Scuba Diving club,
Southern California
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Oxygen Toxicity |
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 effect on the central nervous system
( the Paul Bert effect), results in:
· 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 susceptibility to O2
toxicity include:
· 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
Q.
We often see long lists of drugs that will
increase the risk of CNS abd pulmonary oxygen toxicity? Are there any drugs or
therapeutic measures that can be taken to reduce the risks of acute oxygen
toxicity?
A.
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
Antioxidants
Chlorpromazine
Gamma-aminobutyric acid
Ganglionic blocking drugs
Glutathione
Hypothyroidism
Reserpine
Starvation
Succinate
Trisaminomethane
Intermittent exposure
Disulfiram
Hypothermia
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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Reference
Minibox |
Contact
Ernest S. Campbell, M.D., FACS
31681 Shoal Water Drive
Ono Island, AL, 36561
E-Mail Address
scubadoc@scuba-doc.com
Website Address: http://www.scuba-doc.com/
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Posted August 30, 2003