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Respiratory Diseases in Relation to Changes in Atmospheric Pressure

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Respiratory Diseases in Relation to Changes in Atmospheric Pressure A n n a l s o f C linical Laboratory Science, Vol. 3 , No. 2 Copyright © 1 9 7 3 , Institute for Clinical Science 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.
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