PDE inhibitors are typically used for short-term management
ofheart failure or long-term management in patients awaiting heart transplant
surgery. Specific PDE inhibitors are inamrinone and milrinone.
Administered I.V., inamrinone is distributed
rapidly, metabolized by the liver, and excreted by the kidneys. It’s rarely
used because secondary thrombocytopenia may occur as an adverse reaction.
Milrinone is also administered I.V. It’s
distributed rapidly and ex-creted by the kidneys, primarily as unchanged drug.
PDE inhibitors improve cardiac output by
strengthening contrac-tions. These drugs are thought to help move calcium into
the car-diac cell or to increase calcium storage in the sarcoplasmic
reticu-lum. By directly relaxing vascular smooth muscle, they also de-crease
peripheral vascular resistance (afterload) and the amount of blood returning to
the heart (preload).
Inamrinone and milrinone are used to manage heart
failure in pa-tients who haven’t responded adequately to treatment with
car-diac glycosides, diuretics, or vasodilators. Prolonged use of these drugs
may increase the patient’s risk of complications and death. (See Adverse reactions to PDE inhibitors.)
PDE inhibitors may
interact with disopyramide, causing hy-potension.
Because PDE inhibitors
reduce serum potassium levels, taking them with a potassium-wasting diuretic may
lead to hypokalemia.