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606 INDUSTRIAL HYGIENE AND OCCUPATIONAL MEDICINE Arterial blood examination (table 1) showed a fall in p02 and O2 saturation, and an increase in the alveolar-arterial oxygen pressure difference. Chloramphenicol (chloromycetin) was started on September 19 because of an infection of the upper respiratory tract, and ACTH therapy was started on September 27 (table 1). Subsequent measurements of lung function showed a rather marked increase in maximum breathing and a slight increase in vital capacity. Exercise tolerance improved, and the patient no longer required intermittent oxygen therapy. However, she still had visible cyanosis. Cortisone was administered in the period between October 6 and 18 but apparently produced little additional improvement. The eosinophil count showed a good fall, and 17-ketosteroids excretion was significantly increased, indicating adrenal stimulation by ACTH (table 1). Table 1 (case 1).--Results 0} Studies of Pulmonary Function Patient P. P., woman Age, 53 yr. Height, 178 cm. Weight, 65.2 Kg. Body surface area, 1.82 M.2 All respiratory volumes, BTPS * Diagnosis: Pulmonary fibrosis--cause unknown Minute volume, L./min............................................................. ...... Respiratory rate, resp./min.................................................... ....... Tidal volume, L......................................................................... Inspiratory reserve volume, L.............................................. ....... Expiratory reserve volume, L.............................................. Vital capacity, L....................................................................... Expected vital capacity, L.................................................... Residual volume, L.................................................................... Residual volume -5- total volume, %................................ ....... Alveolar ventilation, L./min................................................ Respiratory dead space, L................................................... Maximum breathing capacity, L./min.............................. Expected maximum, breathing capacity, L./min.......... ....... Total capacity, L...................................................................... June 19, 1950 12.5 20 0.26 50.4 83 Sept. 26, 1950 13.05 24 0.55 0.36 0.76 1.67 2.92 1.14 40.6 4.74 0.300 70 83 2.81 Oct. 6, 1950 12.96 17 0.76 0.66 0.64 2.06 2.92 1.37 40.0 5.80 0.244 101 84 3.43 Oct. 18, 1950 11.13 13 0.86 0.93 0.34 2.13 Nov. 3, 1950 11.73 17 0.69 1.03 0.34 2.06 1.52 41.6 7.66 0.292 115 84 3.65 1.18 36.5 5.12 0.375 104 84 3.24 Alveolar pOa, mm. Hg........................................................... 101 111 120 117 Arterial pCh, mm. Hg............................................................. 34 44 50 45 Arterial pCC>2, mm. Hg.............................'............................ 46 38 32 36 Alveolar-arterial difference, mm. Hg.................................. ....... 48 67 67 70 72 Serum CO2, vol. %......................................... .......................... 56.00 55.76 67.81 7.34 7.42 7.51 7.43 Arterial blood CO2 content, vol. %.................................... 44.62 . 42.96- 44.31 40.00 Arterial blood O2 content, vol. %...................................... 16.89 19.48 19.95 19.85 Arterial blood Oa capacity, vol. %.................................... Arterial blood O2 saturation, %......................................... ....... 77 24.18 69 24.39 79 22.92 86 24.00 82 Hematocrit, RBO, %............................................................... 59.5 .59.5 55.6 si j/ Therapy: ACTH 9/27/60-10/19/50--80 mg./day; cortisone 10/10/50-10/17/50--100 mg./day. Eosinophil count: 176-U/mm.3 17-KetosteroIds excretion: 9.7-22 mg./24 hr. * The significance of BTPS Is explained In the text under the heading "Methods." v. Case 2 (N. A., P.B.B.H. No. 6B-475).--Fifteen years before admission this 16 year old boy had an eczema which persisted for four years, before it subsided, and he began to have bouts of coughing and wheezing associated with insomnia and asthenia. Two months before admission nocturnal orthopnea developed with persistent asthma which failed to respond to 1: 100 epine phrine hydrochloride inhalation. Essential physical findings at admission on March 6, 19S0 were a respiratory rate of 25 and a barrel-shaped chest with many inspiratory and expiratory wheezes, squeaks and groans. He was moderately dyspneic without cyanosis. Following control observations, a brief course of ACTH therapy was given. .~ Charts 2 and 3 describe the pulmonary compartments and vital capacity, and show the temporary increase in residual volume, during an asthmatic attack; the effects of epinephrine on the vital capacity and maximum breathing capacity are also demonstrated. The third column of chart 2 . shows the improvement due to ACTH, manifested by reduction in the residual volume and increase in the vital capacity. One week, after cessation of ACTH therapy, the