Dobutamine is preferred over dopamine in a patient with acute heart failure and low cardiac output primarily because dobutamine:

• A Activates dopaminergic receptors causing renal vasodilation
• B Releases norepinephrine from nerve terminals
• C Produces greater inotropic effect relative to heart rate increase and avoids tachycardia better ✓
• D Selectively stimulates beta-2 receptors in the myocardium

Explanation

Dobutamine predominantly stimulates beta-1 receptors in the heart with relatively balanced alpha-1 and beta-2 activity, producing a strong inotropic effect with less tachycardia and less peripheral vasoconstriction than dopamine at equivalent inotropic doses. Dopamine activates dopaminergic D1 receptors for renal vasodilation and also releases norepinephrine — effects absent with dobutamine. Dobutamine acts on beta-1 receptors (not beta-2) in the myocardium.

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

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