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The occurrence of the shock syndrome following acute myocardial infarction carries with it a high mortality rate.1 Stead and Ebert2 attributed the hypotension to cardiac failure, whereas Schwartz3 and Levine4 each treated a case successfully with antishock measures. Brofman and Hellerstein have recently reported with Caskey5 the 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.6 It 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
Fink TR, d'Angio CJ, Biloon S. CLINICAL STUDY OF SHOCK FOLLOWING MYOCARDIAL INFARCTION. JAMA. 1953;151(14):1163–1165. doi:10.1001/jama.1953.02940140007003
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