Why this drug is interesting

Isoprenaline is a pure beta agonist — β₁ and β₂ with essentially no alpha activity. That combination makes it an excellent chronotrope and a poor vasopressor: it speeds the heart up while dilating the periphery, so the blood pressure response is unpredictable and can fall even as the rate rises.

It occupies an unusual and shrinking niche. It is a bridge to a pacing wire, used when transcutaneous pacing is unavailable, ineffective or intolerable, and atropine has not worked. The half-life is one to several minutes, so it is entirely titratable — and entirely dependent on the infusion continuing to run.

Indications — and the one that is not

The licensed indications are narrow: "short-term treatment of permanent bradycardia due to atrio-ventricular block while pending a pacemaker or when a pacemaker is contraindicated", and "short-term treatment of Adams-Stokes syndrome."¹ The label adds that isoprenaline should not be used routinely, and that it must only be given by clinicians trained in anaesthesia, cardiology or intensive care, in a monitored or critical care setting.

It is worth being clear about what this drug is for: it buys time. The definitive treatments are transcutaneous or transvenous pacing and, in due course, a permanent pacemaker. Starting isoprenaline should be accompanied by a conversation with cardiology, not substituted for one.

Where it also appears

Polymorphic VT with a long QT (torsades) — the Resuscitation Council algorithm lists isoprenaline as an option alongside pacing, to increase the underlying rate and shorten the QT. Note that in this setting magnesium comes first and amiodarone must be avoided
Beta-blocker overdose, occasionally, though glucagon and high-dose insulin have the stronger claim
After cardiac transplant the denervated heart does not respond to atropine; aminophylline is the recommended alternative, with isoprenaline and pacing also used

Preparation and infusion

Route

A large peripheral vein or central venous access. Monitor the insertion site for phlebitis and extravasation. ECG and observation monitoring are mandatory throughout.

Rate table — 2 mg in 500 mL (4 µg/mL)

Dose	Rate
0.5 µg/min	8 mL/h* — exactly 7.5, rounded up on the printed table
1 µg/min	15 mL/h
2 µg/min	30 mL/h
3 µg/min	45 mL/h
4 µg/min	60 mL/h
5 µg/min	75 mL/h — involve a senior clinician above this
6 µg/min	90 mL/h
7 µg/min	105 mL/h
8 µg/min	120 mL/h
9 µg/min	135 mL/h
10 µg/min	150 mL/h

Titration

Start at 0.5 µg/min, increasing to 1 µg/min if required
Then consider increasing in steps of 1 µg/min every 2–3 minutes, until the desired heart rate is reached or adverse effects limit it
If the dose exceeds 5 µg/min, a senior clinician or critical care must be made aware

Three sources, three dosing conventions

This is a drug where the numbers you have been taught depend entirely on which document you were taught from. All three below are current, and they are not expressed in the same units.

Source	Dose	Notes
UK SmPC¹	Start 0.01 µg/kg/min, increments of 0.01, maximum 0.15 µg/kg/min	Weight-based. Target heart rate 50–60 bpm
Local infusion guidelines	0.5–10 µg/min, start 0.5, steps of 1 µg/min every 2–3 min	Not weight-based. Senior review above 5 µg/min
RCUK 2025 bradycardia algorithm	5 µg/min starting dose	"If treatment with atropine is ineffective, consider second-line drugs. These include isoprenaline (5 micrograms min⁻¹ starting dose), and adrenaline (2–10 micrograms min⁻¹)."²

The ceilings agree; the starting doses differ tenfold

At 70 kg the SmPC's maximum of 0.15 µg/kg/min is 10.5 µg/min, so the licensed ceiling and the 0.5–10 µg/min convention describe almost the same envelope. That is where the agreement ends.

Where they diverge is the starting dose, and they diverge by an order of magnitude. The SmPC starts at 0.01 µg/kg/min — 0.7 µg/min at 70 kg. Infusion guidelines start at 0.5 µg/min. RCUK's 5 µg/min is explicitly a starting dose, which is ten times the infusion-guideline start and around seven times the SmPC's. It is not a mid-range figure, and reading it as one is the error this table exists to prevent.

In practice, in a patient who is symptomatic but not peri-arrest, starting low and titrating every 2–3 minutes is the safer approach and is what the SmPC and infusion guidance both describe. RCUK's higher starting figure belongs to an algorithm written for a patient with adverse signs in whom atropine has already failed. Know which of those two situations you are in. And in a very small or very large adult, do the per-kilogram calculation.

Pharmacology

Mechanism

Isoprenaline is a synthetic catecholamine and a potent non-selective agonist at β₁ and β₂ adrenoceptors, with negligible α activity. β₁ stimulation raises heart rate, conduction velocity through the AV node and contractility; β₂ stimulation produces vasodilatation in skeletal muscle and bronchodilatation.

Kinetics

Onset: Immediate on starting the infusion
Plasma half-life: 1 to several minutes, depending on infusion rate
Metabolism: By catechol-O-methyltransferase in liver, lungs and other tissues
Excretion: Urine, as unchanged drug and metabolites

The very short half-life is the drug's principal safety feature and its principal hazard. Adverse effects resolve within minutes of stopping — but so does the therapeutic effect, and an infusion that tissues, kinks or runs through will produce a return of the bradycardia in about the same time.

Contraindications, cautions and adverse effects

Cautions from the label

ECG monitoring is required, with dose reduction if there is ventricular myocardial hyperexcitability — polymorphic extrasystoles, repetitive bursts or ventricular tachycardia
Hypovolaemia — correct it first; isoprenaline vasodilates
Cardiovascular disorders, especially coronary insufficiency, arrhythmias and hypertension
Patients under the effect of digitalis
Diabetes — β₂ stimulation raises glucose
Hyperthyroidism — and the label says administration "should be avoided in cases of uncontrolled hyperthyroidism"
Convulsive disorders
Caution when doses are sufficient to reach a heart rate greater than 130 beats per minute
Patients who respond to sympathomimetic amines in an unusual manner

Adverse effects

Arrhythmias — the effect that most often limits the dose
Palpitations, tremor, sweating, flushing
Hypotension — from β₂ vasodilatation
Headache, nausea
Myocardial ischaemia, in a susceptible patient

Escalating the rate in a patient whose symptoms are not improving, in the hope that more will help, is the commonest way to convert a bradycardia into a tachyarrhythmia. If 5 µg/min is not working, the answer is usually pacing, not 8 µg/min.

Practical use in the ED

Confirm the bradycardia is causing the symptoms. Syncope, confusion, hypotension, ischaemia or an AKI from hypoperfusion — not just a low number on the monitor.
Work through the RCUK algorithm first. Atropine 500 µg IV, repeated to a maximum of 3 mg. Remember RCUK’s instruction: "do not give atropine to patients with high-degree atrioventricular block and wide QRS. It is ineffective and may worsen the block" — there, the answer is pacing. It should also not be used after cardiac transplant.
Decide about pacing in parallel, not afterwards. Isoprenaline is a bridge. If nobody is arranging the wire, the bridge leads nowhere.
Start low and titrate slowly. 0.5 µg/min, then 1, then 1 µg/min steps every 2–3 minutes. Watch the rhythm as much as the rate.
Escalate the conversation, not just the dose, above 5 µg/min.

Critical appraisal

The evidence base is thin and old. Isoprenaline's place in bradycardia rests on physiology and long practice rather than trials. There is no randomised comparison against transcutaneous pacing, and none is likely.
The dosing units are a genuine safety problem. A drug that is expressed in µg/min in one document, µg/kg/min in another, and as a single number in a third, is a drug that will eventually be given at ten times the intended rate. Whichever convention your department uses, the rate table should be attached to the infusion.
It has been quietly displaced. Reliable transcutaneous pacing and prompt transvenous wires have narrowed the indication considerably. The result is that most clinicians will start this infusion rarely, which is precisely when a written preparation and rate table earns its place.
The blood pressure effect is under-taught. Trainees learn isoprenaline as "the drug that speeds the heart up" and are surprised when the pressure falls. Framing it as an inodilator with chronotropic dominance predicts the observed behaviour better.

References

1
Isoprenaline Hydrochloride 1 mg/5 ml concentrate for solution for infusion — Summary of Product Characteristics. electronic Medicines Compendium. Sections 4.1, 4.2, 4.4, 4.5. Verified 24 Aug 2026. Compare Midomil 0.2 mg/ml, emc.
2
Resuscitation Council UK. Adult advanced life support guidelines, 2025 — bradycardia. resus.org.uk — local copies at lifesupport.resusdoc.uk. Source of the 5 µg/min figure and of the atropine sequence.
3
The preparation, rate table and titration steps above follow the infusion guidance in routine UK hospital use for isoprenaline 2 mg in 500 mL. Check your own local guideline before prescribing — the concentration is standard but the escalation thresholds are not.
4
Isoprenaline — dosing and safety monograph. BNF, NICE. bnf.nice.org.uk

Isoprenaline

At a glance