Vasopressin in shock states

There is growing evidence that in end-stage shock or during cardiac arrest, inappropriately low endogenous vasopressin plasma levels may be responsible for pathologic vasodilatation, inadequate organ perfusion, and poor outcome. The purpose of this article is to review recent publications featuring arginine vasopressin as a potent vasoconstrictor in various shock states such as systemic vasodilatation, severe hypovolemia, or cardiac arrest.

Several retrospective investigations give evidence that vasopressin at a dosage of 2-6 U/h is effective in reversing catecholamine-resistant vasodilatory shock due to sepsis or after cardiopulmonary bypass, but prospective randomized controlled trials are warranted. In experimental hypovolemic cardiac arrest or therapy-resistant (irreversible) hypovolemic shock, vasopressin may be an intriguing therapy, although human evidence is not available. Animal data gives strong evidence that vasopressin given during cardiopulmonary resuscitation improves both return of spontaneous circulation and neurological outcome. Clinical experience on the use of vasopressin for in-hospital cardiopulmonary resuscitation with short response time showed equipotency with epinephrine; in patients with out-of-hospital ventricular fibrillation, vasopressin showed improved 24 h survival in comparison with epinephrine. After the large European multicenter study completed in summer 2002, we will hopefully be able to better determine the role of vasopressin versus epinephrine in the management of adult cardiac arrest.

Vasopressin administration is emerging as a rational and promising therapy in the management of various shock states and cardiac arrest.