January 10, 1920


JAMA. 1920;74(2):106-107. doi:10.1001/jama.1920.02620020038018

Whatever may be the cause or causes of surgical shock—which it would be too venturesome to debate at this juncture—considerable evidence is now available pointing to a loss of circulating fluid.1 In the early studies of shock, when fall of blood pressure appeared to be the most conspicuous symptom, remedial measures were directed toward inducing the blood vessels to acquire a better tonus in order to restore the efficiency of the circulation. It must be admitted frankly that most of these have failed in general to accomplish anything more than very transitory advantage. Stimulants and vasoconstrictor drugs were naturally first to be tested, and, like related methods of physical therapy, they proved to be of little importance. Subsequently, attention was turned more directly to the impaired volume of the blood in shock, even though no external hemorrhage had occurred. Gasser, Erlanger and Meek2 point out, in one of

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