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C. A. McKINLAY, M.D.

Arch Intern Med. 1924;34(2):168-176.

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

While a growing number of reports indicate extensive study of the vital capacity of the lungs in cardiac and pulmonary disease, fewer are available in hyperthyroidism. In consideration of increased circulatory demands and cardiac stress, as well as the increased total ventilation of the lungs in hyperthyroidism, this report was thought to be justified. Frequent references to the reduction of vital capacity of the lungs in cardiac decompensation that occurs even before the physical signs of circulatory stasis have become apparent have been found. Since the work of Hutchison¹ it has been suggested by Siebech² that the reduction of vital capacity is due to engorgement of pulmonary vessels with alveolar fixation; by Ulrich and Nathanson³ that it may be present before signs of edema appear at the lung bases; by Burton-Opitz⁴ that a marked decrease in vital capacity actually signifies cardiac decompensation; and by McClure and Peabody⁵ and by Levine⁶ . . . [Full Text PDF of this Article]

Author Affiliations
MINNEAPOLIS

From the Department of Medicine, University of Minnesota.

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