If O2 is breathed at a high partial pressure for long periods it becomes toxic, particularly to the lungs and the brain.
Limit the partial pressure of O2 in the mixture breathed. When using 100% O2, observe the depth/time limits.
PULMONARY OXYGEN TOXICITY
These often start with a tickling sensation in the throat which is worse on inspiration and which may provoke coughing. After a few hours of continued O2 exposure, the tickle is gradually replaced by a sensation of substernal burning and coughing becomes uncontrollable. Shortness of breath eventually prevents even mild exertion. In sensitive individuals, three hours 100% O2 at 2 Bar (abs) may provoke the first signs of toxicity.
Reduce the concentration of O2 in the mixture, preferably to 0.2 Bar (abs). Depending on their severity, symptoms will gradually diminish over a few hours and complete resolution can be expected within a few days.
CEREBRAL OXYGEN TOXICITY
Symptoms and Signs
These are highly variable. Furthermore, there is no fixed O2 exposure at which toxicity becomes apparent. Instead, susceptibility varies both between individuals and in the same person from day to day. It is not unusual for the first sign of cerebral O2 toxicity to be a grand mal convulsion. This generally occurs in two phases. First, there is a period of body rigidity - the "Tonic" phase which may last for up to a minute. It is dangerous to attempt to surface the casualty at this stage because spasm of the glottis and respiratory muscles will result in inadequate exhalation and may therefore provoke pulmonary barotrauma. The tonic phase is followed by the "Clonic" phase during which the casualty undergoes true convulsions. This can last for widely varying periods of time.
Symptoms which may precede the onset of a grand mall convulsion include: lip twitching, dizziness, nausea, ringing or roaring in the ears, tunnel vision, a choking sensation, difficulty and tremor.
1 . If a convulsion occurs underwater, the diver's depth should be kept as constant as possible until at least the tonic phase of the convulsions subsides.
2. If a diver surfaces because of oxygen convulsion or must be surfaced to prevent drowning, the possibility of arterial gas embolism should be considered in the event of subsequent neurological abnormalities.
3. Remove the apparatus and suit.
4. Place the casualty in fresh air to recover.
5. If there are any further convulsions, restrain the casualty sufficiently to prevent self injury. Do not force the mouth open, but if necessary, keep his airway open using the Head Tilt-Neck Lift Manoeuvre when the convulsion has subsided.
6. The casualty must be kept under observation by his fellow divers or sick bay for at least 12 hours; loss of memory almost invariably occurs, but this is normally limited to short term memory and resolves quickly.
NOTE: Paradoxically, the symptoms of cerebral O2 toxicity may be made transiently worse when the inspired PO2 falls. This is the so-called (Off Phenomenon). Consequently the onset may be delayed by up to 5 minutes after leaving the water, coming off O2, or during a decompression stop where the partial pressure of O2 is reduced.
Nitrogen under pressure acts like an anaesthetic drug. The severity of the effect depends on the depth and duration of the dive, the rate of compression and experience of the diver. Some drugs, particularly alcohol and sedatives, may add to the narcosis.
a. Limit the depths of dive corresponding to the experience of the diver. (Existing depth restrictions take account of this).
b. Deep dives should be preceded by a work-up. This does not prevent narcosis but enables the diver to learn to control the effect.
c. Deep dives (deeper than 54m) should be conducted using helium rather than nitrogen as the inert gas in the mixture.
Symptoms and Signs
a. Slurred speech.
c. Inability to concentrate.
d. Feeling of well-being (Raptures of the deep).
a. Decrease the depth of dive.
b. In serious cases, which are very rare, the diver should surface.
NOTE: Symptoms and signs are similar to those of drunkenness. There is no danger from the narcotic effect, which will wear off rapidly on reducing depth. The hazard is that a narcosed diver may act inappropriately, sustain an injury or drown when his concentration is impaired.
CARBON MONOXIDE POISONING
air contaminated by exhaust fumes or other sources of carbon monoxide. Carbon
monoxide self-poisoning is used as a suicide technique and chamber operators are likely to treat such cases, which are generally more severe than the CO poisoning which occasionally occurs in divers.
a. Always ensure that the air intake drawing air from compressors are upwind of any exhaust fumes.
b. If possible, avoid air intakes drawing air from inside compartments; intakes should be sited in the open.
c. Gas must be obtained from authorised, reputable sources.
Symptoms and Signs
Symptoms are similar to those of hypoxia, but also include; pallor (the classical cherry red lips are rather rare), severe headache, dizziness, nausea and vomiting, and dimness of vision.
NOTE: To some extent, the symptoms of CO poisoning may be masked at depth by the raised P02. Therefore, although the rate at which CO is absorbed increases with depth, the symptoms are likely to become more severe during the ascent phase of the dive.
a. Allow the patient to breathe 100% 02 if available.
b. Where there is loss of consciousness, early referral to a Medical Officer is required. Deeply unconscious patients needing ventilatory assistance should be intubated and stabilised prior to recompression.
c. Treatment Table 62 may be used for deeply unconscious cases and less serious poisonings may be treated by Table 61. Alternatively, the Adelaide table may be used.
This consists of 60 minutes at 2.8 Bar (abs) with a bleed to the surface over 30 minutes.
The patient breaths 100% 02 throughout the table without taking air breaks.
NOTE: In cases of suspected CO poisoning in divers the source of gas should be isolated, and samples sent for analysis as soon as possible.