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April 22, 1944


JAMA. 1944;124(17):1202-1203. doi:10.1001/jama.1944.02850170038009

The common factor in the production of shock is a discrepancy between the effective circulating blood volume and the actual volume capacity of the vascular bed. The development of this fundamental change is primarily responsible for the impressive clinical symptomatology with low temperature, feeble and rapid pulse, cold skin, exhaustion and lowered arterial pressure. However, when this clinical syndrome appears, shock is often irreversible and therapy ineffective. Hence it becomes necessary to establish clinical criteria which will express the earliest, asymptomatic phase of the disparity between blood volume and vascular bed.

Many clinicians still believe that a low or falling arterial pressure constitutes an early and obligatory feature of shock. Blalock,1 Moon,2 Harkins3 and others have repeatedly pointed out that arterial pressure is a completely inadequate guide to the state of circulatory deficiency in incipient shock. Frequently the reactive vasoconstriction leads to an elevation of arterial pressure

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