Acute decompensated heart failure: Note: May consider in select patients with a low cardiac index and hypotension or end-organ hypoperfusion. Patients with severe hypotension may require initial stabilization with vasopressor therapy (eg, norepinephrine). Optimal goal of therapy is not well established; typically titrate to maintain end-organ perfusion (AHA [van Diepen 2017]).
Continuous infusion: IV: Initial: 2 to 5 mcg/kg/minute; titrate based on clinical end point (eg, BP, end-organ perfusion); usual dosage range: 2 to 10 mcg/kg/minute; maximum dose: 20 mcg/kg/minute (ACCF/AHA [Yancy 2013]; AHA [van Diepen 2017]; Dunlay 2021; Lewis 2019).
Inotropic support (off-label use): Note: In patients with shock (eg, sepsis) who fail to meet hemodynamic goals with vasopressor therapy (eg, norepinephrine), dobutamine may be added to vasopressor therapy if there is continued hypoperfusion despite volume resuscitation (AHA [Peberdy 2010]; SSC [Dellinger 2013]; SSC [Evans 2021]).
Continuous infusion: IV: Initial: 2 to 5 mcg/kg/minute; titrate based on clinical end point (eg, BP, end-organ perfusion); usual dosage range: 2 to 10 mcg/kg/minute; however, doses as low as 0.5 mcg/kg/min have been used in less severe cardiac decompensation; maximum dose: 20 mcg/kg/minute (AHA [Peberdy 2010]; Annane 2007; Manaker 2021; Mouncey 2015; SSC [Dellinger 2013]; manufacturer’s labeling).
Stress echocardiography, routine (diagnostic agent) (off-label use): Continuous infusion: IV: Initial: 5 mcg/kg/minute; increase at 3-minute intervals to 10 mcg/kg/minute, then 20 mcg/kg/minute, then 30 mcg/kg/minute, and then 40 mcg/kg/minute. May coadminister atropine in patients who do not achieve target heart rate (ASE [Pellikka 2020]; ASNC [Henzlova 2016]).
Stress echocardiography, viability assessment (diagnostic agent) (off-label use): Continuous infusion: IV: Initial: 2.5 mcg/kg/minute; increase at 5-minute intervals in 2.5 mcg/kg/minute increments until contractile response is noted, up to a maximum dose of 10 mcg/kg/minute (AHA [Garcia 2020]; ASE [Pellikka 2020]; Ling 2006).
There are no dosage adjustments provided in the manufacturer's labeling.
There are no dosage adjustments provided in the manufacturer’s labeling.
(For additional information see "Dobutamine: Pediatric drug information")
Hemodynamic support: Infants, Children, and Adolescents: Continuous IV or intraosseous infusion: Initial: 0.5 to 1 mcg/kg/minute, titrate gradually every few minutes until desired response achieved; usual range: 2 to 20 mcg/kg/minute (PALS [Kleinman 2010])
There are no dosage adjustments provided in the manufacturer's labeling.
There are no dosage adjustments provided in the manufacturer's labeling.
Refer to adult dosing.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Solution, Intravenous, as hydrochloride:
Generic: 1 mg/mL (250 mL); 2 mg/mL (250 mL); 4 mg/mL (250 mL); 250 mg/20 mL (20 mL); 500 mg/40 mL (40 mL [DSC])
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous, as hydrochloride:
Generic: 12.5 mg/mL (20 mL)
Always administer via infusion device; administer into large vein.
Parenteral: Administer as a continuous IV infusion via an infusion device; administer into large vein.
Rate of infusion (mL/hour) = dose (mcg/kg/minute) x weight (kg) x 60 minutes/hour divided by the concentration (mcg/mL)
Note: Premixed solutions available.
IV infusion: 250 mg in 500 mL (concentration: 500 mcg/mL), 500 mg in 250 mL (concentration: 2,000 mcg/mL), or 1,000 mg in 250 mL (concentration: 4000 mcg/mL) of D5W or NS
Note: Premixed solutions available.
IV infusion: 1,000 mcg/mL, 2,000 mcg/mL, or 4,000 mcg/mL
Cardiogenic shock: Short-term management of patients with cardiac decompensation.
Inotropic support; Stress echocardiography (diagnostic agent)
DOBUTamine may be confused with DOPamine
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.
1% to 10%:
Cardiovascular: Increased heart rate (10%), increased systolic blood pressure (8%), ventricular premature contractions (5%), angina pectoris (1% to 3%), chest pain (1% to 3%), palpitations (1% to 3%)
Central nervous system: Headache (1% to 3%)
Gastrointestinal: Nausea (1% to 3%)
Respiratory: Dyspnea (1% to 3%)
Frequency not defined:
Cardiovascular: Hypotension, ventricular ectopy
Endocrine & metabolic: Decreased serum potassium
<1%, postmarketing, and/or case reports: Cardiomyopathy (stress), eosinophilia, hypersensitivity reaction, localized phlebitis
Hypersensitivity to dobutamine or sulfites (some contain sodium metabisulfate), or any component of the formulation; hypertrophic cardiomyopathy with outflow tract obstruction (formerly known as idiopathic hypertrophic subaortic stenosis).
Note: When utilized for stress testing, additional contraindications according to the American Society of Nuclear Cardiology include patients with recent (<2 to 4 days) myocardial infarction, unstable angina, severe aortic stenosis, atrial tachyarrhythmias with uncontrolled ventricular response, prior history of ventricular tachycardia, uncontrolled hypertension (>200/110 mm Hg), and aortic dissection or large aortic aneurysm (ASNC [Henzlova 2016]).
Concerns related to adverse effects:
• Arrhythmias: Ventricular arrhythmias, including nonsustained ventricular tachycardia and supraventricular arrhythmias, have been reported (Tisdale 1995). Observe closely for arrhythmias in patients with decompensated heart failure; sudden cardiac death has been observed (O’Connor 1999; Pickworth 1992; Young 2000). Ensure that ventricular rate is controlled in atrial fibrillation/flutter before initiating; may increase ventricular response rate.
• BP effects: An increase in BP is more common due to augmented cardiac output, but occasionally a patient may become hypotensive.
• Heart failure complications: An increased risk of hospitalization and death has been observed with prolonged use in New York Heart Association Class III/IV heart failure patients (O’Connor 1999).
• Tachycardia: May cause dose-related increases in heart rate.
• Ventricular ectopy: May exacerbate ventricular ectopy (dose related).
Disease-related concerns:
• Aortic stenosis: Ineffective therapeutically in the presence of mechanical obstruction such as severe aortic stenosis.
• 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).
• Hypovolemia: If needed, correct hypovolemia first to optimize hemodynamics.
• Active myocardial ischemia/myocardial infarction (post): Use with caution in patients with active myocardial ischemia or recent myocardial infarction; can increase myocardial oxygen demand.
Concurrent drug therapy issues:
• Monoamine oxidase inhibitors: Use with extreme caution in patients taking monoamine oxidase inhibitors; prolong hypertension may result from concurrent use.
Dosage form specific issues:
• Sodium sulfite: Product may contain sodium sulfite.
Special populations:
• Elderly: Use with caution in elderly patients; start at lower end of the dosage range.
Substrate of COMT
AtoMOXetine: May enhance the hypertensive effect of Sympathomimetics. AtoMOXetine may enhance the tachycardic effect of Sympathomimetics. Risk C: Monitor therapy
Beta-Blockers: May diminish the therapeutic effect of DOBUTamine. Risk C: Monitor therapy
Calcium Salts: May diminish the therapeutic effect of DOBUTamine. Risk C: Monitor therapy
Cannabinoid-Containing Products: May enhance the tachycardic effect of Sympathomimetics. 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
Guanethidine: May enhance the arrhythmogenic effect of Sympathomimetics. Guanethidine may enhance the hypertensive effect of Sympathomimetics. 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
Ozanimod: May enhance the hypertensive effect of Sympathomimetics. Risk C: Monitor therapy
Solriamfetol: Sympathomimetics may enhance the hypertensive effect of Solriamfetol. Sympathomimetics may enhance the tachycardic effect of Solriamfetol. 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
Dobutamine should not be used as a diagnostic agent for stress testing during pregnancy; use should be avoided when other options are available (ESC [Regitz-Zagrosek 2018]). Medications used for the treatment of cardiac arrest in pregnancy are the same as in the non-pregnant female. Appropriate medications should not be withheld due to concerns of fetal teratogenicity. Dobutamine use during the post-resuscitation phase may be considered; however, the effects of inotropic support on the fetus should also be considered. Doses and indications should follow current Advanced Cardiovascular Life Support (ACLS) guidelines (AHA [Jeejeebhoy 2015 ]).
It is not known if dobutamine is present in breast milk.
Blood pressure, ECG, heart rate, CVP, RAP, MAP; serum glucose, renal function; urine output; if pulmonary artery catheter is in place, monitor CI, PCWP, and SVR; ScvO2 or SvO2
Consult individual institutional policies and procedures.
Dobutamine, a racemic mixture, stimulates myocardial beta1-adrenergic receptors primarily by the (+) enantiomer and some alpha1 receptor agonism by the (-) enantiomer, resulting in increased contractility and heart rate, and stimulates both beta2- and alpha1-receptors in the vasculature. Although beta2 and alpha1 adrenergic receptors are also activated, the effects of beta2 receptor activation may equally offset or be slightly greater than the effects of alpha1 stimulation, resulting in some vasodilation in addition to the inotropic and chronotropic actions (Leier 1988; Majerus 1989; Ruffolo 1987). Lowers central venous pressure and wedge pressure, but has little effect on pulmonary vascular resistance (Leier 1977; Leier 1978).
Onset of action: IV: 1 to 10 minutes
Peak effect: 10 to 20 minutes
Metabolism: In tissues and hepatically to inactive metabolites
Half-life elimination: 2 minutes
Excretion: Urine (as metabolites)
Solution (DOBUTamine in D5W Intravenous)
2 mg/mL (per mL): $0.06 - $0.18
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