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 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.
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)
Mechanism of Action
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
Renal, hepatic, plasma; 75% to inactive metabolites by monoamine oxidase and 25% to norepinephrine (active)
Urine (as metabolites)
Clearance: Neonates: Varies and appears to be age related; prolonged clearance with combined hepatic and renal impairment
Onset of Action
Adults: Within 5 minutes
Duration of Action
Adults: <10 minutes
Use: Labeled Indications
Hemodynamic support: Adjunct in the treatment of shock (eg, MI, open heart surgery, renal failure, cardiac decompensation) that persists after adequate fluid volume replacement when indicated
Cardiogenic shock: To maintain systemic perfusion and preserve end-organ performance in patients with cardiogenic shock. Vasopressor therapy is indicated in patients with hemodynamic instability (eg, systolic blood pressure <90 mm Hg or evidence of end organ hypoperfusion) or the following etiologies of cardiogenic shock: Right ventricular failure, aortic regurgitation, mitral regurgitation, ventricular septal defect after MI, or bradycardia. Note: Norepinephrine is preferred over dopamine for most of these etiologies of cardiogenic shock due to lower likelihood for causing arrhythmias. However, in the case of shock due to bradycardia or aortic regurgitation, then dopamine is preferred (ACCF/AHA [Yancy 2013], AHA [van Diepen 2017]).
Inotropic support in advanced heart failure: Bridge therapy in stage D HF unresponsive to guideline-directed medical therapy and device therapy in patients awaiting heart transplant or mechanical circulatory support; short-term management of hospitalized patients with severe systolic dysfunction presenting with low blood pressure and significantly depressed cardiac output; long-term management (palliative therapy) in select patients with stage D heart failure unresponsive to guideline-directed medical therapy and device therapy who are not candidates for heart transplant or mechanical circulatory support (ACCF/AHA [Yancy 2013]).
Sepsis and septic shock: Suggested for use as an alternative vasopressor to norepinephrine only in highly selected patients (eg, patients with low risk of tachyarrhythmias and absolute or relative bradycardia) (SCCM [Rhodes 2017]).
Use: Off Label
Heart block unresponsive to atropine or pacing; Symptomatic bradycardia
Hypersensitivity to sulfites (commercial preparation contains sodium bisulfite); pheochromocytoma; uncorrected tachyarrhythmias; ventricular fibrillation
Dosage and Administration
Hemodynamic support: IV infusion:
Dosage range: 2 to 20 mcg/kg/minute; titrate to desired response (maximum: 50 mcg/kg/minute; however, doses >20 mcg/kg/minute may not have a beneficial effect on blood pressure and may increase the risk of tachyarrhythmias); infusion may be gradually increased by 5 to 10 mcg/kg/minute increments until optimal response is obtained
Cardiogenic shock (off-label dose): IV: 0.5 to 20 mcg/kg/minute (AHA [van Diepen 2017])
Inotropic support in advanced heart failure: IV infusion: 5 to 15 mcg/kg/minute; lower doses are preferred (ACCF/AHA [Yancy 2013]).
ACLS guideline recommendations (to treat hypotension especially if associated with symptomatic bradycardia in the immediate post-cardiac arrest care setting) (off-label use): Initial: 5 to 10 mcg/kg/minute; titrate to effect (AHA [Peberdy 2010])
Note: If dosages >20 to 30 mcg/kg/minute are needed, a more direct-acting vasopressor may be more beneficial (ie, epinephrine, norepinephrine).
Hemodynamic effects of dopamine are dose dependent (however, this is relative and there is overlap of clinical effects between dosing ranges):
Low-dose: 1 to 5 mcg/kg/minute, results in increased renal blood flow and urine output. Note: The use of low-dose dopamine to prevent or treat acute kidney injury is not recommended (KDIGO 2012).
Intermediate-dose: 5 to 10 mcg/kg/minute, results in increased renal blood flow, heart rate, cardiac contractility, and cardiac output
High-dose: >10 mcg/kg/minute, alpha-adrenergic effects begin to predominate, resulting in vasoconstriction, increased blood pressure, in addition to increased heart rate, cardiac contractility, and cardiac output due to beta-adrenergic effects.
Refer to adult dosing.
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
IV: Administer as a continuous infusion with the use of an infusion pump. Administer into large vein to prevent the possibility of extravasation (central line administration); 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). Vials (concentrated solution) must be diluted prior to use.
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)
Protect from light. Solutions that are darker than slightly yellow should not be used.
Alpha1-Blockers: May diminish the vasoconstricting effect of Alpha-/Beta-Agonists. Similarly, Alpha-/Beta-Agonists may antagonize Alpha1-Blocker vasodilation. Monitor therapy
AtoMOXetine: May enhance the hypertensive effect of Sympathomimetics. AtoMOXetine may enhance the tachycardic effect of Sympathomimetics. 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. Consider therapy modification
Bretylium: May enhance the therapeutic effect of Alpha-/Beta-Agonists (Direct-Acting). Monitor therapy
Cannabinoid-Containing Products: May enhance the tachycardic effect of Sympathomimetics. Exceptions: Cannabidiol. Monitor therapy
Chloroprocaine: May enhance the hypertensive effect of Alpha-/Beta-Agonists. Monitor therapy
CloZAPine: May diminish the therapeutic effect of Alpha-/Beta-Agonists. 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. Consider therapy modification
COMT Inhibitors: May decrease the metabolism of COMT Substrates. Monitor therapy
Doxofylline: Sympathomimetics may enhance the adverse/toxic effect of Doxofylline. Monitor therapy
Erdafitinib: May increase the serum concentration of OCT2 Substrates. Monitor therapy
Ergot Derivatives: May enhance the hypertensive effect of Alpha-/Beta-Agonists. Ergot Derivatives may enhance the vasoconstricting effect of Alpha-/Beta-Agonists. Exceptions: Ergoloid Mesylates; Nicergoline. Avoid combination
Guanethidine: May enhance the arrhythmogenic effect of Sympathomimetics. Guanethidine may enhance the hypertensive effect of Sympathomimetics. 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. Consider therapy modification
Inhalational Anesthetics: May enhance the arrhythmogenic effect of DOPamine. Management: Avoid use of dopamine in patients receiving halogenated hydrocarbon anesthetics. If concomitant treatment cannot be avoided, monitor for arrhythmia. Dopamine induced ventricular arrhythmia may be reversible with propranolol based on animal data. 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. Consider therapy modification
Lurasidone: DOPamine may enhance the hypotensive effect of Lurasidone. 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. Consider therapy modification
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. Consider therapy modification
Solriamfetol: DOPamine may enhance the hypertensive effect of Solriamfetol. Monitor therapy
Spironolactone: May diminish the vasoconstricting effect of Alpha-/Beta-Agonists. Monitor therapy
Sympathomimetics: May enhance the adverse/toxic effect of other Sympathomimetics. 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. Consider therapy modification
Tedizolid: May enhance the hypertensive effect of Sympathomimetics. Tedizolid may enhance the tachycardic effect of Sympathomimetics. 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. Consider therapy modification
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
Ophthalmic: Increased intraocular pressure, mydriasis
Miscellaneous: Tissue necrosis
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.
- 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.
- 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]).
Blood pressure, ECG, heart rate, CVP, RAP, MAP; serum glucose, renal function; urine output; if pulmonary artery catheter is in place, monitor CI, PCWP, SVR, and PVR
Consult individual institutional policies and procedures.
Pregnancy Risk Factor
Adverse events have been observed in some animal reproduction studies. It is not known if dopamine crosses the placenta. Medications used for the treatment of cardiac arrest in pregnancy are the same as in the non-pregnant woman. Appropriate medications should not be withheld due to concerns of fetal teratogenicity. Dopamine use during the post-resuscitation 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 (Jeejeebhoy [AHA] 2015).
What is this drug used for?
- It is used to treat heart failure (weak heart).
- It is used to treat low blood pressure.
- It may be given to you for other reasons. Talk with the doctor.
Frequently reported side effects of this drug
- Goose bumps
Other side effects of this drug: Talk with your doctor right away if you have any of these signs of:
- Fluid and electrolyte problems like mood changes, confusion, muscle pain or weakness, abnormal heartbeat, severe dizziness, passing out, fast heartbeat, increased thirst, seizures, loss of strength and energy, lack of appetite, unable to pass urine or change in amount of urine passed, dry mouth, dry eyes, or nausea or vomiting.
- Shortness of breath
- Chest pain
- Slow heartbeat
- Fast heartbeat
- Abnormal heartbeat
- Severe dizziness
- Passing out
- Severe headache
- Vision changes
- Cool extremities
- Pale extremities
- Skin discoloration
- Unable to pass urine
- Change in amount of urine passed
- Severe injection site redness, burning, pain, edema, or irritation
- Signs of a significant reaction like wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat.
Note: This is not a comprehensive list of all side effects. Talk to your doctor if you have questions.
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