ResusDocDrug Monographs

Reference material for UK healthcare professionals. Doses and licensing change — verify against the current SmPC and local policy before use.

Drug monographs / Dopamine

Dopamine

Dopamine is largely a drug of historical interest in UK emergency practice, which is precisely why the reasons for its decline are worth knowing.

VasopressorInotropeShockCritical careCardiology

At a glance

ClassCatecholamine; dopaminergic, β₁ and α₁ depending on rate
PresentationConcentrate 40 mg/mL — must be diluted
Licensed start2–5 µg/kg/min, increased in 5–10 µg/kg/min steps
Upper rangeUp to 50 µg/kg/min; higher has been used
AccessUse as large a vein as possible; central preferred
Renal doseAbandoned — no renal protective effect
Versus noradrenalineMore arrhythmia (SOAP II); not first line
ContraindicatedPhaeochromocytoma · hyperthyroidism · uncorrected tachyarrhythmia

Why this drug is interesting

Dopamine is the drug most likely to be described to you in terms of three neat dose ranges — dopaminergic, then beta, then alpha — as though the receptors switch on in sequence as the rate climbs. It is a memorable model. It is also substantially wrong at the level of the individual patient, where plasma concentrations at a given weight-based rate vary several-fold and the ranges overlap comprehensively.

It is worth a monograph for two reasons. The first is that it remains in use in some settings and appears in older protocols. The second is that its decline is one of the clearest worked examples in critical care of a physiologically attractive idea being dismantled by trials — twice, for two different reasons.

Dose-dependent effects — with the caveat attached

Approximate ratePredominant effectConsequence
1–5 µg/kg/minDopaminergic (DA₁)Renal and mesenteric vasodilatation, natriuresis
5–10 µg/kg/minβ₁ predominatesIncreased contractility and heart rate
>10 µg/kg/minα₁ predominatesVasoconstriction, rising systemic vascular resistance

Licensed dosing

  • Initial rate 2–5 µg/kg/min, increased gradually in increments of 5–10 µg/kg/min until the optimum individual dose is reached1
  • Up to 50 µg/kg/min may be required; the label notes even higher doses have been used
  • Use as large a vein as possible. The concentrate must be diluted before administration and given through a metering device
  • Safety and efficacy in children have not been established
  • Correct hypovolaemia before starting. Use low doses in shock due to acute myocardial infarction
  • In patients previously treated with MAO inhibitors, the starting dose should be one tenth of the usual dose

The two things trials took away

Renal-dose dopamine does not protect kidneys

For years, low-dose dopamine was given to critically ill patients with the aim of preserving renal function, on the reasoning that DA₁-mediated renal vasodilatation and natriuresis would prevent acute kidney injury. It increases urine output, which made it look as though it was working.

It causes more arrhythmia than noradrenaline

SOAP II randomised patients in shock to dopamine or noradrenaline as first-line vasopressor. There was no significant difference in the primary outcome of 28-day mortality, but there were significantly more arrhythmic events with dopamine, and a subgroup analysis suggested worse outcomes with dopamine in cardiogenic shock.3

That result, more than any other, is why dopamine is no longer a default first-line vasopressor. The mortality signal is a subgroup finding and should be read as one; the arrhythmia finding is the primary safety observation and is the more solid ground.

Where it still has a place

The licensed indication is broad — "correction of haemodynamic imbalances in low-perfusion circulatory insufficiency associated with myocardial infarction, trauma, septicaemia, cardiac failure and open heart surgery"1 — but practice has narrowed considerably.

  • Symptomatic bradycardia, as a chronotropic infusion where atropine has failed and pacing is not immediately available — an alternative to isoprenaline or adrenaline
  • Settings where central venous access is not available, since dopamine has historically been considered more tolerable peripherally than noradrenaline — though this argument has weakened as peripheral noradrenaline has become common practice
  • Where it is what is stocked. In some prehospital and resource-limited settings dopamine is the vasopressor available, and a drug you have beats one you do not

Contraindications and adverse effects

Contraindications

  • Hypersensitivity to dopamine or excipients
  • Phaeochromocytoma
  • Hyperthyroidism
  • Uncorrected atrial or ventricular tachyarrhythmia, or ventricular fibrillation
  • Cyclopropane and halogenated hydrocarbon anaesthetics should be avoided

Adverse effects

  • Tachyarrhythmia — the effect that displaced the drug
  • Ectopic beats, palpitations, angina, widened QRS
  • Peripheral vasoconstriction and digital ischaemia at higher rates
  • Tissue necrosis on extravasation
  • Nausea and vomiting, headache
  • Suppression of prolactin and thyroid-stimulating hormone release during prolonged infusion — an endocrine effect that is easy to forget in a long critical care stay

Excess administration of potassium-free solutions may cause significant hypokalaemia, and the volume of diluent can contribute to fluid overload — both labelled warnings, and both relevant to a patient on a prolonged infusion.

Critical appraisal

  1. Dopamine is the best teaching example in the vasopressor formulary of a surrogate endpoint misleading everyone. Renal-dose dopamine increased urine output, which felt like renal protection, and was given to a great many patients for years on that basis. The trial that stopped it did not find a small effect — it found none.
  2. The three-band dose model persists because it is memorable, not because it is accurate. It should be taught with its variability attached, or trainees will believe they can select a receptor by setting a pump rate.
  3. SOAP II is frequently over-read. It was neutral for mortality overall; the arrhythmia difference was the robust finding and the cardiogenic shock signal was a subgroup. "Dopamine kills people" is not what the trial showed, and overstating it makes the genuine safety point harder to defend.
  4. Its decline is a good thing that has left a small gap. Peripheral noradrenaline has largely closed it. But dopamine's tolerance of peripheral administration and its chronotropy still give it occasional utility, and pretending it has no role at all is its own kind of error.

References

  1. 1
    Dopamine Hydrochloride 40mg/ml Concentrate for Solution for Infusion — Summary of Product Characteristics, ADVANZ Pharma. electronic Medicines Compendium. Sections 4.1–4.4, 4.8. Verified 24 Aug 2026.
  2. 2
    Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh J (ANZICS Clinical Trials Group). Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial. Lancet 2000;356(9248):2139–43. PubMed
  3. 3
    De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock (SOAP II). N Engl J Med 2010;362(9):779–89. PubMed
  4. 4
    Resuscitation Council UK. Adult bradycardia algorithm, 2025 Resuscitation Guidelines. resus.org.uk — local copies at lifesupport.resusdoc.uk
  5. 5
    Dopamine hydrochloride — dosing and safety monograph. BNF, NICE. bnf.nice.org.uk

Last reviewed 2026-08-24 · Author: Dr Nirmalya Hore