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Gas Toxicity During Diving

by Alfred A. Bove, MD, PhD

Various physiologic (eg, O 2 , N 2 , CO 2 ) and nonphysiologic (eg, carbon monoxide) gases can cause symptoms during diving.

Oxygen toxicity

O 2 toxicity typically occurs when the partial pressure of O 2 exceeds 1.4 atmospheres (atm), equivalent to about 57 m (187 ft) depth when air is breathed. Symptoms include paresthesias, focal seizures, vertigo, nausea, vomiting, and constricted vision. About 10% of patients have generalized seizures or syncope, which typically results in drowning. Risk is increased when divers breathe mixtures of O 2 and N 2 (nitrox) that have an increased percentage of O 2 .

Nitrogen narcosis

When compressed air is breathed at depths of > 30 m (> 100 ft), the elevated partial pressure of N 2 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 clinical. Treatment entails immediate but controlled ascent. Nitrogen narcosis can be prevented by using helium to dilute O 2 for deep diving because helium lacks the narcotic properties of N 2 . However, using pure helium/O 2 mixtures in very deep dives (> 180 m [> 600 ft]) increases the risk of developing high-pressure neurologic syndrome (see High-pressure neurologic syndrome).

Carbon dioxide poisoning

CO 2 poisoning may be caused by any of the following:

  • Inadequate respiratory effort (hypoventilation)

  • A tight wetsuit

  • Overexertion

  • Regulator malfunction

  • Deep diving

  • Air supply contamination by exhaled gases (as occurs with a CO 2 scrubber failure in a rebreather air supply)

Hypoventilation can increase blood CO 2 levels and cause shortness of breath and sedation. Severe CO 2 poisoning can cause nausea, vomiting, dizziness, headache, rapid breathing, flushing, confusion, seizures, and loss of consciousness.

Mild CO 2 poisoning is suspected if divers frequently have dive-related headaches or low air-use rates.

CO 2 intoxication usually resolves during ascent; thus, ABG testing after a dive typically does not detect any increase in CO 2 levels. Treatment is gradual ascent and termination of the diving exercise or correction of the precipitating cause.

Carbon monoxide poisoning

Carbon monoxide can enter a diver’s air 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 (COHb) level in blood; pulse oximetry readings are nondiagnostic and usually normal because pulse oximeters cannot distinguish between oxyhemoglobin and COHb. The diver’s air supply can be tested for carbon monoxide.

Treatment is with high-flow 100% O 2 , best given via a nonrebreather mask, which decreases the half-life of COHb from 4 to 8 h in room air to 40 to 80 min. For severe cases, hyperbaric O 2 therapy may be considered if readily available. COHb levels will drop quickly in the hyperbaric chamber (half-life 15 to 30 min); however, the benefit of hyperbaric O 2 therapy is controversial. Some studies indicate that hyperbaric O 2 therapy lessens neurologic sequelae, but others do not support this finding.

High-pressure neurologic syndrome

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/O 2 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.

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