Dopamine Other names: Dopamine hydrochloride

Patients who have been treated with MAO inhibitors prior to dopamine hydrochloride should be given reduced doses; the starting dose should be 10% of the usual dose.

It is not recommended to use dopamine with alpha and beta blockers. The cardiac effects of dopamine hydrochloride are antagonised by β-adrenergic blocking agents such as propranolol acebutolol, atenolol, bisoprolol, nadolol, nebivolol, and metoprolol, and the peripheral vasoconstriction caused by high doses of dopamine hydrochloride is antagonised by α adrenergic blocking agents (e.g. doxazosin, prazosin, terazosin).

The clearance of dopamine hydrochloride is affected by renal and hepatic dysfunction – decreasing by 2-fold in the presence of either. In younger children, particularly neonates, clearance is highly variable, close monitoring is advised.

Tricyclic antidepressants (e.g. amitriptyline, desipramine, doxepin, imipramine, nortriptyline) and guanethidine may potentiate the pressor response to dopamine hydrochloride.

It is not recommended to use dopamine with diuretic agents (e.g. bumetanide, torsemide, and furosemide). Dopamine hydrochloride may increase the effect of diuretic agents.

The combination of dopamine hydrochloride with ergot alkaloids (e.g., ergotamine) should be avoided because of the possibility of excessive peripheral vasoconstriction, increasing the risk of gangrene.

It is not recommended to use dopamine with metoclopramide as metoclopramide can impair the dopamine hydrochloride effect.

Administration of IV phenytoin to patients receiving dopamine hydrochloride has resulted in hypotension, bradycardia and cardiac arrest; it is recommended that phenytoin should be used with extreme caution, if at all, in patients receiving dopamine hydrochloride.

When dopamine is used in patients with a history of occlusive vascular disease, particular attention should be paid to the status of blood circulation in the extremities.

Patients with a history of peripheral vascular disease should be closely monitored for any changes in colour or temperature of the skin of the extremities. If change of skin colour or temperature occurs and is thought to be the result of compromised circulation to the extremities, the benefits of continued dopamine infusion should be weighed against the risk of possible necrosis. These changes may be reversed by decreasing the rate or discontinuing the infusion. IV administration of phentolamine mesylate 5-10 mg may reverse the ischaemia.

Dopamine is not recommended in patients with narrow angle glaucoma.

Dopamine hydrochloride is selectively used in paediatric patients with low cardiac output syndrome (LCOS) and low systemic vascular resistance (SVR) to improve cardiac output. Its use in patients with elevated SVR or elevated pulmonary vascular resistance (PVR) is generally limited due to the potential to worsen vascular resistance abnormalities. The decision to administer dopamine hydrochloride in cardiac surgery should always be made based on the patient’s specific clinical condition.

Dopamine hydrochloride can increase pulmonary vascular resistance, particularly at higher doses. When administering dopamine hydrochloride in patients with increased pulmonary arterial pressure, close haemodynamic monitoring is recommended and doses above 10 μg/kg/min should be avoided. In acute pulmonary hypertension dopamine hydrochloride should only be administered if considered necessary based on an individual assessment of the haemodynamic and clinical state of the patient.

Based on signals of an increased mortality with the first line use of dopamine in paediatric and adult patients with septic shock, first line administration of dopamine in paediatric patients with sepsis is not recommended.

There are limited amount of data from the use of dopamine hydrochloride in pregnant woman. Animal studies are insufficient with respect to reproductive toxicity. Dopamine is not recommended during pregnancy and in women of childbearing potential not using contraception.

It is not known if dopamine hydrochloride is excreted in human milk. However, because of the short plasma half-life of dopamine hydrochloride at therapeutic doses no effects on the breastfed infants are anticipated. Therefore, dopamine can be used during breast-feeding.

Fertility

No data available.

Not relevant.

Summary of the safety profile

Except for vasoconstrictive effects caused by inadvertent infusion of dopamine hydrochloride into the umbilical artery, adverse reactions unique to the paediatric population have not been identified.

Tabulated list of adverse reactions

The data in the following table is extracted from clinical studies and post-marketing experience pertaining to the adult population. The frequency of adverse events cannot be estimated in the paediatric population. The adverse reactions are listed below by SOC (System Organ Class) and by frequency, most frequent reactions first, with the following guidelines: very common (≥1/10), common (≥1/100 to <1/10), uncommon (≥1/1 000 to <1/100), rare (≥1/10 000 to <1/1 000), very rare (<1/10 000) and not known (cannot be estimated from the available data). Within each frequency grouping, adverse reactions are presented in the order of decreasing seriousness.

Adverse reactions identified in clinical studies and post-marketing:

^* Anaphylactic reactions and severe life-threatening asthmatic episodes may be due to Sodium metabisulphite sensitivity.

Description of selected adverse reactions

Suppression of pituitary function

Due to activation of D2 receptors in the pituitary gland, dopamine suppresses the release of prolactin and thyroid-stimulating hormone (TSH), the latter resulting in a decrease of T4 release from the thyroid gland. Conversely, dopamine discontinuation may lead to a rebound effect with overshooting release of prolactin, TSH and T4.

Increase in hypoxemia

Dopamine may contribute to hypoxemia by several mechanisms, e.g. by ventilation-perfusion mismatch, i.e., increased blood flow even to hypoventilated alveolar areas (pulmonary “shunt” formation), specifically in ventilator-dependent patients. Moreover, dopamine may increase systemic oxygen consumption (VO2).