【中文品名】米力农
【药效类别】强心药
【通用药名】MILRINONE
【别　　名】Primacor，Corotrope，Win-47203
【化学名称】 1,6-Dihydro-2-methyl-6-oxo[3,4'-bipyridine]-5-carbonitrile
【CA登记号】[78415-72-2]
【结 构 式】

【分 子 式】C12H9N3O
【分 子 量】211.22
【收录药典】
【开发单位】Steriling (美国)
【首次上市】1987年，美国
【性　　状】白色结晶。微溶于水。mp>300℃。
【用　　途】
强心药，用于治疗顽固性心力衰竭和已发生洋地黄中毒的心力衰竭患者。本品能明显改善心力衰竭患者全身血流动力学各种参数，无血小板减少和低血压副作用。
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【用途】
强心药，具有增强心肌收缩力和直接扩张血管的作用
新型非苷类非儿茶酚胺类强心药，作用与氨吡酮相似，正性肌力作用强，约为氨力农的20～50倍，并有明显的扩张血管平滑肌作用，能降低心脏负荷，还能极好地改善肾脏和肌肉供血。口服和静脉均有效，无严重不良反应。用于慢性心力衰竭及充血性心力衰竭等严重的心力衰竭。

【米力农注射液】
米力农注射液磷酸二酯酶抑制剂，为氨力农的同类药物，作用机理与氨力农相同，兼有正性肌力作用和血管扩张作用。本品正性肌力作用主要是通过抑制磷酸二酯酶，使心肌细胞内环磷酸腺苷（CAMP）浓度增高，细胞内钙增加，心肌收缩力加强，心排血量增加。而与肾上腺素b1受体或心肌细胞Na+、K+ -ATP酶无关其血管扩张作用可能是直接作用于小动脉或所致，从而可降低心脏前、后负荷，降低左心室充盈压，改善左室功能，增加心脏指数，但对平均动脉压和心率无明显影响。本品对伴有传导阻滞的患者较安全。本品口服时不良反应较重，不宜长期应用。

【药代动力学】
静脉给药5～15分钟起生效，清除半衰期为2～3小时。蛋白结合率70%。

【作用与用途】
本品可使高血性心力衰竭患者体循环血管阻力、肺动脉平均压和肺毛细血管楔嵌压显著降低、心输出量、心脏指数和每搏指数增加，但不增加心肌耗氧量。 　　
适用于充血性心力衰竭短期静脉用药。

【用法】
可用适量生理盐水或葡萄糖液稀释后，先按37.5μg/kg-50μg/kg缓慢静脉注射10分钟(注射过快，可能出现室性早搏)，继续以0.375μg～0.75μg/kgmin静脉滴注，此后根据临床效应调整用量。

【副作用】
少数病人可有低血压、窦性心动过速、室性心律失常、血小板计数减少、肝、肾功能异常、及头痛、头晕、恶心、呕吐等。

【药物相互作用】
与常用强心药、利尿药、血管扩张药合用，临床未见不良相互作用，与多巴胺、多巴酚丁胺合用有协同作用。

【禁忌症】
严重室性心律失常。对本品过敏者。

【注意事项】
①用药期间应监测心电图，心率及血压，必要时调整用量。 　　
②本品有较强的血管扩张作用，严重低血压或血容量不足者应慎用。 　　
③不宜用于重度辨膜狭窄症。 　　
④可能加重肥厚性心肌病的流出道梗阻。 　　
⑤合并用强利尿药时，应注意纠正血容量不足与电介质平衡。 　　
⑥对房颤或房扑患者，本品可增加房室传导、导致心室率增快，宜先用或联合应用控制心室率的药物。 　　
⑦肝肾功能损害严重者慎用。 　　
⑧尚无用于孕妇哺乳及儿童的经验，使用时权衡利弊。 　　
⑨用药期间应监测血小板计数。

【原产地英文商品名】Milrila 10mg/10ml/vial 5vials/box
【原产地英文药品名】Milrinone
【原产地英文化合物名称】1,6-Dihydro-2-methyl-6-oxo-[3,4'-bipyridine]-5-carbonitrile
【中文参考商品译名】Milrila 10毫克/10毫升/瓶 5瓶/盒
【中文参考药品译名】米力农
【生产厂家中文参考译名】安斯泰来
【生产厂家英文名】Astellas

milrinone lactate in dextrose (Milrinone Lactate and Dextrose monohydrate)  injection 
[B. Braun Medical Inc.]

Single Dose
PAB® Plastic Container

For intravenous infusion only.

DESCRIPTION

Milrinone Lactate in 5% Dextrose Injection is a sterile, aqueous solution of milrinone in 5% dextrose. It is administered by the intravenous route. It is premixed and requires no further dilution.

Milrinone is a member of a new class of bipyridine inotropic/vasodilator agents with phosphodiesterase inhibitor activity, distinct from digitalis glycosides or catecholamines. Milrinone lactate is designated chemically as 1,6-dihydro-2-methyl-6-oxo-[3,4'-bipyridine]-5-carbonitrile lactate.

Milrinone is an off-white to tan crystalline compound with a molecular formula of C12H9N3O. It is slightly soluble in methanol, and very slightly soluble in chloroform and in water. As the lactate salt, it is stable and colorless to pale yellow in solution.

The molecular structures of milrinone lactate and dextrose (hydrous) are as follows:

The PAB Container is Latex-free, PVC-free, and DEHP-free.

The PAB plastic container system provides a ready-to-use dilution of milrinone in a volume of 100 mL of 5% Dextrose Injection. Each mL contains milrinone lactate equivalent to 200 mcg milrinone. The nominal concentration of Lactic Acid USP is 0.282 mg/mL. Each mL also contains 49.4 mg Dextrose, Anhydrous, USP in Water for Injection, USP. The pH is adjusted to between 3.2 and 4.0 with lactic acid and/or sodium hydroxide.

The solution contains no preservative and is intended only for use as a single-dose injection. When smaller doses are required the unused portion should be discarded.

The PAB plastic container system is a copolymer of ethylene and propylene formulated and developed for parenteral drugs. The copolymer contains no plasticizers and exhibits virtually no leachability. The safety of the plastic container has been confirmed by biological evaluation procedures.

The material passes Class Vl testing as specified in the U.S. Pharmacopeia for Biological Tests – Plastic Containers. These tests have shown that the container is nontoxic and biologically inert. The container-solution unit is a closed system and is not dependent upon entry of external air during administration. No overwrap is necessary.

CLINICAL PHARMACOLOGY

Milrinone is a positive inotrope and vasodilator, with little chronotropic activity different in structure and mode of action from either the digitalis glycosides or catecholamines.

Milrinone, 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 milrinone 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 milrinone 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 milrinone produces increases in the slope of the left ventricular pressure-dimension relationship, indicating a direct inotropic effect of the drug. Milrinone 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, milrinone 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.

Pharmacokinetics

Following intravenous injections of 12.5 mcg/kg to 125 mcg/kg to congestive heart failure patients, milrinone had a volume of distribution of 0.38 liters/kg, a mean terminal elimination half-life of 2.3 hours, and a clearance of 0.13 liters/kg/hr. Following intravenous infusions of 0.20 mcg/kg/min to 0.70 mcg/kg/min to congestive heart failure patients, the drug had a volume of distribution of about 0.45 liters/kg, a mean terminal elimination half-life of 2.4 hours, and a clearance of 0.14 liters/kg/hr. These pharmacokinetic parameters were not dose-dependent, and the area under the plasma concentration versus time curve following injections was significantly dose-dependent.

Milrinone has been shown (by equilibrium dialysis) to be approximately 70% bound to human plasma protein.

The primary route of excretion of milrinone in man is via the urine. The major urinary excretions of orally administered milrinone 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 milrinone is approximately 0.3 liters/min, indicative of active secretion.

Pharmacodynamics

In patients with heart failure due to depressed myocardial function, milrinone produced a prompt dose and plasma concentration related increase in cardiac output and decreases in pulmonary capillary wedge pressure and vascular resistance, which were accompanied by mild-to-moderate increases in heart rate. Additionally, there is no increased effect on myocardial oxygen consumption. In uncontrolled studies, hemodynamic improvement during intravenous therapy with milrinone was accompanied by clinical symptomatic improvement, but the ability of milrinone to relieve symptoms has not been evaluated in controlled clinical trials. The great majority of patients experience improvements in hemodynamic function within 5 to 15 minutes of the initiation of therapy.

In studies in congestive heart failure patients, milrinone when administered as a loading injection followed by a maintenance infusion produced significant mean initial increases in cardiac index of 25 percent, 38 percent, and 42 percent at dose regimens of 37.5 mcg/kg/0.375 mcg/kg/min, 50 mcg/kg/0.50 mcg/kg/min, and 75 mcg/kg/0.75 mcg/kg/min, respectively. Over the same range of loading injections and maintenance infusions, pulmonary capillary wedge pressure significantly decreased by 20 percent, 23 percent, and 36 percent, respectively, while systemic vascular resistance significantly decreased by 17 percent, 21 percent, and 37 percent. Mean arterial pressure fell by up to 5 percent at the two lower dose regimens, but by 17 percent at the highest dose. Patients evaluated for 48 hours maintained improvements in hemodynamic function, with no evidence of diminished response (tachyphylaxis). A smaller number of patients have received infusions of milrinone for periods up to 72 hours without evidence of tachyphylaxis.

The duration of therapy should depend upon patient responsiveness.

Milrinone has a favorable inotropic effect in fully digitalized patients without causing signs of glycoside toxicity. Theoretically, in cases of atrial flutter/fibrillation, it is possible that milrinone may increase ventricular response rate because of its slight enhancement of AV node conduction. In these cases, digitalis should be considered prior to the institution of therapy with milrinone.

Improvement in left ventricular function in patients with ischemic heart disease has been observed. The improvement has occurred without inducing symptoms or electrocardiographic signs of myocardial ischemia.

The steady-state plasma milrinone concentrations after approximately 6 to 12 hours of unchanging maintenance infusion of 0.50 mcg/kg/min are approximately 200 ng/mL. Near maximum favorable effects of milrinone on cardiac output and pulmonary capillary wedge pressure are seen at plasma milrinone concentrations in the 150 ng/mL to 250 ng/mL range.

INDICATIONS AND USAGE

Milrinone Lactate in 5% Dextrose Injection is indicated for the short-term intravenous treatment of patients with acute decompensated heart failure. Patients receiving milrinone should be observed closely with appropriate electrocardiographic equipment. The facility for immediate treatment of potential cardiac events, which may include life-threatening ventricular arrhythmias, must be available. The majority of experience with intravenous milrinone has been in patients receiving digoxin and diuretics. There is no experience in controlled trials with infusions of milrinone for periods exceeding 48 hours.

CONTRAINDICATIONS

Milrinone Lactate in 5% Dextrose Injection is contraindicated in patients who are hypersensitive to milrinone.

Solutions containing dextrose may be contraindicated in patients with hypersensitivity to corn products.

WARNINGS

Whether given orally or by continuous or intermittent intravenous infusion, milrinone has not been shown to be safe or effective in the longer (greater than 48 hours) treatment of patients with heart failure. In a multicenter trial of 1088 patients with Class III and IV heart failure, long-term oral treatment with milrinone was associated with no improvement in symptoms and an increased risk of hospitalization and death. In this study, patients with Class IV symptoms appeared to be at particular risk of life-threatening cardiovascular reactions. There is no evidence that milrinone given by long-term continuous or intermittent infusion does not carry a similar risk.

The use of milrinone both intravenously and orally has been associated with increased frequency of ventricular arrhythmias, including nonsustained ventricular tachycardia. Long-term oral use has been associated with an increased risk of sudden death. Hence, patients receiving milrinone should be observed closely with the use of continuous electrocardiographic monitoring to allow the prompt detection and management of ventricular arrhythmias.

PRECAUTIONS

General

Milrinone should not be used in patients with severe obstructive aortic or pulmonic valvular disease in lieu of surgical relief of the obstruction. Like other inotropic agents, it may aggravate outflow tract obstruction in hypertrophic subaortic stenosis.

Supraventricular and ventricular arrhythmias have been observed in the high-risk population treated. In some patients, injections of milrinone and oral milrinone have been shown to increase ventricular ectopy, including nonsustained ventricular tachycardia. The potential for arrhythmia, present in congestive heart failure itself, may be increased by many drugs or combinations of drugs. Patients receiving milrinone should be closely monitored during infusion.

Milrinone produces a slight shortening of AV node conduction time, indicating a potential for an increased ventricular response rate in patients with atrial flutter/fibrillation which is not controlled with digitalis therapy.

During therapy with milrinone, blood pressure and heart rate should be monitored and the rate of infusion slowed or stopped in patients showing excessive decreases in blood pressure.

If prior vigorous diuretic therapy is suspected to have caused significant decreases in cardiac filling pressure, milrinone should be cautiously administered with monitoring of blood pressure, heart rate, and clinical symptomatology.

USE IN ACUTE MYOCARDIAL INFARCTION

No clinical studies have been conducted in patients in the acute phase of post myocardial infarction. Until further clinical experience with this class of drugs is gained, milrinone is not recommended in these patients.

Laboratory Tests

Fluid and Electrolytes

Fluid and electrolyte changes and renal function should be carefully monitored during therapy with milrinone. Improvement in cardiac output with resultant diuresis may necessitate a reduction in the dose of diuretic. Potassium loss due to excessive diuresis may predispose digitalized patients to arrhythmias. Therefore, hypokalemia should be corrected by potassium supplementation in advance of or during use of milrinone.

Drug Interactions

No untoward clinical manifestations have been observed in limited experience with patients in whom milrinone was used concurrently with the following drugs: digitalis glycosides; lidocaine, quinidine; hydralazine, prazosin; isosorbide dinitrate, nitroglycerin; chlorthalidone, furosemide, hydrochlorothiazide, spironolactone; captopril; heparin, warfarin, diazepam, insulin; and potassium supplements.

Chemical Interactions

There is an immediate chemical interaction which is evidenced by the formation of a precipitate when furosemide is injected into an intravenous line of an infusion of milrinone. Therefore, furosemide should not be administered in intravenous lines containing milrinone.

Carcinogenesis, Mutagenesis, Impairment of Fertility

Twenty-four months of oral administration of milrinone to mice at doses up to 40 mg/kg/day (about 50 times the human oral therapeutic dose in a 50 kg patient) was unassociated with evidence of carcinogenic potential. Neither was there evidence of carcinogenic potential when milrinone was orally administered to rats at doses up to 5 mg/kg/day (about 6 times the human oral therapeutic dose) for twenty-four months or at 25 mg/kg/day (about 30 times the human oral therapeutic dose) for up to 18 months in males and 20 months in females. Whereas the Chinese Hamster Ovary Chromosome Aberration Assay was positive in the presence of a metabolic activation system, results from the Ames Test, the Mouse Lymphoma Assay, the Micronucleus Test, and the in vivo Rat Bone Marrow Metaphase Analysis indicated an absence of mutagenic potential. In reproductive performance studies in rats, milrinone had no effect on male or female fertility at oral doses up to 32 mg/kg/day.

Animal Toxicity

Oral and intravenous administration of toxic dosages of milrinone to rats and dogs resulted in myocardial degeneration/fibrosis and endocardial hemorrhage, principally affecting the left ventricular papillary muscles. Coronary vascular lesions characterized by periarterial edema and inflammation have been observed in dogs only. The myocardial/endocardial changes are similar to those produced by beta-adrenergic receptor agonists such as isoproterenol, while the vascular changes are similar to those produced by minoxidil and hydralazine. Doses within the recommended clinical dose range (up to 1.13 mg/kg/day) for congestive heart failure patients have not produced significant adverse effects in animals.

Pregnancy

Teratogenic Effects

Pregnancy Category C

Oral administration of milrinone to pregnant rats and rabbits during organogenesis produced no evidence of teratogenicity at dose levels up to 40 mg/kg/day and 12 mg/kg/day, respectively. Milrinone did not appear to be teratogenic when administered intravenously to pregnant rats at doses up to 3 mg/kg/day (about 2.5 times the maximum recommended clinical intravenous dose) or pregnant rabbits at doses up to 12 mg/kg/day, although an increased resorption rate was apparent at both 8 mg/kg/day and 12 mg/kg/day (intravenous) in the latter species. There are no adequate and well-controlled studies in pregnant women. Milrinone-should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Nursing Mothers

Caution should be exercised when milrinone is administered to nursing women, since it is not known whether it is excreted in human milk.

Pediatric Use

Safety and effectiveness in pediatric patients have not been established.

Geriatric Use

There are no special dosage recommendations for the elderly patient. Ninety percent of all patients administered milrinone in clinical studies were within the age range of 45 to 70 years, with a mean age of 61 years. Patients in all age groups demonstrated clinically and statistically significant responses. No age-related effects on the incidence of adverse reactions have been observed. Controlled pharmacokinetic studies have not disclosed any age-related effects on the distribution and elimination of milrinone.

ADVERSE REACTIONS

Cardiovascular Effects

In patients receiving milrinone in Phase II and III clinical trials, ventricular arrhythmias were reported in 12.1%: Ventricular ectopic activity, 8.5%; nonsustained ventricular tachycardia, 2.8%; sustained ventricular tachycardia, 1% and ventricular fibrillation, 0.2% (2 patients experienced more than one type of arrhythmia). Holter recordings demonstrated that in some patients injection of milrinone increased ventricular ectopy, including nonsustained ventricular tachycardia. Life-threatening arrhythmias were infrequent and when present have been associated with certain underlying factors such as preexisting arrhythmias, metabolic abnormalities (e.g. hypokalemia), abnormal digoxin levels and catheter insertion. Milrinone was not shown to be arrhythmogenic in an electrophysiology study. Supraventricular arrhythmias were reported in 3.8% of the patients receiving milrinone. The incidence of both supraventricular and ventricular arrhythmias has not been related to the dose or plasma milrinone concentration.

Other cardiovascular adverse reactions include hypotension, 2.9% and angina/chest pain, 1.2%.

In the post marketing experience, there have been rare cases of "torsades depointes" reported.

CNS Effects

Headaches, usually mild to moderate in severity, have been reported in 2.9% of patients receiving milrinone.

Other Effects

Other adverse reactions reported, but not definitely related to the administration of milrinone include hypokalemia, 0.6%; tremor, 0.4%; and thrombocytopenia, 0.4%.

Isolated spontaneous reports of bronchospasm and anaphylactic shock have been received; and in the post-marketing experience, liver function test abnormalities and skin reactions such as rash have been reported.

OVERDOSAGE

Doses of milrinone may produce hypotension because of its vasodilator effect. If this occurs, administration of milrinone should be reduced or temporarily discontinued until the patient's condition stabilizes. No specific antidote is known, but general measures for circulatory support should be taken.

DOSAGE AND ADMINISTRATION

CAUTION: DO NOT ADMIX WITH OTHER DRUGS.

MUST NOT BE USED IN SERIES CONNECTIONS.

Milrinone Lactate in 5% Dextrose Injection should not be used for administering a loading dose. The information regarding loading doses for milrinone shown below is for informational purposes only.

A loading dose of milrinone lactate injection (1 mg [base]/mL) should be administered followed by a continuous infusion (maintenance dose) according to the following guidelines:

LOADING DOSE

50 mcg/kg: Administer slowly over 10 minutes

The table below shows the loading dose in milliliters (mL) of milrinone (1 mg/mL) by patient body weight (kg).

Loading Dose (mL) Using 1 mg/mL Concentration

Patient Body Weight (kg)
kg	30	40	50	60	70	80	90	100	110	120
mL	1.5	2.0	2.5	3.0	3.5	4.0	4.5	5.0	5.5	6.0

The loading dose may be given undiluted, but diluting to a rounded total volume of 10 or 20 mL (see Maintenance Dose for diluents) may simplify the visualization of the injection rate.

MAINTENANCE DOSE

	Infusion Rate	Total Daily Dose (24 Hours)
Minimum	0.375 mcg/kg/min	0.59 mg/kg	Administer as a continuous intravenous infusion.
Standard	0.50 mcg/kg/min	0.77 mg/kg
Maximum	0.75 mcg/kg/min	1.13 mg/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." 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.

The maintenance dose in mL/hr by patient body weight (kg) may be determined by reference to the following table.

Milrinone Infusion Rate (mL/hr) Using 200 mcg/mL Concentration

Maintenance Dose	Patient Body Weight (kg)
(mcg/kg/min)	30	40	50	60	70	80	90	100	110	120
0.375	3.4	4.5	5.6	6.8	7.9	9.0	10.1	11.3	12.4	13.5
0.400	3.6	4.8	6.0	7.2	8.4	9.6	10.8	12.0	13.2	14.4
0.500	4.5	6.0	7.5	9.0	10.5	12.0	13.5	15.0	16.5	18.0
0.600	5.4	7.2	9.0	10.8	12.6	14.4	16.2	18.0	19.8	21.6
0.700	6.3	8.4	10.5	12.6	14.7	16.8	18.9	21.0	23.1	25.2
0.750	6.8	9.0	11.3	13.5	15.8	18.0	20.3	22.5	24.8	27.0

When administering milrinone by continuous infusion, it is advisable to use a calibrated electronic infusion device.

Dosage Adjustment in Renally Impaired Patients

Data obtained from patients with severe renal impairment (creatinine clearance = 0 to 30 mL/min) but without congestive heart failure have demonstrated that the presence of renal impairment significantly increases the terminal elimination half-life of milrinone. Reductions in infusion rate may be necessary in patients with renal impairment. For patients with clinical evidence of renal impairment, the recommended infusion rate can be obtained from the following table:

Creatinine Clearance (mL/min/1.73 m2)	Infusion Rate (mcg/kg/min)
5	0.20
10	0.23
20	0.28
30	0.33
40	0.38
50	0.43

The PAB® plastic container system contains milrinone equivalent to 200 mcg/mL milrinone in 5% Dextrose Injection.

Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. Do not use if cloudy or precipitated or if the seals are not intact.

If administration is controlled by a pumping device, care must be taken to discontinue pumping action before the container runs dry or air embolism may result.

Use sterile equipment. It is recommended that the intravenous administration apparatus be replaced at least once every 24 hours.

Directions for Use of PAB® Plastic Container System

CAUTION: DO NOT ADMIX WITH OTHER DRUGS.

MUST NOT BE USED IN SERIES CONNECTIONS.

For intravenous infusion only.

Store the individual container in the storage carton until ready to use.

Aseptic technique is required.

1. Caution – Before use, perform the following checks:

   (a)

   Read the label. Ensure solution is the one ordered and is within the expiration date.

   (b)

   Inspect the solution in good light for cloudiness, haze or particulate matter; check the container for leakage or damage. Any container which is suspect should not be used.

Check for minute leaks by squeezing solution container firmly. Use only if solution is clear and container and seals are intact.

Single dose plastic container. Discard unused portion.

Consult Package Insert for complete product information.

2.

Caution – IV admixtures containing this solution and other drugs should be avoided. Additives should not be introduced into this solution. If used with a primary intravenous fluid system, the primary solution should be discontinued during milrinone infusion.

3.

To Attach Administration Set
Remove the set port closure. Hold the container below the set port and grasp cap between thumb and forefinger, then roll cap upward (see Figure A). Push the spike into and through the diaphragm of the port (see Figure B). Continue with Directions for Use for the administration set. Suspend the container using the hole in the lower flap.

 

HOW SUPPLIED

Milrinone Lactate 20 mg (base)/100 mL (200 mcg (0.2 mg)[base]/mL) in 5% Dextrose Injection is supplied sterile and nonpyrogenic in 100 mL fill PAB® plastic containers packaged 4 per carton, 6 cartons per case (24 per case).

NDC	Cat. No.	Size
0264-3000-32	D6083-52	100 mL

Exposure of pharmaceutical products to heat should be minimized. Avoid excessive heat. Protect from freezing. It is recommended that the product be stored at room temperature 25°C (77°F); however, brief exposure up to 40°C (104°F) does not adversely affect the product.

Store the individual container in the storage carton until ready to use.