W. B. YOUMANS, M.D., Ph.D.
From time to time physicians have noted certain similarities between the syndrome produced by a systemic arteriovenous fistula and the cardiovascular effects produced by chronic thiamine deficiency.1 Not only do the circulatory patterns in these two conditions resemble each other, but also the circulatory changes produced by therapy with large doses of thiamine in patients with beriberi heart disease are similar in several respects to those associated with closure of an arteriovenous fistula.1 It has become common practice to refer to the circulatory failure of the type produced by beriberi and arteriovenous fistula as high output failure, in recognition of
YOUMANS WB. MECHANISM OF HIGH OUTPUT CIRCULATORY FAILURE(MECHANISM OF HIGH OUTPUT CIRCULATORY FAILURE*). Ann Intern Med. 1954;41:747–756. doi: 10.7326/0003-4819-41-4-747
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Published: Ann Intern Med. 1954;41(4):747-756.
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