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.
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 infusion: IV: 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 infusion: IV: 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 (SSC [Evans 2021]; SSC [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; SSC [Evans 2021]; SSC [Rhodes 2017]). In general, maintain goal mean arterial pressure (MAP) (eg, ~65 mm Hg); consider use if patient is in shock or has hypoperfusion during or after fluid resuscitation (SSC [Dellinger 2013]; SSC [Levy 2018]; SSC [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 infusion: IV: 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 (AHA/ACC/HFSA [Heidenreich 2022]).
Continuous infusion: IV: 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 (AHA/ACC/HFSA [Heidenreich 2022]; Hollenberg 2011).
(For additional information see "Dopamine: Pediatric drug information")
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]; manufacturer's labeling). Note: Dopamine has a dose-dependent effect; doses at lower end of this range are preferred, as inotropic actions predominate at lower doses and vasoconstrictive actions predominate at higher doses (ACCM/SCCM [Davis 2017]; PALS [Kleinman 2010]).
Refer to adult dosing.
The recommendations for dosing in patients with obesity are based upon the best available evidence and clinical expertise. Senior Editorial Team: Jeffrey F. Barletta, PharmD, FCCM; Manjunath P. Pai, PharmD, FCP; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC.
Class 1, 2, and 3 obesity (BMI ≥30 kg/m2):
Continuous infusion: IV: Use ideal body weight for initial dose calculations, then titrate to hemodynamic effect and clinical response (Erstad 2021; expert opinion). During therapy, clinicians should not change dosing weight from one weight metric to another (ie, ideal body weight to/from actual body weight) (Erstad 2021; expert opinion). Refer to adult dosing for indication specific doses.
Rationale for recommendations:
There is a paucity of studies evaluating the influence of obesity on dopamine dosing or pharmacokinetics. One observational study evaluating patients with obesity and overall mortality showed a trend in lower dopamine doses at 6 hours with increasing obesity (Arabi 2013). Other observational studies, including phenylephrine, epinephrine and norepinephrine, suggest non–weight-based dosing strategies may result in lower overall cumulative dose requirements and increased drug exposure to second line agents in some patients and may not be advantageous in time to achieving hemodynamic stability (Adams 2017; Radosevich 2016; Vadiei 2017). However, it is difficult to show outcome differences between weight-based and non–weight-based dosing because of dose titration to target BP, particularly in the context of retrospective studies. Furthermore, there is substantial variability in response in critically ill patients, irrespective of weight. Due to the short onset of action and small volume of distribution, rapid titration to clinical effect after initial dosing is possible (Erstad 2021).
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)
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)
Parenteral: Continuous IV infusion: Vials (concentrated solution) must be diluted prior to administration; premixed IV solutions (800 mcg/mL, 1,600 mcg/mL, 3,200 mcg/mL) are available. 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 minimize the possibility of extravasation (central line administration); administration into an umbilical arterial catheter is not recommended (Domonoske 2017). If central line is not available, may administer for a short duration through a peripheral IV catheter placed in a large vein or via intraosseous access using a more dilute solution or with a second carrier fluid; once central access is available, begin central line infusion and wait for pharmacologic effect prior to stopping peripheral administration (AAP [Shenoi 2020]; ACCM/SCCM [Davis 2017]; SCCM/ESICM [Weiss 2020]). Frequent monitoring of the IV catheter site is recommended to rapidly identify extravasation (Reynolds 2014). Refer to institutional policies and procedures; catheter placement/size and vasopressor concentration may vary depending on institution. Do not administer sodium bicarbonate (or any alkaline solution) through an IV line containing dopamine; inactivation of dopamine may occur (AAP [Shenoi 2020]). Avoid abrupt discontinuation; reduce infusion flow rate slowly.
Rate of infusion (mL/hour) = [dose (mcg/kg/minute) × weight (kg) × 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; Reynolds 2014).
Note: Premixed solutions available.
IV infusion: 400 mg in 250 mL (concentration: 1600 mcg/mL) or 800 mg in 250 mL (concentration: 3200 mcg/mL) of D5W or NS
Note: Premixed solutions available.
IV infusion: 800 mcg/mL, 1,600 mcg/mL, or 3,200 mcg/mL.
Hypotension or shock: Treatment of severe hypotension or shock (eg, septic shock and other vasodilatory shock states, cardiogenic shock, decompensated heart failure, post–cardiac arrest) that persists during and after adequate fluid volume replacement.
Bradycardia or atrioventricular block, symptomatic (unresponsive to atropine)
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 are derived from product labeling unless otherwise specified.
Postmarketing:
Cardiovascular: Angina pectoris, atrial fibrillation, bradycardia, cardiac conduction disorder, ectopic beats, hypertension, hypotension, palpitations, tachycardia, vasoconstriction, ventricular arrhythmia, widened QRS complex on ECG
Dermatologic: Peripheral gangrene (with prolonged or high dose, can occur with low doses with concomitant occlusive vascular disease), piloerection
Gastrointestinal: Nausea, vomiting
Genitourinary: Azotemia
Nervous system: Anxiety, headache
Respiratory: Dyspnea
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.
Substrate of COMT, OCT1, OCT2
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
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 (Systemic): 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
Ergot Derivatives (Vasoconstrictive CYP3A4 Substrates): May enhance the vasoconstricting effect of Alpha-/Beta-Agonists. Risk X: Avoid combination
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
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]).
It is not known if dopamine is present in breast milk.
Note: General monitoring parameters are below; individualize monitoring and consult institutional policies and procedures.
BP, heart rate, ECG; hemodynamic parameters as appropriate (eg, CVP, RAP, CI, PCWP, SVR, ScvO2 or SvO2); end-organ perfusion (eg, urine output, mental status); infusion site for blanching/extravasation; intravascular volume status.
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 kidney 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): $0.06
1.6 mg/mL 5% (per mL): $0.06 - $0.07
3.2 mg/mL 5% (per mL): $0.09
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