The following adverse reactions have been observed, but there are not enough data to support an estimate of their frequency.

Cardiovascular System

ventricular arrhythmia (at very high doses)
ectopic beats
tachycardia
anginal pain
palpitation
cardiac conduction abnormalities
widened QRS complex
bradycardia
hypotension
hypertension
vasoconstriction

Respiratory System

dyspnea

Gastrointestinal System

nausea
vomiting

Metabolic/Nutritional System

azotemia

Central Nervous System

headache
anxiety

Dermatological System

piloerection

Other

Gangrene of the extremities has occurred when moderate to high doses were administered for prolonged periods or in patients with occlusive vascular disease receiving low doses of dopamine HCl.

A few cases of peripheral cyanosis have been reported.

Cyclopropane or halogenated hydrocarbon anesthetics increase cardiac autonomic irritability and may sensitize the myocardium to the action of certain intravenously administered catecholamines, such as dopamine. The interaction appears to be related both to pressor activity and to the beta adrenergic stimulating properties of these catecholamines, and may produce ventricular arrhythmias. Therefore, EXTREME CAUTION should be exercised when administering dopamine HCl to patients receiving cyclopropane or halogenated hydrocarbon anesthetics. Results of studies in animals indicate that dopamine induced ventricular arrhythmias during anesthesia can be reversed by propranolol.

Because dopamine is metabolized by monoamine oxidase (MAO), inhibition of this enzyme prolongs and potentiates the effect of dopamine. Patients who have been treated with MAO inhibitors within two to three weeks prior to the administration of dopamine should receive initial doses of dopamine HCl not greater than one-tenth (1/10) of the usual dose.

Concurrent administration of low-dose dopamine HCl and diuretic agents may produce an additive or potentiating effect on urine flow.

Tricyclic antidepressants may potentiate the cardiovascular effects of adrenergic agents.

Cardiac effects of dopamine are antagonized by beta-adrenergic blocking agents, such as propranolol and metroprolol. The peripheral vasoconstriction caused by high doses of dopamine HCl is antagonized by alpha-adrenergic blocking agents. Dopamine-induced renal and mesenteric vasodilation is not antagonized by either alpha- or beta-adrenergic blocking agents.

Butyrophenones (such as haloperidol) and phenothiazines can suppress the dopaminergic renal and mesenteric vasodilation induced with low-dose dopamine infusion.

The concomitant use of vasopressors, vasoconstricting agents (such as ergonovine) and some oxytocic drugs may result in severe hypertension.

Administration of phenytoin to patients receiving dopamine HCl has been reported to lead to hypotension and bradycardia. It is suggested that in patients receiving dopamine HCl, alternatives to phenytoin should be considered if anticonvulsant therapy is needed.

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