How oxygen is dissolved in the blood
The higher the total dose, calculated from the product of partial pressure and time, the higher the probability of CNS poisoning. Since the critical limit can be exceeded when diving with oxygen-enriched mixtures, acute oxygen poisoning is possible when diving with nitrox or technical diving. Oxygen cramps have also been described during recreational diving with compressed air at great depths (from 60 meters) - depths in which a diver with compressed air should not normally stay.
Symptoms of acute oxidosis are: restlessness, metallic taste on the tongue, uncontrolled twitching of the facial muscles, tunnel vision, drowsiness, nausea and finally generalized cramps. At high oxygen partial pressures, these symptoms appear within a few minutes. The harbingers of an impending oxygen spasm are usually too short to be able to react adequately under water. With a few exceptions (divers with full face masks), an oxygen spasm underwater is followed by drowning. Even with quick help from the buddy, a spasm underwater cannot be controlled, nor does one win the race to the surface before drowning. During a seizure, the glottis is tightly closed so that no air can escape from the lungs. When surfacing quickly, the lungs are over-inflated or even ruptured. This - along with the expected decompression sickness - would admittedly be preferable to drowning, but this race to the surface is not won.
Observations in patients from hyperbaric medicine show that the affected person often reflexively removes the mask before the cramp begins. At this point, however, the patient is no longer clearly conscious. Even if the oxygen supply is reduced to a normal level at this moment, the spasm will continue unaffected for its full length. Underwater, divers often take the mouthpiece of the regulator out of their mouth or remove the mask shortly before a cramp. Attempts to reinsert the mouthpiece always fail because the teeth are clenched firmly and the jaw can no longer be opened.
Chronic oxygen poisoning: longer exposure times to oxygen or oxygen-rich mixtures (> 24 h) can lead to damage - even at low partial pressures (<1 bar). In diving, this is basically only of importance in the case of repeated recompression therapy after decompression sickness, since a diver hardly has the long exposure times underwater that are necessary for this.
The target organ is usually the lungs. With increasing pressure, the exposure time is reduced in order to cause the same lung damage. From earlier times one also knows the impairment of the retina with prolonged oxygen administration in premature infants in the incubator, which led to blindness (retrolental fibrosis). The damage to the lungs is also known as the "Lorrain-Smith effect". The effect was named after the British doctor James Lorrain Smith (1862-1931). The mechanism behind this consists of edema formation (fluid accumulation) in the small alveoli (alveolar edema) and damage to the surfactant factor, which leads to alveolar collapse. This reduces the lung surface area available for gas exchange.
The symptoms of pulmonary oxygen toxicity begin with irritation of the throat and occasional coughing, which can increase to an uncontrollable painful cough and tightness in the chest, dizziness, inefficiency and pain when breathing. The lung tissue is increasingly damaged. The structural changes are initially reversible, but after long exposure times they can also become permanent and incurable and - ultimately due to insufficient oxygen supply to the body - even lead to death.
Today, 0.5 bar is regarded as the tolerable upper limit of the oxygen partial pressure, which can be breathed over long periods of time without harmful effects. Therefore, the oxygen partial pressure of 0.5 bar must not be exceeded during saturation dives. For dives with compressed air, which are limited to 50 m water depth, the partial pressure is max. 6 bar x 0.21 = 1.26 bar. This oxygen partial pressure would require an exposure time of about 8 hours to damage the lungs on the order of 2%. However, since the diving time for a depth of 50 m is limited to about 1 hour due to decompression requirements, chronic oxygen poisoning can be excluded when diving with compressed air. It is different when treating serious diving accidents in pressure chambers, where deliberately high oxygen partial pressures could cause neurological symptoms of poisoning, especially if the diver is physically exhausted or - due to the severity of DCS II - repetitive recompression therapies are necessary. In order to be able to carry out an imputed risk assessment of oxygen damage, the so-called "UPTD" (Unit Pulmonary Toxic Dose) has been introduced in diving and hyperbaric medicine. A UPTD is calculated as follows: 1 UPTD = ambient pressure 1 bar with 100% oxygen for 1 minute. Based on animal models it is known that with 615 UPTDs the first impairment of lung function must be expected. This must be taken into account in the therapy protocol.
The oxygen tolerance and the oxygen sensitivity are individually different - what one can put away without any problems is already too much for some others. The oxygen tolerance varies not only between the individual people, but also individually from day to day and depends on the physical condition and daily form. For example, the tolerance is significantly greater at rest than when working hard under water, for example, which is expressed in the different tolerance limits in a pressure chamber in contrast to wet diving in the water. Lack of sleep, dehydration, the influence of alcohol and excitement all increase sensitivity.
This puts the so-called oxygen tolerance tests, which were already carried out by the British government in 1942/43, into perspective.
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