Vasoactive Medications Reference

Primary effect: Potent vasoconstriction via α1 — increases MAP and SVR. Mild positive inotropy via β1.

Receptor activity: Predominantly α1 agonist with modest β1 activity. Heart rate effect is variable; reflex bradycardia may occur due to increased afterload.

Common clinical use: First-line vasopressor for septic shock (Surviving Sepsis Campaign recommendation). Also used for other distributive and vasodilatory shock states.

Primary effect: Dose-dependent α and β stimulation — potent vasoconstriction plus strong positive inotropy and chronotropy. At low doses, β2 effects may predominate causing vasodilation.

Receptor activity: Full α1, β1, and β2 agonist. Increases HR, contractility, and BP. Increases myocardial oxygen demand significantly.

Common clinical use: Anaphylaxis (first-line IM/IV). Cardiac arrest (ACLS — 1 mg IV every 3–5 min). Second-line vasopressor in refractory septic shock. Can cause hyperglycemia and tachyarrhythmias.

Primary effect: Dose-dependent receptor activity.

• Low dose (1–5 mcg/kg/min): Dopaminergic — renal and mesenteric vasodilation (historically called “renal dose”; not proven to protect kidneys)
• Moderate dose (5–10 mcg/kg/min): β1 — increased HR and contractility
• High dose (> 10 mcg/kg/min): α1 — vasoconstriction, increased BP and SVR

Common clinical use: Hemodynamically unstable bradycardia (alternative to atropine in ACLS). Dopamine is less preferred than norepinephrine for septic shock due to higher arrhythmia risk and increased mortality in some studies.

Primary effect: Positive inotrope — increases cardiac contractility and cardiac output. Mild decrease in SVR via β2. May slightly increase heart rate. Does NOT primarily increase BP — may actually lower it due to vasodilation.

Receptor activity: Predominantly β1 agonist with some β2. Minimal α1 activity. Improves cardiac output without major vasoconstriction.

Common clinical use: Cardiogenic shock or acute decompensated heart failure with low cardiac output. Often combined with a vasopressor (norepinephrine) to maintain MAP while improving contractility. Not a vasopressor.

Primary effect: Direct smooth muscle vasoconstriction through V1 receptors — increases SVR and MAP without adrenergic receptor activity. Does not increase HR or contractility.

Receptor activity: Acts on vasopressin V1 receptors in vascular smooth muscle and V2 receptors in renal tubules (antidiuretic effect). Non-adrenergic mechanism makes it useful in catecholamine-refractory shock.

Common clinical use: Added to norepinephrine in septic shock to increase MAP and reduce norepinephrine requirements. Fixed-dose infusion (0.03–0.04 units/min) — not typically titrated. Can cause skin ischemia, decreased cardiac output, and hyponatremia with prolonged use.

Primary effect: Pure α1 agonist — potent peripheral vasoconstriction, increases SVR and MAP. No direct effect on heart rate or contractility. Reflex bradycardia may occur.

Receptor activity: Selective α1 agonist with no β receptor activity. Increases afterload without increasing cardiac oxygen demand through β stimulation.

Common clinical use: Vasodilatory shock when tachycardia is a concern (e.g., septic shock with tachyarrhythmia). Intraoperative hypotension. Spinal anesthesia-induced hypotension. Less preferred than norepinephrine for septic shock as primary agent — may reduce cardiac output in some patients due to increased afterload without inotropic support.