Difference between revisions of "Dopamine"
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Dopamine is a catecholamine with dopaminergic and adrenergic activity. Its primary indication is for the treatment of hypotension and bradycardia in the setting of shock and cardiac arrest. It is also used in the treatment of symptomatic bradycardia that is not responsive to atropine or pacing. It may be used as a palliative infusion for patients with chronic heart failure. | '''Dopamine''' is a catecholamine with dopaminergic and adrenergic activity. Its primary indication is for the treatment of hypotension and bradycardia in the setting of shock and cardiac arrest. It is also used in the treatment of symptomatic bradycardia that is not responsive to atropine or pacing. It may be used as a palliative infusion for patients with chronic heart failure. | ||
== 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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=== Absolute contraindications<!-- List absolute contraindications for use of the drug. If none, this section may be removed. --> === | === Absolute contraindications<!-- List absolute contraindications for use of the drug. If none, this section may be removed. --> === | ||
* Pheochromocytoma | * [[Pheochromocytoma]] | ||
* Ventricular tachycardia | * Ventricular tachycardia | ||
* Ventricular fibrillation | * Ventricular fibrillation | ||
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=== Precautions<!-- List precautions for use of the drug. If none, this section may be removed. --> === | === Precautions<!-- List precautions for use of the drug. If none, this section may be removed. --> === | ||
* Asthma | * [[Asthma]] | ||
* Hypovolemia | * Hypovolemia | ||
* Occlusive vascular disease | * Occlusive vascular disease | ||
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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. --> ==== | ||
Dopamine is an endogenous catecholamine, the metabolic precursor to norepinephrine in the catecholamine synthetic pathway. Dopamine’s affinity for its receptors is dose-dependent. Low infusion rates (0.5 to 2 micrograms/kg per minute) act on dopaminergic D1 and D2 receptors in the visceral vasculature to produce vasodilation and increased blood flow to the kidneys, intestines, heart, and brain. Intermediate infusion rates (from 2 to 10 micrograms/kg/min) continue to stimulate dopaminergic receptors, but also activates beta-1 receptors, increasing myocardial contractility and electrical conductivity in the heart leading to increased cardiac output. Higher doses cause potent vasoconstriction and increased blood pressure via the adrenergic receptors alpha-1, beta-1, and beta-2.<ref name=":0">{{Citation|title=Dopamine Hydrochloride and Dextrose Injection|url=http://dx.doi.org/10.31003/uspnf_m28028_05_01|publisher=U.S. Pharmacopeial Convention|access-date=2024-01-09}}</ref> <ref>{{Cite journal|last=Overgaard|first=Christopher B.|last2=Džavík|first2=Vladimír|date=2008-09-02|title=Inotropes and Vasopressors|url=http://dx.doi.org/10.1161/circulationaha.107.728840|journal=Circulation|volume=118|issue=10|pages=1047–1056|doi=10.1161/circulationaha.107.728840|issn=0009-7322}}</ref><ref>{{Cite journal|last=Stratton|first=Leeanne|last2=Berlin|first2=David A.|last3=Arbo|first3=John E.|date=2017-02|title=Vasopressors and Inotropes in Sepsis|url=http://dx.doi.org/10.1016/j.emc.2016.09.005|journal=Emergency Medicine Clinics of North America|volume=35|issue=1|pages=75–91|doi=10.1016/j.emc.2016.09.005|issn=0733-8627}}</ref> | Dopamine is an endogenous catecholamine, the metabolic precursor to [[norepinephrine]] in the catecholamine synthetic pathway. Dopamine’s affinity for its receptors is dose-dependent. Low infusion rates (0.5 to 2 micrograms/kg per minute) act on dopaminergic D1 and D2 receptors in the visceral vasculature to produce vasodilation and increased blood flow to the kidneys, intestines, heart, and brain. Intermediate infusion rates (from 2 to 10 micrograms/kg/min) continue to stimulate dopaminergic receptors, but also activates beta-1 receptors, increasing myocardial contractility and electrical conductivity in the heart leading to increased cardiac output. Higher doses cause potent vasoconstriction and increased blood pressure via the adrenergic receptors alpha-1, beta-1, and beta-2.<ref name=":0">{{Citation|title=Dopamine Hydrochloride and Dextrose Injection|url=http://dx.doi.org/10.31003/uspnf_m28028_05_01|publisher=U.S. Pharmacopeial Convention|access-date=2024-01-09}}</ref> <ref>{{Cite journal|last=Overgaard|first=Christopher B.|last2=Džavík|first2=Vladimír|date=2008-09-02|title=Inotropes and Vasopressors|url=http://dx.doi.org/10.1161/circulationaha.107.728840|journal=Circulation|volume=118|issue=10|pages=1047–1056|doi=10.1161/circulationaha.107.728840|issn=0009-7322}}</ref><ref>{{Cite journal|last=Stratton|first=Leeanne|last2=Berlin|first2=David A.|last3=Arbo|first3=John E.|date=2017-02|title=Vasopressors and Inotropes in Sepsis|url=http://dx.doi.org/10.1016/j.emc.2016.09.005|journal=Emergency Medicine Clinics of North America|volume=35|issue=1|pages=75–91|doi=10.1016/j.emc.2016.09.005|issn=0733-8627}}</ref> | ||
==== Adverse effects<!-- Describe any potential adverse effects of the drug. --> ==== | ==== Adverse effects<!-- Describe any potential adverse effects of the drug. --> ==== | ||
Latest revision as of 18:32, 10 January 2024
Dopamine
| Clinical data | |
| Drug class |
Endogenous catecholamine |
|---|---|
| Uses |
Treatment of hypotension and bradycardia |
| Contraindications |
pheochromocytoma, ventricular tachycardia, ventricular fibrillation, corn or sulfite hypersensitivities |
| Routes of administration |
Intravenous |
| Dosage | |
| Pharmacodynamics | |
| Mechanism of action |
Dopaminergic and adrenergic agonism |
| Adverse effects |
Arrhythmia and ectopy, tachycardia, hypotension, hypertension, headahce, vomiting, dyspnea, peripheral vasoconstriction and tissue necrosis |
| Pharmacokinetics | |
| Onset of action |
5 minutes |
| Duration of action |
10 minutes |
| Metabolism |
MAO and COMT activity in liver, kidneys, plasma |
| Physical and chemical data | |
| Formula |
C8H11NO2 |
| Molar mass |
153.18 g/mol |
| Article quality | |
| Editor rating | |
| User likes | 0 |
Dopamine is a catecholamine with dopaminergic and adrenergic activity. Its primary indication is for the treatment of hypotension and bradycardia in the setting of shock and cardiac arrest. It is also used in the treatment of symptomatic bradycardia that is not responsive to atropine or pacing. It may be used as a palliative infusion for patients with chronic heart failure.
Uses
- Hemodynamic support or treatment of hypotension from shock (septic, cardiogenic, anaphylactic, or neurogenic), open-heart surgery, or renal failure
- Treatment of symptomatic bradycardia unresponsive to atropine and/or external pacing
- Treatment of chronic heart failure
Contraindications
Absolute contraindications
- Pheochromocytoma
- Ventricular tachycardia
- Ventricular fibrillation
- Corn or sulfite hypersensitivities
Precautions
- Asthma
- Hypovolemia
- Occlusive vascular disease
- Raynaud’s phenomenon
- Thromboangiitis obliterans
- Geriatric patients
- Pregnancy or breast-feeding
Pharmacology
Pharmacodynamics
Mechanism of action
Dopamine is an endogenous catecholamine, the metabolic precursor to norepinephrine in the catecholamine synthetic pathway. Dopamine’s affinity for its receptors is dose-dependent. Low infusion rates (0.5 to 2 micrograms/kg per minute) act on dopaminergic D1 and D2 receptors in the visceral vasculature to produce vasodilation and increased blood flow to the kidneys, intestines, heart, and brain. Intermediate infusion rates (from 2 to 10 micrograms/kg/min) continue to stimulate dopaminergic receptors, but also activates beta-1 receptors, increasing myocardial contractility and electrical conductivity in the heart leading to increased cardiac output. Higher doses cause potent vasoconstriction and increased blood pressure via the adrenergic receptors alpha-1, beta-1, and beta-2.[1] [2][3]
Adverse effects
- Ventricular arrhythmias
- Atrial fibrillation
- PVCs and PACs
- Sinus tachycardia
- Hypotension
- Hypertension
- Headache
- Vomiting
- Dyspnea
- Anxiety
- Piloerection
- Azotemia
- Peripheral vasoconstriction and tissue necrosis
Pharmacokinetics
- Widely distributed throughout the body, but does not cross the blood-brain barrier
- Metabolized in the liver, kidneys, and plasma by monoamine oxidase and catechol-O-methyltransferase[1]
- 25% is taken up into adrenergic nerve terminals, where it is hydroxylated to form norepinephrine[1]
- Excretion of metabolites and conjugates in the urine
- Onset of action: 5 minutes
- Duration of action: 10 minutes
Chemistry and formulation
Dopamine is the prototypical endogenous catecholamine.
History
References
- ↑ 1.0 1.1 1.2 Dopamine Hydrochloride and Dextrose Injection, U.S. Pharmacopeial Convention, retrieved 2024-01-09
- ↑ Overgaard, Christopher B.; Džavík, Vladimír (2008-09-02). "Inotropes and Vasopressors". Circulation. 118 (10): 1047–1056. doi:10.1161/circulationaha.107.728840. ISSN 0009-7322.
- ↑ Stratton, Leeanne; Berlin, David A.; Arbo, John E. (2017-02). "Vasopressors and Inotropes in Sepsis". Emergency Medicine Clinics of North America. 35 (1): 75–91. doi:10.1016/j.emc.2016.09.005. ISSN 0733-8627. Check date values in:
|date=(help)
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