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The occurrence of the shock syndrome following acute myocardial infarction carries with it a high mortality rate.1Stead and Ebert2attributed the hypotension to cardiac failure, whereas Schwartz3and Levine4each treated a case successfully with antishock measures. Brofman and Hellerstein have recently reported with Caskey5the successful use of a new vasoconstrictor, phenyl tertiary butylamine sulfate, in such cases. Yet on reviewing physiological factors they state that venous return to the heart in this syndrome is more than adequate and such shock cannot be attributed to the mechanisms that are thought to be important in traumatic shock.6It is the purpose of this paper to report a study of 15 cases of the syndrome seen in 1949 and 1950, treated on the basis of clinical findings. It was expected that the response to such empirical therapy would serve to clarify the nature of
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Fink et al. (Sat,) studied this question.
synapsesocial.com/papers/6a1551aa5347fbb1739f95f2 — DOI: https://doi.org/10.1001/jama.1953.02940140007003
Theodore R. Fink
Carl J. d'Angio
Sol Biloon
Journal of the American Medical Association
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