A patient with acute decompensated heart failure already receiving maximally tolerated oral beta-blocker therapy requires inotropic support. Compared with dobutamine, milrinone offers the specific advantage that:
- A It raises systemic vascular resistance, improving coronary perfusion
- B It increases myocardial cyclic AMP only through beta-1 receptor stimulation
- C Its inotropic effect does not depend on beta-adrenergic receptor signaling, so efficacy is preserved despite concurrent beta-blockade ✓
- D It inhibits phosphodiesterase type 5 selectively in the pulmonary circulation
Explanation
Milrinone inhibits phosphodiesterase type 3 in cardiac and vascular smooth muscle, raising intracellular cyclic AMP independently of the beta receptor. Because its site of action is downstream of the receptor, chronic beta-blockade does not blunt its positive inotropic or vasodilating effects, unlike dobutamine, which acts directly at beta-1 receptors and may require higher doses under beta-blockade. Milrinone lowers rather than raises vascular resistance, giving it the label inodilator, and PDE5 inhibition is the domain of sildenafil, not milrinone.
Reference: Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.