What is the primary action of milrinone as an inotropic agent?

Milrinone primarily acts as a phosphodiesterase (PDE) inhibitor, specifically inhibiting PDE type 3. This action leads to an increase in intracellular cyclic adenosine monophosphate (cAMP) levels. Elevated cAMP levels facilitate enhanced calcium influx into the cardiomyocytes, which subsequently increases myocardial contractility and improves cardiac output. This mechanism is particularly useful in managing heart failure, where increasing contractility can help improve the heart's pumping efficiency.

The increase in cAMP also results in vasodilation of the systemic and pulmonary vascular beds, contributing to a reduction in preload and afterload, which can relieve some of the strain on a failing heart. This dual mechanism of action—improving contractility while promoting vasodilation—makes milrinone a valuable agent in the treatment of acute decompensated heart failure.

In contrast, other actions listed in the alternatives do not accurately describe milrinone’s primary mechanism. Enhancing calcium release from the sarcoplasmic reticulum is not the direct action of milrinone; rather, it is the result of increased cAMP levels. Inhibiting sodium-potassium ATPase is a mechanism associated with digoxin, not milrinone. Blocking beta receptors would