The occurrence of arterial hypoxia with polycythemia usually results from some known type of pulmonary disease or from an abnormal communication between the right and left sides of the circulation. Although arterial oxygen unsaturation has been observed in patients with polycythemia vera (1)(2)(3)(4) Physical examination revealed an alert, cyanotic, slightly orthopneic man who weighed 290 pounds and was 67 inches in height. A few rales were heard at the right posterior lung base. The heart was in gallop rhythm, and the pulmonic second sound was accentuated. Mild edema of the abdominal wall and marked edema of the lower extremities was present.The significant laboratory findings were as follows: red blood cells 6.77 million per cu. mm.; hemoglobin 20 gm. per cent; hematocrit 69 per cent; white blood cells 6,000 per cu. mm. with a normal differential count and normal cellular morphology; platelets 150,000 per cu. mm. The bone marrow showed hyperplasia of the erythroid series, and reticulocytes were 1 per cent of the red blood cells. The blood uric acid was 9.6 mg. per cent. The urinary 17-ketosteroid excretion was 8 mg. in twenty-four hours (normal). X-ray of the chest showed cardiac enlargement and enlargement of the pulmonary vessels. Angiocardiography showed filling of the cardiac chambers in normal sequence. The sella turcica appeared normal by X-ray. An electrocardiogram showed evidence of right ventricular hypertrophy.

A 25-year-old farm worker developed acute bronchopneumonia after heavy exposure to a respiratory irritant in a silo. He recovered from the acute episode but then experienced chronic dyspnea and fatigue. Pulmonary function testing showed small lung volumes with a normal ratio of 1 s forced expiratory volume/forced vital capacity (restrictive defect). This defect improved markedly with bronchodilator treatment and changed to a mixed obstructive/restrictive defect with methacholine challenge. We believe that this is an example of the reactive airways dysfunction syndrome manifested by a restrictive rather than obstructive defect. Constriction of airways at the bronchiole or alveolar duct level is the most likely cause of the syndrome.

Treadmill exercise responses of oxygen uptake (VO2), CO2 production (VCO2), and venoarterial CO2 difference (Cv-Ca), measured by CO2 rebreathing (Defares technique) at 1 and 3 min of exercise, were studied in two separate series of control (apparently healthy) and coronary artery disease (CAD) subjects. In the 1-min series there were 21 controls and 15 CAD subjects. In the 3-min series there were 21 controls and 18 CAD subjects. All were males, ages 30--60 yr, and the CAD subjects had histories of myocardial infarction. In both series VO2 at 1 min and power requirement (P ) = 1,000 (VO2-1-1,000) was estimated where P =weight (kg) X grade (fractional) X walking speed (m/min). In the 1-min series (P = 1,000) all measurements were made at 45--60 s in separate test runs. In the 3-min series P was 750 kg.m/min, VCO2 and VO2 were measured at 2.5--3 min exercise, and Cv-Ca was measured at 3--3.25 min in the same test run. Data indicate that the average cardiac output (Q) for control subjects was 15 l/min in both series with lower values for CAD subjects. At 1 min reduced Q was accompanied by reduced VO2 or VCO2 and increased Cv-Ca, whereas at 3 min reduced Q was accompanied by increased Cv-Ca.