PROTECTIVE MECHANISMS IN SHOCK

Aii important unresolved problem iii the operative management of surgical patients is that posed by the seemingly inevitable progression of severe, protracted hypotension to a “point of no return,” despite blood replacement and drug therapy. During the early phases of the hypotensive reaction to hemorrhage, compensatory readjustinents prevail and the condition can readily be alleviated hy blood replacement. With time, however, there develops a set of deconipensatory reactions that progressively undermine the precarious homeostatic balance and make the iiidividual less responsive to blood replacement measures. In experimental shock it is possible, with graded hemorrhage, to achieve a “state of irreversibility” that resembles the condition encountered following various traumatic injuries. More recently, it has been found possible to combat successfully the lethal tendency even in this forin of severe This report is concerned with experimental findings in this area. An effective approach to the problein has been to use the behavior of the terminal vascular bed as an index of the general trend of circulatory readjustment measure^.^ The pattern of vascular behavior has indicated the existence of two discrete phases iii response to both heiiiorrhage and trauma. Initially, there appears a series of compensatory adjustments characterized hy increased vasomotor activity, heightened sensitivity, and selective restriction of blood flow to the most central and direct channels. The attendant vasoconstriction is not uniform, either in degree or extent; it appears earliest in the skin, skeletal musculature, and the kidneys, and it is sustained by stimuli froin central chemcireceptors and baroreceptors without direct reference to the status of the circulation through the tissue proper. In instances where these readjustments are sufficient to sustain peripheral blood flow at near normal levels, the metabolic effects associated with more profound shock are circumvented. Recovery, either spontaneous or f ollowing transfusion, is invariable. However, when the blood pressure drops to extremely low levels despite maximal compensatory activities, widely different cellular disturbances occur and ultimately result in serious derangement of the circulation. With protracted hypotension, the compensatory behavior is progressively replaced in the vascular bed by a decompeiisatory tendency, manifested by a failure to sustain the ischemic restricted pattern of blood flow, by a hyporeactivity of the muscular elements, and by a venous stagiiation to the point of almost complete stasis. The longer the decompensatory tendency is permitted to develop, the less favorable is the prognosis for recovery as a result of blood replacement