POSTGRAD. MED. J. (1966), 42, 636.

ASPECTS OF UNDERWATER MEDICINEE. E. P. BARNARD, M.B., B.S.,

Surgeon Lieutenant Commander, R.N.Royal Naval Physiological Laboratory, Alverstoke, Hants.

Two OF the most interesting theoretical aspects ofdiving or working at increased ambient pressuresare inert-gas narcosis and decompression sickness,both due, in different ways, to the behaviour of theso-called 'inert' gases dissolved in the fluids of thebody.The inert gases dissolve according to the gas

laws so that the tissues of the body are in equilib-rium with the alveolar gas pressures. At atmosphericpressure the PN2 of the tissues is about 573 mm. Hg.and the total quantity dissolved is approximately 1litre (B.T.P.).

If the ambient pressure is increased the quantityof nitrogen dissolved and the tissue PN2 will beproportionately increased at equilibrium. Howeverthe process of achieving a fresh equilibrium aftersuch an increase in pressure is not instantaneous.The quantity of gas dissolved after some finitetime is described by an exponential function which,in this context, is usually defined by its 'half-time';that is the time taken to reach 50% of the quantitydissolved at equilibrium (or 0.693 times the timeconstant of the exponential).

Inert-Gas NarcosisNitrogenThe degree of impairment due to narcosis has

been shown by Barnard, Hempleman and Trotter(1962) to be approximately proportional to thepartial pressure of the nitrogen breathed, butsymptoms are not normally detected at pressuresbelow 4 ats. abs. It has been recently suggested byPoulton, Catton and Carpenter (1964) that someimpairment of performance may be found at 2 ats.abs.; however these findings await confirmation.The symptoms are variable, but numbness of the

lips and cheeks, increased excitability and euphoriaare the most common manifestations. At increasingpressures excitement may give way to somnolence,judgement is markedly affected and at 10 ats. abs.most men are incapable of useful work and mayeven be stuporous. When the subject is decom-pressed the narcosis is relieved, but some subjectsshow amnesia for the time spent at pressure.

Present address: University Department ofPharmacology,South Parks Road, Oxford.

While there is no accurate estimate of theanaesthetic pressure for nitrogen, two divers becameunconscious almost immediately when exposed toair at 31 ats.abs. (Keller, 1964).Helium

Behnke, Thomson and Motley (1935) were thefirst to show that nitrogen was the cause of thesymptoms described and Behnke and Yarbrough(1939) the first to demonstrate that these symptomswere absent if the nitrogen in the breathing mixturewas replaced by helium. This finding had the immedi-ate practical advantage that it allowed diving to beextended beyond 10 ats.abs. (300 feet of sea water).There is however another good reason for abandon-ing air and this is the toxic effect of oxygen atraised pressures. The accepted safe upper limit forthe Po2 in breathing mixtures is 2 ats.abs., which isreached at a total pressure of about 10 ats.abs.when breathing air. In order to dive deeper there-fore, the oxygen percentage in the mixture must bereduced and the nitrogen replaced by some otherinert gas.Of the inert gases available to act as diluents for

the essential oxygen, only helium, neon and hydrogenappear to be less narcotic than nitrogen.Recent work by Bennett (1965) seems to show that

neon is intermediate in its narcotic propertiesbetween nitrogen and helium. Regarding theposition of hydrogen, although oxy-hydrogenmixtures have been used in diving by Zetterstrom(1948) it is not known whether hydrogen ismore or less narcotic than helium or even whetherit should be regarded as physiologically inert.This lack of information is partly due to thetechnical difficulties of handling potentially explosivemixtures of hydrogen and oxygen.From this brief outline therefore it should be

clear why oxy-helium mixtures are used in deep-diving and, also that, if no superior gas can befound the limits to which one can dive will dependupon the depth at which helium narcosis appears.

Recent observations at the Royal NavalPhysiological Laboratory during the course ofdives between 10 and 25 ats.abs. suggest that oxy-helium mixtures produce effects which are firstdetected at about 16 ats.abs.

BARNARD: Aspects of Underwater Medicine

The most noticeable sign is a coarse tremor,particularly of the hands, which tends to improveafter about an hour. The divers may also reportfeeling weak, clumsy, nauseated or dizzy; feelingswhich also improve with time. Since these effectsare different from those of nitrogen, both in theirnature and in their behaviour with time, it is probablethat they are due to a combination of factors. Itseems likely however that at least part of the effectis due to the narcotic action of helium.The precise mechanism by which inert gases

produce these narcotic effects is not known butMiller, Paton and Smith (1965) show evidencewhich favours the 'lipid solubility' or 'non-aqueousphase' theories rather than 'aqueous phase' theories;and the evidence assembled by Bennett (1965)points to the synapses within the central nervoussystem as the sites of action.

Decompression Sickness (Dysbarism)The term decompression sickness includes caisson

disease, diver's 'bends' and similar conditionswhich occur in aviators. While the aetiologyremains obscure, a fall in ambient pressure, i.e. adecompression, invariably preceeds the onset; it istherefore an occupational disease almost entirelyrestricted to men of working age and unknownbefore the invention of the diving suit and thecaisson in the first half of the nineteenth century.The time of onset is variable; even in severe

cases there seems to be a short latent period of theorder of five minutes. In divers and caisson workersmost symptoms come on within two hours followingdecompression; but in deep-diving numerous casesoccur during decompression, (Barnard, 1966) andthe onset may be delayed for many hours in caissonworkers. The situation in aviators is slightlydifferent since symptoms are usually caused by lossof cabin pressure when at altitude and the time ofonset is related to the length of time for whichoxygen has been breathed prior to decompression.A further point of difference is that symptoms inaviators are caused by decompression of the normalamount of nitrogen dissolved in the body at 1ats.abs.; whereas in divers and caisson workerssymptoms are caused by decompression of thegreatly increased amounts of gas dissolved atraised pressures.

In spite of these differences it is possible tocatalogue the types of decompression sicknesswithout referring to the type of exposure whichcaused them. The classification of decompressionsickness is however most unsatisfactory and that ofGolding, Griffiths, Hempleman, Paton and Walder(1960) into two types, Type 1 cases being cases of'bend' pain and Type II cases, all others, is noadvance on the present odd collection of traditionalnames.

Minor CasesThis group is understandably the most difficult to

diagnose, symptoms such as general malaise orsleepiness are common after diving and mildpyrexia may also occur. More definite however areitching of the skin, 'itches,' particularly of theexposed areas of the face and the backs of thehands; and mild aches and pains, 'niggles' varyingin intensity and site but gradually improving. Apartfrom the signs due to lesions of the nervous systemthe only other signs are restricted to the skin. Thecommonest of these called 'marbling' frequentlyappears as florid red, white and blue marking onthe skin. These markings seem to be due to dilatedstagnant veins with large areas of arteriolar flareand small areas of contracted capillaries. Thatcapillary damage occurs is shown by the presence ofsmall petechial haemorrhage after the 'marbling'has faded.A rare sign, which has occurred twice in the same

individual, is induration of the skin. It occurredduring an attack of a more severe type of decom-pression sickness and was fully developed withinfive minutes. The loose skin of the face and of theupper chest and back became swollen, firm, tenderand hot. No crepitus could be felt, and the indur-ation, which appeared to be due to an inflammatoryreaction, gradually disappeared in the course ofabout ten days.

Local oedema may sometimes be seen in a limbwhich is the site of 'bend'-pain, but this usuallydisappears when the 'bend' is treated.

'Bends': The commonest symptom in divers andcaisson workers is pain in the limbs. These painsvary from mild persistent aches to intense sharppains causing sweating and distress. The pain isfrequently localised in or near to a joint, usually toan area including the whole joint, but sometimes toa precise site such as the insertion of the ligamentumpatellae.

Characteristically the pain increases in intensityfrom the time of onset and may be associated withtransient pains in other sites. The intensity of thepain increases with exercise, it cannot be 'workedoff,' although some relief may be obtained from ahot bath or from local pressure.Abdominal pain (of a similar nature) also occurs

and must be distinguished from the effects ofexpanded gas within the lumen of the gut, whichgives rise to 'colicky' pain.

Cases of 'bends' rarely show any abnormality onphysical examination, the diagnosis usually beingmade on the history alone; however one may findreduced tendon jerks on the affected side or araised skin temperature over a painful joint.

'Chokes': This is characterised by substernaldiscomfort or pain and difficulty in taking a deep

October 1966 637

POSTGRADUATE MEDICAL JOURNAL

breath. The attack is frequently 'triggered' by thefirst cigarette after a dive and consists of a paroxysmof coughing, the subject perhaps becoming cyanosedand needing urgent treatment. Cases of 'chokes'seem particularly liable to lead to shock especiallyif treatment is inadequate.

Nervous DisordersAlmost any type of nervous disorder seems to

present at some time or another as a manifestationof decompression sickness.

Sensory symptoms are perhaps most frequent,patches of paraesthesia or anaesthesia, feelings ofwarmth or burning sensations and disorders ofproprioception may be seen both together orseparately. There is a tendency for sensory symp-toms to precede any motor loss, but isolated lowermotor neurone type paralysis may come on withoutany alteration of sensation.The distribution or extent of sensory symptoms is

frequently difficult to correlate with any singlelesion which could be postulated on the basis of theanatomical pathways, for instance, anaesthesia ofthe tips of all digits on both hands has been observed.This may of course be due to multiple lesions,which might be expected if the aetiological agent isgas-bubbles, but the distribution of such bubbles ina symmetrical manner is just as difficult to explain.

Hemiplegia and paraplegia are the most commonsevere neurological involvements but quadriplegiahas also been reported. These paralyses show apeculiarity which may be of some value in differen-tial diagnosis, in that recovery is usually muchfaster and more complete than is usual in otherconditions. Many divers have made almost completefunctional recovery following an incident which atthe time might have been indistinguishable fromcomplete transection of the cord.Due to the protean nature of decompression

sickness and the way in which symptoms mayresolve without treatment, there may be realdifficulty in distinguishing between cases of multiplesclerosis and decompression sickness, even if thehistory of diving is known. Diagnosis can be madeif such patients are given a therapeutic test ofresponse to pressure. The pressure must be adequatei.e. at least 6 ats.abs., the time at pressure needs tobe at least two hours and the only conclusive resultof the test is relief. This test is more likely to giveinformation if it is used early, preferably with 24hours of onset, but it is still worth trying afterseveral days. Failure to respond may be due to theirreversibility of damage.

'Cerebral Bends': These are not common, but maypresent either as sudden loss of consciousness,perhaps followed by some degree of paralysis or asan alteration in mood, behaviour or personality.

The onset is normally soon enough after the decom-pression to make the diagnosis obvious.

'Staggers': Cases occur in which the labyrinth iseffected, sometimes associated with a cochlearlesion on the same side. The patient presents withvertigo, nausea or vomiting, unsteadiness of gaitand 'Rombergism' and there may also be some deaf-ness. If treated soon enough recovery is complete.

Visual Disturbance: The development of tempor-ary scotomata has been reported, particularly inaviators, by Flinn and Womack (1963). Suchcomplaints are rare in divers, who however seem toget mild visual disturbances, similar to 'fortificationspectra,' quite frequently. It is possible that raisedoxygen partial pressures are responsible for thesesymptoms.

Avascular Necrosis of BoneAlthough this disorder has been recognised as a

risk of caisson working or tunnelling for many yearsit is only recently that large-scale surveys have beenundertaken, notably by the Medical ResearchCouncil, in order to discover its incidence. Thelesions are usually discovered on radiography andoccur in the long bones particularly in the upper endof the humerus, femur and tibia in descending orderof frequency. The lesions may be either in the shaftor in the head of the bone and they are frequentlybilateral. They consist of discrete areas of necrosissurrounded by new bone. Lesions of the shaft mayby asymptomatic while those of the head maypresent with secondary arthritic changes, or follow-ing collapse of the joint surface.

Post-Decompression ShockThis condition is more common in aviators but

is sometimes seen in divers or tunnel workers. Thelikelihood of its occurrence seems to be related tothe adequacy of treatment. It occurs in aviatorsafter they have been recompressed back to 1atmosphere and should be treated by further recom-pression to greater pressures, while in divers ortunnel workers it is usually seen following unsuccess-ful attempts at treatment. Cases of post-decompression shock may occur in men with 'bends'treated with morphine or similar alkaloids, whichalthough they relieve the pain do not preventfurther damage. In early cases the pulse rate maybe normal or slightly raised and the blood pressurewithin normal limits while sitting or lying. Howeverthere is usually marked postural hypotension sothat the patient is unable to stand, but may feelnormal when lying down. These symptoms seemto be due to gross haemoconcentration followingfluid loss into the tissues and treatment is by recom-pression in the early stages or by a combination ofrecompression and intravenous infusion of plasmain more severe cases.

638 October 1966

October 1966 BARNARD: Aspects of Underwater Medicine 639

IncidenceDecompression sickness is, in theory at least,

completely preventible. However, cases do occurand these supply the only information from whichone can assess the degree of failure of a particulardecompression procedure.The current practice is to calculate crude incidence

figures, defined as the ratio of the cases observed tothe total number of exposures. This figure is ofcourse quite satisfactory for an employer whoneeds to know how many man-hours are being lostdue to decompression sickness, but it concealsrelationships which might lead to a better under-standing of the problem and a consequent improve-ment in the procedure.

Tunnel working in Great Britain produces anincidence of only about 1 %, remarkably low incomparison with that in experimental diving, butthis figure only represents those men who reportfor treatment. If the results of experimental divingare in any way comparable, then of all the men whohave signs or symptoms, only about one third askfor or receive treatment. To pretend that thesecases which are ignored represent successes isincorrect as is perhaps most clearly shown byrecent studies of avascular necrosis of bone (M.R.C.1966).Even if revised regulations for compressed air

workers completely abolished all cases of 'bend' painand yet produced avascular necrosis in 10% of themen at risk they would still be inadequate.

In calculating the incidence of decompressionsickness one must therefore include all manifest-ations of decompression sickness, as far as they canbe discovered. However, even if all cases could berecorded there is a further complication due to thefactor of acclimatisation (Paton and Walder, 1954).The effect of acclimatisation is seen as a greatersusceptibility to 'bends' in men when they are firstintroduced into compressed air compared withthose who have been exposed repeatedly. Apartfrom other factors the effect of introducing newmen will be to produce a fluctuating incidence ofwhich the crude incidence represents the mean.

Since the pressure to which men are exposedvaries throughout the construction of a tunnel,the decompression routine, which is determined bythe maximum working pressure of each shift mayalter from shift to shift. Now there is no certaintythat the decompression routines for differentpressures are equally safe, they tend in fact to becomeless adequate at pressures above 35 p.s.i.

Since in practice it is not possible to ensure thatall men remain acclimatised, in order to have anyclear idea of the effectiveness of a decompressionprocedure we must know the incidence of decom-pression sickness, for the particular routine inquestion, in unacclimatised men. This is the only

index which avoids the interference of factorsother than individual differences in susceptibility.

Individual SusceptibilityThe simplest situation in which to compare the

susceptibility of individuals is in so-called 'no-stop'dives, which are dives followed by direct ascent tothe surface. For dives deeper than about 33 feet ofsea water (2 ats.abs.) there is an exposure timebeyond which direct ascent is no longer possiblewith safety, and the maximum exposure at eachdepth which just allows direct ascent may beplotted as the no-stop curve (Fig. 1).

In all longer exposures ascent can be made to apoint short of the surface but the decompressionmust be prolonged to avoid decompression sickness.These prolonged decompressions may consist of aseries of 'stops' as in most diving schedules, or of amore or less continuous reduction of pressure asin the decompression procedures of tunnel workers.The most detailed no-stop curve available is

that produced by Eaton and Hempleman (1962)using goats as subjects (Fig. 2). This curve, althoughvery similar to that for men, shows several curiousfeatures. The first of these is that there is a differencebetween the most susceptible and the most resistantanimal of about 30 feet for both short deep divesand long shallow dives. The second is that ananimal may alter its relative position within thesample, being more resistant at one end of thecurve and more susceptible at the other. Thus theindividual susceptibility of an animal is related tothe type of exposure, but the variation in sus-ceptibility between animals is constant and inde-pendent of the type of exposure.

Obviously if these findings can be applied tomen they have a practical effect upon any selectionprocedure; since only exposures similar to workingconditions are likely to produce comparable

7 ^e-_, tl46truat

2<

tDI

0 s0-I~~~~~~~~~ISztNtteus

FIG 1.-No-stop curve for men. After Albano (1961).The points plotted represent the threshold exposuresfor the production of decompression sickness whenbreathing air.

640 POSTGRADUATE MEDICAL JOURNAL October 1966

Zn-,~~ ~ ~ ~ ~ 10

IrI F~

2 1

2

1 _ _ _ _ _ _ _ _ _ _ _ _

Q 44 6rIIL I ONOULS.

FIG. 2.-'No-stop' curve for goats. After Eaton &Hempleman (1962). The incidence of decompressionsickness is shown for air exposures between 15minutes and six hours.

results. This is particularly difficult in divers whoneed to work throughout a large range of depthsand times and means in effect that there are nosatisfactory ways of selecting those who might bemore resistant to decompression sickness.A further point arises from these experiments

since it was found that for a constant time, increasingthe depth of exposure led to a markedly skewdistribution of individual susceptibility, mostindividuals being found near the lower limit asshown by the position of the 50% incidence. Whileit is possible to convert this into a more 'normal'distribution by plotting the incidence against thelogarithm of the pressure, this is of little help inunderstanding the underlying causes of the situation.One possible explanation is that the distribution

only appears skew due to the suppression of sub-clinical or mild cases, which are difficult to diagnosein goats. Some support for this view is evidencedby the way in which an increase in the severity ofexposure tends to alter the type of decompressionsickness found in men, from mild itching or fleetingaches and pains towards true 'bends.' If only'bends' were considered as a true end-point then allthe premonitory symptoms would be suppressed inthe way suggested.

40)

/

l/Ij

0 03oo ' 40O 50

2~~~~~~~~~~l-[1 9T-

FIG. 3.-Saturation curve for air derived from the no-stop curve for men.

SaturationThere are two common ways of talking about the

uptake of gas, the first, describing the rate ofuptake by the 'half-time,' has already beenmentioned; the second in general use is to describethe quantity in excess of normal as a percentage ofthe excess gas dissolved at equilibrium, frequentlycalled saturation.The obsession with the time taken to 'saturate'

which is found in diving literature derives from apreoccupation with the no-stop curve and itspossible interpretations, particularly with the firstassumption in attempts to derive a 'saturationcurve' from the meagre data.

Inspection of a more complete curve shows thatit appears to be asymptotic and that a dive to 33 feetmay apparently be prolonged indefinitely withoutany increase in risk. The basic assumption is thatthis particular dive represents the condition ofsaturation and hence that all shorter dives on thecurve represent different degrees of partialsaturation.To calculate a saturation curve from these data a

further assumption must be made, namely that theonset of decompression sickness is caused by thepresence of the same number of gas molecules inevery case. Without knowing what this number iswe can express it as the quantity of excess gasdissolved after a saturation dive to 33 feet, or moresimply as 33 footsworth. The percentage saturation isthen given by the simple expression:

33 x 100% Satn = (Fig. 3)

Depth in feet

October 1966 BARNARD: Aspects of Underwater Medicine 641

This is an extremely roundabout way of derivingan uptake curve for inert gas: it is obviouslysimpler to measure the uptake and eliminationdirectly. However since we are not quite sure howa certain quantity of gas acts to produce a certaindegree of risk, we must try to correlate the inform-ation given by these two different methods.The first difficulty in such an attempt is that

there seems only to be general agreement by thevarious authors as to the order of magnitude of thetime constants concerned. Lundin (1953) refers to'the conflicting results obtained by different investi-gators using the nitrogen elimination during oxygenbreathing as a means to establish the role of nitrogenin producing decompression sickness.'The problem seems to arise from the fact that

any desaturation curve is not a simple exponentialbut can be represented as the sum of several ex-ponentials. It is usual to analyse an experimentallyproduced curve by semilogarithmic analysis into twoor more exponentials with different time constants.In spite of the fact that some authors, notablyJones (1951), analyse the elimination curve intofour or five components, it seems that the accuracyof the measurements and the large errors involvedin lung-rinsing, make an analysis into more thantwo or three components of limited value.

If however one takes as a crude measure of sucha curve the half-time for the total curve, then fornitrogen elimination this time is between 60 minutesand 100 minutes, whereas the saturation curve,obtained from a very limited number of values,gives a half-time of about one hour. This is perhapsas good agreement as one could expect from thedata available. What is of perhaps more interestcurrently however is the rate of uptake and elimin-ation of helium.Behnke and Willmon (1941) gave some measure-

ments which showed that helium was eliminatedmuch more quickly than nitrogen, the crude half-time lying between 15 and 25 minutes for men atrest. While recent experiments at the Royal NavalPhysiological Laboratory would predict a similarlyrapid rate of uptake by inference from no-stopdives, there are some findings of Duffner, Snyderand Smith (1959) which are in direct contradiction,since they imply that helium and nitrogen areexchanged at the same rate.

It seems that this situation is unlikely to beresolved until further work on the uptake andelimination of inert gases give more reliableinformation.

TreatmentThere is still no satisfactory basis on which to

calculate decompression procedures whether fornormal use or for use as treatment tables whendecompression sickness develops. Even the pre-

ceding discussion on the uptake of inert gas doesno more than attempt to put into figures what PaulBert (1878) put in words, that decompressionsickness is caused by the presence of inert gas,which it is thought produces bubbles of free gas ifthe decompression is too severe. A discussion ofbubbles has purposely been omitted since theevidence is no more precise than the originalsuggestion. However the greatest argument infavour of bubbles as the aetiological agent is theresponse to pressure of cases of decompressionsickness.The general treatment for all cases of decom-

pression sickness is recompression. The decom-pression schedules used after taking the patient topressure are nearly all modifications of thoseproposed by Van der Aue, White, Hayter, Brinton,Kellar and Behnke (1945). These involve returningthe patient to an arbitrary pressure of 4 or 6 ats.abs.according to the type of case. A second method,which is in many ways preferable, is to return thepatient to the pressure of relief. This method wasin use for many years and is still used in tunnelworkers; it has also been used with success for mendeveloping symptoms, at greater pressures than 6ats.abs. for which no ready-made procedures exist.Implicit in this method is that a pressure of reliefcan always be found, that is to say pressure cures,and as a result of the accumulated experience of thelast century it can be said that this is so, but thatdelay in starting treatment or inadequate recom-pressions are the commonest causes of failure.

Instances of death due to decompression sicknessstill arise; there is therefore a need for improvedtreatment, but if we knew enough to make treat-ment completely effective we should have solvedthe problems which would make prevention certain.

REFERENCES

ALBANO, G. (1961): Ricerche Sperimentale sulla Decom-pressione nell'uomo, Med. Sport, 1, 259.

BARNARD, E. E. P., HEMPLEMAN, H. V. and TROTrER, C.(1962): Mixture Breathing and Nitrogen Narcosis,Roy. Nav. Personnel Committee, U.P.S. Report No.208.

BARNARD, E. E. P. (1966): The Treatment of BendsDeveloping at Extreme Pressures. (In preparation).

BEHNKE, A. R., THOMSON, R. M. and MOTLEY, E. P.(1935): Psychologic Effects from Breathing Air at 4Atmospheres Pressure, Amer. J. Physiol., 112, 554.

BEHNKE, A. R. and YARBROUGH, 0. D. (1939): Res-piratory Resistance, Oil-Water Solubility and MentalEffects of Argon Compared with Helium andNitrogen, Amer. J. Physiol., 126, 409.

BEHNKE, A. R. and WILLMON, T. L. (1941): GaseousNitrogen and Helium Elimination from the BodyDuring Rest and Exercise, Amer. J. Physiol., 131, 619.

642 POSTGRADUATE MEDICAL JOURNAL October 1966

BENNETT, P. B. (1966): The Aetiology of CompressedAir Intoxication and Inert Gas Narcosis. Oxford,Pergamon.

BERT, P. (1878): La Pression Barometrique. Recherchesde Physiologie Experimentale. Paris: G. Masson.

DUFFNER, G. J., SNYDER, J. F. and SMITH, L. L. (1959):Adaption of Helium Oxygen to Mixed Gas SCUBA.U.S.N. Exp. Diving Unit. Report 3 - 59.

EATON, W. J. and HEMPLEMAN, H. V. (1962): TheIncidence of Bends in Goats after Direct Ascent fromRaised Pressures of Air. Roy. Nav. PersonnelCommittee. U.P.S. Report 209.

FLINN, D. C. and WOMACK, G. J. (1963): NeurologicalManifestations of Dysbarism. J. Aerospace Medicine,34. No. 10, 956.

GOLDING, F. CAMPBELL, GRIFFrrHS, P. D. HEMPLEMAN,H. V., PATON, W. D. M. and WALDER, D. N. (1960):Decompression Sickness During Construction of theDartford Tunnel, Brit. J. Industr. Med., 17, 167.

JONES, H. B. (1951): Gas Exchange of Blood-TissuePerfusion Factors in Various Body Tissues. InDecompression Sickness by J. F. Fulton. p. 278.Philadelphia: Saunders.

KELLER, H. (1964): Personal Communication.LUNDIN, G. (1953): Nitrogen Elimination duringOxygen Breathing, Acta. physiol. scand., 30, supp.111. 130.

MEDICAL RESEARCH COUNCIL (1966): Bone Lesions inCompressed Air Workers. Report of DecompressionSickness Panel. J. Bone Jt. Surg. 48.B, 207.

MILLER, K. W., PATON, W. D. M. and SMITH, E. B.(1965): Site of Action of General Anaesthetics, Nature(Lond.), 206, 574.

PATON, W. D. M. and WALDER, D. N. (1954): CompressedAir Illness, Spec. Rep. Ser. med. Res. Coun. (Lond.),No. 281.

POULTON, E. C., CATTON, M. J. and CARPENTER, A.(1964): Efficiency at Sorting Cards in CompressedAir, Brit. J. industr. Med., 21, 242.

VAN DER AUE, 0. E., WHITE, W. A., HAYTER, R.,BRINTON, E. S., KELLAR, R. J. and BEHNKE, A. R.(1945): Physiological Factors Underlying the Pre-vention and Treatment of Decompression Sickness.U. S. Navy N.M.R.I. Project X-443. Report No. 1.

ZETTERSTROM, A. (1948): Deep Sea Diving withSynthetic Gas Mixtures, Milit. Surg., 103. 104.