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J. BAILEY CARTER, M.D.; EUGENE F. TRAUT, M.D.

Arch Intern Med. 1943;72(6):757-766.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Profound circulatory changes occur in both primary and secondary anemia.

With a decrease in the hemoglobin content of the blood the output of the heart is increased.¹ This is the outstanding compensatory mechanism for the loss of oxygen-carrying power of the blood. The cardiac rate is also increased in anemia.² Although the cardiac acceleration is moderate, rarely more than 120 per minute, it results in a certain increase in cardiac output. This increase in minute volume output is due, likewise, in part, to lowering of the viscosity of the blood.1c Nevertheless, the increased cardiac output observed in anemia is due mainly to the increased systolic output of the heart. This increase in cardiac output is directly proportional to the decrease in hemoglobin content of the blood. A 200 per cent and a 300 per cent increase are reported to occur with hemoglobin levels of 30 per cent and . . . [Full Text PDF of this Article]

Author Affiliations
Assistant Professor, Department of Medicine, University of Illinois; Professor of Medicine, Cook County Graduate School of Medicine; Assistant Professor, Department of Medicine, University of Illinois; Professor of Medicine, Cook County Graduate School of Medicine CHICAGO

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