Dobutamine is preferred over dopamine in acute decompensated heart failure without hypotension because:

• A Dobutamine stimulates cardiac D1 receptors increasing cAMP independently of adrenergic receptors
• B Dobutamine does not increase heart rate, whereas dopamine produces marked reflex tachycardia
• C Dobutamine's predominant β1 agonism increases contractility with minimal vasoconstriction; dopamine at higher doses activates α1 receptors increasing afterload on the failing heart ✓
• D Dobutamine has selective renal vasodilation preventing oliguria in heart failure

Explanation

Dobutamine is a synthetic catecholamine with predominantly β1-adrenergic agonism (positive inotropy, modest chronotropy) and mild β2 (peripheral vasodilation). At doses used in heart failure, it increases cardiac output without significantly increasing systemic vascular resistance. Dopamine at > 5–10 μg/kg/min activates α1 receptors, raising SVR and afterload, which is deleterious in the failing heart. Dopamine's 'renal dose' selective D1 effect is now considered unreliable.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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Written and medically reviewed by the StethoPrep medical team.