Document 6Rmmgao12kwyzj0LORjG80X5R

614 HEINZ SPECHT If. Critical Altitudes Practically, the gases in contact with the alveolar surface are di both water vapor and carbon dioxide in the ratio of their combin'dpressures to the total barometric pressure. It is found experimentally t altitude of about 41,500 feet is critical for hypoxic symptoms when p_ur.'e is being breathed.11 When pure oxygen is being inhaled, if one assumes .'a dioxide pressure of 40 mm. Hg and a water vapor pressure of 47 pressure of oxygen at 41,500 feet can be no greater than 45 mm. Hg, equivSI a hemoglobin saturation of not more than 80 per cent. This conditiomis|^;t when breathing ambient air at a level not strictly definable unless iidsiuS* concerning the ventilation rate and respiratory quotient are made, but iffij found that the critical level for unacclimatized individuals is at about','"fa 16,000 feet.11 ' The altitudes at which perceptible impairment, that is, objectivei ' strable impairment, is effected under the two conditions given above ya. the tests used to demonstrate it. Thus, effects on night vision are foUn_s. low levels and necessitate the use of oxygen from the ground up forJnlfff even though low-level flying is to be carried out.11 This finding from perience should be one of the first to be applied to civilian flight, ggf? passenger transport where hazard to the pilot is carried over direct numbers of individuals. At 10,000 to 12,000 feet the ability to adapt .tfiSgsi' night vision and the ability of discrimination of objects is cut to nbout'Jm when "breathing "ambient-air;11'The~ addition"of~eEOUglroxygen to"raiji^Jheli: g pressure to that at ground level will correct this deficiency. In generahjji|| " oxygen is to be recommended at 10,000 feet if operations are carried onifngj? ^ hours. The exact time of onset of deficiency for different individuals vav.eV deal ancLprophylaxis is based on the most conservative interval for safetyj gin of 6 hours at 10,000 to 12,000 feet, 2 hours at 12,000 to 15,000:<feet|||!| above 15,000 feet have been found to be''compatible with reasohab^o^afetiv' selected groups of men, as in the military services,11 but morerecon'tl'j^f;j?> of oxygen on all flights above 10,000 feet has been ordered.70 ConsidfefStjl(i*ftffli` should be exercised in transferring these values to civilian flying, psjTeciwi pilots of private craft. 5. Decompression Sickness ' In discussing the effects of ascent it was indicated that the cn^ctjloi) from-inert-gas due-to-the supersaturation caused bv ascent-tf)-a-Mt#de^v.J^ifii delayed. This necessitates the discussion of these effects as they apjiqaRjjJjc sustained low pressure. The similarity of this condition to'-Ltfiat:;fou,:'/ decompressing to 1 atm. from high pressures is great enough to ennb'epf general approach to be carried over directly. EFFECTS OF ABNORMAL ATMOSPHERIC PRESSURE 615 Jnsi'gthe terminology of these effects has been rather uncritical in its *j^ffi^PTes8ed-air experience, workers in low-pressure studies have ^specific interpretations of the names for the phenomena which nSj^th'evdevelopment of intravascular bubbles is called "aeroembolism," jS'&iva-cular bubbles are relegated to the category of "bends," which discs'Jboth'phenomena in compressed-air terminology except for bubbles in - -Mfich1 in both cases are called "chokes." Reference is made to these <5nTy|oe6ause they appear in the literature of both fields and often constijpj^detail of symptomatology. In view of the fact that the theory that "JpapEthe cause of the pain and other sequelae to decompression is Xi|some reason by investigators,11'80,84 the term "aeroembolism" has prdEjlept to some criticism. It is admitted, however, that in the fulminatJlpifj'dScompression sickness bubbles are found both intra- and extra- B^^Mnd: they certainly play a large part in the derangement of the body |j||i^whether primary or secondary in point of time.69,84-?7 The fact that i=ion brings immediate relief lends great weight to the bubble theory jjssion sickness, whether of extra- or intravascular caharcter.11 Jpi arance of bubbles in the vascular system has been shown to occur SaM&iiHSjOOO feet with great regularity even in the presence of oxygen fm^tnrpughout the ascent.88 These observations indicate that the removal , Jp'from the body is not fast enough to prevent the formation of Sge|-'gas phases and that once these bubbles are formed they continue immlithey can be demonstrated _as circulating or embolic entities and !sues. Attempts to demonstrate bubbles within cells, particularly J?||ining fat inclusions, have been largely unsuccessful,84,87 and even Iffii'bubbles have not been observed in experimental animals after IppfOO feet,88 despite the fact that rather large gas accumulations be||||mas8es, under the skin, and near the joints have been demonstrated nSJubjects.84 Another disconcerting fact concerning the etiology of itfroih decompression sickness is that bends pain5 can be reduced by the jSbJjarterial vessels leading to the region affected.11 This is not compatible ^mltelic theory or local ischemia unless the action involves the compres- jSs)JS|jjgVOr other sensory nerves that are stimulated by the local- effects feipifein the vessels. The fact that as- little as 50 mm.- Hgspressure over lEpflfia] to the site of bends pain will relieve the symptom indicates llgr&jiae mechanism is not yet explainable by the mechanisms carried omrcn tnpressed-air studies.11 . ^^feivey, Bull. New York Acad. Med., 21, 505 (1945). '^^dieS^tsls:ttaid^S^GeislirMaval-M.e<L-Researclv-Jrtstv-Researohr-Projeot-X~SS4r 5.0,'^n (1915). Also in/. Cellular Comp. Physiol., 27, 27 (1946). and H. R. Catchpole, Naval Med. Research Inst., Research Project X-S84, ^^aiij:(i945). ." Whitaker, L. R. Blinks, W. E. Berg, V. C. Twitty, and M. Harris, J. Gen. Physiol/,' 11915!