The most common cause of hypoxia is an interruption of the
breathing gas supply. This situation is obvious, and is treated by immediately
reestablishing the gas supply, or shifting to an alternate gas supply. Shifting the
diver to a gas with insufficient oxygen can also cause hypoxia. Analysis of diving
accidents caused by divers breathing insufficient oxygen indicates that the first
sign of trouble is an unresponsive diver. The immediate cause of the problem
usually is not obvious. Always know the oxygen content of the diver’s breathing
gas! If a diver becomes unresponsive during a mixed-gas dive, hypoxia should be
assumed until it is ruled out.
- If the diver is in the water, shift to an alternate gas supply containing sufficient
oxygen.
-
Administer 100 percent oxygen at the surface.
-
If the diver has lost consciousness or appears abnormal in any way, seek medical
advice immediately.
Because the first sign of hypoxia may be
unconsciousness, it may be difficult to differentiate hypoxia from arterial gas
embolism in an ascending diver. However, recompression treatment for arterial
gas embolism should also correct the hypoxia.
Refer to Volume 4 for
information on treatment of hypoxia arising in specific operational environments
for MK 16 dives and diving involving closed-circuit oxygen rebreathers.
Carbon monoxide poisoning can result from an air
supply contaminated by exhaust fumes. It is treated the same way as low oxygen
content of breathing gas. The early signs of carbon monoxide poisoning are:
Divers with these symptoms can be treated with 100 percent oxygen at the surface.
Divers with symptoms (i.e. severe headache, mental status changes, any neurological
symptoms, rapid heart rate) should be treated at 60 fsw on oxygen. When
carbon monoxide poisoning is suspected, isolate the suspect breathing gas source,
and forward gas samples for analysis as soon as possible.
Carbon dioxide toxicity, or hypercapnia,
may occur with or without a deficiency of oxygen. The diver may have no
warning of hypercapnia and may become confused and even slightly euphoric
before losing consciousness. The inspired carbon dioxide itself does not usually
cause permanent injury. Injury from hypercapnia is usually due to secondary
effects such as drowning or injury caused by decreased mental function or unconsciousness. Because the first sign of hypercapnia may be unconsciousness and it
may not be readily apparent whether the cause is hypoxia or hypercapnia, rule out
hypoxia first.
Carbon dioxide buildup can be caused by:
-
Inadequate ventilation of UBAs
-
Controlled or skip-breathing
-
Excessive breathing resistance
-
Excessive dead space in equipment such as a failure of mushroom valves in
scuba mouthpiece
-
Failure or expenditure of the carbon dioxide absorbent material in a closedcircuit
or semiclosed-circuit UBA
To treat hypercapnia, lower the inspired carbon dioxide
level by:
1. Increasing helmet ventilation
2. Decreasing the level of exertion
3. Shifting to an alternate breathing source
4. Aborting the dive if defective equipment is the cause
Divers surfacing unconscious should be treated for suspected arterial gas
embolism.
Refer to Volume 4
for information on treatment of hypercapnia in specific operational environments
for MK 16 diving operations and diving involving closed-circuit oxygen
rebreathers.
Oxygen toxicity affects the lungs (Pulmonary Oxygen
Toxicity) or the central nervous system (CNS Oxygen Toxicity). Pulmonary
oxygen toxicity may occur during long oxygen exposures such as recompression
treatments, special 100-percent oxygen UBA operations, and saturation dives.
Refer to paragraph 21-5.5.6.2 for information on pulmonary oxygen toxicity.
During in-water diving operations,
the most common and most serious form of oxygen toxicity involves the
central nervous system (CNS). The symptom of CNS oxygen toxicity that has the
most serious consequence is the oxygen convulsion. The convulsion itself is not
harmful and there will be no long-term residual effects provided injury or
drowning can be prevented.
CNS oxygen toxicity is usually not encountered
unless the partial pressure of oxygen approaches or exceeds 1.6 ata.
However, oxygen convulsion may be encountered at lower oxygen partial pressure.
Symptoms of CNS oxygen toxicity may occur singly or together, in no
particular order. There may be no warning of an impending convulsion. Signs and
symptoms of CNS oxygen toxicity include:
V: Visual symptoms. Tunnel vision, a decrease in 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. This is the most frequent and
obvious symptom.
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
that occurs with little or no warning.
A tethered diver who thinks he has symptoms of
oxygen toxicity shall inform the Diving Supervisor. The Diving Supervisor shall
take action to lower the oxygen partial pressure by:
1. Decreasing diver depth 10 feet.
2. Discontinuing 100 percent oxygen and vent with a gas of lower oxygen
content.
Free-swimming divers on a 100-percent
oxygen UBA shall alert their diving partner and surface if possible.
If a diver convulses, the UBA should be ventilated
immediately with a gas of lower oxygen content, if possible. If depth control
is possible and the gas supply is secure (helmet or full face mask), the diver’s
depth must be kept constant until the convulsion subsides. If an ascent must take
place, it should be done as slowly as possible. A diver surfacing unconscious
because of an oxygen convulsion or to avoid drowning must be treated as if
suffering from arterial gas embolism. Convulsing divers in the recompression
chamber should be protected from physical harm. When the convulsion subsides,
the diver should be kept with head back and chin up to ensure an adequate airway
until consciousness is regained. Forcing the mouth open to insert a bite block is unnecessary. CNS oxygen toxicity occurring during recompression therapy is
discussed fully in paragraph 21-5.5.6.1.
Refer to
Volume 3 for information about treatment of CNS oxygen toxicity in specific
operational environments for surface-supplied helium-oxygen diving, and to
Volume 4 for MK 16 diving operations and 100-percent oxygen rebreather dives.
Narcosis is a state of stupor or unconsciousness caused by
breathing inert gases at pressure while diving. The most common form, nitrogen
narcosis, is caused by breathing compressed air at depth.
Symptoms of nitrogen narcosis may occur
singly or together, in no particular order. Signs and symptoms include:
-
Loss of judgment or skill
-
A false feeling of well-being
-
Lack of concern for job or safety
-
Apparent stupidity
-
Inappropriate laughter
-
Tingling and vague numbness of lips, gums, and leg
The only effective way to counteract the
narcotic effect of nitrogen is to lower the nitrogen partial pressure. Specifically:
1. The diver should ascend or be brought to a shallower depth.
2. If mental acuity is not restored, the dive shall be aborted.
When diving MK 16 UBA (maintaining a constant
ppO2 of 0.75) with N2O2 as the diluent, nitrogen narcosis becomes a significant
factor at deep depths.
Hyperventilation is rapid breathing in excess of metabolic
requirements, usually as the result of a conscious voluntary effort or by apprehension.
Hyperventilation excessively lowers the carbon dioxide levels in the blood
and increases the blood oxygen level slightly. This, in turn, may lead to a
biochemical imbalance that gives rise to dizziness and twitching or tingling of the
extremities, which may be mistaken for CNS oxygen toxicity. Usually, this
twitching is also accompanied by some degree of spasm of the small muscles of
the hands and feet which allows a sure diagnosis to be made. Treatment is to slow
down the breathing rate by direction and reassurance, which allows the condition
to correct itself. Refer to Chapter 3 for more information on the signs, symptoms,
and treatment of hyperventilation.
The increased density of the breathing gas at
depth, combined with physical exertion, may lead to shortness of breath that may
become severe and cause panic in some divers.
Dyspnea is usually associated with carbon dioxide buildup in the body, but may
occur without it. When dyspnea occurs, the diver must rest until the shortness of
breath subsides. This may take several minutes. If dyspnea does not subside with
rest, or if it returns with even slight exertion, it may be due to carbon dioxide
buildup. In open-circuit UBAs, ventilation rates should be checked to make sure
they are adequate; the helmet should be ventilated if necessary. Adequate ventilation
rates are at least 4 acfm for moderate work and 6 acfm for very hard work.
Ventilation should not drop below 1 acfm, even at rest.
`
In demand systems, excessive dead space from a damaged oral-nasal may be the
cause. In closed or semiclosed UBAs, the CO2 absorbent canister may be spent. If these causes are likely, the dive must be aborted to correct them.
