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2. 0. 0 RESPIRATORY GASES 2. 1. 0 Oxygen Except for the limitations of depth and duration imposed by oxygen toxici- ty, pure oxygen might be the ideal gas for use in deep diving. It is not cumula- tive, being consumed so rapidly in the tissues that at normal rates of decompres- sion it is probably not possible to produce oxygen bends, even though oxygen is not eliminated from the body tissues. Where diving duration at a particular depth exceeds the practical useful period for pure oxygen, it has been considered advisable to determine the highest permissible concentrations of oxygen which can be used as a diluent of an inert gas to minimize inert gas narcosis and bends without re-introducing the problem of oxygen toxicity. This approach requires definitive knowledge of oxygen toler- ance as affected by depth, exertion and other factors. However, while oxygen tolerance is thus a factor in "mixed gas", pure oxygen, and even possibly air diving, only crude estimates of oxygen tolerance at various depths and work rates are currently available upon which to base methods of extending useful div- ing depth and duration. In general it is known that at rest, oxygen tolerance at 60 feet exceeds the limits for "no-decompression" diving at this depth. No information is available regarding resting oxygen tolerance between a depth of 60 feet of sea water and sea level, where central nervous system oxygen tolerance is known to be at least 24 hours. Exercise comparable in degree to that of underwater swimming does shorten the latent period to the onset of oxygen toxicity, with the beginnings of convulsive reaction at about 40 minutes at 35 feet. One of the great deficiencies of information in the attempt to extend practical mixed-gas or oxygen diving is the void of information regarding the ultimate limits of oxygen tolerance during exercise between depths of 30 feet and 20 feet of sea water. Information pres- ently available indicates only that toxic effects have not occurred at these depths with exposures as long as approximately 1 and 2 hours, respectively. There is as yet no indication whether oxygen toxicity can be produced at these pressures with normal levels of underwater activity, or whether the ultimate tolerance is close to the arbitrary time limits currently employed. It is not yet known whether exercise shortens the latent period of oxygen toxicity in all subjects. The considerable variability of oxygen tolerance in and among normal individuals presents difficulties in the study of this condition, and, to some extent, limits the full use of oxygen in diving. Recent evidence suggests that changes in arterial pCO2 (carbon dioxide tension), through an effect upon the rate of cerebral circulations, and thus upon cerebral oxygenation, may be one of the most likely causes of individual variations in oxygen tolerance. Pos- sibly through better understanding of the factors involved in producing it, this individual variability may be reduced or a means devised for detecting the most susceptible individuals. At rest, the effects of high oxygen partial pressures upon respiration, 5
blood gas transport, and cerebral circulation indicate that oxygen may exert certain of its effects through actions on normal carbon dioxide exchange. This, together with the apparent ability of altered inspired, arterial, or central levels of pCC>2 to modify the response to high inspired oxygen pressures, indicates that studies of the physiological or toxic reactions to oxygen must be closely corre- lated with studies of the concurrent alterations of carbon dioxide exchange. The effects of high oxygen pressures upon the respiratory and circulatory responses to various levels of exercise have only just begun to be investigated. The physi- ological responses to oxygen during exercise appear at this stage to be consid- erably different from those at rest. Here again, studies to date indicate that interrelationships of the levels of exercise, carbon dioxide exchange, inspired pO£, respiratory responses, and circulatory alteration are mutually interdepend- ent. The composite effect upon oxygen tolerance varies considerably with changes in any one of these factors. The details of these relationships require much further study. 2.1.1 Effects of Inert Gases on Oxygen Toxicity It has recently become questionable whether, as had been heretofore con- sidered, the tension of an "inert" gas such as nitrogen is without influence upon the tolerance to a particular high tension of oxygen. Preliminary studies suggest that convulsive seizures occur earlier in the presence of nitrogen than they do in its absence, even though inspired pOz is the same. Exercise hyperventilation is relatively low at high ambient pressures when mixtures of oxygen and nitrogen are inhaled; it is yet not certain whether the associated extremely high alveolar pCO2, oxygen, or both are responsible for the seizures. Nor is it known whether nitrogen, through a narcotic action, directly alters the cortical response to high pOz, or whether any action of high nitrogen tensions per se is related to alterna- tion of pulmonary ventilation and alveolar pCC^. The degree to which such ef- fects may be altered by increasing diving depth and duration or even whether other as yet unknown actions of "inert" gases can modify oxygen tolerance is still unanswered. The various hydrostatic and inertial forces and changes in gas density en- countered underwater may conceivably affect pulmonary ventilation and circula- tion and, through such effects, alter carbon dioxide exchange and oxygen toler- ance. Essentially, no information is available regarding these questions. 2.1.2 Intermittent High and Low Oxygen Tension Most studies of oxygen toxicity have involved continuous exposures to pure oxygen at high pressure. If oxygen toxicity develops slowly, as indicated by the very long latent period at moderate pressures, and is rapidly reversed on lowering oxygen tension, as also appears to be the case, an alternation of high and low oxygen tensions in the respired gas mixture might conceivably extend greatly the working time at increased ambient pressure. Field experiments in man during World War II suggested that this occurred. Recent, better-controlled studies in guineapigsat 3.0atmospheres indicate that the latent period for the first signs of oxygen intolerance is extended from about 4 hours breathing oxygen continuously, to about 19 hours on a schedule of oxygen inhalation for 30 minutes, alternating with normal inspired pO2 for ten minutes. Since such a schedule not
only greatly extends oxygen tolerance but appears to permit nitrogen elimination during the periods of oxygen breathing, simultaneous solution of the problems of bends and oxygen intolerance may be possible. No controlled studies of this na- ture have as yet been carried out in man. 2.1. 3 Biochemical and Bioelectric Phenomena A considerable advance was made during World War II in delineating ef- fects of high oxygen pressures upon enzyme systems, particularly of brain tis- sue. Additional studies of this nature, making effective use of recent advances in enzyme chemistry, could add to the excellent past work and extend compre- hension of the biochemical basis for oxygen intolerance. It appears particularly desirable, now that physiological effects of high oxygen upon men are being studied quantitatively, to attempt establishment of a link of technique or experi- mental condition between in vitro and in vivo studies to facilitate ultimate corre- lation of data obtained through these different approaches. Thus far no systematic neurophysiological studies of oxygen toxicity have been made, though numerous workers have demonstrated measureable bioelec- tric phenomena in parts of the neuraxis during exposure to high oxygen pressures. It is possible that measurement of bioelectric phenomena may provide an early and sensitive index of oxygen intolerance in studies of oxygen toxicity, or of its modification by agents such as drugs or other gases. 2. 1.4 Pulmonary Effects of Oxygen There is no evidence for the occurrence of pulmonary irritation in humans subjected to inhalation of oxygen at high ambient pressures. Total length of exposure of human subjects has, however, rarely exceeded two hours at 2 to 4 atmospheres. Nevertheless, one of the principal results of the more prolonged exposure of certain laboratory animals to oxygen is pulmonary pathology. Cer- tainly with common experimental animals (rats, guinea pigs, rabbits, cats, and dogs) pulmonary damage, rather than central nervous system toxicity, is quite frequently the factor limiting exposure. The damage becomes severe with in- creased duration of exposure to high oxygen pressures. At autopsy the lungs of these animals present the picture of severe congestion with edema and atelectas- is. The gross appearance resembles that of liver or spleen. There is much evidence supporting an endocrine influence on the degree of pulmonary irritation by oxygen, both hypophysectomy and adrenalectomy providing a significant de- gree of protection. The pulmonary changes can in a large measure be reversed by positive pressure insufflation of the lungs. The indication thus is that a prin- cipal component of the oxygen effect may be diffuse atelectasis. Since pulmonary changes can decrease the oxygenation of arterial blood, the central nervous form of oxygen toxicity may be prevented in animals susceptible to pulmonary effects of high oxygen pressures. Much work remains to be done in elucidating the mechanism of the pulmonary damage, and ways of alleviating it must be found in order to permit more definitive studies in animals of the central nervous system effects of high oxygen pressures.
2.2.0 Carbon Dioxide Carbon dioxide, produced by the body at a high rate during exercise, has powerful physiological and toxic effects of its own. It can also indirectly affect the diver through modification of oxygen tolerance. Until recently, carbon diox- ide was considered as a factor in diving only if important amounts were inhaled, e. g., because of high apparatus dead space, inadequate helmet wash-out or inad- equate carbon dioxide absorption in rebreathing systems. These causes of direct carbon dioxide excess are primarily related to the design of breathing apparatus and are still common where equipment design or maintenance is deficient. In general, the inhalation of carbon dioxide appears to exert such effects as respira- tory stimulation, cerebral vasodilation, headache, and, if inspired tension ex- ceeds the equivalent of 10% CO2 at sea level, can lead to confusion and uncon- sciousness. Still higher inspired levels (20% to 30%) produce myoclonic twitch- ings or convulsions not dissimilar in appearance to those of oxygen toxicity. The latent period for such carbon dioxide convulsions (one to two minutes) is ex- tremely short as compared with that for oxygen convulsions. 2. 2.1 Carbon Dioxide and Oxygen Toxicity When carbon dioxide is inhaled with oxygen, oxygen tolerance is de- creased, apparently due in part to the increase in oxygen delivery to the brain re- sulting from cerebral vasodilation by high carbon dioxide tensions. The primary and secondary effects of inhaled carbon dioxide have been subjected to relatively little study under positive pressure. While the relationships of respiratory re- sponses to increased inhaled carbon dioxide under resting conditions at sea level are becoming more clear, circulatory responses even under these conditions are less well understood. The maximum increase in cerebral circulation which can be produced by carbon dioxide is not yet known, nor is it completely clear whether inspired carbon dioxide dilates the cerebral vessels through a direct ac- tion upon cerebral arterioles or through other mechanisms. Information regard- ing the effects of increasing inspired carbon dioxide concentrations upon judg- ment, reflexes and motor performance is inadequate for determining safe levels of carbon dioxide inhalation in diving. The underlying biochemical and neuro- physiological mechanisms of carbon dioxide convulsions also require study, par- ticularly in regard to interrelationships with the convulsions of oxygen toxicity. Just as high levels of inspired carbon dioxide or the pulmonary retention of carbon dioxide can diminish oxygen tolerance, it appears from the results of animal studies that hyperventilation, with a resultant lowering of arterial carbon dioxide tension, can increase oxygen tolerance. These observations may have considerable relationship to the powerful cerebral vasoconstrictor action of hy- pocapnea. As one of the few presently evident possibilities for lowering brain tissue pC>2 at a given inspired oxygen tension, the effects of hypocapnea com- bined with hyperoxia upon cerebral hemodynamics, cerebral gas exchange, and the tolerance to high oxygen tensions deserve study. Cerebral blood flow begins to be increased when carbon dioxide concen- trations above 2% are inspired at sea level. However, the minimal inspired ten- sion of carbon dioxide which will decrease oxygen tolerance is not yet known, nor is the lowest oxygen tension which will produce toxic symptoms in the pres- 8
ence of maximal cerebral vasodilation by carbon dioxide. While either exercise or carbon dioxide can decrease tolerance to oxygen, no studies of the combined effects of exercise and high inspired carbon dioxide tensions upon oxygen toler- ance have been made. For all of these studies a base line of tolerance and its variance when pure oxygen is breathed must be established. 2. 2.2 Carbon Dioxide Autointoxication During the past few years it has become apparent that carbon dioxide may produce toxic effects in diving, not only by reinhalation from defective apparatus, but through its inadequate elimination from the body. Carbon dioxide autointoxi- cation presumably occurs whenever pulmonary ventilation is low with respect to the rate of metabolic carbon dioxide production. Conceivably factors such as re- sistance to breathing, training, partial depression of the respiratory centers, and breathholding may lead to inadequate removal of carbon dioxide from the lungs, blood and tissues, resulting in a critical degree of hypercapnea. This problem, now only in the early stages of investigation at positive pressure, has an important relationship, not only to primary carbon dioxide intoxication as a possible cause of "shallow water blackout" or even convulsions, but also to the pharmacology of oxygen toxicity and nitrogen narcosis, the physiology of respira- tory resistance and exercise, and probably numerous other aspects of diving. Considerable information bearing upon this subject should arise in the course of general sea-level studies of the physiology of pulmonary ventilation, carbon diox- ide and oxygen, exercise, respiratory control and even the respiratory effects of narcotic and stimulant drugs. The ultimate delineation of the scope of this prob- lem will require further study at increased ambient pressures. 2.3.0 Nitrogen Whenever a diver is at depth breathing air or any other nitrogen-oxygen mixture, he is exposed to unusual partial pressures of nitrogen. Such exposure can involve two major untoward effects: namely, 1) solution of this "inert" gas in the blood and tissues while under pressure may give rise to decompression problems on subsequent ascent; and, 2) increased nitrogen pressures may cause depression of the central nervous system even though gaseous nitrogen is gener- ally considered inert. The overt manifestation of the latter effect is called nitro- gen narcosis or compressed air-intoxication. In recent years, it has achieved popular recognition as "Rapture of the Depths". The subjective experience is not unlike alcohol intoxication or mild nitrous oxide anesthesia. The mechanism of this effect is no better understood than that of other narcotic gases. 2. 3.1 Individual Differences in Susceptibility to Nitrogen Narcosis Individuals differ in their susceptibility to nitrogen narcosis, but most divers are aware of some mental impairment at a depth of 100 feet when breath- ing air. Performance of tasks which require much thought, judgment, or manual skill makes the impairment more evident. On approaching 300 feet, the average diver is virtually useless, and this depth is accepted as the practical limit for useful air dives. Even with deep-sea diving equipment and good telephone com- munication with the surface, impairment of the diver's sensorium is a definite hindrance in working dives beyond 150 feet. In diving with self-contained under-
water breathing apparatus (SCUBA), the same degree of impairment can affect performance even more adversely and can jeopardize the diver's safety as well. 2. 3.2 Central Nervous System Effects Even though the existence of a central narcotic effect of nitrogen has been recognized for many years, much more information is required. The actual types, degrees, and consequences of functional impairment produced by nitrogen at various partial pressures remain ill-defined. The extent of individual varia- tion in susceptibility needs to be ascertained, and reliable means of identifying unusually susceptible individuals are needed. If there are any indulgence or ab- stinence influences which cause proneness to nitrogen narcosis to increase or de- crease, these have not been identified. Practical methods of improving perform- ance under increased nitrogen pressures would be of considerable value; this approach has received essentially no attention. Recent investigations indicate that the depressant action of nitrogen may include the more elemental functions of the brain as well as the mental processes. Depression of respiration with retention of carbon dioxide has been observed in working divers exposed to increased nitrogen pressures. The consequences of this apparent medullary depression may include not only direct carbon dioxide autointoxication but also increased susceptibility to oxygen poisoning in the use of nitrogen-oxygen mixtures. These effects appear possible even when the influence of nitrogen upon the higher centers is not subjectively pronounced. The exact mechanism of the observed phenomena is still uncertain, and the possibility of actions on the circulation and other functions has not been ruled out. The inter- relationships with oxygen toxicity may prove to be complex. The extent of indi- vidual differences in susceptibility to this form of nitrogen depression has barely been explored, but it appears that experienced divers may be unusually suscepti- ble. The observations suggesting medullary depression require verification and further study. The possibility of effects on functions other than respiration must be investigated. The exact significance of any nitrogen depression of the lower centers must be defined quantitatively relative to both oxygen toxicity and carbon dioxide intoxication. Understanding of both aspects will require further study of its mechanisms as well as a delineation of its effects and consequences. Individual differences and means of personnel selection also require study, es- pecially in view of apparent peculiarities of divers in regard to respiratory con- trol. Since these depressant phenomena jeopardize the utility of nitrogen-oxygen mixtures in essential diving operations, means of circumvention must be sought. Certainly the effects of nitrogen will remain a physiological problem of distinct practical importance as long as air or other nitrogen-oxygen mixtures are used in diving. 2.4. 0 Helium Helium lacks the depressant effects of nitrogen. At least, these effects are slight even at considerable diving depths. The respiratory depression ob- served with nitrogen at depth is not seen when helium is substituted, and the preservation of mental clarity with helium is well known. 10
At present, helium is the only "non-depressant", inert gas which is known to be a fully practical substitute for nitrogen in breathing mixtures. The technique of helium-oxygen diving, as currently employed, is highly successful in making useful dives possible at greater depths than are possible with air. The current record depths are 561 feet (pressure tank) and 500 feet (open sea). There is no known physiological reason why these records cannot be exceeded. 2.4.1 Decompression Contrary to original expectations and to information still to be found in textbooks, the use of helium does not eliminate or greatly lessen the problem of decompression in most diving situations. It provides such an advantage in long, deep dives, but in the depth-time range of practical SCUBA diving the use of hel- ium actually appears to increase the amount of decompression time required. According to present knowledge, a dive which requires less than one hour of total decompression time will generally yield a better ratio of working time to decompression time if nitrogen is used rather than helium. 2. 4. 2 Breathing Resistance In addition to its lack of depressant effects, helium also reduces the re- spiratory resistance encountered in SCUBA circuits and in the diver's own air- ways at depth. Since excessive work-of-breathing may limit the degree of physi- cal exertion possible in deep dives, this may be a real advantage of helium-oxygen breathing. It is not yet known whether the elimination of carbon dioxide from the lungs is significantly interfered with by increased gas density at depth. Should this be the case, the use of helium would be desirable from this standpoint also. If medullary depression by nitrogen is involved in the enhanced susceptibility to oxygen poisoning observed in the use of nitrogen-oxygen mixtures, the operational objectives of "mixed gas" diving may have to be sought with helium. Then the main problems related to helium will be those concerned with decompression. To what extent increased decompression time, apparently required by the use of hel- ium in the SCUBA depth-duration range, would limit advance, remains to be seen. 2.5.0 Toxic Inhalants 2. 5.1 Carbon Monoxide The SCUBA diver is susceptible to harm from any noxious substance which finds its way into his gas cylinders or breathing circuit. Among the possi- bilities, carbon monoxide is probably the most serious. Its presence can come about either through intake of exhaust gas by the compressor or through forma- tion of carbon monoxide by the breakdown of lubricating oil in the compressor it- self. The former is particularly possible with portable gasoline-driven air com- pressors used in the field. The latter is a potential danger wherever an oil- lubricated compressor must be used. The toxicity of carbon monoxide at sea level is proportional to the amount of carboxyhemoglobin formed. While at depth, a diver may tolerate considerably higher ratios of carboxyhemoglobin because, due to the increased partial pres- sure of oxygen at depth, some of his oxygen transport requirements are met by 11
oxygen in simple solution. However, since the reconversion of carboxyhemo- globin to oxyhemoglobin is relatively slow, he may be Jn immediate difficulty on ascent. If the carboxyhemoglobin formation resulting from a given inspired con- centration of carbon monoxide is proportional to the ambient pressure, the per- missible concentration in diving may be exceedingly small. However, it is not certain that this relationship applies since the equilibrium ratio of carboxyhemo- globin to oxyhemoglobin at high pressures has not been established. It is con- ceivable that high ambient pressures may influence the initial rate of carboxy- hemoglobin formation but not the equilibrium amount, since the oxygen tension of respired air is also increased under these circumstances. Without definite information on this subject is is impossible to specify the safe limits of carbon monoxide content for gases used in SCUBA or even to assess the actual impor- tance of this potential hazard. It is also impossible to be certain whether avail- able methods of carbon monoxide analysis which can be used in the field are suf- ficiently sensitive, whether practical methods of removing the gas are adequate, or whether the use of certain types of compressors should be interdicted entirely. 2. 5. 2 Oil Vapor Oil vapor is a common contaminant of SCUBA air supplies. Any oil- lubricated compressor will yield air containing at least a trace and badly designed or poorly maintained compressors may produce a large amount of oil vapor. It is known that lipoid pneumonia and related disorders can result from inhalation of oil vapor. The possibility of carcinogenesis from oil constituents, while proba- bly remote, cannot be ignored completely. Although many divers have undoubted- ly had considerable exposure to inspired oil vapor, there has been little clinical evidence of harm. However, a search for such evidence, especially of delayed and chronic effects, might be illuminating. At the present time, it is not even possible to say whether oil vapor is a serious diving hazard. 2. 5. 3 Miscellaneous Inhalants The effects of any noxious gas, fume, or vapor which contaminates a div- er's gas supply might be intensified by increased ambient pressure. For exam- ple, even jokes about "compressed smog" may have an element of unpleasant truth. Ozone has not been exonerated as a pulmonary irritant. A variety of other- wise ill-explained diving accidents or sequelae may have their explanation in con- taminants. For example, divers using certain open circuit units consistently re- ported symptoms closely resembling "metal-fume fever" following otherwise un- exceptional dives. It is possible that certain methods of treating the interior of cylinders could give rise to such an effect. Although the incidence of accidents from causes such as those mentioned above is fortunately small, many questions arise. It would be highly desirable to know the interrelationship between the toxicity of carbon monoxide and increased ambient pressure. Definite information about the tolerable amount of oil vapor and the possible effects of other contaminants would be worthwhile. Meanwhile it remains necessary to seek means of preventing contamination of air supplies and reliably removing noxious agents. 12
