To prevent sloughing and necrosis in ischemic areas, the area should be infiltrated as soon as possible with 10 to 15 mL of sodium chloride 0.9% injection containing phentolamine 5 to 10 mg, an adrenergic blocking agent. Pediatric dosage of phentolamine should be 0.1 to 0.2 mg/kg up to a maximum of 10 mg per dose. 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.
Hemodynamic support: Continuous IV infusion: 2 to 20 mcg/kg/minute; titrate gradually by 5- to 10-mcg/kg/minute increments until optimal response is obtained
The hemodynamic effects of dopamine are dose-dependent:
Low dosage: 1 to 5 mcg/kg/minute, increased renal blood flow and urine output
Intermediate dosage: 5 to 15 mcg/kg/minute, increased renal blood flow, heart rate, cardiac contractility, cardiac output, and blood pressure
High dosage: >15 mcg/kg/minute, alpha-adrenergic effects begin to predominate, vasoconstriction, increased blood pressure
Hemodynamic support: Infants, Children, and Adolescents: Continuous IV or intraosseous infusion: 2 to 20 mcg/kg/minute, titrate gradually by 5- to 10-mcg/kg/minute increments until optimal response is obtained (PALS [Kleinman 2010])
The hemodynamic effects of dopamine are dose-dependent:
Low dosage: 1 to 5 mcg/kg/minute, increased renal blood flow and urine output
Intermediate dosage: 5 to 15 mcg/kg/minute, increased renal blood flow, heart rate, cardiac contractility, cardiac output, and blood pressure
High dosage: >15 mcg/kg/minute, alpha-adrenergic effects begin to predominate, vasoconstriction, increased blood pressure
(For additional information see "Dopamine: Drug information")
Note: Hemodynamic effects of dopamine are dose dependent (however, this is relative and there is overlap of clinical effects between dosing ranges) (Hollenberg 2011; Rhodes 2017; Russell 2021).
Low dose: Augments renal dopamine receptors, which may increase renal blood flow and urine output. The use of low-dose dopamine to prevent or treat acute kidney injury is not recommended.
Intermediate dose: Dopamine and beta-adrenergic effects predominate, resulting in increased renal blood flow, heart rate, cardiac contractility, and cardiac output.
High dose: Alpha-adrenergic effects begin to predominate, resulting in vasoconstriction and increased blood pressure, in addition to increased heart rate, cardiac contractility, and cardiac output due to beta-adrenergic effects.
Bradycardia or atrioventricular block, symptomatic (unresponsive to atropine) (off-label use):
Continuous IV infusion: Initial: 5 mcg/kg/minute; increase by 5 mcg/kg/minute every 2 minutes until desired effect; maximum dose: 20 mcg/kg/minute (ACC [Kusumoto 2019]; AHA [Panchal 2020]; AHA/CPR 2020).
Hypotension or shock:
Cardiogenic shock (alternative agent):
Note: Typically, not the preferred initial agent in cardiogenic shock; consider other inotropic and/or vasopressor options; caution with the use of dopamine due to increased arrhythmias and possibly mortality in this population (AHA [van Diepen 2017]; De Backer 2010). Optimal goal of therapy not well established, but typically titrate to maintain end-organ perfusion (AHA [van Diepen 2017]).
Continuous IV infusion: Usual dosage range: 0.5 to 20 mcg/kg/minute; titrate based on clinical end point (eg, end-organ perfusion) (AHA [van Diepen 2017]).
Septic shock and other vasodilatory shock states (alternative agent):
Note: Not recommended for septic shock except as an alternative to norepinephrine in patients with bradycardia who have a low risk of tachyarrhythmias (SCCM [Evans 2021]; SCCM [Rhodes 2017]). Compared to norepinephrine, dopamine is associated with an increased risk of tachyarrhythmias and potentially worse outcomes (eg, increased mortality, kidney failure) (Avni 2015; De Backer 2012; SCCM [Evans 2021]; SCCM [Rhodes 2017]). In general, maintain goal mean arterial pressure (MAP) (eg, ~65 mm Hg); consider use if patient is hypotensive or has elevated lactate (eg, ≥4 mmol/L) during or after fluid resuscitation (Levy 2018; SCCM [Dellinger 2013]; SCCM [Rhodes 2017]).
Continuous infusion: IV: Initial: 2 to 5 mcg/kg/minute; titrate to goal MAP up to a dose of 20 mcg/kg/minute (De Backer 2010; Manaker 2021).
Post–cardiac arrest shock (alternative agent):
Note: Typically, not the preferred initial agent in post–cardiac arrest shock due to risk of tachyarrhythmias; consider other inotropic and/or vasopressor options (De Backer 2010; Russell 2021). Optimal goal of therapy is not well established, but typically titrate to MAP >65 mm Hg and preferably >80 mm Hg to optimize cerebral and end-organ perfusion (AHA [Callaway 2015]; Russell 2021).
Continuous IV infusion: Usual dosage range: 5 to 20 mcg/kg/minute; titrate based on clinical end points (eg, MAP, end-organ perfusion) (AHA [Peberdy 2010]; manufacturer's labeling).
Inotropic support:
Note: May consider in patients with severe systolic dysfunction with decreased end-organ perfusion (ACCF/AHA [Yancy 2013]).
Continuous IV infusion: 5 to 15 mcg/kg/minute; doses at lower end of this range are preferred as inotropic actions predominate at lower doses and vasoconstrictive actions predominate at higher doses (ACCF/AHA [Yancy 2013]; Hollenberg 2011).
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Solution, Intravenous, as hydrochloride:
Generic: 0.8 mg/mL (250 mL, 500 mL); 1.6 mg/mL (250 mL, 500 mL); 3.2 mg/mL (250 mL); 40 mg/mL (5 mL, 10 mL); 80 mg/mL (5 mL [DSC]); 160 mg/mL (5 mL [DSC])
Solution, Intravenous, as hydrochloride [preservative free]:
Generic: 40 mg/mL (5 mL, 10 mL)
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous:
Generic: 0.8-5 MG/ML-% (250 mL); 1.6-5 MG/ML-% (250 mL, 500 mL); 3.2-5 MG/ML-% (250 mL, 500 mL)
Parenteral: Administer as a continuous IV infusion with the use of an infusion pump or an intraosseous infusion until IV access can be obtained in pediatric patients (PALS [Kleinman 2010]). Administer into large vein to prevent the possibility of extravasation (central-line administration); administration into an umbilical arterial catheter is not recommended. Some experts recommend that low-dose dopamine infusion may be administered peripherally while trying to establish central access; once central access is available, begin central line infusion and wait for pharmacologic effect prior to stopping peripheral administration (Brierley 2009; Dellinger 2013). Monitor continuously for free flow; use infusion device to control rate of flow; when discontinuing the infusion, gradually decrease the dose of dopamine (sudden discontinuation may cause hypotension).
Rate of infusion (mL/hour) = dose (mcg/kg/minute) x weight (kg) x 60 minutes/hour divided by concentration (mcg/mL)
Vesicant; ensure proper needle or catheter placement prior to and during infusion; avoid extravasation. If extravasation occurs, stop infusion immediately and disconnect (leave cannula/needle in place); gently aspirate extravasated solution (do NOT flush the line); remove needle/cannula; elevate extremity. Initiate phentolamine (or alternative) antidote (see Management of Drug Extravasations for more details). Apply dry warm compresses (Hurst 2004).
IV: Administer as a continuous infusion via an infusion pump. Central line administration is preferred; extravasation may cause severe ischemic necrosis. If central line is not available, may administer for a short duration (<72 hours) through a peripheral IV catheter placed in a large vein at a proximal site (eg, in or proximal to antecubital fossa). Frequent monitoring of the IV catheter site is recommended to rapidly identify extravasation (Cardenas-Garcia 2015; Evans 2021; Lewis 2019; Medlej 2018; Tian 2020). Refer to institutional policies and procedures; catheter placement/size and vasopressor concentration may vary depending on institution.
Vesicant; ensure proper needle or catheter placement prior to and during infusion; avoid extravasation.
Extravasation management: If extravasation occurs, stop infusion immediately and disconnect (leave cannula/needle in place); gently aspirate extravasated solution (do NOT flush the line); remove needle/cannula; elevate extremity. Initiate phentolamine (or alternative) antidote. Apply dry warm compresses (Hurst 2004; Reynolds 2014).
Phentolamine: Dilute 5 to 10 mg in 10 to 20 mL NS and administer into extravasation site as soon as possible after extravasation; may readminister if patient remains symptomatic (Reynolds 2014)
Alternatives to phentolamine:
Nitroglycerin topical 2% ointment (based on limited data): Apply a 1-inch strip to the site of ischemia; may repeat every 8 hours as necessary (Reynolds 2014).
Terbutaline (based on limited case reports): Infiltrate extravasation area using a solution of terbutaline 1 mg diluted in 10 mL NS (large extravasation site; administration volume varied from 3 to 10 mL) or 1 mg diluted in 1 mL NS (small/distal extravasation site; administration volume varied from 0.5 to 1 mL) (Reynolds 2014; Stier 1999)
Note: Premixed solutions available.
IV infusion: 1600 mcg/mL or 3200 mcg/mL
Note: Premixed solutions available.
IV infusion: 1600 mcg/mL or 3200 mcg/mL
Store vials at 20°C to 25°C (68°F to 77°F) and premixed single-use containers at 20°C to 25°C (68°F to 77°F). Protect from light. Avoid excessive heat; brief exposure of premixed single-use containers of up to 40°C (104°F) does not adversely affect the product. Protect from freezing. Dopamine has been found to be stable for a minimum of 24 hours after dilution in a compatible solution. Avoid contact or simultaneous administration with alkalies (including sodium bicarbonate), oxidizing agents, or iron salts.
Increase cardiac output, blood pressure, and urine flow as an adjunct in the treatment of shock or hypotension which persists after adequate fluid volume replacement (FDA approved in all ages); has also been used in low dosage to increase renal perfusion
DOPamine may be confused with DOBUTamine, Dopram
The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drugs which have a heightened risk of causing significant patient harm when used in error.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Frequency not defined.
Cardiovascular: Angina pectoris, atrial fibrillation, bradycardia, ectopic beats, hypertension, hypotension, palpitations, tachycardia, vasoconstriction, ventricular arrhythmia, ventricular conduction, widened QRS complex on ECG
Central nervous system: Anxiety, headache
Dermatologic: Gangrene (high dose), piloerection
Endocrine & metabolic: Increased serum glucose (usually not above normal limits)
Gastrointestinal: Nausea, vomiting
Genitourinary: Azotemia
Ophthalmic: Increased intraocular pressure, mydriasis
Renal: Polyuria
Respiratory: Dyspnea
Miscellaneous: Tissue necrosis
Hypersensitivity to sulfites (commercial preparation contains sodium bisulfite); pheochromocytoma; uncorrected tachyarrhythmias; ventricular fibrillation
Concerns related to adverse effects:
• Arrhythmias: May cause increases in heart rate, increasing the risk of tachycardia and other tachyarrhythmias including ventricular arrhythmias (Tisdale 1995). In heart transplant candidates, institute appropriate measures to protect patient against risks of sudden cardiac death (Young 2000).
• Extravasation: Vesicant; ensure proper needle or catheter placement prior to and during infusion. Avoid extravasation; infuse into a large vein if possible. Avoid infusion into leg veins. Watch IV site closely. [US Boxed Warning]: If extravasation occurs, infiltrate the area with diluted phentolamine (5 to 10 mg in 10 to 15 mL of saline) with a fine hypodermic needle. Phentolamine should be administered as soon as possible after extravasation is noted to prevent sloughing/necrosis.
Disease-related concerns:
• Cardiovascular disease: Use with caution in patients with cardiovascular disease, cardiac arrhythmias and/or occlusive vascular disease.
• Active myocardial ischemia/post-myocardial infarction: Use with caution in patients with active myocardial ischemia or recent myocardial infarction; may increase myocardial oxygen consumption.
• Electrolyte imbalance: Correct electrolyte disturbances, especially hypokalemia or hypomagnesemia, prior to use and throughout therapy to minimize the risk of arrhythmias (ACC/AHA/ESC [Zipes 2006]; Tisdale 1995).
• Shock: The use of dopamine in adult patients with shock (majority of patients had septic shock) demonstrated a higher incidence of adverse events (eg, tachyarrhythmias) (De Backer 2010). Higher 28-day mortality was also seen in patients with septic shock with the use of dopamine as compared to norepinephrine (De Backer 2012; Vasu 2012).
Concurrent drug therapy issues:
• Monoamine oxidase inhibitors (MAO-I): Use with extreme caution in patients taking MAO inhibitors; prolong hypertension may result from concurrent use.
Dosage form specific issues:
• Sodium metabisulfite: Product may contain sodium metabisulfite.
Other warnings/precautions:
• Appropriate use: Assure adequate circulatory volume to minimize need for vasoconstrictors when used in hemodynamic support. Avoid hypertension; monitor blood pressure closely and adjust infusion rate.
• Long-term therapy: According to the ACCF/AHA 2013 heart failure guidelines, long-term use of intravenous inotropic therapy without a specific indication or for reasons other than palliation is potentially harmful (ACCF/AHA [Yancy 2013]).
Substrate of COMT, OCT2
Alpha1-Blockers: May diminish the vasoconstricting effect of Alpha-/Beta-Agonists. Similarly, Alpha-/Beta-Agonists may antagonize Alpha1-Blocker vasodilation. Risk C: Monitor therapy
Atomoxetine: May enhance the hypertensive effect of Sympathomimetics. Atomoxetine may enhance the tachycardic effect of Sympathomimetics. Risk C: Monitor therapy
Benzylpenicilloyl Polylysine: Alpha-/Beta-Agonists may diminish the diagnostic effect of Benzylpenicilloyl Polylysine. Management: Consider use of a histamine skin test as a positive control to assess a patient's ability to mount a wheal and flare response. Risk D: Consider therapy modification
Bretylium: May enhance the therapeutic effect of Alpha-/Beta-Agonists (Direct-Acting). Risk C: Monitor therapy
Bromocriptine: May enhance the hypertensive effect of Alpha-/Beta-Agonists. Management: Consider alternatives to this combination when possible. If combined, monitor for hypertension and tachycardia, and do not coadminister these agents for more than 10 days. Risk D: Consider therapy modification
Cannabinoid-Containing Products: May enhance the tachycardic effect of Sympathomimetics. Risk C: Monitor therapy
Chloroprocaine: May enhance the hypertensive effect of Alpha-/Beta-Agonists. Risk C: Monitor therapy
CloZAPine: May diminish the therapeutic effect of Alpha-/Beta-Agonists. Risk C: Monitor therapy
Cocaine (Topical): May enhance the hypertensive effect of Sympathomimetics. Management: Consider alternatives to use of this combination when possible. Monitor closely for substantially increased blood pressure or heart rate and for any evidence of myocardial ischemia with concurrent use. Risk D: Consider therapy modification
COMT Inhibitors: May increase the serum concentration of COMT Substrates. Risk C: Monitor therapy
Doxofylline: Sympathomimetics may enhance the adverse/toxic effect of Doxofylline. Risk C: Monitor therapy
Erdafitinib: May increase the serum concentration of OCT2 Substrates. Risk C: Monitor therapy
Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): May enhance the vasoconstricting effect of Alpha-/Beta-Agonists. Risk X: Avoid combination
Fexinidazole: May increase the serum concentration of OCT2 Substrates. Management: Avoid use of fexinidazole with OCT2 substrates when possible. If combined, monitor for increased OCT2 substrate toxicities. Risk D: Consider therapy modification
Guanethidine: May enhance the arrhythmogenic effect of Sympathomimetics. Guanethidine may enhance the hypertensive effect of Sympathomimetics. Risk C: Monitor therapy
Hyaluronidase: May enhance the adverse/toxic effect of DOPamine. Management: Avoid the use of hyaluronidase to enhance dispersion or absorption of dopamine. Use of hyaluronidase for other purposes in patients receiving dopamine may be considered as clinically indicated. Risk D: Consider therapy modification
Inhalational Anesthetics: May enhance the arrhythmogenic effect of DOPamine. Risk C: Monitor therapy
Kratom: May enhance the adverse/toxic effect of Sympathomimetics. Risk X: Avoid combination
Linezolid: May enhance the hypertensive effect of Sympathomimetics. Management: Reduce initial doses of sympathomimetic agents, and closely monitor for enhanced pressor response, in patients receiving linezolid. Specific dose adjustment recommendations are not presently available. Risk D: Consider therapy modification
Lisuride: May enhance the hypertensive effect of Alpha-/Beta-Agonists. Risk X: Avoid combination
Monoamine Oxidase Inhibitors: May enhance the hypertensive effect of DOPamine. Management: Initiate dopamine at no greater than one-tenth (1/10) of the usual dose in patients who are taking (or have taken within the last 2 to 3 weeks) monoamine oxidase inhibitors. Monitor for an exaggerated hypertensive response to dopamine. Risk D: Consider therapy modification
Ozanimod: May enhance the hypertensive effect of Sympathomimetics. Risk C: Monitor therapy
Pergolide: May enhance the hypertensive effect of Alpha-/Beta-Agonists. Risk C: Monitor therapy
Serotonin/Norepinephrine Reuptake Inhibitors: May enhance the tachycardic effect of Alpha-/Beta-Agonists. Serotonin/Norepinephrine Reuptake Inhibitors may enhance the vasopressor effect of Alpha-/Beta-Agonists. Management: If possible, avoid coadministration of direct-acting alpha-/beta-agonists and serotonin/norepinephrine reuptake inhibitors. If coadministered, monitor for increased sympathomimetic effects (eg, increased blood pressure, chest pain, headache). Risk D: Consider therapy modification
Solriamfetol: Sympathomimetics may enhance the hypertensive effect of Solriamfetol. Sympathomimetics may enhance the tachycardic effect of Solriamfetol. Risk C: Monitor therapy
Spironolactone: May diminish the vasoconstricting effect of Alpha-/Beta-Agonists. Risk C: Monitor therapy
Sympathomimetics: May enhance the adverse/toxic effect of other Sympathomimetics. Risk C: Monitor therapy
Tafenoquine: May increase the serum concentration of OCT2 Substrates. Management: Avoid use of OCT2 substrates with tafenoquine, and if the combination cannot be avoided, monitor closely for evidence of toxicity of the OCT2 substrate and consider a reduced dose of the OCT2 substrate according to that substrate's labeling. Risk D: Consider therapy modification
Tedizolid: May enhance the hypertensive effect of Sympathomimetics. Tedizolid may enhance the tachycardic effect of Sympathomimetics. Risk C: Monitor therapy
Tricyclic Antidepressants: May enhance the vasopressor effect of Alpha-/Beta-Agonists. Management: Avoid, if possible, the use of alpha-/beta-agonists in patients receiving tricyclic antidepressants. If combined, monitor for evidence of increased pressor effects and consider reductions in initial dosages of the alpha-/beta-agonist. Risk D: Consider therapy modification
Vasopressin: Alpha-/Beta-Agonists (Direct-Acting) may enhance the hypertensive effect of Vasopressin. The effect of other hemodynamic parameters may also be enhanced. Risk C: Monitor therapy
Medications required for the treatment of critically ill pregnant patients should not be withheld due to concerns of fetal teratogenicity (ACOG 2019; AHA [Jeejeebhoy 2015]). Medications used for the treatment of cardiac arrest in pregnancy are the same as in the nonpregnant patients. Dopamine use during the postresuscitation phase may be considered; however, the effects of vasoactive medications on the fetus should also be considered. Doses and indications should follow current Advanced Cardiovascular Life Support guidelines (AHA [Jeejeebhoy 2015]).
Blood pressure, ECG, heart rate, CVP, MAP, urine output; if pulmonary artery catheter is in place, monitor Cl, PWCP, SVR, RAP, and PVR; monitor for skin color and temperature changes
Stimulates both adrenergic and dopaminergic receptors, lower doses are mainly dopaminergic stimulating and produce renal and mesenteric vasodilation, higher doses also are both dopaminergic and beta1-adrenergic stimulating and produce cardiac stimulation and renal vasodilation; large doses stimulate alpha-adrenergic receptors
Note: Children: Dopamine has exhibited nonlinear kinetics in children; with dose changes, may not achieve steady-state for ~1 hour rather than 20 minutes
Onset of action: Adults: Within 5 minutes
Duration: Adults: <10 minutes
Metabolism: Renal, hepatic, plasma; 75% to inactive metabolites by monoamine oxidase and 25% to norepinephrine (active)
Half-life elimination: ~2 minutes
Excretion: Urine (as metabolites)
Clearance: Neonates: Varies and appears to be age related; clearance is more prolonged with combined hepatic and renal dysfunction
Solution (DOPamine HCl Intravenous)
40 mg/mL (per mL): $0.70 - $0.71
Solution (DOPamine in D5W Intravenous)
0.8 mg/mL 5% (per mL): $0.05
1.6 mg/mL 5% (per mL): $0.06
3.2 mg/mL 5% (per mL): $0.09
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