DOPAMINE Drug Interactions: What You Need to Know

Drug Interactions 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 HCl should receive initial doses of dopamine HCl no greater than one-tenth (1/10) of the usual dose. Concurrent administration of dopamine HCl and diuretic agents may produce an additive or potentiating effect on urine flow. Tricyclic antidepressants may potentiate the pressor response to adrenergic agents. Cardiac effects of dopamine are antagonized by beta-adrenergic blocking agents , such as propranolol and metoprolol. 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. Haloperidol appears to have strong central antidopaminergic properties. Haloperidol and haloperidol-like drugs suppress the dopaminergic renal and mesenteric vasodilation induced at low rates of dopamine infusion. 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. This interaction appears to be related both to pressor activity and to beta-adrenergic stimulating properties of these catecholamines and may produce ventricular arrhythmias and hypertension. Therefore, EXTREME CAUTION should be exercised when administering dopamine HCl to patients receiving cyclopropane or halogenated hydrocarbon anesthetics. It has been reported that results of studies in animals indicate that dopamine-induced ventricular arrhythmias during anesthesia can be reversed by propranolol. The concomitant use of vasopressors and some oxytocic drugs may result in severe persistent hypertension.

See

Labor and Delivery below. 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 used if anticonvulsant therapy is needed. Pregnancy: Teratogenic Effects: Animal studies have revealed no evidence of teratogenic effects due to dopamine. However, in one study, administration of dopamine HCl to pregnant rats resulted in a decreased survival rate of the newborn and a potential for cataract formation in the survivors. There are no adequate and well-controlled studies in pregnant women and it is not known if dopamine crosses the placental barrier. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if, in the judgment of the physician, the potential benefit justifies the potential risk to the fetus.

CONTRAINDICATIONS Dopamine hydrochloride should not be used in patients with pheochromocytoma. Dopamine hydrochloride should not be administered in the presence of uncorrected tachyarrhythmias or ventricular fibrillation. Solutions containing dextrose may be contraindicated in patients with known allergy to corn or corn products.

AND PRECAUTIONS

• Tissue ischemia : Severe peripheral and visceral vasoconstriction can occur. Address hypovolemia prior to use, monitor extremities, and infuse into large vein. ( 5.1 )
• Cardiac arrhythmias : Monitor closely. ( 5.2 )
• Hypotension after abrupt discontinuation : Gradually reduce infusion rate while expanding blood volume with intravenous fluids. ( 5.3 )
• Severe hypersensitivity reactions due to sodium metabisulfite excipient : May cause anaphylaxis including life-threatening or less severe asthmatic episodes in susceptible individuals. ( 5.4 )

5.1 Tissue Ischemia Administration of dopamine to patients who are hypotensive from hypovolemia can result in severe peripheral and visceral vasoconstriction, decreased renal perfusion and hypouresis, tissue hypoxia, lactic acidosis, and poor systemic blood flow despite &quot;normal&quot; blood pressure. Address hypovolemia prior to initiating Dopamine HCl in Dextrose Injection <span class="opacity-50 text-xs">[see Dosage and Administration (2.2) ]</span> . Gangrene of the extremities has occurred in patients with occlusive vascular disease or who received prolonged or high dose infusions. Monitor for changes to the skin of the extremities in susceptible patients. Extravasation of Dopamine HCl in Dextrose Injection may cause necrosis and sloughing of surrounding tissue. To reduce the risk of extravasation, infuse into a large vein <span class="opacity-50 text-xs">[see Dosage and Administration (2.1) ]</span> , check the infusion site frequently for free flow, and monitor for signs of extravasation.

Emergency

Treatment of Extravasation To prevent sloughing and necrosis in areas in which extravasation has occurred, infiltrate the ischemic area as soon as possible, using a syringe with a fine hypodermic needle with:

• 5 to 10 mg of phentolamine mesylate in 10 to 15 mL of 0.9% Sodium Chloride Injection in adults
• 0.1 to 0.2 mg/kg of phentolamine mesylate up to a maximum of 10 mg per dose in pediatric patients. Sympathetic blockade with phentolamine causes immediate and conspicuous local hyperemic changes if the area is infiltrated within 12 hours.

5.2 Cardiac Arrhythmias Dopamine may cause arrhythmias. Monitor patients with arrhythmias and treat appropriately.

5.3 Hypotension after Abrupt Discontinuation Sudden cessation of the infusion rate may result in marked hypotension. Gradually reduce the infusion rate while expanding blood volume with intravenous fluids.

5.4 Severe Hypersensitivity Reactions due to Sodium Metabisulfite Excipient Dopamine HCl in Dextrose Injection, contains sodium metabisulfite, a sulfite that may cause allergic-type reactions including anaphylactic symptoms and life-threatening or less severe asthmatic episodes in certain susceptible people. The overall prevalence of sulfite sensitivity in the general population is unknown and probably low. Sulfite sensitivity is seen more frequently in asthmatic than in non-asthmatic people.