SandboxAlonso

{{DrugProjectFormSinglePage |authorTag=Alonso Alvarado, M.D. [1] |genericName=Dopamine |aOrAn=a |drugClass=Adrenergic receptor agonist |indicationType=treatment |indication=hemodynamic imbalances present in the shock syndrome due to myocardial infarctions, trauma, endotoxic septicemia, open heart surgery, renal failure, and chronic cardiac decompensation as in congestive heart failure |hasBlackBoxWarning=Yes |adverseReactions=chest pain, hypertension, palpitations, tachyarrhythmia, injection site reaction, piloerection, nausea, vomiting, headache, mydriasis, anxiety, oliguria, dyspnea |blackBoxWarningTitle=IMPORTANT |blackBoxWarningBody=Antidote for Peripheral Ischemia: To prevent sloughing and necrosis in ischemic areas, the area should be infiltrated as soon as possible with 10 to 15 mL of saline solution containing 5 to 10 mg of phentolamine, an adrenergic blocking agent. A syringe with a fine hypodermic needle should be used, and the solution liberally infiltrated throughout the ischemic area. Sympathetic blockade with phentolamine causes immediate and conspicuous local hyperemic changes if the area is infiltrated within 12 hours. Therefore, phentolamine should be given as soon as possible after the extravasation is noted. |fdaLIADAdult======Condition 1=====

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|contraindications=* Patients with pheochromocytoma.

• Uncorrected tachyarrhythmias or ventricular fibrillation.

|warnings=* Do no add dopamine to any alkaline diluent solution, since the drug is inactivated in alkaline solution.

• Patients who have been treated with monoamine oxidase (MAO) inhibitors prior to the administration of dopamine will require substantially reduced dosage. * Contains sodium metabisulfite, a sulfite that may cause allergic-type reactions including anaphylactic symptoms and life-threatening or less severe asthmatic episodes in certain susceptible people. The overall prevalence of sulfite sensitivity in the general population is unknown, and probably low. Sulfite sensitivity is seen more frequently in asthmatic than in nonasthmatic people.

Precautions

• Careful monitoring required: Close monitoring of the following indices-urine flow, cardiac outputand blood pressure during dopamine infusion is necessary as in the case of any adrenergic agent.
• Avoid hypovolemia: Prior to treatment with dopamine, hypovolemia should be fully corrected, if possible with either whole blood or plasma as indicated. Monitoring of central venous pressure of left ventricular filling pressure may be helpful in detecting and treating hypovolemia.
• Hypoxia, Hypercapnia, Acidosis: These conditions which may also reduce the effectiveness and/or increase the incidence of adverse effects of dopamine, must be identified and corrected prior to, or concurrently with administration of dopamine HCl.
• Ventricular Arrhythmias: If an increased number of ectopic beats are observed, the dose should be reduced if possible.
• Decreased Pulse Pressure: If a disproportionate rise in the diastolic pressure (i.e., a marked decrease in the pulse pressure) is observed in patients receiving dopamine, the infusion rate should be decreased and the patient observed carefully for further evidence of predominant vasoconstrictor activity, unless such an effect is desired.
• Hypotension: At lower infusion rates, if hypotension occurs, the infusion rate should be rapidly increased until adequate blood pressure is obtained. If hypotension persists, dopamine HCl should be discontinued and a more potent vasoconstrictor agent such as norepinephrine should be administered.
• Extravasation: Dopamine should be infused into a large vein whenever possible to prevent the possibility of extravasation into tissue adjacent to the infusion site. Extravasation may cause necrosis and sloughing of surrounding tissue. Large veins of the actecubital fossa are preferred to veins in the dorsum of the hand or ankle. Less suitable infusion sites should be used only if the patient’s condition requires immediate attention. The physician should switch to more suitable sites as rapidly as possible. The infusion site should be continuously monitored for free flow.
• Occlusive vascular disease: Patients with a history of occlusive vascular disease (for example, atheroscierosis, arterial embolism, and Raynaud’s disease, cold injury, diabetic endarteritis, and Buergers disease) should be closely monitored for any changes in color or temperature of the skin in the extremities. If a change in skin color or temperature occurs and is thought to be the result of compromised circulation to the extremities, the benefits of continued dopamine infusion should be weighed against the risk of possible necrosis. This condition may be reversed by either decreasing or discontinuing the rate of infusion.

Weaning: When discontinuing the infusion, it may be necessary to gradually decrease the dose of dopamine HCl while expanding blood volume with IV fluids, since sudden cessation may result in marked hypotension. |clinicalTrials=======Central Nervous System======

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|postmarketing=(Description) |drugInteractions=* Cyclopropane or halogenated hydrocarbon anesthetics increase cardiac autonomic irritability and may sensitize the myocardium to the action of certain intravenously administered catecholamines, such as dopamine. The interaction appears to be related both to pressor activity and to the beta adrenergic stimulating properties of these catecholamines, and may produce ventricular arrhythmias. Therefore, extreme caution should be exercised when administering dopamine HCl to patients receiving cyclopropane or halogenated hydrocarbon anesthetics. Results of studies in animals indicate that dopamine induced ventricular arrhythmias during anesthesia can be reversed by propranolol.

• Because dopamine is metabolized by monoamine oxidase (MAO), inhibition of this enzyme prolongs and potentiates the effect of dopamine. Patients who have been treated with MAO inhibitors within two to three weeks prior to the administration of dopamine should receive initial doses of dopamine HCl not greater than one-tenth (1/10) of the usual dose.
• Concurrent administration of low-dose dopamine HCl and diuretic agents may produce an additive or potentiating effect on urine flow.
• Tricyclic antidepressants may potentiate the cardiovascular effects of adrenergic agents.
• Cardiac effects of dopamine are antagonized by beta-blocking agents, such as propranolol and metroprolol. The peripheral vasoconstriction caused by high doses of dopamine HCl is antagonized by alpha-blocking agents. Dopamine-induced renal and mesenteric vasodilation is not antagonized by either alpha- or beta-adrenergic blocking agents.
• Butyrophenones (such as haloperidol) and phenothiazines can suppress the dopaminergic renal and mesenteric vasodilation induced with low-dose dopamine infusion.
• The concomitant use of vasopressors, vasoconstricting agents (such as ergonovine) and some oxytocic drugs may result in severe hypertension.
• Administration of phenytoin to patients receiving dopamine HCl has been reported to lead to hypotension and bradycardia. It is suggested that in patients receiving dopamine HCl, alternatives to phenytoin should be considered if anticonvulsant therapy is needed.

|FDAPregCat=C |useInPregnancyFDA=Teratogenicity studies in rats and rabbits at dopamine hydrochloride dosages up to 6 mg/kg/day intravenously during organogenesis produced no detectable teratogenic or embryotoxic effects, although maternal toxicity consisting of mortalities, decrease body weight gain, and pharmacotoxic signs were observed in rats. In a published study, dopamine hydrochloride administered at 10 mg/kg subcutaneously for 30 days, markedly prolonged metestrus and increased mean pituitary and ovary weights in female rats. Similar administration to pregnant rats throughout gestation or for 5 days starting on gestation day 10 or 15 resulted in decreased body weight gains, increased mortalities and slight increases in cataract formation among the offspring. There are no adequate and well-controlled studies in pregnant women, and it is not known if dopamine hydrochloride crosses the placental barrier. Dopamine hydrochloride should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. |useInLaborDelivery=In obstetrics, if vasopressor drugs are used to correct hypotension or are added to a local anesthetic solution the interaction with some oxytocic drugs may cause severe hypertension. |useInNursing=It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when dopamine is administered to a nursing mother. |useInPed=Safety and effectiveness in children have not been established. Dopamine HCl has been used in a limited number of pediatric patients, but such use has been inadequate to fully define proper dosage and limitations for use. Peripheral gangrene has been reported in neonates and children. |administration=Intravenous |monitoring=Close monitoring of the following indices-urine flow, cardiac output and blood pressure during dopamine infusion is necessary as in the case of any adrenergic agent. |IVCompat======Cardiovascular System=====

• Ventricular arrhythmia (at very high doses)
• Ectopic beats
• Tachycardia
• Anginal pain
• Palpitation
• Cardiac conduction abnormalities
• Widened QRS complex
• Bradycardia
• Hypotension
• Hypertension
• Vasoconstriction

Respiratory System

• Dyspnea

Gastrointestinal System

• Nausea
• Vomiting

Metabolic/Nutritional System

• Azotemia

Central Nervous System

• Headache
• Anxiety

Dermatological System

• Piloerection

Other

• Gangrene of the extremities has occurred when moderate to high doses were administered for prolonged periods or in patients with occlusive vascular disease receiving low doses of dopamine HCl.
• A few cases of peripheral cyanosis have been reported.

|overdose=In case of accidental overdosage, as evidenced by excessive blood pressure elevation, reduce rate of administration or temporarily discontinue dopamine until patient’s condition stabilizes. Since the duration of action of dopamine is quite short, no additional remedial measures are usually necessary. If these measures fail to stabilize the patient’s condition, use of the short-acting alpha-blocking agent, phentolamine, should be considered. |drugBox={{Drugbox2

For other uses, see SandboxAlonso (disambiguation).

Dopamine

Clinical data
Synonyms	2-(3,4-Dihydroxyphenyl)ethylamine; 3,4-Dihydroxyphenethylamine; 3-hydroxytyramine; DA; Intropin; Revivan; Oxytyramine
[[Regulation of therapeutic goods |Template:Engvar data]]	US FDA: Dopamine
Routes of administration	Intravenous Injection
ATC code	C01CA04 (WHO)
Legal status
Legal status	In general: ℞ (Prescription only)
Pharmacokinetic data
Metabolism	ALDH, DBH, MAO-A, MAO-B, COMT
Excretion	Renal
Identifiers
IUPAC name 4-(2-Aminoethyl)benzene-1,2-diol
CAS Number	51-61-6 Y 62-31-7 (hydrochloride)
PubChem CID	681
IUPHAR/BPS	940
DrugBank	DB00988 Y
ChemSpider	661 Y
UNII	VTD58H1Z2X
KEGG	D07870 Y
ChEBI	CHEBI:18243 Y
ChEMBL	ChEMBL59 Y
E number	{{#property:P628}}
ECHA InfoCard	{{#property:P2566}}
Chemical and physical data
Formula	C8H11NO2
Molar mass	153.18 g/mol
3D model (JSmol)	Interactive image
Density	1.26 g/cm3
Melting point	128 °C (262.4 °F)
Boiling point	decomposes
SMILES c1cc(c(cc1CCN)O)O
InChI InChI=1S/C8H11NO2/c9-4-3-6-1-2-7(10)8(11)5-6/h1-2,5,10-11H,3-4,9H2 Y Key:VYFYYTLLBUKUHU-UHFFFAOYSA-N Y
(verify)

|mechAction=Dopamine is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). It is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system, especially in the nigrostriatal tract, and in a few peripheral sympathetic nerves.

Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings. |structure=Dopamine hydrochloride injection is a clear, practically colorless, aqueous, additive solution for intravenous infusion after dilution. Each mL contains either 40 mg, 80 mg, or 160 mg dopamine HCl, USP (equivalent to 32.3 mg, 64.6 mg and 129.2 mg dopamine base respectively) in Water for Injection, USP, containing 9 mg sodium metabisulfite as an antioxidant. The pH range (2.5 to 5.0) may be adjusted with citric acid and/or sodium citrate. The solution is sterile and nonpyrogenic. Dopamine HCl, a naturally occurring catecholamine, is an inotropic vasopressor agent. Its chemical name is 3,4 dihydroxyphenethylamine hydrochloride and its chemical structure is:

This image of the FDA label is provided by the National Library of Medicine.

Dopamine HCl is sensitive to alkalis, iron salts and oxidizing agents. dopamine must be diluted in an appropriate, sterile parenteral solution before intravenous administration. |PD=The predominant effects of dopamine are dose-related, although actual response of an individual patient will largely depend on the clinical status of the patient at the time the drug is administered. At low rates of infusion (0.5-2 mcg/kg/min) dopamine causes vasodilation that is presumed to be due to a specific agonist action on dopamine receptors (distinct from alpha and beta adrenoceptors) in the renal, mesenteric, coronary, and intracerebral vascular beds. At these dopamine receptors, haloperidol is an antagonist. The vasodilation in these vascular beds is accompanied by increased glomerular filtration rate, renal blood flow, sodium excretion, and urine flow. Hypotension sometimes occurs. An increase in urinary output produced by dopamine is usually not associated with a decrease in osmolarity of the urine.

At intermediate rates of infusion (2-10 mcg/kg/min) dopamine acts to stimulate the beta1- adrenoceptors, resulting in improved myocardial contractility, increased SA rate and enhanced impulse conduction in the heart. There is little, if any, stimulation of the beta2-adrenoceptors (peripheral vasodilation). Dopamine causes less increase in myocardial oxygen consumption than isoproterenol, and its use is not usually associated with a tachyarrhythmia. Clinical studies indicate that it usually increases systolic pressure and pulse pressure with either no effect or a slight increase in diastolic pressure. Blood flow to the peripheral vascular beds may decrease while mesenteric flow increases due to increased cardiac output. At low and intermediate doses, total peripheral resistance (which would be raised by alpha activity) is usually unchanged.

At higher rates of infusion (10-20 mcg/kg/min) there is some effect on alpha-adrenoceptors, with consequent vasoconstrictor effects and a rise in blood pressure. The vasoconstrictor effects are first seen in the skeletal muscle vascular beds, but with increasing doses they are also evident in the renal and mesenteric vessels. At very high rates of infusion (above 20 mcg/kg/min), stimulation of alpha-adrenoceptors predominates and vasoconstriction may compromise the circulation of the limbs and override the dopaminergic effects of dopamine, reversing renal dilation and natriuresis. |PK=Dopamine’s onset of action occurs within five minutes of intravenous administration, and with dopamine’s plasma half-life of about two minutes, the duration of action is less than ten minutes. If monoamine oxidase (MAO) inhibitors are present, however, the duration may increase to one hour. The drug is widely distributed in the body but does not cross the blood-brain barrier to a significant extent. Dopamine is metabolized in the liver, kidney, and plasma by MAO and catechol-O-methyltransferase to the inactive compounds homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid. About 25% of the dose is taken up into specialized neurosecretory vesicles (the adrenergic nerve terminals), where it is hydroxylated to form norepinephrine. It has been reported that about 80% of the drug is excreted in the urine within 24 hours, primarily as HVA and its sulfate and glucuronide conjugates and as 3,4-dihydroxyphenylacetic acid. A very small portion is excreted unchanged. |nonClinToxic=Long-term animal studies have not been performed to evaluate carcinogenic potential of dopamine hydrochloride.

Dopamine hydrochloride at doses approaching maximal solubility shows no clear genotoxic potential in the Ames test. Although there was a reproducible dose-dependent increase in the number of revertant colonies with strains TA100 and TA98, both with and without metabolic activation, the small increase was considered inconclusive evidence of mutagenicity. In the L5178Y TK+/− mouse lymphoma assay, dopamine hydrochloride at the highest concentrations used of 750 mcg/mL without metabolic activation, and 3000 mcg/mL with activation, was toxic and associated with increases in mutant frequencies when compared to untreated and solvent controls; at the lower concentrations no increases over controls were noted.

No clear evidence of clastogenic potential was reported in the in vivo mouse or male rat bone marrow micronucleus test when the animals were treated intravenously with up to 224 mg/kg and 30 mg/kg of dopamine hydrochloride, respectively. |clinicalStudies======Poor Perfusion of Vital Organs=====

Clinical studies have shown that when dopamine is administered before urine flow has diminished to levels approximating 0.3 mL/minute, prognosis is more favorable. Nevertheless, in a number of oliguric or anuric patients, administration of dopamine resulted in an increase in urine flow which in some cases reached normal levels. Dopamine may also increase urine flow in patients whose output is within normal limits and thus may be of value in reducing the degree of preexisting fluid accumulation. It should be noted that at doses above those optimal for the individual patient urine flow may decrease, necessitating reduction of dosage. Concurrent administration of dopamine and diuretic agents may produce an additive or potentiating effect. |howSupplied=* Packages of 25 vials: 200 mg/5 mL Vial (40 mg/mL) (NDC 0517-1805-25) (color-coded WHITE)

• Packages of 25 vials: 400 mg/5 mL Vial (80 mg/mL) (NDC 0517-1905-25)(color-coded GREEN)
• Packages of 25 vials: 800 mg/5 mL Vial (160 mg/mL) (NDC 0517-1305-25) (color-coded YELLOW)

|storage=* Store at 20° to 25°C (68° to 77°F); excursions permitted to 15° to 30°C (59° to 86°F).

• Avoid contact with alkalis (including sodium bicarbonate), oxidizing agents or iron salts.

|fdaPatientInfo=There is limited information regarding Patient Counseling Information of aminocaproic acid in the drug label. |alcohol=Alcohol-SandboxAlonso interaction has not been established. Talk to your doctor about the effects of taking alcohol with this medication. |brandNames=* Intropin |lookAlike=* Dopamine - Dobutamine |nlmPatientInfo=(Link to patient information page) |drugShortage=Drug Shortage }} {{#subobject:

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