Difference between revisions of "Dobutamine"
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Dobutamine is a direct-acting sympathomimetic with preferential activation of beta-1 adrenergic receptors accounting for most of its ionotropic and chronotropic effects. It is also active at beta-2 and alpha-1 adrenergic receptors. Its primary indication is the treatment of low cardiac output secondary to CHF, cardiogenic shock, septic shock, or following cardiac surgery; Dobutamine is also the preferred agent for pharmacologic cardiac stress testing in patients who cannot tolerate an exercise stress test. | '''Dobutamine''' is a direct-acting sympathomimetic with preferential activation of beta-1 adrenergic receptors accounting for most of its ionotropic and chronotropic effects. It is also active at beta-2 and alpha-1 adrenergic receptors. Its primary indication is the treatment of low cardiac output secondary to CHF, cardiogenic shock, septic shock, or following cardiac surgery; Dobutamine is also the preferred agent for pharmacologic cardiac stress testing in patients who cannot tolerate an exercise stress test. | ||
==Uses<!-- Describe uses of the drug. If appropriate, add subsections for each indication. -->== | ==Uses<!-- Describe uses of the drug. If appropriate, add subsections for each indication. -->== | ||
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====Mechanism of action<!-- Describe the mechanism of action for the primary uses of the drug. -->==== | ====Mechanism of action<!-- Describe the mechanism of action for the primary uses of the drug. -->==== | ||
Dobutamine is a direct-acting synthetic catecholamine. It is formulated as a racemic mixture of 2 enantiomers, the positive enantiomer is predominantly a beta-agonist (beta-1 greater than beta-2), while the negative enantiomer has partial alpha-1 agonist effects. Dobutamine binding to beta-1 adrenergic receptors enhances voltage-gated calcium channel expression on cardiac myocytes and increases myocardial contractility, leading to larger stroke volumes and increased cardiac output. This increased cardiac output activates baroreceptors, which decrease systemic vascular resistance, resulting in minimal change to arterial blood pressure. | Dobutamine is a direct-acting synthetic catecholamine. It is formulated as a racemic mixture of 2 enantiomers, the positive enantiomer is predominantly a beta-agonist (beta-1 greater than beta-2), while the negative enantiomer has partial alpha-1 agonist effects. Dobutamine binding to beta-1 adrenergic receptors enhances voltage-gated calcium channel expression on cardiac myocytes and increases myocardial contractility, leading to larger stroke volumes and increased cardiac output. This increased cardiac output activates baroreceptors, which decrease systemic vascular resistance, resulting in minimal change to arterial blood pressure. Dobutamine also has minor beta-2 and alpha-1 adrenergic stimulatory effects. <ref>{{Cite journal|last=Ruffolo|first=Robert R.|date=1987-10|title=Review: The Pharmacology of Dobutamine|url=http://dx.doi.org/10.1097/00000441-198710000-00005|journal=The American Journal of the Medical Sciences|volume=294|issue=4|pages=244–248|doi=10.1097/00000441-198710000-00005|issn=0002-9629}}</ref> | ||
====Adverse effects<!-- Describe any potential adverse effects of the drug. -->==== | ====Adverse effects<!-- Describe any potential adverse effects of the drug. -->==== | ||
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==History<!-- Describe the historical development of the drug. -->== | ==History<!-- Describe the historical development of the drug. -->== | ||
Dobutamine was developed by Drs. Tuttle and Mills in 1975, after they modified the structure of | Dobutamine was developed by Drs. Tuttle and Mills in 1975, after they modified the structure of [[isoprenaline]]. <ref>{{Cite journal|last=Tuttle|first=R R|last2=Mills|first2=J|date=1975-01|title=Dobutamine: development of a new catecholamine to selectively increase cardiac contractility.|url=http://dx.doi.org/10.1161/01.res.36.1.185|journal=Circulation Research|volume=36|issue=1|pages=185–196|doi=10.1161/01.res.36.1.185|issn=0009-7330}}</ref> | ||
==References== | ==References== | ||
[[Category:Drug reference]] | [[Category:Drug reference]] | ||
[[Category:Positive chronotropes]] | |||
<references /> | <references /> | ||
Latest revision as of 17:19, 10 January 2024
Dobutamine
| Clinical data | |
| Drug class |
Synthetic catecholamine |
|---|---|
| Uses |
Low cardiac output, pharmacologic cardiac stress echocardiography |
| Contraindications |
Corn hypersensitivity, idiopathic hypertrophic subaortic stenosis |
| Routes of administration |
IV |
| Dosage | |
| Pharmacodynamics | |
| Mechanism of action |
beta-1 agonism (primary), beta-2 agonism and alpha-1 agonism (secondary) |
| Adverse effects |
Hypertension, hypotension, arrhythmia, hypokalemia, nausea, headache, chest pain |
| Pharmacokinetics | |
| Onset of action |
1-2 minutes |
| Metabolism |
Liver metabolism by catechol-O-methyltransferase and glucuronidation to inactive metabolites |
| Clearance |
90 mL/kg/min |
| Physical and chemical data | |
| Formula |
C18H23NO3 |
| Molar mass |
301.38 |
| Article quality | |
| Editor rating | |
| User likes | 0 |
Dobutamine is a direct-acting sympathomimetic with preferential activation of beta-1 adrenergic receptors accounting for most of its ionotropic and chronotropic effects. It is also active at beta-2 and alpha-1 adrenergic receptors. Its primary indication is the treatment of low cardiac output secondary to CHF, cardiogenic shock, septic shock, or following cardiac surgery; Dobutamine is also the preferred agent for pharmacologic cardiac stress testing in patients who cannot tolerate an exercise stress test.
Uses
- Low cardiac output secondary to congestive heart failure, cardiogenic shock, septic shock, or following cardiac surgery[1]
- Stress echocardiography, preferred alternative test for evaluation of myocardial ischemia if the patient is unable to exercise, though this use is off-label[2]
Contraindications
Absolute contraindications
- Corn hypersensitivity, as premixed bags contain dextrose
- Idiopathic hypertrophic subaortic stenosis
Precautions
- Acute myocardial infarction and coronary artery disease, as dobutamine may worsen myocardial ischemia
- Atrial fibrillation, ventricular arrhythmias, as dobutamine increases AV conduction and can precipitate or worsen ectopic activity[3]
- Hypertension
- Hypotension and hypovolemia
- Renal failure, as continuous infusions may result in myoclonia[4]
- Premature neonates, as dobutamine has been shown to be less effective than dopamine in this population[1]
- Geriatric patients
- Pregnancy and breast feeding[1]
- Sulfite hypersensitivity, as some preparations include sulfites[1]
Pharmacology
Pharmacodynamics
Mechanism of action
Dobutamine is a direct-acting synthetic catecholamine. It is formulated as a racemic mixture of 2 enantiomers, the positive enantiomer is predominantly a beta-agonist (beta-1 greater than beta-2), while the negative enantiomer has partial alpha-1 agonist effects. Dobutamine binding to beta-1 adrenergic receptors enhances voltage-gated calcium channel expression on cardiac myocytes and increases myocardial contractility, leading to larger stroke volumes and increased cardiac output. This increased cardiac output activates baroreceptors, which decrease systemic vascular resistance, resulting in minimal change to arterial blood pressure. Dobutamine also has minor beta-2 and alpha-1 adrenergic stimulatory effects. [5]
Adverse effects
- Hypertension
- Hypotension due to decreased systemic vascular resistance
- Tachycardia
- Rapid ventricular response or premature ventricular contractions
- Hypokalemia
- Nausea
- Headaches
- Chest pain
- Palpitations
- Shortness of breath
Pharmacokinetics
- Onset of action: 1-2 minutes, though peak effect can take up to 10 minutes
- Plasma half-life: 2 minutes
- Metabolized in the liver catechol-O-methyltransferase and by glucuronidation to inactive metabolites, excretion of metabolites via the kidneys
Chemistry and formulation
History
Dobutamine was developed by Drs. Tuttle and Mills in 1975, after they modified the structure of isoprenaline. [6]
References
- ↑ 1.0 1.1 1.2 1.3 Dobutamine in Dextrose Injection, U.S. Pharmacopeial Convention, retrieved 2024-01-08
- ↑ Pellikka, Patricia A.; Arruda-Olson, Adelaide; Chaudhry, Farooq A.; Chen, Ming Hui; Marshall, Jane E.; Porter, Thomas R.; Sawada, Stephen G. (2020-01). "Guidelines for Performance, Interpretation, and Application of Stress Echocardiography in Ischemic Heart Disease: From the American Society of Echocardiography". Journal of the American Society of Echocardiography. 33 (1): 1–41.e8. doi:10.1016/j.echo.2019.07.001. ISSN 0894-7317. Check date values in:
|date=(help) - ↑ David, Shukri; Zaks, Jeffrey M. (1986-02). "Arrhythmias Associated with Intermittent Outpatient Dobutamine Infusion". Angiology. 37 (2): 86–91. doi:10.1177/000331978603700203. ISSN 0003-3197. Check date values in:
|date=(help) - ↑ Wierre, L.; Decaudin, B.; Barsumau, J.; Vairon, M. X.; Horrent, S.; Odou, P.; Azar, R. (2004-04-21). "Dobutamine-induced myoclonia in severe renal failure". Nephrology Dialysis Transplantation. 19 (5): 1336–1337. doi:10.1093/ndt/gfh132. ISSN 0931-0509.
- ↑ Ruffolo, Robert R. (1987-10). "Review: The Pharmacology of Dobutamine". The American Journal of the Medical Sciences. 294 (4): 244–248. doi:10.1097/00000441-198710000-00005. ISSN 0002-9629. Check date values in:
|date=(help) - ↑ Tuttle, R R; Mills, J (1975-01). "Dobutamine: development of a new catecholamine to selectively increase cardiac contractility". Circulation Research. 36 (1): 185–196. doi:10.1161/01.res.36.1.185. ISSN 0009-7330. Check date values in:
|date=(help)
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