Adenosine

Why this drug is interesting

Adenosine has the shortest half-life of any drug in routine emergency use — under 10 seconds — and that single property dictates everything about how it is given.¹ It is not a drug where technique is a refinement; technique is the entire therapy. A dose delivered slowly, or into a distal vein without a flush, is metabolised in transit and never reaches the AV node in a concentration capable of blocking it.

It is also both a treatment and a diagnostic test. Transient AV block either terminates a re-entrant circuit that uses the node, or unmasks the underlying atrial rhythm in a tachycardia that does not — which makes the rhythm strip during administration as valuable as the outcome.

The UK dose discrepancy

The current RCUK 2025 adult tachyarrhythmia algorithm is unambiguous. For a regular narrow-complex tachycardia where vagal manoeuvres have failed, it directs:

adenosine (if no pre-excitation) 6 mg rapid IV bolus, if unsuccessful give 12 mg, if unsuccessful give 18 mg

Resuscitation Council UK, Adult tachyarrhythmia algorithm, 2025³

Does the starting dose matter?

There is reasonable evidence that starting at 12 mg rather than 6 mg converts more patients first time — reported termination rates of around 79% versus 56% for the initial dose — without a clear increase in adverse effects. Cumulative conversion after 6 mg followed by 12 mg reaches roughly 93%. This is an active question in the literature rather than a settled one, and it is part of why practice has drifted upward from the licensed escalation.

The practical resolution: use the RCUK 2025 escalation, and know that the third dose exceeds the licence. The clinically important variable remains delivery technique, not the choice between 12 and 18 mg at the third step.

Pharmacology

Mechanism

Adenosine is an endogenous purine nucleoside present throughout the body. Acting at A1 receptors in the AV node, it opens acetylcholine-sensitive potassium channels and inhibits calcium influx, hyperpolarising nodal tissue and transiently blocking conduction through the AV node. At A2 receptors on vascular smooth muscle it causes vasodilatation — the source of the flushing, headache and chest discomfort.

The therapeutic logic follows directly. In AV nodal re-entrant tachycardia and AV re-entrant tachycardia, the AV node forms part of the re-entry circuit; block it and the circuit terminates. In atrial flutter, atrial tachycardia and atrial fibrillation, the node is a bystander; blocking it slows ventricular response briefly and reveals the underlying atrial activity without terminating anything.

Kinetics

Half-life

Estimated at under 10 seconds in vitro, possibly shorter in vivo¹

Metabolism

Rapid uptake into erythrocytes and vascular endothelial cells; deaminated to inosine and phosphorylated to AMP

Clearance mechanism

An efficient salvage and recycling system rather than hepatic or renal elimination

Implication

No dose adjustment for renal or hepatic impairment

Indications and administration

Licensed for rapid conversion to sinus rhythm of paroxysmal supraventricular tachycardias, including those associated with accessory bypass tracts (Wolff-Parkinson-White syndrome), and as an aid to the diagnosis of broad or narrow complex supraventricular tachycardias.¹

Technique — the part that actually determines success

1. Continuous ECG monitoring with a running rhythm strip, and resuscitation equipment immediately available. The strip is diagnostic data you cannot recover afterwards.
2. Large-bore cannula in a large, proximal vein — antecubital fossa or above. The SmPC specifies a large-bore cannula for peripheral administration.
3. If using an IV line, inject as proximally as possible and follow immediately with a rapid saline flush.
4. Rapid bolus over about 2 seconds, then the flush without pause. A two-syringe technique or a three-way tap makes this achievable single-handed.
5. Elevate the arm to speed venous return.
6. Warn the patient — see below.

Paediatric dosing

• First bolus 0.1 mg/kg (maximum 6 mg)
• Increments of 0.1 mg/kg as needed to achieve termination, to a maximum of 12 mg

Vagal manoeuvres first

In the stable patient, a properly performed modified Valsalva — the strain followed by supine repositioning and passive leg raise — converts a meaningful proportion of SVT and should precede adenosine. It costs nothing and spares the patient an unpleasant experience.

Contraindications and the pre-excitation problem

Contraindications

• Hypersensitivity to adenosine or excipients
• Sick sinus syndrome, second- or third-degree AV block — except in patients with a functioning pacemaker
• Chronic obstructive lung disease with evidence of bronchospasm, e.g. asthma
• Long QT syndrome
• Severe hypotension
• Decompensated heart failure

Atrial fibrillation with an accessory pathway

Recent heart transplant

Patients less than one year from heart transplantation show increased sensitivity to adenosine, reflecting denervation supersensitivity.¹ Severe bradycardia has been reported, some cases occurring in early post-transplant patients. Use a substantially reduced dose or an alternative agent, with expert input.

Other cautions

Left main coronary stenosis, uncorrected hypovolaemia, stenotic valvular disease, pericarditis or effusion, autonomic dysfunction, carotid artery stenosis, recent myocardial infarction, severe heart failure and minor conduction defects. Cerebrovascular events and myocardial infarction have been reported following adenosine administration.

Interactions

Adverse effects

Almost all of adenosine's adverse effects share one redeeming feature: they last as long as the drug does, which is a matter of seconds.

• Chest tightness or pain, dyspnoea, and a sense of impending doom — very common, transient, and the reason for forewarning
• Flushing and headache — A2-mediated vasodilatation
• Transient asystole or profound bradycardia at the point of conversion — expected on the rhythm strip and usually self-limiting within seconds
• Bronchospasm — the reason for the respiratory contraindication
• Nausea, light-headedness, apprehension
• Atrial fibrillation may be precipitated transiently after conversion
• Rarely: severe bradycardia, hypotension, respiratory failure, and asystole or cardiac arrest requiring immediate discontinuation

Critical appraisal

1. The evidence for efficacy in AVNRT and AVRT is strong and long-standing, with conversion rates typically above 90% when the drug is delivered correctly. Failures in practice are disproportionately technique failures.
2. Guideline and licence have diverged, and teaching material lags both. RCUK moved to 6-12-18 in 2025 while the SmPC still stops at 12 mg. Plenty of e-learning and departmental posters still show the 2021 6-12-12. Clinicians should know which version they are looking at and that the top dose is off-label.
3. The optimal starting dose is genuinely unsettled. Comparative data favouring an initial 12 mg over 6 mg are accumulating but come largely from observational and single-centre work; the guideline recommendation of 6 mg has not yet moved. This is a reasonable thing for a department to have a considered local position on.
4. Modified Valsalva deserves more prominence than it gets. The REVERT trial demonstrated a substantially higher conversion rate for the modified technique over standard Valsalva, and it precedes adenosine at no cost and no risk. It is under-used relative to its evidence.
5. Diagnostic use in broad-complex tachycardia is contested. Adenosine can help distinguish SVT with aberrancy from VT, but a broad-complex tachycardia should be treated as VT until proven otherwise, and the pre-excited AF hazard means the diagnostic gain is not free. Many electrophysiologists would rather you cardioverted.
6. The patient experience is systematically under-weighted. Adenosine is briefly one of the more unpleasant experiences in emergency medicine. That is an acceptable trade for terminating a tachycardia — but it is a reason to attempt vagal manoeuvres properly first, and to explain what is coming.

References

1. 1
   Adenosine 3 mg/ml Solution for Injection — Summary of Product Characteristics. electronic Medicines Compendium. Sections 4.1–4.5, 5.2. Verified 20 Aug 2026.
2. 2
   Adenosine — dosing and safety monograph. BNF, NICE. bnf.nice.org.uk
3. 3
   Resuscitation Council UK. Adult tachyarrhythmia algorithm, 2025. resus.org.uk — also mirrored at lifesupport.resusdoc.uk. The 2025 revision escalates to 18 mg; earlier (2021) material gives a second 12 mg instead.
4. 4
   Appelboam A, Reuben A, Mann C, et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet 2015;386(10005):1747–53.
5. 5
   Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. Eur Heart J 2020;41(5):655–720. Eur Heart J Gives adenosine as a 6–18 mg intravenous bolus range.
6. 6
   Comparative data on initial adenosine dose: see e.g. comparison of initial adenosine dose conversion rate for SVT in the emergency department, Am J Emerg Med 2024 (PubMed), and Sert et al., initial 12 mg versus 6 mg adenosine for SVT in the emergency department, Acad Emerg Med 2026.