By Richard Taylor
The terms CNS, OTU and UPTD all deal with oxygen toxicity within the human body. The terms OTU and UPTD mean the same thing, so we will break this down into two separate sections.
CNS stands for '˜Central Nervous System' and is used when we are discussing the oxygen toxicity effect to our central nervous system. It is actually the CNS percentage that we refer to and this will be what we look at first. A secondary concern, and one which in general as divers has little or no effect on us, is the '˜Whole Body' or '˜Pulmonary' toxicity which is discussed when dealing with OTU's, Oxygen Tolerance Units. To begin with though we need to understand the basics of of our oxygen system.
Oxygen as a gas is what keeps us alive. It is absorbed through our lungs into the body and delivered to the tissues via the arterial system where it is metabolised in the long run producing carbon dioxide (CO2). This waste is then delivered back to the lungs via the veinial system and exhaled (a much more in depth explanation is available in most good medical books). However, as much as oxygen is our life giving gas, too much of it can be harmful. It is this excessive amount of oxygen that we look out for.
Breathed under pressure each of the components of air, oxygen and nitrogen, effect an increased pressure proportional to the total pressure, this being their '˜Partial Pressure', PPO2 for oxygen and PPN2 for Nitrogen. The greater the partial pressure of the gas then the greater the amount that is breathed by the diver and therefore the greater the amount metabolised into the body. The human body has a threshold at which too much oxygen is unable to be safely metabolised and it is at this point that oxygen becomes toxic.
The most important concern to us as divers is Central Nervous System toxicity. Also known as the Paul Bert Effect, after the French researcher who first documented the physiological effects of exposure to high pressures of oxygen (1878 in '˜La Pression Barometrique'), CNS toxicity is monitored by taking the amount of exposure to a given partial pressure of oxygen as a percentage of the total maximum recommended. This maximum recommended allowed doseage is published by NOAA (the National Oceanic & Atmospheric Association) as a set of tables widely accepted and used by the Nitrox and Technical Diving training agencies. These '˜NOAA Oxygen Exposure Tables' are recommended limits only as the exposure tolerance varies from diver to diver. Much of today's knowledge on CNS Toxicity stems from research undertaken in the 1940's by the Royal Navy (for more details read '˜Oxygen and the Diver' by Kenneth Donald, SPA Ltd 1992).
There is much research continuing today on CNS Toxicity and as to date there has been no satisfactory consistent warning of the onset it is only through the limits to exposure that CNS Toxicity can be avoided. Among the warning symptons are twitching (especially lips), nausea, dizziness and dysphoria. The onset of convulsions will result in a Grand Mal seizure and unconciousness, an effect which will place the diver at serious risk of drowning. Diving beyond the depth limit of the mixture being breathed will increase the chance of suffering from a CNS Toxicity convulsion.
The second effect is more relevent to commercial divers who undertake long exposures to increased oxygen pressures than to us as recreational diver. Whole Body, or Pulmonary Oxygen, Toxicity causes progressive respiratory distress, leading to respiratory failure and death. The net result is that the lungs' vital capacity to transfer the oxygen is destroyed along with the pulmonary capillaries and alveolar lining cells. This effect can be tracked via the '˜Oxygen Toxicity Clock' and the REPEX method (Repetive Exposure Tables, R. W. Hamilton 1989). Here repetitive exposure to oxygen partial pressures above 0.5 bar can be tracked in relation to a recommended maximum equivelent in minutes to breathing 100% oxygen at sea level, 1 bar. The Oxygen Tolerence Units allowed ( OTU's or Unit Pulmonary Toxicity Dose, UPTD) will decrease with each repetitive days diving.
Also known as the Lorrain Smith Effect, who identified this effect in 1899, much of today's knowledge was again gained by the research undertaken conducted by Professor Donald during the Second World War. The symptoms are chest tightness, cough, chest pain and shortness of breath. Intermittent rather than continuous exposure to high oxygen partial pressures will alleviate this risk. As recreational scuba divers it is most likely that the relatively short dive times and numerous surface intervals we undertake will accumulate only a minimal number of OTU's. However, repetitive multi day diving with high partial pressurs of oxygen sould be planned to include the OTU Repex Tables and limits.
(Note: for a more detailed description of Oxygen Toxicity refer to '˜Diving and Subaquatic Medicine' 3rd Ed 1992 by Carl Edmunds et al, from which some of the above is taken)