Drug class: Selective beta-1-Adrenergic Agonists
VA class: AU100
CAS number: 62-31-7

Medically reviewed by Drugs.com on Feb 21, 2024. Written by ASHP.

Introduction

Dopamine, an endogenous catecholamine that is the immediate precursor of norepinephrine, is a sympathomimetic agent with prominent dopaminergic and β₁-adrenergic effects at low to moderate doses and α-adrenergic effects at high doses.

Uses for DOPamine

Shock

Used as adjunctive therapy to correct hemodynamic imbalances (e.g., increase cardiac output and BP) in the treatment of shock.

Pressor therapy is not a substitute for replacement of blood, plasma, fluids, and/or electrolytes. Correct blood volume depletion as fully as possible before administration.

The Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock recommend norepinephrine as the vasopressor of choice in adults with septic shock; although dopamine was used widely in the past, more recent evidence indicates that the drug is associated with a greater risk of adverse effects (e.g., arrhythmias) and possibly also an increased risk of death compared with norepinephrine. In these guidelines, dopamine is considered an alternative to norepinephrine only in highly selected patients with septic shock (e.g., those with low risk of tachyarrhythmias and bradycardia).

Also used to provide vasopressor support in other types of shock (e.g., cardiogenic, hemorrhagic), generally as a temporary measure until underlying cause can be treated.

Some evidence suggests that dopamine may be associated with increased risk of mortality compared with norepinephrine in patients with cardiogenic shock. Early revascularization is standard of care in patients with cardiogenic shock; individualize use of vasopressors in this setting.

Some experts state dopamine may be considered for treatment of drug-induced hypovolemic shock when patient is unresponsive to fluid volume expansion and inotropic and/or vasopressor support is required.

May increase cardiac output, BP, and urine flow in shock; however, exact effects are dose related and based on patient's clinical status at time of administration. In low or intermediate doses, usually does not produce sufficient peripheral vasoconstriction to increase BP. If hypotension persists, a more potent vasoconstrictor such as norepinephrine may be required.

Appears to be most effective when therapy is begun shortly after the signs and symptoms of shock appear and before physiologic parameters such as BP and myocardial function undergo severe deterioration and before urine flow has decreased to <0.3 mL/minute.

Advanced Cardiovascular Life Support

Used in ACLS^{† [off-label]} for treatment of symptomatic bradycardia in adults, particularly if associated with hypotension; although not a first-line drug, may be considered in patients who are unresponsive to atropine, or as a temporizing measure while awaiting a pacemaker.

Also used during resuscitation for management of patients in cardiac arrest. Principal goal of pharmacologic therapy during cardiac arrest is to facilitate the return of spontaneous circulation (ROSC), and epinephrine is the drug of choice for this use. Vasoactive drugs such as dopamine may be used for hemodynamic support following resuscitation.

Acute Renal Failure

Low-dose (“renal dose,” e.g., <5 mcg/kg per minute) therapy does not appear to prevent or ameliorate acute (e.g., oliguric) renal failure in critically ill patients despite some evidence of increased renal and mesenteric perfusion from selective dopaminergic effects. Currently available data do not support any benefit from such therapy, and routine use of low-dose (“renal dose”) dopamine therapy for prevention or amelioration of acute renal failure in critically ill patients not recommended.

In addition, low-dose dopamine infusions are not without risk and may be associated with adverse effects (e.g., suppression of respiratory drive, increased cardiac output and myocardial oxygen consumption, arrhythmias, hypokalemia, hypophosphatemia, gut ischemia, disruption of metabolic and immunologic homeostasis).

Heart Failure

May be used for inotropic support in patients with refractory heart failure^{† [off-label]}. Because parenteral inotropes can be potentially harmful (e.g., increased risk of arrhythmias) in patients with heart failure, some experts recommend that such use be reserved for patients with severe systolic dysfunction who have low cardiac index and evidence of systemic hypoperfusion and/or congestion, or for palliative therapy in those with end-stage heart failure. To minimize risk of adverse effects, use lowest possible dosage and evaluate regularly for need for continued inotropic therapy.

Low-dose dopamine infusion has been used in combination with loop diuretics to augment diuresis and improve renal blood flow in patients with acute decompensated heart failure^{† [off-label]}; however, current evidence does not support routine use of dopamine for this purpose.

DOPamine Dosage and Administration

Administration

Administer by IV infusion.

Also has been administered by intraosseous infusion^{† [off-label]} during ACLS.

IV Infusion

For solution and drug compatibility information, see Compatibility under Stability.

Infuse IV into a large vein, preferably the antecubital vein, using an infusion pump or other apparatus to control the rate of flow and avoid inadvertent administration of a bolus dose.

Use less suitable veins (e.g., hand or ankle vein) only when required, but switch to a preferred vein as soon as possible.

Continuously monitor infusion site for free flow.

Avoid extravasation. (See Boxed Warning and also see Extravasation under Cautions.)

A controlled-infusion device, preferably a volumetric pump, should be used; do not administer via an ordinary, gravity-controlled IV administration set.

Dopamine in 5% dextrose in flexible containers (e.g., LifeCare) should not be used in series connections.

Consult manufacturer's labeling for proper methods of administration and other associated precautions.

Dilution

Must dilute the commercially available injection concentrate for IV infusion prior to administration; alternatively, may use commercially available prediluted solutions of dopamine hydrochloride in 5% dextrose.

Individualize concentration according to patient dosage and fluid requirements. Consult manufacturer's prescribing information for suggested dilutions.

Rate of Administration

Avoid bolus administration.

Rate of IV infusion varies according to individual dose requirements. (See Dosage under Dosage and Administration.)

Dosage

Individualize and carefully adjust dosage to achieve the desired hemodynamic and renal response as indicated by heart rate, BP, urine flow, and, whenever possible, measurement of central venous or pulmonary wedge pressure and cardiac output. Once optimal hemodynamic effects have been achieved, use lowest possible dosage to maintain these effects.

When discontinuing therapy, it may be necessary to gradually decrease the dose while expanding blood volume with IV fluids to prevent a recurrence of hypotension. Sudden discontinuance can precipitate marked hypotension. (See Hypotension under Cautions.) In patients who have been receiving moderate to high doses, some clinicians recommend that the final dosage should not be less than 5 mcg/kg per minute in order to avoid hypotension.

Pediatric Patients

Shock

IV

Studies have not been conducted to specifically inform dosage recommendations in pediatric patients; however, clinical experience indicates that dosing in pediatric patients is generally similar to that in adults.

ACLS† [off-label]

IV or Intraosseous†

Usual infusion rate for postresuscitation stabilization is 2–20 mcg/kg per minute. Although dosages >5 mcg/kg per minute stimulate the cardiac β-adrenergic receptors, this effect may be reduced in infants. Infusion rates >20 mcg/kg per minute may result in excessive vasoconstriction.

Adults

Shock

IV

Usually, initiate at a rate of 2–5 mcg/kg per minute; may increase by 1–4 mcg/kg per minute at 10- to 30-minute intervals until the optimal response is attained. In more severely ill patients, initiate at 5 mcg/kg per minute, and gradually increase in increments of 5–10 mcg/kg per minute up to 20–50 mcg/kg per minute as needed.

In patients with occlusive vascular disease, some experts recommend initial rate of ≤1 mcg/kg per minute because of risk of local ischemia (e.g., gangrene). Monitor closely for any signs or symptoms of compromised circulation; if this occurs, decrease rate or discontinue infusion.

If MAO inhibitors were used within the previous 2–3 weeks, initiate dopamine at no greater than 10% of the usual dose. (See MAO Inhibitors under Cautions.)

Titrate dosage to achieve desired hemodynamic effects. Most patients can be maintained at <20 mcg/kg per minute; however, infusion rates >50 mcg/kg per minute have been used safely in advanced states of circulatory decompensation.

ACLS†

IV

Usual initial dosage range for symptomatic bradycardia is 2–10 mcg/kg per minute; titrate according to patient response. Infusion rates >10 mcg/kg per minute are associated with vasoconstrictive effects.

For postresuscitation stabilization, dosage of 5–10 mcg/kg per minute has been recommended.

Heart Failure†

IV

Some clinicians recommend initial rate of 0.5–2 mcg/kg per minute in patients with severe, refractory heart failure. Usual dosage range is 5–10 mcg/kg per minute.

To minimize risk of adverse effects, use lowest possible dosage and evaluate patient regularly for the need for continued inotropic therapy.

Special Populations

Hepatic Impairment

No specific dosage recommendations.

Renal Impairment

No specific dosage recommendations.

Geriatric Patients

Initial dosage usually should be at the low end of the range.

Cautions for DOPamine

Contraindications

• Pheochromocytoma.

• Uncorrected tachyarrhythmias or VF.

Warnings/Precautions

Warnings

MAO Inhibitors

Metabolized by MAO; therefore, inhibition of this enzyme prolongs duration of dopamine effects. Patients recently (within 2–3 weeks) treated with MAO inhibitors will require substantially reduced dopamine dosage. (See Dosage under Dosage and Administration.)

Alkalinizing Substances

Inactivated in alkaline solutions; do not administer with any alkaline diluent solution (e.g., sodium bicarbonate).

Sensitivity Reactions

Sulfites

Some formulations contain sulfites, which may cause allergic-type reactions (including anaphylaxis and life-threatening or less severe asthmatic episodes) in certain susceptible individuals.

General Precautions

Monitoring

Monitor BP and urine flow and, when possible, cardiac output and pulmonary wedge pressure. (See Hypovolemia and also Hypoxia, Hypercapnia, and Acidosis under Cautions.) Decrease rate or temporarily interrupt infusion if excessive vasoconstriction, decreased urine output, increased heart rate, or an arrhythmia occurs and observe the patient closely.

Extravasation

Extravasation may cause tissue necrosis and sloughing of surrounding tissues; avoid extravasation. Infuse IV into a large vein. (See Boxed Warning.)

Continuously monitor infusion site for free flow.

Hypovolemia

Pressor therapy is not a substitute for replacement of blood, plasma, fluids, and/or electrolytes. Correct blood volume depletion as fully as possible before dopamine therapy is instituted.

May be used in an emergency as an adjunct to fluid replacement or as a temporary supportive measure to maintain coronary and cerebral artery perfusion until volume replacement can be completed, but dopamine must not be used as sole therapy in hypovolemic patients.

Monitor central venous pressure or left ventricular filling pressure; in addition, monitor central venous or pulmonary arterial diastolic pressure to avoid overloading the cardiovascular system, diluting serum electrolyte concentrations, and precipitating congestive heart failure or pulmonary edema.

Hypoxia, Hypercapnia, and Acidosis

Must be identified and corrected prior to, or concurrently with, dopamine administration. Can reduce the effectiveness and/or increase the toxicity of dopamine.

Vasoconstriction

At high rates of infusion, vasoconstrictive effects of dopamine may cause compromised limb circulation and reversal of renal dilation and natriuresis.

If a disproportionate increase in diastolic pressure occurs, decrease rate of infusion and observe the patient carefully for further evidence of predominant vasoconstrictor activity, unless such an effect is desired.

Hypotension

If hypotension occurs, infusion rate should be increased rapidly in order to increase BP. If hypotension persists, discontinue dopamine and administer a drug with greater vasoconstricting properties (e.g., norepinephrine).

Occlusive Vascular Disease

Carefully monitor patients with a history of occlusive vascular disease (e.g., atherosclerosis, arterial embolism, Raynaud’s disease, cold injury, diabetic endarteritis, or Buerger’s disease) for decreased circulation to the extremities indicated by changes in color or temperature of the skin or pain in the extremities.

Correct by decreasing the rate of infusion or discontinuing dopamine; however, these changes occasionally have persisted and progressed after discontinuing the drug.

Some clinicians recommend IV administration of 5–10 mg of phentolamine mesylate if discoloration of the extremities occurs.

Weigh potential benefits of continuing dopamine against possible risk of necrosis.

Ventricular Arrhythmias

Ventricular arrhythmias may occur; monitor patient and reduce dosage if increased number of ectopic beats observed.

Specific Populations

Pregnancy

Category C.

No adequate and well-controlled studies in pregnant women; use during pregnancy only when potential benefits justify potential risks to fetus.

When used in ACLS, may decrease blood flow to uterus; however, the woman must be resuscitated for survival of the fetus.

If a vasopressor (e.g., dopamine) is used during labor in conjunction with oxytocic drugs, the vasopressor effect may be potentiated and result in severe hypertension. (See Specific Drugs and Laboratory Tests under Interactions.)

Lactation

Not known whether dopamine is distributed into human milk. Caution if used in nursing women.

Pediatric Use

Manufacturer states safety and efficacy of IV dopamine not established in children; however, the drug has been used in pediatric patients of all age groups from neonate onward.

Except for vasoconstrictive effects caused by inadvertent infusion of dopamine into the umbilical artery, adverse effects unique to the pediatric population have not been identified, nor have adverse effects identified in adults been found to be more common in pediatric patients.

Has been administered at rates as high as 125 mcg/kg per minute in some neonates, but the usual dosage in children has been similar to that in adults on a mcg/kg per minute basis.

In pediatric patients, dopamine is recommended as an appropriate drug for the treatment of shock that is unresponsive to fluids when systemic vascular resistance is low.

Geriatric Use

Insufficient experience in patients ≥65 years of age to determine whether geriatric patients respond differently than younger adults.

No differences in responses between geriatric and younger patients have been identified.

Initial usual dosage should be at the low end of the dosage range, and caution should be exercised since renal, hepatic, and cardiovascular dysfunction and concomitant disease or other drug therapy are more common in this age group than in younger adults.

Common Adverse Effects

Dopamine may cause cardiac conduction abnormalities (e.g., ventricular arrhythmia, atrial fibrillation, widened QRS complex, ectopic heartbeats), tachycardia, angina, palpitation, bradycardia, vasoconstriction, hypotension, hypertension, dyspnea, nausea, vomiting, headache, anxiety, azotemia, piloerection, and gangrene of the extremities.

Drug Interactions

Specific Drugs and Laboratory Tests

DOPamine Pharmacokinetics

Absorption

Bioavailability

Rapidly metabolized in the GI tract after oral administration.

Onset

Within 5 minutes following IV administration.

Duration

<10 minutes.

Distribution

Extent

Widely distributed but does not cross the blood-brain barrier to a substantial extent.

Apparent volume of distribution in neonates ranges from 0.6–4 L/kg.

Not known whether dopamine crosses the placenta or is distributed into milk.

Elimination

Metabolism

Via the liver, kidneys, and plasma by MAO and catechol-O-methyltransferase (COMT) to the inactive compounds homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid.

In patients receiving MAO inhibitors, the duration of action of dopamine may be as long as 1 hour.

About 25% of a dose of dopamine is metabolized to norepinephrine within the adrenergic nerve terminals.

Elimination Route

In urine principally as HVA and its sulfate and glucuronide conjugates and as 3,4-dihydroxyphenylacetic acid; a very small fraction of a dose is excreted unchanged.

Half-life

Plasma half-life: About 2 minutes.

Special Populations

Neonates: Elimination half-life of 5–11 minutes.

Critically ill infants and children: Clearance reportedly ranges from 48–168 mL/kg per minute, with the higher values reported in the younger patients.

Stability

Storage

Parenteral

Injection Concentrate for IV Infusion

20–25°C.

Injection for IV Infusion

20–25°C. Do not freeze.

Compatibility

Parenteral

Incompatible with sodium bicarbonate and other alkaline solutions.

Avoid contact with oxidizing agents and iron salts.

Solution CompatibilityHID

Stable for at least 24 hours in dextrose 5%, dextrose 5% in sodium chloride 0.9%, dextrose 5% in sodium chloride 0.45%, dextrose 5% in lactated Ringer’s injection, lactated Ringer's, 0.9% sodium chloride, and sodium lactate (1/6)M.

Drug Compatibility

Additives should not be introduced into the infusion container (e.g., LifeCare ) of commercially available premixed solutions for IV infusion.

Actions

• Stimulates adrenergic receptors of the sympathetic nervous system.

• Principally a direct stimulatory effect on β₁-adrenergic receptors.

• Acts on specific dopaminergic receptors in the renal, mesenteric, coronary, and intracerebral vascular beds to cause vasodilation.

• Little or no effect on β₂-adrenergic receptors.

• Main effects depend on the dose administered.

• In low doses (0.5–2 mcg/kg per minute), acts predominantly on dopaminergic receptors causing vasodilation in renal, mesenteric, coronary, and intracerebral vascular beds. Renal vasodilation results in increased renal blood flow, urine flow, and GFR.

• At intermediate doses (2–10 mcg/kg per minute), stimulates β₁-adrenergic receptors, resulting in improved myocardial contractility; blood flow to peripheral vascular beds may decrease while mesenteric blood flow is increased because of increased cardiac output.

• At doses of 10–20 mcg/kg per minute, α-adrenergic receptors are stimulated with consequent vasoconstrictor effects and an increase in BP.

• At doses >20 mcg/kg per minute, α-adrenergic effects become more prominent compromising peripheral circulation and overriding the drug's dopaminergic effects; renal vasoconstriction may decrease previously augmented renal blood flow and urine output.

Advice to Patients

• Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.

• Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.

• Importance of informing patients of other important precautionary information. (See Cautions.)

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

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