Inert gas narcosis (IGN) was comprehensively reviewed in 2003, and interested readers are referred to that work for more detail1. The first recorded description of symptoms suggestive of air intoxication related to hyperbaric exposure was by Junod, who, in 1835, reported that ‘thoughts have a peculiar charm and in some persons, symptoms of intoxication are present’. He was conducting research into the physiological effects of compression and rarefaction of air. J. B. Green in 1861 observed sleepiness, impaired judgement and hallucinations in divers breathing compressed air at 5.8 ATA, sufficient to warrant an immediate return to the surface. Paul Bert, in 1878, also noted that divers became intoxicated at great depth. In 1903, Hill and McLeod described impairment of intellectual functioning in caisson workers at 5.5 ATA. Damant, in 1930, likened the mental abnormalities and memory defects observed in men at 10 ATA to alcoholic intoxication and postulated that it was caused by the high partial pressure of oxygen.
Hill and Phillips suggested in 1932 that the effects could be psychological as a result of claustrophobia or perhaps caused by impurities in the air from the compressors (Case report 15.1). The Royal Navy appointed a committee to investigate the problems of deep diving and submarine escape, and their report in 1933 contained a section entitled ‘semi-loss of consciousness’. Between 7 and 11.6 ATA, divers answered hand signals but in many cases failed to obey them. After return to surface, the divers could not remember the events of the dive. It was noted that all divers regained full consciousness during the return to 1 ATA. The report also noted great individual variation in divers’ reactions but was unable to elucidate the problem.
CASE REPORT 15.1: DESCRIPTIONS OF DIVERS ABOUT THEIR EXPERIENCES AT BETWEEN 250 AND 300 FEET AS REPORTED BY HILL AND PHILLIPS
‘You notice the dark more although it may not be darker; the light is a comfort and company. You notice things more if there is nothing to do; I get comfort from seeing the fish, it takes your mind off everything else’.
When asked for a description, an old hand at diving gave the following account: ‘You have to be more careful in deep water; in deep water you know that you are concentrating… You think of each heave as you turn a spanner… If you go down with a set purpose it becomes an obsession; it will become the main thing and you will forget everything else’. He described how he thinks very deliberately; he says, ‘I have finished my job, what shall I do next? – Of course, I have finished and now I must go up’. He described how he was aware of every action: ‘If my hand goes out I think of my hand going out’. He gave the following as an analogy: ‘if I saw a thing of value, say half-a-crown, in the street, I would pick it up. Down below I would look at it and think, “What is that, shall I pick it up? Yes, I will pick it up” and then I feel my hand go out’.
‘I left the ladder determined to get to the bottom. At 250 feet I got a recurrence of the tingling and a feeling of lying on my back. I decided to rest a couple of minutes and then go on. I slid 10 feet and felt I was going unconscious. I made signals to be pulled up and kept repeating them. I lost the use of my limbs and let go everything. While hanging on to the rope I saw my own face in the front glass; it was outside the glass and looked all greenish; I was dressed in my shore-going suit. I heard the order, “Pull the diver up”, again and again, as if someone in the suit was saying it’.
‘Suddenly I came over rather “funny”; it was a distinct “different” feeling; I stood up, the tank wire in my right hand, and thinking it was a touch of CO2, I began to breathe deep and hearty, thinking of course that in a couple of minutes I would be able to resume work. Then I seemed to go quite limp, a feeling of “no life or energy”. This was new and strange to me, whether it was a part of CO2, I didn’t know, because I had never experienced a real dose of CO2; anyhow, after stopping and doing the drill for CO2, I thought I would be alright, but suddenly something definitely seemed to say – snap inside my head and I started to, what I thought, go mad at things’.
Description of interview of above diver after an aborted deep dive:
Practically no hypnoidal effort was required to produce the horrors of that morning’s dive, and the picture of stark, mad terror….left an impression which is very difficult to describe. The impression was of sitting in the stalls and watching the acting of Grand Guignol. To such a pitch did he arouse his emotions that he clawed his face to remove the imaginary face-glass and tore his clothes which he mistook for his diving suit (Hill I, Phillips AE. Deep-sea diving. Journal of the Royal Navy Medical Service 1932;18:157–173).
It was not until 1935 that Behnke, Thomson and Motley proposed the now generally held theory of the cause of this compressed air intoxication. They stated that the narcosis was the result of the raised partial pressure of the metabolically inactive gas, nitrogen. At a depth of 30 metres (4 ATA), compressed air produced a state of ‘euphoria, retardation of the higher mental processes and impaired neuromuscular co-ordination’. This effect was progressive with increasing pressure so that at 10 ATA, stupefaction resulted. Unconsciousness developed between 10 and 15 ATA. They also invoked the Meyer-Overton hypothesis (see the later section on aetiology) to relate the narcotic effect to the high ratio of solubility of nitrogen in oil to water. It was not long after this major breakthrough that Behnke and Yarbrough reported that the substitution of helium for the nitrogen in compressed air eliminated narcosis.
The nitrogen partial pressure theory was not universally accepted. The 1933 Deep Diving Committee Report had raised the possibility that carbon dioxide retention was implicated. Case and Haldane, in 1941, reported that the addition of carbon dioxide to compressed air worsened the mental symptoms, although up to 6 per cent concentrations at 1 ATA had little mental effect. Bean, in 1947, demonstrated a reduction in arterial pH during compression and later also showed increased alveolar carbon dioxide concentrations. He explained these changes as being caused by reduced diffusion of carbon dioxide in the increased density of the air. He postulated that carbon dioxide was an alternative cause of depth narcosis. Seusing and Drube later supported Bean’s views as recently as 1961. Also in 1961, Buhlmann believed that increased airway resistance led to hypoventilation and hypercapnia.
Rashbass in 1955 and Cabarrou in 1959 had already refuted the carbon dioxide theory, by observing signs of narcosis despite methods to ensure normal alveolar carbon dioxide levels. Later work (by Hesser, Adolfson and Fagraeus) showed that the effects of nitrogen and carbon dioxide are additive in impairing performance. Normal arterial carbon dioxide and oxygen levels, while the diver is breathing air and helium-oxygen at various depths, demonstrate the key role of nitrogen in the production of this disorder and the relative insignificance of carbon dioxide.