Efficacy of the Use of Vasopressin as a Primary Vasoconstrictor in Critically Ill Patients

1.2 Hypothesis - Literature Review The treatment of circulatory shock due to vasoparalysis in critically ill patients is based on the administration of fluids and vasopressors. In recent years a new vasopressor, vasopressin, has been recommended to be added to septic patients in need of low to moderate doses of noradrenaline to reduce the negative effects of circulating in elevated concentrations catecholamines. The aim of the present study is to investigate the degree of multiorganic failure improvement in patients with an early administration of vasopressin (as the first vasoconstrictor drug) versus noradrenaline on the outcome of critically ill patients in need of hemodynamic support with vasoactive drugs.

Vasopressin is an endogenous peptide that through V1 receptors causes selective vasoconstriction in non-vital organs and increases blood flow to the myocardium and brain. Vasopressin via V2 receptors causes vasodilation in coronary vessels as well as in cerebral vessels.

Noradrenaline (or norepinephrine) "is a potent peripheral vasoconstrictor which acts both on arterial and venous substrates (alpha-adrenergic effect) and as a cardiac inotropic stimulator. These effects result in an increase in systemic arterial pressure and blood flow in the coronary arteries".

Several studies have shown that the addition of vasopressin may allow the total norepinephrine / noradrenaline dose to be reduced. Vasopressin levels are thought to increase in the initial phase of shock in response to hypotension but then decrease over the following 48 to 72 hours resulting in relative vasopressin deficiency. However, a subgroup analysis in the Vasopressin and Septic Shock Trial (VASST) showed extremely low baseline vasopressin levels in patients with septic shock, so the lack of vasopressin is obvious. At the same time, the same subanalysis found a survival benefit in patients given vasopressin when the norepinephrine dose was less than 15 μg/min.

Two further studies showed that starting vasopressin very early (within four hours of initiating treatment with noradrenaline) in combination with noradrenaline: allowed earlier achievement and maintenance of Mean Arterial Pressure, improved organ function and led to a shorter length of hospital stay compared to noradrenaline. Rydz et al., showed that earlier initiation of vasopressin (within 7.3 h of starting noradrenaline) was associated with a greater likelihood of patients showing improvement in their multiorgan failure score and/or survival compared with those who had a delay in starting vasopressin.