Milrinone (Primacor ®)
|The authors make no claims of the accuracy of the information contained herein; and these suggested doses and/or guidelines are not a substitute for clinical judgment. Neither GlobalRPh Inc. nor any other party involved in the preparation of this document shall be liable for any special, consequential, or exemplary damages resulting in whole or part from any user's use of or reliance upon this material. PLEASE READ THE DISCLAIMER CAREFULLY BEFORE ACCESSING OR USING THIS SITE. BY ACCESSING OR USING THIS SITE, YOU AGREE TO BE BOUND BY THE TERMS AND CONDITIONS SET FORTH IN THE DISCLAIMER.|
Standard Dilutions [Amount of drug] [Infusion volume] [Infusion rate]
|Remove 50 ml from 250ml bag.
(Final volume =250 ml)
[50 mg] [200 ml] [Titrate]
Also available as a pre-pack:
200 mL (200 mcg/mL) NDC 0024-1203-22 in 5% Dextrose Injection single units.
Exposure of pharmaceutical products to heat should be minimized. Avoid excessive heat. Protect from freezing. It is recommended that the Flexible Containers be stored at room temperature, 25 C (77 F), however, brief exposure up to 40 C (104 F) does not adversely affect the product.
Stability / Miscellaneous
|EXP: 3 DAYS (RT).
Dosing: initially give loading dose: 50 mcg/kg IV over 10 minutes, followed by continuous infusion: 0.375 to 0.75 mcg/kg/min (usually 0.5 mcg/kg/min).
Venodilator: 0 Arterial dilator: ++ Inotropic effect: +++
Recommended infusion rates: renal insufficiency
PRIMACOR, at relevant inotropic and vasorelaxant concentrations, is a selective inhibitor of peak III cAMP phosphodiesterase isozyme in cardiac and vascular muscle. This inhibitory action is consistent with cAMP mediated increases in intracellular ionized calcium and contractile force in cardiac muscle, as well as with cAMP dependent contractile protein phosphorylation and relaxation in vascular muscle. Additional experimental evidence also indicates that PRIMACOR is not a beta-adrenergic agonist nor does it inhibit sodium-potassium adenosine triphosphatase activity as do the digitalis glycosides.
Clinical studies in patients with congestive heart failure have shown that PRIMACOR produces dose-related and plasma drug concentration-related increases in the maximum rate of increase of left ventricular pressure. Studies in normal subjects have shown that PRIMACOR produces increases in the slope of the left ventricular pressure-dimension relationship, indicating a direct inotropic effect of the drug. PRIMACOR also produces dose-related and plasma concentration-related increases in forearm blood flow in patients with congestive heart failure, indicating a direct arterial vasodilator activity of the drug.
Both the inotropic and vasodilatory effects have been observed over the therapeutic range of plasma milrinone concentrations of 100 ng/mL to 300 ng/mL.
In addition to increasing myocardial contractility, PRIMACOR improves diastolic function as evidenced by improvements in left ventricular diastolic relaxation.
The acute administration of intravenous milrinone has also been evaluated in clinical trials in excess of 1600 patients, with chronic heart failure, heart failure associated with cardiac surgery, and heart failure associated with myocardial infarction. The total number of deaths, either on therapy or shortly thereafter (24 hours) was 15, less than 0.9%, few of which were thought to be drug-related.
PRIMACOR has been shown (by equilibrium dialysis) to be approximately 70% bound to human plasma protein.
The primary route of excretion of PRIMACOR in man is via the urine. The major urinary excretions of orally administered PRIMACOR in man are milrinone (83%) and its 0-glucuronide metabolite (12%). Elimination in normal subjects via the urine is rapid, with approximately 60% recovered within the first two hours following dosing and approximately 90% recovered within the first eight hours following dosing. The mean renal clearance of PRIMACOR is approximately 0.3 liters/min, indicative of active secretion.
INDICATIONS AND USAGE
DOSAGE AND ADMINISTRATION
Note: PRIMACOR Flexible Containers (200 mcg/mL in 5% Dextrose Injection) are for intravenous infusion only and should not be used for a loading dose. Dosage recommendations using a 1mg/mL concentration of milrinone are included for informational purposes only. The loading dose should be administered using a milrinone 1mg/mL vial.
The table below shows the loading dose in milliliters (mL) of milrinone (1mg/mL) by patient body weight (kg).
The infusion rate should be adjusted according to hemodynamic and clinical response. Patients should be closely monitored. In controlled clinical studies, most patients showed an improvement in hemodynamic status as evidenced by increases in cardiac output and reductions in pulmonary capillary wedge pressure.
Note: See Dosage Adjustment in Renally Impaired Patients at top of page.... Dosage may be titrated to the maximum hemodynamic effect and should not exceed 1.13 mg/kg/day. Duration of therapy should depend upon patient responsiveness.
Revised March 2007B
©2007 sanofi-aventis U.S. LLC
Source: [package insert]
The authors make no claims of the accuracy of the information contained herein; and these suggested doses are not a substitute for clinical judgment. Neither GlobalRPh Inc. nor any other party involved in the preparation of this program shall be liable for any special, consequential, or exemplary damages resulting in whole or part from any user’s use of or reliance upon this material.PLEASE READ THE DISCLAIMER CAREFULLY BEFORE ACCESSING OR USING THIS SITE. BY ACCESSING OR USING THIS SITE, YOU AGREE TO BE BOUND BY THE TERMS AND CONDITIONS SET FORTH IN THE DISCLAIMER. Read the disclaimer