A patient with acute decompensated heart failure has a low cardiac output despite adequate filling pressures and blood pressure of 100/65 mmHg. Dobutamine infusion is inadequate. Milrinone is added. The hemodynamic profile of milrinone differs from dobutamine chiefly because milrinone:
- A Acts through beta-1 receptor stimulation, increasing cAMP selectively in myocardium
- B Inhibits phosphodiesterase type 3 in cardiac myocytes and vascular smooth muscle, producing inotropy plus vasodilation ✓
- C Increases intracellular calcium via Na+/Ca2+ exchanger inhibition, sparing the vasculature
- D Stimulates dopamine-1 receptors, causing selective renal vasodilation
Explanation
Milrinone is a phosphodiesterase type 3 inhibitor that raises cAMP independently of beta receptors. Because PDE3 exists in both cardiac myocytes and vascular smooth muscle, it produces a combined positive inotropic, lusitropic and arteriovenous vasodilator ('inodilator') response, lowering filling pressures while raising output. Dobutamine achieves inotropy via beta-1 stimulation and is subject to beta-receptor downregulation in chronic heart failure. Option A describes dobutamine itself, option C is fictitious, and fenoldopam, not milrinone, is the D1 agonist.
Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.