Note: Hemodynamic effects of dopamine are dose dependent (however, this is relative and there is overlap of clinical effects between dosing ranges) (Ref).
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 (Ref).
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 (Ref). Optimal goal of therapy not well established, but typically titrate to maintain end-organ perfusion (Ref).
Continuous infusion: IV: Usual dosage range: 0.5 to 20 mcg/kg/minute; titrate based on clinical end point (eg, end-organ perfusion) (Ref).
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 (Ref). Compared to norepinephrine, dopamine is associated with an increased risk of tachyarrhythmias and potentially worse outcomes (eg, increased mortality, kidney failure) (Ref). 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 (Ref).
Continuous infusion: IV: Initial: 2 to 5 mcg/kg/minute; titrate to goal MAP up to a dose of 20 mcg/kg/minute (Ref).
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 (Ref). 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 (Ref).
Continuous infusion: IV: Usual dosage range: 5 to 20 mcg/kg/minute; titrate based on clinical end points (eg, MAP, end-organ perfusion) (Ref).
Note: May consider in patients with severe systolic dysfunction with decreased end-organ perfusion (Ref).
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 (Ref).
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 (Ref). During therapy, clinicians should not change dosing weight from one weight metric to another (ie, ideal body weight to/from actual body weight) (Ref). 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 (Ref). 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 (Ref). 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 (Ref).
Refer to adult dosing.
(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 (Ref). 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 (Ref).
The following adverse drug reactions are derived from product labeling unless otherwise specified.
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
Nervous system: Anxiety, headache
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. If extravasation occurs, infiltrate the area with diluted phentolamine (5 to 10 mg in 10 mL of saline) with a fine hypodermic needle. Phentolamine should be administered as soon as possible after extravasation is noted to prevent sloughing/necrosis (Stefanos 2023).
• 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).
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.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
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)
Solution, Intravenous, as hydrochloride [preservative free]:
Generic: 40 mg/mL (5 mL, 10 mL)
Solution (DOPamine HCl Intravenous)
40 mg/mL (per mL): $0.70 - $0.86
Solution (DOPamine in D5W Intravenous)
0.8 mg/mL 5% (per mL): $0.06
1.6 mg/mL 5% (per mL): $0.07
3.2 mg/mL 5% (per mL): $0.09 - $0.10
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
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 (Ref). 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; leave cannula/needle in place temporarily but do NOT flush the line; gently aspirate extravasated solution, then remove needle/cannula; elevate extremity; apply dry, warm compresses; initiate phentolamine (or alternative) antidote (Ref).
Phentolamine: SUBQ: Dilute 5 to 10 mg in 10 mL NS and administer into extravasation site as soon as possible after extravasation; if IV catheter remains in place, administer initial dose intravenously through the infiltrated catheter; may repeat in 60 minutes if patient remains symptomatic (Ref).
Alternatives to phentolamine:
Nitroglycerin topical 2% ointment: Apply a 1-inch strip to the site of ischemia to cover the affected areas; may repeat every 8 hours as necessary (Ref).
Large extravasations: SUBQ: Infiltrate affected extravasation area with terbutaline 1 mg using a solution of terbutaline 1 mg diluted in 10 mL NS; may repeat dose after 15 minutes (Ref).
Small extravasations: SUBQ: Infiltrate affected extravasation area with 0.5 mg using a solution of terbutaline 1 mg diluted in 1 mL NS; may repeat dose after 15 minutes (Ref).
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 (Ref). Administer into large vein to minimize the possibility of extravasation (central line administration); administration into an umbilical arterial catheter is not recommended (Ref). 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 (Ref). Frequent monitoring of the IV catheter site is recommended to rapidly identify extravasation (Ref). 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 (Ref). 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 (Ref).
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.
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
Levothyroxine: May enhance the adverse/toxic effect of Sympathomimetics. Specifically, the risk of coronary insufficiency may be increased in patients with coronary artery disease. Levothyroxine may enhance the therapeutic effect of Sympathomimetics. Sympathomimetics may enhance the therapeutic effect of Levothyroxine. Risk C: Monitor therapy
Linezolid: May enhance the hypertensive effect of Sympathomimetics. Management: Consider initial dose reductions of sympathomimetic agents, and closely monitor for enhanced blood pressure elevations, in patients receiving linezolid. 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.
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟