Gas Toxicity During Diving
(See also Overview of Diving Injuries.)
Oxygen toxicity typically occurs when the partial pressure of oxygen exceeds 1.4 atmospheres (atm), equivalent to about 57 m (187 ft) depth when air is breathed. Symptoms include paresthesias, seizures, vertigo, nausea, vomiting, and constricted (tunnel) vision. About 10% of patients have generalized seizures or syncope, which typically results in drowning. Risk is increased when divers breathe mixtures of oxygen and nitrogen (nitrox) that result in an inspired pressure of oxygen exceeds 1.3 atmospheres.
When compressed air is breathed at depths of > 30 m (> 100 ft), the elevated partial pressure of nitrogen can exert an anesthetic-like effect similar to that of nitrous oxide. Nitrogen narcosis (rapture of the deep) causes symptoms and signs similar to those of alcohol intoxication (eg, impaired intellectual and neuromuscular performance, changes in behavior and personality). Impairment of judgment can lead to drowning. Hallucinations and loss of consciousness can occur at depths of > 91 m (> 300 ft).
Because divers recover rapidly during ascent, diagnosis is often based on history. Treatment entails immediate but controlled ascent. Nitrogen narcosis can be prevented by using helium to dilute oxygen for deep diving because helium lacks the narcotic properties of nitrogen. However, using pure helium/oxygen mixtures in very deep dives (> 180 m [> 600 ft]) increases the risk of developing high-pressure neurologic syndrome.
Carbon dioxide poisoning may be caused by any of the following:
Hypoventilation can increase blood carbon dioxide levels and cause shortness of breath and sedation. Severe carbon dioxide poisoning can cause nausea, vomiting, dizziness, headache, rapid breathing, flushing, confusion, seizures, and loss of consciousness.
Mild carbon dioxide poisoning is suspected if divers frequently have dive-related headaches or low air-use rates.
Carbon dioxide intoxication usually resolves during ascent; thus, arterial blood gas (ABG) testing after a dive typically does not detect any increase in carbon dioxide levels. Treatment is gradual ascent and termination of the diving exercise or correction of the precipitating cause.
Carbon monoxide can enter a diver’s air supply if the air compressor intake valve is placed too close to engine exhaust or if the lubricating oil in a malfunctioning compressor becomes hot enough to partially combust (flashing), producing carbon monoxide.
Symptoms include nausea, headache, weakness, clumsiness, and mental changes. Severe carbon monoxide poisoning can cause seizures, syncope, or coma.
Diagnosis is by detecting an elevated carboxyhemoglobin level in blood; pulse oximetry readings are nondiagnostic and usually normal because standard pulse oximeters cannot distinguish between oxyhemoglobin and carboxyhemoglobin. However, pulse carbon monoxide oximetry can detect elevated carboxyhemoglobin. The diver’s air supply can also be tested for carbon monoxide.
Treatment is with high-flow 100% oxygen, best given via a nonrebreather mask, which decreases the half-life of carboxyhemoglobin in room air from 4 to 6 hours to 30 to 150 minutes. For severe cases, in which there are neurologic manifestations or where carboxyhemoglobin is ≥ 25%, hyperbaric oxygen therapy should be considered. Carboxyhemoglobin levels will drop quickly in the hyperbaric chamber (half-life 15 to 30 minutes), and most studies show that persistent sequelae are reduced by hyperbaric oxygen treatment. Although carboxyhemoglobin elevation confirms the diagnosis, tissue hypoxia is augmented by carbon monoxide binding to other hemoproteins such as myoglobin and cytochrome a and a3. Thus, carboxyhemoglobin level does not correlate with clinical severity and should not be used as a treatment target.
A poorly understood syndrome of neuromuscular and cerebral abnormalities can develop at ≥ 180 m (≥ 600 ft), particularly when divers are compressed rapidly while breathing helium/oxygen mixtures. Symptoms include nausea, vomiting, fine tremors, incoordination, dizziness, fatigue, somnolence, myoclonic jerking, stomach cramps, and decrements in intellectual and psychomotor performance.
Diagnosis is clinical. Prevention is usually accomplished by slowing the rate of compression and/or adding a small amount of a narcotic gas (eg, 5% nitrogen) to the breathing mix.