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Cirrhosis of the Liver and Decreased Arterial Oxygen Saturation
WALTER H. ABELMANN, M.D.;
GERTRUDE E. KRAMER, M.D.;
JEAN M. VERSTRAETEN, M.D.;
MICHAEL A. GRAVALLESE, JR., M.D.;
WILLIAM F. McNEELY, M.D.
Arch Intern Med. 1961;108(1):34-40.
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Unsaturation of arterial blood for oxygen in patients with cirrhosis of the liver was first reported by Snell in 1935.1 In a later study Keys and Snell2 presented evidence for a shift of the hemoglobin dissociation curve of whole blood to the right and a decreased affinity of hemoglobin for oxygen in such patients. They concluded that this accounted for the abnormally low saturation. It is the purpose of the present communication to present evidence for an alternate explanation of unsaturation of arterial blood in patients with cirrhosis of the liver.
Arterial unsaturation is usually produced either by a reduced diffusing capacity of the lungs or by increased venous admixture. The latter includes true anatomic venous admixture from intracardiac or extracardiac right-to-left shunts, as well as physiologic venous admixture due to perfusion of alveoli, which are poorly or not at all ventilated. Before the hypothesis of Keys and
. . . [Full Text PDF of this Article]
Author Affiliations
BOSTON
Established Investigator of the American Heart Association (Dr. Abelmann).; From the Thorndike Memorial Laboratory and Second and Fourth (Harvard) Medical Services, Boston City Hospital, and the Department of Medicine, Harvard Medical School.
Footnotes
Submitted for publication July 27, 1960.
This work was done during the tenure of a Fulbright Fellowship (Dr. Verstraeten).
Supported in part by grants-in-aid from the Massachusetts Heart Association (Greater Boston Chapter) and the Life Insurance Medical Research Fund.
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