Therapy for vasodilatory shock: Arginine vasopressin

Abstract

V ASODILATORY SHOCK is a condition of hypotension with end-organ hypoperfusion resulting from a decrease in systemic vascular resistance. This vasodilatory state is a well-known characteristic of septic shock, but it is also observed in the late phase of hemorrhagic shock and as a complication of cardiopulmonary bypass. 1-3 Catecholamine vasopressors, the only clinically used vasoconstrictors, can be effective, but their action is frequently diminished in vasodilatory shock, and side effects are prominent at increased doses. ~-4 Thus, the morbidity and mortality from catecholamine-resistant hypotension in vasodilatory shock remains high, and alternative treatments could be useful. The mechanisms responsible for vasodilation in the various syndromes associated with vasodilatory shock continues to be elucidated. We and others have shown that the vasodilatory shock of sepsis is mediated in part by vasodilatory mechanisms such as the inappropriate release of nitric oxide (NO) and the opening of adenosine triphosphate (ATP)-sensitive potassium channels (K+ATP) on vascular smooth muscle. 56 The possibility that vasoconstrictor mechanisms, such as arginine vasopressin (AVP), might be defective and thus contribute to vasodilatory shock has not been as well studied. Our incidental observation of a marked vasopressor response to exogenous AVP in a patient with vasodilatory septic shock contrasted with the decreased effectiveness of catecholamine vasoconstrictors in this patient. This led us to examine the role of AVP in the hypotension of vasodilatory shock. We discovered that the baroreflex-mediated secretion of vasopressin is defective not only in septic shock but in a variety of vasodilatory shock