ascend to lower the carbon dioxide partial pressure in both
the rig and in the diver’s lungs. If unconsciousness occurs, take the actions
described above for hypoxia.
WARNING
Hypoxia and hypercapnia may give the diver little or no warning prior to onset of
unconsciousness.
Chemical Injury. 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.
Causes of Chemical Injury. A caustic alkaline solution results when water
leaking into the canister comes 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 the upper airway.
Symptoms of Chemical Injury. Before actually inhaling the caustic solution, the
diver may experience labored 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.
Management of a Chemical Incident. 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 diluent bypass valve continuously.
3. If the dive is a no-decompression dive, make a controlled ascent to the surface,
exhaling through the nose to prevent overpressurization.
4. If the dive requires decompression, shift to the EBS or another alternative
breathing supply. If it is not possible to complete the planned
decompression,
surface the diver and treat for omitted decompression as outlined in paragraph
17-10.6.Refer to the appropriate operations and maintenance manual for specific emergency
procedures.
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.
A chemical injury may cause the diver to have difficulty breathing properly on
ascent. He should be observed for signs of an arterial gas embolism and should be
treated if necessary. A victim of a chemical injury should be evaluated by a physician
or corpsman as soon as possible. Respiratory distress which may result from
the chemical trauma to the air passages requires immediate hospitalization.
NOTE Performing a careful dip test during predive setup is essential to detect
system leaks. Additionally, dive buddies shall check each other’s
equipment carefully before leaving the surface at the start of a dive.
Decompression Sickness in the Water. Decompression sickness may develop in
the water during MK 16 diving. The symptoms of decompression sickness may be
joint pain or may be more serious manifestations such as numbness, loss of
muscular function, or vertigo.
Managing decompression sickness in the water will be difficult in the best of
circumstances. Only general guidance can be presented here. Management decisions
must be made on site, taking into account all known factors. The advice of a
Diving Medical Officer should be sought whenever possible.
Diver Remaining in Water. If the diver signals that he has decompression sickness
but feels that he can remain in the water:
1. Dispatch the standby diver to assist.
2. Have the diver descend to the depth of relief of symptoms in 10-fsw
increments, but no deeper than two increments (i.e., 20 fsw).
3. Raise the oxygen partial pressure in the rig manually to 1.3 ata.
4. Compute a new decompression profile by multiplying all stops by 1.5. If
recompression went deeper than the depth of the first stop on the original
decompression schedule, use a stop time equal to 1.5 times the first stop in the
original decompression schedule for the one or two stops deeper than the
original first stop.
5. Ascend on the new profile, controlling the rig manually at 1.3 ata until leaving
the 20-fsw stop.
6. Lengthen stops as needed to control symptoms. Do not combine the 20-fsw
and 10-fsw stops.
7. Upon surfacing, transport the diver to the nearest chamber. If he is
asymptomatic, treat on Treatment Table 5. If he is symptomatic, treat in
accordance with the guidance given in Volume 5, Chapter 21 (Figure 21-3).
Diver Leaving the Water. If the diver signals that he has decompression sickness
but feels that he cannot remain in the water:
1. Surface the diver at a moderate rate (not to exceed 30 fpm).
2. If a recompression chamber is on site (i.e., within 30 minutes), recompress the
diver immediately. Guidance for treatment table selection and
use is given in
Chapter 21.
If a recompression chamber is not on site, follow the management guidance given
in Volume 5.MK 16 DIVING EQUIPMENT REFERENCE DATA
Figure
17-12 outlines the capabilities and logistical requirements of the MK 16 UBA mixed-gas diving system. Minimum required equipment for the pool phase
of diving conducted at Navy diving schools and MK 16 RDT&E commands may
be modified as necessary. Any modification to the minimum required equipment
listed herein must be noted in approved lesson training guides or SOPs.
