Respiratory Diseases in Relation to Changes in Atmospheric Pressure

BROOKS H. HURD, M.D.

Director of Laboratories, Grant Hospital and Clinical Associate Professor of Pathology, ■ Ohio State University, Columbus, OH 43215

ABSTRACT In this paper are reviewed the present status of respiratory diseases in relation to high and low altitude environments.

High Altitude Sickness in mountaineers occurred on their initial Intkoduction exposure to high altitude without proper acclimatization time. Men living at high Mountain sickness occurs in both an altitudes have a higher total blood volume acute form and a chronic form. Only re and a greater proportion of pulmonary cently has this been studied to any degree; blood volume than that present in sea level however, the first description was by a inhabitants. Persons going to high altitudes Peruvian in 1897.8 In 1937, Hurtado de tend to develop greater blood volume in scribed a case of pulmonary edema in an the pulmonary bed. Houston had reported Indian who became acutely ill after return mountaineers who have described cases of ing home from sea level to the high alti rapid death attributed to pneumonia. This tude.7 In 1945, a 39 year old man was occurred in healthy persons who were en examined who had developed pulmonary gaged in strenuous exercise over 14,000 edema after going to a height of 11,550 feet. feet. Death in 12 to 24 hours resulted if In 1949, a 29 year old man was described the symptoms were severe and remained who died from an acute pulmonary illness untreated. in La Oroya, Peru, at an elevation of 12,250 feet. Lundberg, in 1952, described several The period of acclimatization should be cases of acute pulmonary edema. Mountain gradual in going to different altitudes and sickness or high altitude pulmonary edema should last from 3 to 7 days. Persons who occurs in individuals who quickly go from develop high altitude pulmonary edema sea level to altitudes of 9,000 to 15,000 feet. have stayed at sea level any where from Natives who have lived at high altitudes two days to two months. There seems to for a considerable time and then visit at be an individual predisposition to high alti sea level are most susceptible when they tude pulmonary edema.15 During acclima return to their mountain homes. Young tization, undue physical exertion should be children are also particularly susceptible avoided for the first 48 hours. Mountain under these circumstances. Most episodes sickness can be divided into two types, the 8 6 HURD acute form or Soroche and the chronic form was first described in 1924 and the pathol or Monge’s disease. The onset of early ogy has been described only recently.3 A symptoms varies from 6 to 36 hours after 48 year old woman who lived at 14,300 feet reaching a high altitude area. Most patients developed a syndrome of right cardiac in develop symptoms in the first 24 hours. The sufficiency, anasarca, and prominent cyano symptoms come on either during sleep or sis. Before her death, her hemoglobin was prolonged exercise. Infection is not a prob 21.6 g and the red blood count was 7.42 lem in the patient with the occurrence of million. The anatomic findings of impor high altitude pulmonary edema. tance included: (1) severe right heart hypertrophy, (2) the right ventricle weigh Sy m p t o m s a n d F in d in g s ing 67 percent of the total ventricular weight, ( 3 ) a marked degree of musculari- The early symptoms consist of headache, zation of the peripheral pulmonary arteries, restlessness, increasing dyspnea, dry cough, (4) multiple fresh and partially organized palpitations, precordial discomfort, and thrombi were present in the medium sized nausea. Severe respiratory distress develops and smaller peripheral arteries and arteri after several hours.17 This is followed by oles of the lung and (5) a moderate degree dyspnea, wet cough, foamy sputum, cold of muscular hypertrophy of the intermedi perspiration, anxiety, diffuse muscular and ate and proximal pulmonary arteries was joint aching, thirst and sensory distur noted. The pathogenesis of high altitude bances. Marked dyspnea may develop pulmonary edema has been studied for when lying down and is accompanied by many years with gradual increase in the; cyanosis in severe cases. Most of the pa amount of available information. tients have marked facial pallor. On physi cal examination, the lungs are full of wet E t io l o g y rales. Tachycardia is present and there is hypotension. Most cases have leukocytosis. The cause is apparently a change in Electrocardiographic findings are the same hemodynamics of the pulmonary vascular as in acute right ventricular strain. The bed. Patients have pulmonary hypertension, average sinus tachycardia of 124 beats per but normal left atrial pressure. Hultgren minute was usually present. The tracing has reported normal pulmonary capillary tends to show elevated P-waves and depres pressure and, therefore, it is considered that sion of the T-wave. After recovery, the a contributing factor is vasoconstriction at electrocardiogram returns to normal and is a precapillary level. Increased capillary similar to the tracings of other persons permeability must still be considered an living at high altitude. other contributory factor. This may aid the X-ray findings are usually that of spotty, development of hyaline membrane de mottled edema scattered through the lung scribed in the autopsied cases. The degree fields with a tendency for the apices and of anoxemia is more marked in newcomers bases to be free. The X-ray findings usually to high altitude than in regular residents. clear after 48 hours of treatment and the The development of pulmonary edema patients are clinically improved before the while sleeping is considered a postural x-ray picture clears. The pulmonary artery effect. Hurtado also noted a fall in the may be prominent during an attack; how arterial oxygen while the patients were ever, the heart size remains unchanged. sleeping at high altitude. The increase in The chronie form of mountain sickness pulmonary blood volume is probably also occurs in Indian natives who develop an a factor. The changes producing high alti intolerance to high altitudes. This condition tude pulmonary edema appear to be a RESPIRATORY DISEASE-----A T M O SPH ER IC PR ESSU R E 8 7 magnification of the hemodynamic changes Hultgren gave the normal pulmonary ar noted during rapid exposure to low tem terial pressure as 13.8 ± 1.9 mm Hg.13 He perature and hypoxia. considered that high altitude pulmonary edema was still of debatable etiology in P athological F in d in g s 1971. Four hemodynamic abnormalities were cited which are consistently observed: The pathology of acute high altitude pul (1) elevated pulmonary arterial pressure, monary edema has been reported by Arias- (2) normal or decreased pulmonary artery Stella2 with a mortality rate of 12.7 percent wedge pressure, (3) an excessive degree of in a series of 86 cases. The autopsy findings arterial desaturation, not corrected by 100 described cyanosis of the face and anterior percent oxygen and (4) a normal or de aspects of the thorax and hands. The tra creased cardiac output. Hultgren studied a chea and bronchi were full of abundant group of individuals with right heart cath seromucous secretion which was sometimes eterization performed first at sea level and blood tinged. The lungs were heavy and then, several weeks later, repeated at high did not collapse when the thorax was altitude. The studies at high altitude were opened. There was abundant white, pink done following rapid ascent; expired sam and foamy fluid exuding from the lungs. ples of air and blood were examined at the The right ventricular wall was thickened. same time. Exposure to high altitude pro Microscopically, alveolar edema alternated duced a remarkable increase in the pulmo with emphysema in all lobes of the lung. nary artery pressure. Pulmonary artery Alveolar hyaline membranes were present pressure was considerably increased over as well as recent thromboses which were wedge pressure, whereas at sea level they frequently seen in precapillary septal ves had been equal. Hultgren considered that sels. The pulmonary artery had thickening there was a 3 to 5 fold increase in pulmo of the media and peripheral arterioles nary vascular resistance. Increased oxygen showed frequent muscularization. Cellular inhalation partially relieved the elevated elements were very scanty in the edema pulmonary artery pressure. During exer fluid of the alveoli. The hyaline membranes cise, while breathing oxygen in high con were histochemically similar to those seen centration, pulmonary artery pressure was in hyaline membrane disease or in placental significantly decreased. The stroke volume fibrinoid. These patients were not affected of cardiac output was reduced but the by primary cardiac nor pulmonary disease. heart rate was increased at high altitude. Children living at high altitudes have Hultgren concluded that the patients who evidence of right ventricular hypertrophy were prone to develop high altitude pulmo by vectorcardiogram. An accidentally killed nary edema tend to develop grossly abnor child showed, at autopsy, right ventricular mal pulmonary hypertension.13 This was hypertrophy and pulmonary arterioles with due to increased pulmonary vascular re the prominent muscular wall.20 Sime et al sistance since pulmonary blood flow and reported right heart catheterization in 32 pulmonary capillary wedge pressure were healthy children living at a high altitude of over 14,000 feet. The degree of arterial un normal. The nature of the increased resist saturation in these children was the same ance is not known definitely. A portion of as in adults at that altitude. Pulmonary the resistance can be accounted for by hy wedge and right atrial mean pressures were poxic pulmonary vasoconstriction. normal. The child living at high altitude The development of the widespread fi tends to maintain a pulmonary arterial brin deposits may also contribute to the structure of fetal type. development of edema. The peripheral 8 8 HURD venous constriction has been shown to be weakness, rash and pruritus, vertigo, visual exaggerated in persons susceptible to high disturbances, paralysis, and dyspnea. A par altitude pulmonary edema. adoxical response may occur with rapid deterioration during the recompression pe T r e a t m e n t riod.19 The pathogenesis of the condition Treatment consists of prompt administra develops from too rapid decompression tion of oxygen by mask and bed rest. It is with the development of intravaseular gas imperative that there be as little delay in bubbles. It has been noted, experimentally, treatment as possible. Supportive treatment that partial or complete constriction of with digitalis preparations and diuretics has muscular arteries following gas injection not proven beneficial. Occasionally, if it is lasts several minutes. Next there is then feasible, the patient must be removed to a a resulting vasodilatation and increased lower altitude. The pulmonary congestion is blood flow.6 The presence of gas micro usually gone in 24 to 48 hours and progress nuclei within the blood is recognized. examination several weeks later reveals no These may be produced in areas of reduced evidence of residual symptoms nor signs. hydrostatic pressure owing to muscular contraction.10 Workers regularly employed Decompression Sickness seem to develop acclimatization, and the I ntroduction frequency of bends decreases. This suggests the possibility that micronuclei may be dis Decompression sickness has been recog sipated by repeated pressure-decompres- nized for many years. Robert Boyle, in sion cycles.10 Several authors conclude that 1670, first recorded gas bubbles in tissues there is a large element of chance in the of animals. These were demonstrated by development of decompression sickness.21 placing small animals in a decompression Occurrence of pulmonary fat embolism is chamber and withdrawing the air.6 Decom also observed with decompression.9 It is pression is also known as caisson disease doubtful that this observed fat embolism is and dysbarism. Workers call the disease the of serious consequence. Recent studies have bends, the staggers or the chokes. The con shown that decompression sickness may dition can develop during a transition from occur in workers exposed to relatively low a high pressure to normal pressure or from pressures in the range of 11 to 16 psi.4 normal pressure to low pressure such as encountered in high altitude flying.6 There Workers who are to be examined for are two types of the bends: Type 1, better work in compressed air must be carefully designated as mild, and Type 2, designated examined according to requirements set up as serious. The respiratory form is known by various state agencies. Constant facil as the chokes, the neurological form as the ities for recompression and for first aid staggers and a circulatory manifestation has treatment must also be available 24 hours been known as the shocks. Minor effects, a day.4 such as debilitating fatigue, rash, pruritus Behnke has noted that there is a marked and paresthesias, may be experienced. The increase in susceptibility to decompression manifestations of decompression sickness sickness between the ages of 18 and 28 are similar in the diver, the aviator and the years. In addition, susceptibility to the ill tunnel worker, although the aviator is more ness increases with increase in amount of prone to develop the chokes.4 Most of the body fat. Serious problems may develop symptoms develop within one hour after from pulmonary abnormalities. These in decompression. The most characteristic clude congenital cysts, scar tissue, vesicles symptoms are pain, paresthesias, muscular and emphysematous bullae. Their presence RESPIRATORY DISEASE-----ATMOSPHERIC PRESSURE 8 9 may result in air embolism or pneumo much more decompression time than the thorax. The workers must also be screened tables from the British Ministry of Labor. carefully to rule out those with obstructive The states of Washington and California lung disease. The intravenous bubbles con give even greater length of times for de tain mainly nitrogen, but occasionally they compression. The serious aseptic necrosis of may contain oxygen.19 bone is seen particularly about the heads of Evaluation of the auditory tubes and the humerus and femur. These bones, if in auditory acuity is important.4 During com volved, show areas of density in the head, pression, it is necessary to resort to vol neck and medullary shafts. Juxta-articular untary procedures, such as the Valsalva involvement leads to serious crippling com maneuver, swallowing and yawning, to plications. The adoption of the new decom equalize pressure on both sides of the pression tables, as proposed by Sealey, has tympanic membrane. Upper respiratory effectively eliminated this serious complica tract infections impair the ability to accom tion of compressed-air workers. The possi modate to pressure changes. Dysbarism has ble occurrence of a chronic neurological produced little disturbance in hearing defect is extremely rare. within the speaking range. This disease A decompression and prevention of de rarely causes deafness. Upper respiratory compression sickness are not necessarily re and nasal allergies predispose the workers lated entirely to the physical condition of to aerotitis.4 Experimentally, there has been the worker. Haldane had proposed that the a rather marked degree of hemoconcentra- gas could be transported in a state of super tion during decompression. saturation in the circulating blood to the lungs. This probably represented the body’s E t io l o g y tolerance of “silent” gas bubbles.4 Slow de Despite the evidence that intravascular compression, 10 to 15 minutes per foot of bubbles are the initiating cause of decom ascent, allows a low pressure head for dif pression sickness, complete protection is fusion of gases from tissues and subsequent provided by preoxygenation to affect nitro transport in the blood. Transfer of oxygen gen removal prior to rapid altitude ascent. from blood to the tissues results in a space Other associated complicating factors are or oxygen window, through which the inert fat embolism, liberation of proteolytic en gases can be transported from the tissues to zymes, potassium ions and peptides.4 Addi the lungs. The inhalation of pure oxygen at tional changes noted are vasoconstriction, elevated pressures is extremely useful in loss of circulating plasma, hemoconcentra- allowing this window to open.4 Behnke has tion and the development of shock. proposed that prolonged residence in com pressed air, not exceeding 14 psi, would P athological F in d in g s solve most of the medical problems of this condition. A holding facility with pressures Aseptic necrosis of bone has been a se no higher than 12 psi would permit work rious and disabling complication of decom pression sickness. Among the workers who men to leave after a relatively short period built the East River Tunnel, there were 20 of time, if necessary. This system of control deaths. All the men in that construction of decompression sickness, however, must were experienced workers.4 A marked in also meet social obligations of the workers. crease in decompression time with resulting Campbell has reported that certain agents, shortening of work hours has resulted in including fat scattering agents, narcotics, elimination of the serious disabilities. Ta autonomic depressants and diuretics, are bles from the United States Navy give effective in preventing severe decompres w HURD sion sickness.7 Another possibility is that causing fat embolism. Amer. J. Path. 55:203, protective properties of these agents may 1969. 10. E v a n s , A. and W older, D. N.: Significance "be related to sludging of blood as described of gas micronuclei in the aeriology of decom lay Behnke.4 It is believed that the action pression sickness. Nature 222:251-252, 1969. of oxygen is that of a mechanical grádient 11. H a r r i s o n , T. R ., ed.: Principles of Internal Medicine. 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