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  1. Pharmacology. Dopamine is an endogenous catecholamine and the immediate metabolic precursor of norepinephrine. It stimulates alpha- and beta-adrenergic receptors directly and indirectly. In addition, it acts on specific dopaminergic receptors. Its relative activity at these various receptors is dose-related. At low doses (1-5 mcg/kg/min), dopamine causes vasodilation of renal vascular beds thereby increasing renal blood flow and urine output. At intermediate doses (5-10 mcg/kg/min), dopamine stimulates beta-1 activity (increased heart rate and contractility) in addition to increasing renal and mesenteric blood flow through dopaminergic agonist activity. At high infusion rates (10-20 mcg/kg/min), alpha-adrenergic stimulation predominates, resulting in increased peripheral vascular resistance. Dopamine is not effective orally. After IV administration, its onset of action occurs within 5 minutes, and the duration of effect is less than 10 minutes. The plasma half-life is about 2 minutes.

  2. Indications

    1. Dopamine is used to increase blood pressure, cardiac output, and urine flow in patients with shock who have not responded to intravenous fluid challenge, correction of hypothermia, or reversal of acidosis.

    2. Low-dose infusion is most effective for hypotension caused by venodilation or reduced cardiac contractility; high-dose dopamine is indicated for shock resulting from decreased peripheral arterial resistance.

  3. Contraindications

    1. Tachyarrhythmias or ventricular fibrillation. Electrolyte imbalances should be corrected prior to use to minimize the risk of dysrhythmias.

    2. Uncorrected hypovolemia.

    3. Pheochromocytoma.

    4. High-dose infusion is relatively contraindicated in the presence of peripheral arterial occlusive disease with thrombosis and in patients with ergot poisoning. It should also be used with caution in patients with active or recent myocardial infarction.

  4. Adverse effects

    1. Severe hypertension, which may result in intracranial hemorrhage, pulmonary edema, or myocardial necrosis.

    2. Aggravation of tissue ischemia, resulting in gangrene (with high-dose infusion).

    3. Ventricular arrhythmias, especially in patients intoxicated by halogenated or aromatic hydrocarbon solvents or anesthetics.

    4. Tissue necrosis after extravasation (see Item VI. A below for the treatment of extravasation).

    5. Anaphylactoid reaction induced by sulfite preservatives in sensitive patients.

    6. Use in pregnancy. FDA Category C (indeterminate). There may be a dose-related effect on uterine blood flow. This does not preclude its acute, short-term use for a seriously symptomatic patient (Introduction).

  5. Drug or laboratory interactions

    1. Enhanced pressor response may occur in the presence of cocaine and cyclic antidepressants owing to inhibition of neuronal reuptake.

    2. Enhanced pressor response may occur in patients taking monoamine oxidase inhibitors owing to inhibition of neuronal metabolic degradation.

    3. Chloral hydrate and halogenated hydrocarbon anesthetics may enhance the arrhythmogenic effect of dopamine owing to sensitization of the myocardium to the effects of catecholamines.

    4. Alpha- and beta-blocking agents antagonize the adrenergic effects of dopamine; haloperidol and other dopamine antagonists may antagonize the dopaminergic effects.

    5. There may be a reduced pressor response in patients with depleted neuronal stores of catecholamines (eg, chronic disulfiram or reserpine use).

  6. Dosage and method of administration (adults and children)

    1. Avoid extravasation. Caution: The intravenous infusion must be free-flowing, and the infused vein should be observed frequently for the signs of subcutaneous infiltration (pallor, coldness, and induration). If extravasation occurs, immediately infiltrate ...

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