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

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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.

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. 1.0 1.1 1.2 Dopamine Hydrochloride and Dextrose Injection, U.S. Pharmacopeial Convention, retrieved 2024-01-09
  2. 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.
  3. 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)