[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Content Landing]
April 4, 1953


Author Affiliations

New York; Mount Vernon, N. Y.; New York
From the Medical Service of the Morrisania City Hospital, New York.

JAMA. 1953;151(14):1163-1165. doi:10.1001/jama.1953.02940140007003

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.


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

First Page Preview View Large
First page PDF preview
First page PDF preview