What's new in vasopressin?

Abstract

Septic shock is associated with a relative deficiency of the endogenous stress hormone vasopressin. In shock states vasopressin binds to vasopressin receptors on vascular smooth muscle, producing intense vasoconstriction with minimal osmotic effects and resulting in increased blood pressure. Two recent meta-analyses report relative risks (RR) of short-term mortality in favour of vasopressin analogues compared to noradrenaline; however, using different methodologies, one group found this difference to be statistically significant (RR = 0.87, 95 % CI 0.77–0.99) [1] and the other did not (RR = 0.91, 95 % CI 0.79–1.05) [2]. The current Surviving Sepsis Campaign guidelines recommend that vasopressin may be added as an adjunct to noradrenaline in septic shock [3]. This short review aims to give an overview of the latest clinical evidence about vasopressin. The Vasopressin in Septic Shock Trial (VASST) compared vasopressin to noradrenaline (when added to open label vasopressors) and found no difference in 28-day mortality in the whole septic shock population [4]. However, in an a priori defined subgroup of less severe shock (noradrenaline\15 lg/min), a mortality benefit in favour of vasopressin use was present. The potential survival benefit of vasopressin in less severely shocked patients was also seen in those patients who had the lowest lactate levels [5]. The haemodynamic effects of both noradrenaline and vasopressin were similar, with no difference in cardiac or stroke volume index between the two treatment groups, although there was a greater use of inotropes in the vasopressin group [6]. Vasopressin use was associated with a significant reduction in heart rate particularly in the less severe shock subgroup, potentially due to reduced catecholamine use. This is an interesting observation in view of the recent interest in beta-blockers to treat tachycardia in septic shock [7].