Vasopressin and septic shock

• Main Author: Sarah Mousavi (Author)
• Format: Book
• Published: Research Center for Rational Use of Drugs (RCRUD), 2015-10-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

Septic shock continues to be one of the leading causes of death in the Intensive Care Units. When the shock state persists after adequate fluid resuscitation,  vasopressor therapy is required to improve and maintain adequate tissue/organ  perfusion in an attempt to improve survival and prevent the development of multiple organ dysfunction and failure. Various studies have suggested that exogenous administration of arginine vasopressin  may  be  an  effective  adjunctive  therapy  to  traditional  catecholamines for the management of hypotension during septic shock. Vasopressin is both a vasopressor  and  an  antidiuretic  hormone.  It  also  has  hemostatic,  gastrointestinal and thermoregulatory  effects, and is an adrenocorticotropic  hormone secretagogue. Vasopressin  is released from the axonal terminals of magnocellular  neurons in the hypothalamus. Vasopressin mediates vasoconstriction  via V1-receptor activation on vascular smooth muscle and mediates its antidiuretic effect via V2-receptor activation in the renal collecting duct system. Vasopressin  infusion of 0.01 to 0.04 U/min in patients with septic shock increases plasma vasopressin levels. Current guidelines from the Surviving Sepsis Campaign recommend arginine vasopressin 0.03 unit/minute may be added to norepinephrine with the anticipation of an effect equal to higher doses of norepinephrine alone. Clinicians must be knowledgeable about the use of vasopressin in septic shock, including controversial areas where guidelines do not always provide solid recommendations.

Item Description

2322-4630
2322-4509