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It has recently become apparent that a high proportion of individuals who possess S type hemoglobin exhibit significant desaturation of the arterial blood. In 1942 Klinefelter (1) found arterial oxygen saturations of 89 and 91 per cent in two patients, and in 1943 Reinhard, Moore, Dubach, and Wade (2) found values ranging from 74.2 to 90.8 per cent saturation in one patient with sickle cell disease. Leight, Snider, Clifford, and Hellems (3) studied 13 patients with sickle cell disease in 1954, 10 of whom had arterial 02 desaturation. Within the past year reports from this laboratory (4, 5) and from Jensen, Rucknagel, and Taylor (6) indicate that desaturation of arterial blood exists in most people who possess S type hemoglobin. The exact mechanism responsible for this phenomenon has not been elucidated. The various possibilities may be distinguished with fair accuracy by determining alveolar and arterial oxygen tensions and calculating A-a oxygen tension gradients at three levels of oxygenation. If desaturation is due to hypoventilation, no appreciable gradient exists at any level of oxygenation and CO2 retention is usually evident. Any increase in A-a gradient must, therefore, be due to some other mechanism. Lilienthal, Riley, Proemmel, and Franke (7) suggested that one might distinguish between a diffusion defect and veno-arterial admixture by measurement of the effective alveolar-arterial gradient at two levels of oxygenation, one of which produces significant desaturation of arterial blood. Low levels of inspired 02 (12 to 14 per cent) exaggerate the effects of impaired diffusion and minimize the effects of veno-arterial admixture. Veno-arterial admixture, thus delineated, may be either through actual anatomical communications, or the result of reduction in the ventilation-perfusion ratios.

A STUDY OF CARDIOPULMONARY ALTERATIONS IN PATIENTS WITH SICKLE CELL DISEASE AND ITS VARIANTS1