THE MECHANISMS OF PERIPHERAL CIRCULATORY FAILURE

Abstract

Circulatory failure develops whenever the driving pressure in small arteries ia inadequate for overcoming the resistance in the arterioles, capillaries and venules. The type characterized by a progressive decline of arterial as well as effective central venous pressure and designated as peripheral circulatory failure is considered. After a summary of the symptomatology and clinical conditions with which peripheral circulatory failure is associated, the intimate mechanisms are discussed by which 4 conceivable peripheral changes could initiate such failure, viz., primary arteriolar dilatation, primary arteriolar constriction, primary atony and dilatation of capillaries and primary default of a venopressor mechanism. The data indicate that primary arteriolar constriction induced by nervous or humoral agents is not a probable initiating mechanism; primary toxic action on capillaries may be concerned, but the degree of anoxia or asphyxia which obtains is not the humoral factor, if one exists; in toxemic shock the actual circulatory vol. may not be decreased as much as is suspected; initial arteriolar dilatation is still "in the running" as a possible initiating factor; and in addition to initiating and sustaining factors, a precipitating factor, unrelated to the peripheral circulation, may be required to tilt the balance toward an irreversible state of circulatory failure.