Clinical meaning
Vasopressors are vasoactive medications that increase systemic vascular resistance (SVR) and mean arterial pressure (MAP) through stimulation of adrenergic receptors (alpha-1, beta-1) or non-adrenergic receptors (V1 vasopressin receptors). They are classified into catecholamines (norepinephrine, epinephrine, dopamine, phenylephrine) and non-catecholamines (vasopressin, angiotensin II). Alpha-1 receptor stimulation on vascular smooth muscle activates the Gq-phospholipase C-IP3 pathway, increasing intracellular calcium and producing arterial and venous vasoconstriction, thereby raising SVR and MAP. Beta-1 receptor stimulation in the myocardium activates the Gs-adenylyl cyclase-cAMP pathway, increasing heart rate (chronotropy), contractility (inotropy), and conduction velocity (dromotropy), thereby increasing cardiac output. V1 (vasopressin-1a) receptors on vascular smooth muscle couple to Gq proteins and produce vasoconstriction independent of catecholamine pathways, which is particularly valuable in vasodilatory shock where catecholamine receptor downregulation occurs. Dopaminergic (D1) receptors in renal and mesenteric vasculature produce vasodilation at low dopamine doses. The clinician selects vasopressors based on the underlying shock physiology: norepinephrine (first-line for septic shock per Surviving Sepsis Campaign) provides potent alpha-1 with moderate beta-1 stimulation; vasopressin (0.03-0.04 units/min) is added as a catecholamine-sparing adjunct; epinephrine provides combined alpha-1 and beta-1 effects for refractory shock or anaphylaxis; phenylephrine (pure alpha-1) is reserved for situations where tachyarrhythmias preclude beta-1 stimulation; and dopamine's dose-dependent receptor effects make it less predictable. MAP target is typically >=65 mmHg (higher targets of 80-85 mmHg may be considered in chronic hypertension). Vasopressors require central venous access for infusion (though short-term peripheral administration via large-bore proximal IV is acceptable in emergencies), continuous hemodynamic monitoring (arterial line preferred), and careful titration to avoid excessive vasoconstriction causing digital ischemia, mesenteric ischemia, or myocardial oxygen demand-supply mismatch.