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Oxygen Toxicity

Effects of Oxygen at Depth
The effects of oxygen are increased at depth so that the maximum PO2 in diving is 1.6 ATA, and this is achieved at 218 fsw breathing air, 132 fsw breathing 32% O2, and 20 fsw breathing 100% O2.

This is due to the effects of Dalton's Law which states that on descent, the partial pressure of all component gases increase in the same ratio as the total pressure. this results in the creation of the elevated pO2 that causes the convulsions of O2 toxicity and is the direct cause of nitrogen narcosis and along with Boyle's law, is the cause of decompression sickness.
All O2 treatments using 100% O2 are given at 60 feet or shallower, except for gas gangrene and CO poisoning. This effect is also the limiting factor in the use of nitrox (increased O2 percentages) in increasing the bottom time of "tech" divers.

The Paul Bert Effect

  • Muscle twitching and spasm
  • nausea and vomiting
  • dizziness
  • vision (tunnel vision) and hearing difficulties (tinnitus)
  • twitching of facial muscles
  • irritability, confusion and a sense of impending doom
  • trouble breathing, anxiety
  • unusual fatigue
  • incoordination
  • convulsion.

  • Convulsion at depth in water usually results in drowning or arterial gas embolism and is prevented by not using oxygen breathing with SCUBA and by limiting oxygen exposure with hyperbaric oxygen therapy 100% O2 greater than 60 FSW.

    Factors increasing risk of O2 toxicity

  • Increasing exposure time
  • Increasing depth
  • Increasing the percentage of inspired O2 (As in nitrox mixtures)
  • The simple act of immersion setting off the diving reflex
  • Exercise increasing the metabolic rate
  • Increased CO2 in the tissues (May be due to cerebral vasodilation)
  • Cold stress (Shivering is a form of exercise)Systemic diseases that increase the metabolic rate (such as thyroid diseases)
  • Sympathomimetic drugs (Drugs that mimic adrenalin in effect).

  • Sudafed is a medication often used by divers due to it's decongestive effect. It has few side effects but is a sympathomimetic drug (pseudephedrine). Whether or not it should be used in nitrox or rebreather diving is discussed by Dr. E.D. Thalmann in DAN's publication at http://www.diversalertnetwork.org/medical/articles/article.asp?articleid=51

    "In 1962, none other than DAN's Chief Executive Officer, Dr. Peter Bennett, while working as a research physiologist at the Royal Navy Physiological Laboratory in England, published a paper (Life Sciences; 12:721-727, 1962) testing the hypothesis that oxygen toxicity and nitrogen narcosis were caused by similar mechanisms.

    He found that in rats, sympathomimetics seemed to enhance oxygen toxicity. Pseudoephedrine was not tested specifically, but it is a sympathomimetic, so we might infer that it has a similar effect. In addition, our current understanding of the mechanisms which produce oxygen convulsions would predict that sympathomimetic drugs might enhance susceptibility to oxygen convulsions. It has been shown that drugs which inhibit sympathetic stimulation seem to reduce the likelihood of oxygen convulsions in animals. No human studies have ever been done. Thus, at least a theoretical reason exists why pseudoephedrine should be avoided while diving on high PO2 dives."

    Mitigation of oxygen toxicity

    We often see long lists of drugs that will increase the risk of CNS and pulmonary oxygen toxicity? Are there any drugs or therapeutic measures that can be taken to reduce the risks of acute oxygen toxicity?

    This is a question being studied by many for it's benefits in the area of hyperbarics and in the military for reduction of risks for users of closed circuit breathing aparatus.

    Bove, p. 135. "Factors that modify the rate of development of oxygen poisoning"

    Factors that Delay Onset

    Acclimatization to hypoxia
    Adrenergic blocking drugs
    Gamma-aminobutyric acid
    Ganglionic blocking drugs
    Intermittent exposure
    Vitamin E

    Edmonds p. 210, mentions aerosolized [recombinant human manganese] superoxide dismutase as a preventive of pulmonary O2 toxicity. He also mentions glutathione, and disulfiram, GABA, lithium (convulsions in rats),  hyperventilation, hypophysectomy, adrenalectomy, adrenergic blockers, some anesthetics, magnesium and superoxide dismutase.

    Some close relatives of the Carnobacterium in the Antarctic contain millimolar concentrations of intracellular Mn2+ which helps these cells to mitigate oxygen toxicity.

    Damaging or toxic effects of oxygen therapy likely are related to the unbridled formation and release of reactive oxygen species, such as superoxide, hydroxyl radical, and hydrogen peroxide. Superoxide dismutase, catalase, glutathione, and glutathione reductase keep the formation of these radicals in check until the oxygen load overwhelms the enzymes, leading to the detrimental affects on cell membranes, proteins, and enzymes. Other antioxidants used by the body include vitamins C and E, selenium, and glutathione.
    Interleukin 1  and Polyethylene glycol-attached antioxidant enzymes have been shown to reduce the effects of O2 toxicity in rats.

    Due to the other dangers of diving while on drugs, probably the safest measures to take are the intermittent periods of air breathing used quite successfully in the hyperbaric chamber. That this can not be so easily accomplished in the underwater environment should be readily apparent.

    Pulmonary oxygen toxicity (Lorraine Smith effect) is a direct time/dose relationship on the lungs caused by a direct effect of O2 on the lungs, blockage of airways, increased CO2, pulmonary surfactant changes , enzyme interference and an inert as effect. The best treatment is prevention and removal of pure O2 at the first signs of toxicity.

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