1 vial


Each 5ml vial contains 200mg of dopamine
Add 200mg of dopamine (5ml) to 95ml of compatible IV fluid (i.e. 200mg in 100ml)
Compatible with the following IV fluids:
Normal saline Glucose and sodium chloride 5% Dextrose
Store at room temperature
Protect from light
Prepare solution immediately prior to use. Stable in compatible IV fluid for 24 hours at room temperature. Coloured solutions indicate decomposition of dopamine and should not be used

Administered by infusion at rates of 0-20 mcg/kg/min

15mg/kg in 50ml of 5% dextrose or normal saline at 0-20mcg/kg/min (0-4ml/hr)
1ml/hr equal 5mcg/kg/min

Dose as in normal renal function

The predominant effects of dopamine are dose-related, although it should be noted that actual response of an individual patient will largely depend on the clinical status of the patient at the time the drug is administered.

At low rates of infusion (0.5 to 2 mcg/kg/min) dopamine causes vasodilation that is presumed to be due to a specific agonist action on dopamine receptors (distinct from alpha- and beta-adrenoceptors) in the renal, mesenteric, coronary and intracerebral vascular beds. At these dopamine receptors, haloperidol is an antagonist. The vasodilation in these vascular beds is accompanied by increased glomerular filtration rate, renal blood flow, sodium excretion and urine flow. Hypotension sometimes occurs. An increase in urinary output produced by dopamine is usually not associated with a decrease in osmolality of the urine.

At intermediate rates of infusion (2-10 mcg/kg/min), dopamine acts to stimulate the beta1-adrenoceptors, resulting in improved myocardial contractility, increased SA rate and enhanced impulse conduction in the heart. There is little, if any, stimulation of the beta2-adrenoceptors (peripheral vasodilation). Blood flow to the peripheral vascular beds may decrease while mesenteric flow increases due to increased cardiac output. Total peripheral resistance (alpha effects) at low and intermediate doses is usually unchanged.

At higher rates of infusion (10-20 mcg/kg/min), there is some effect on alpha-adrenoceptors, with consequent vasoconstrictor effects and a rise in blood pressure. The vasoconstrictor effects are first seen in the skeletal muscle vascular beds, but with increasing doses, they are also evident in the renal and mesenteric vessels.

At very high rates of infusion (above 20 mcg/kg/min), stimulation of alpha-adrenoceptors predominates and vasoconstriction may compromise the circulation of the limbs and override the dopaminergic effects of dopamine, reversing renal dilation and nariuresis.


  • Idiopathic hypertrophic subaortic stenosis

  • Hypersensitivity to dopamine

Dopamine contains sodium metabisulphite, a sulphite 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 sulphite sensitivity in the general population is unknown and probably low. Sulphite sensitivity is seen more frequently in asthmatic than in non-asthmatic people.

Hypovolemia should be corrected with suitable volume expanders before treatment with dopamine
If an increased number of ectopic beats are observed the dose should be reduced if possible.
At lower infusion rates, if hypotension occurs, the infusion rate should be rapidly increased until adequate blood pressure is obtained. If hypotension persists, dopamine should be discontinued and a more potent vasoconstrictor agent such as noradrenaline should be added.

Laboratory Tests:
No tests additional to routine ICU tests are indicated

Drug/Laboratory Test Interactions:
None known.

Patients who have been receiving monoamine oxidase (MAO) inhibitors prior to the administration of dopamine should receive substantially reduced dosage of the latter.
Concurrent administration of low-dose dopamine and diuretic agents may produce an additive or potentiating effect on urine flow.

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

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:
Gastrointestinal System:
Nausea, vomiting.
Central Nervous System:
Headache, anxiety.
Gangrene of the extremities has occurred when high doses were administered for prolonged periods or in patients with occlusive vascular disease receiving low doses of dopamine.

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