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)

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.