Abstract

IS THIS A NEW role for an old drug? The impression that arginine vasopressin (AVP) is rarely used as a first-line vasoconstrictor after cardiopulmonary bypass (CPB) is confirmed by a review of the published literature. All the patients in the relevant clinical studies found were already receiving catecholamine vasopressors before being treated with AVP (Table 1); this is probably because adrenergic agonists are normally effective and have predictable, titratable effects. AVP has been advocated as a rational therapy in vasodilatory shock, in which catecholamine resistance often occurs. The evidence for the safety and efficacy of vasopressin in vasodilatory shock is sparse, considering vasodilatory shock may occur in 8% of cardiac surgical patients.1 Published supportive evidence is based on case reports, retrospective analysis of case series, and small comparative studies with physiologic endpoints from predominantly one research group. Large, multicenter randomized, controlled trials are needed to assess the effect of AVP on outcome and organ dysfunction in this setting. The absence of such trials may be explained by the lack of research funding into AVP, which is an orphan drug with an expired patent. This article discusses the pathophysiology of vasodilatory states after CPB and provides a critical assessment of the evidence for the use of AVP in this context.

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