Septic shock is often dominated by vasoplegia.
Norepinephrine is usually the first-line vasopressor, but escalating catecholamine doses can bring problems: tachyarrhythmias, increased myocardial oxygen demand, excessive beta stimulation, and worsening lactate interpretation.
Vasopressin offers a different pathway.
Endogenous vasopressin is released from the posterior pituitary in response to hypotension and increased plasma osmolality. In septic shock, levels may be initially elevated but can become relatively deficient over time.
Vasopressin acts primarily at V1 receptors on vascular smooth muscle, producing vasoconstriction through a non-catecholamine mechanism.