A patient with acute decompensated heart failure and low cardiac output is started on milrinone. Its hemodynamic profile differs from digoxin primarily because milrinone:
- A Stimulates beta-1 receptors, increasing contractility at the cost of tachycardia
- B Inhibits phosphodiesterase type 3, raising cAMP in both myocardium and vasculature to produce positive inotropy with vasodilation ✓
- C Inhibits Na+/K+-ATPase, producing inotropy with vasoconstriction
- D Blocks phosphodiesterase type 5, selectively dilating the pulmonary circulation
Correct answer: B. Inhibits phosphodiesterase type 3, raising cAMP in both myocardium and vasculature to produce positive inotropy with vasodilation
Explanation
Milrinone inhibits PDE3, preventing cAMP degradation in cardiac myocytes and vascular smooth muscle. The result is increased contractility plus arterial and venous dilation, the inodilator profile useful in low-output states, especially in patients on beta-blockers where beta-agonists lose efficacy. Unlike digoxin, it does not act via Na+/K+-ATPase, and unlike dobutamine it works independently of beta-receptors, avoiding receptor desensitization issues.
Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.
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