Vascular mechanisms of terminal shock.

Experience during the war has shown conclusively that treatment of early shock with plasma and blood is satisfactory and demands no more improvement than the perfection of technics. These agents are not as effective, however, in the late, so-called "irreversible" or "terminal" phase of shock. The pressing problem therefore is the study of the nature and treatment of terminal shock. In its essence, the problem is one of vascular failure; the approach adopted by our groups, first in Indianapolis and later in Cleveland, lay in a study of the reactions of the whole vascular system. These reactions determine the volume and rate of tissue blood flow. They are basic in this study because the degree of tissue perfusion determines the survival of tissues and the survival of vital tissues determines the survival of the shocked patient. First it is necessary to know something of the relation between the rate of tissue blood flow and the level of arterial pressure. Fortunately, as this study was being undertaken, a patient was seen whose condition all but settled this relationship. At admission, his blood pressure while reclining was 38—0 mm. mercury by auscultation and approximately 30 mm. mercury by intra-arterial puncture. In spite of this, he had few complaints, talked well and clearly, his skin was warm, and there were no signs of shock. Other than extreme hypotension, the only distinct abnormality was failure of urinary secretion. Remarkably, cardiac output was doubled. He failed to show signs of shock because he was able to maintain tissue blood flow by increasing greatly the volume of blood ejected under low pressure into vessels which were not excessively constricted. The abnormality lay basically in a great decrease of peripheral resistance due to the suicidal ingestion of arsenic trioxide. Infusion of angiotonin and fluids seemed in part responsible for recovery so far as hypotension was concerned. Clearly, the level of arterial pressure is not the major determinant of tissue perfusion nor is hypotension coextensive with shock. Rather, the caliber of the arterial blood vessels is a major issue.

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