Vasopressors and septic shock

Abstract

Endothelial dysfunction causes vasodilation and hypotension that characterize septic shock. Many complex molecular pathways lead to major alterations and heterogeneity of the microcirculation. Molecules capable of targeting the mechanisms of the septic vasoplegia are currently in development or under animal experimentation and are still far from a possible clinical use. The vasopressors currently used in clinical practice, vasopressin and its analogue terlipressin and α-adrenergic agonists (norepinephrine, epinephrine) are “blind” vasoconstrictors that do not target vasoplegia where it is dominant. Their effects on blood pressure and organ perfusion pressure are very similar. Their impact on the regional and microcirculation depends on the ratio between the obtained easily measurable macro-hemodynamic effects (cardiac output, blood pressure) and the effect of vasoconstriction on the microcirculation, more difficult to monitor clinically. In this mini-review we discuss the macro- and microcirculatory effects of the different vasopressors in septic shock and examine the published comparative clinical trials to address the following practical questions: what vasopressor should we use, which blood pressure level should we target, and how to monitor its effects?