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Milrinone: pharmacology

Bypyridine derivative, isoenzyme fractionPDE III inhibitor. This inhibitiondecreases the hydrolysis of cAMP, leading to increased intracellular concentration of cAMP in the myocardium and vascular smooth muscle. Increased intracellular concentration of cAMP (little effect on cGMP) results instimulation of protein kinases that phosphorylate substances responsible for uptake, storage, and release of Ca from sarcoplasmic reticulumduring excitation- contraction coupling. Milrinone enhances the effects of catecholamines, which also increase cAMP concentrations through beta-adrenergic stimulation.

Milrinone is a derivative of Amrinone. Has 20 times the inotropic potency of the parent compound. Is active both IV and PO.

Administration: 50 mcg/kg IV over 10 min, followed by 0.375 – 0.75 mcg/kg/min infusion (not to exceed 1.13 mg/kg/day). Onset of action is 5-15 min. 70% bound by plasma proteins. Hepatically metabolized (only 12%), renally excreted (80% unchanged, since most of it is not metabolized), elimination half life 2.7 hrs (on CVVH – 20 hrs). In setting of severe renal dysfunction (GFR < 50 ml/min), the dose should be decreased.

Milrinone: Summary

  • Mechanism of Action: PDE III inhibitor (decreased cAMP breakdown, ultimately leads to increased intracellular Ca++)
  • Adult IV Dosing: 50 mcg/kg IV over 10 min, followed by 0.375 – 0.75 mcg/kg/min
  • Onset Time: 5-15 mins
  • Elimination Half-Time: 2.7 hrs
  • Metabolism/Excretion: hepatic (only 12%), renal (80% excreted unchanged)


  1. Jerrold H Levy, James M Bailey, G Michael Deeb Intravenous milrinone in cardiac surgery. Ann. Thorac. Surg.: 2002, 73(1);325-30 PubMed Link