Detection and recording of paroxysmal arrhythmias remain a clinical challenge. Potential clinical features, such as palpitations or syncope are transient. Consequently, making an exact diagnosis can be difficult if a paroxysmal ECG pattern becomes normal when the patient arrives at the hospital. An exact diagnosis of the underlying arrhythmia is crucial because of its prognostic and therapeutic consequences. Depending on the arrythmia the cardiologist may recommend lifestyle modifications, drug-based therapy, ablation or implantation of a pacemaker or ICD.

Adenosine binds to the A1-receptor thus exerting its effects of depressing sinus node automaticity, slowing or blocking AV node conduction, shortening and hyperpolarizing the atrial action potential as well as decreasing automaticity in Purkinje fibers. Adenosine is impossible to study via classical ADME protocols. It is present in various forms in all cells of the body where it plays an important role in energy production and utilisation. An efficient salvage and recycling system exists in the body, primarily in the erythrocytes and blood vessel endothelial cells. The half-life in vitro is estimated to be <10 seconds. The in vivo half-life may be even shorter.

Adenosine, administered as an intravenous bolus during sinus rhythm, has been shown to unmask latent pre-excitation with high sensitivity and specificity. Often these are only apparent otherwise during atrial arrhythmia or with pacing. By slowing or transiently blocking conduction to the ventricles through an AV node, an accessory pathway can be exposed.

AF or atrial flutter with accessory pathway (WPW), first degree AV block, bundle branch block, left main stem coronary artery stenosis, uncorrected hypovolaemia, stenotic valvular heart disease, stenotic carotid artery disease and cerebral insufficiency, pericarditis, pericardial effusion, left to right shunt, autonomic dysfunction, recent myocardial infarction, heart failure, heart transplant.

Second- or third-degree AV block or sick sinus syndrome (unless device in-situ), Long QT syndrome, severe hypotension, decompensated heart failure, unstable asthma, COPD with evidence of bronchospasm.

As dipyridamole is a known inhibitor of adenosine uptake, it may potentiate the action of Adenosine and should be avoided or stopped 24 hours prior to the test. Aminophylline, theophylline, and other xanthine’s are competitive adenosine antagonists and should be avoided for 24 hours prior to use of adenosine. Caffeine causes most of its biological effects via antagonizing all types of adenosine receptors and should not be consumed for 12 hours prior to elective adenosine provocation.

Since neither the kidney nor the liver are involved in the degradation of exogenous adenosine, Adenosine 3 mg/ml solution for injection's efficacy should be unaffected by hepatic or renal insufficiency.

• Advice patient to avoid caffeine on the day of the test.

• Obtain written consent.

• Baseline observations, 12 lead ECG, weight.

• Insert cannula into large vein.

This test will be performed in the angiography recovery area by EPS consultant, cardiology registrar or arrhythmia nurse only.

Adenosine should be administered by rapid intravenous (IV) bolus injection into a vein.

The dosing regime is at the discretion of the staff performing the test but a suggested protocol is as follows:

Initially 6mg, if no response repeat with 12mg, if no response repeat with 18mg and then 24mg (unlicensed doses of 18mg & 24mg) (Viskin et al, 2001; Obeyesekere et al, 2011). Further doses MUST be discussed with EP Consultant.

The use of a three-way tap can facilitate rapid administration by ensuring that both syringes are connected to the intravenous line and can be given one after the other with minimal delay.

Flush immediately with sodium chloride 0.9% flush to be given directly after the adenosine as a rapid bolus.

The occurrence of angina, severe bradycardia, severe hypotension respiratory failure (potentially fatal), or asystole/cardiac arrest (potentially fatal) or syncope should lead to immediate discontinuation of administration.

Adenosine may trigger convulsions in patients who are susceptible to convulsions. In patients with history of convulsions/seizures, the administration of adenosine should be carefully monitored.

Apprehension (warn patient prior to the test), nausea, flushing, angina, dizziness, dyspnoea, headache, metallic taste, palpitation, hyperventilation, weakness, blurred vision, sweating, bronchospasm, injection site reaction may also occur.

These side effects are generally mild, of short duration (usually less than 1 minute) and well tolerated by the patient.

• Ensure the crash trolley with defibrillator is checked beforehand and is present in the room; but does not need to be attached to the patient (Whinnet et al, 2012).

• Ensure continuous monitoring during the test.

• Record 12 lead ECG prior, during and after the administration of the Adenosine.

• If arrhythmias are observed and the patient is haemodynamically compromised, put out NEWS call 2222 or call the Cardiology Consultant in the Cath lab.

• If the patient has a full cardiac arrest, put out crash call 2222 and commence cardiopulmonary resuscitation.

• Monitoring must continue for up to 30 minutes post procedure or until the ECG has returned to normal. Blood pressure must be documented every 15 minutes.

Clauss, S., Wakili, R., Steinbeck, G. & Kaab, S. (2015) Provocative Testing for Arrhythmias [Online] Available from https://clinicalgate.com/provocative-testing-for-arrhythmias/ [Accessed 16.04.2021].

Mullord, P. & Sargent, A. (2011) Pharmacological conversion of AV nodal re-entry tachycardia with adenosine. British Journal of Cardiac Nursing 6 4 pp178-183.

Obeyesekere, M.N, Klein, J.C. Modi, S., Leong-Sit, P., Gula, L., Yee, R., Skanes, A.C. & Khran, A.D. (2011) How to Perform and Interpret Provocative Testing for the diagnosis of Brugada Syndrome, Long-QT Syndrome, and Catecholaminergic Polymorphic Ventricular Tachycardia Circ Arrhythm Electrophysiology 4 pp958-964.https://www.ahajournals.org/doi/full/10.1161/CIRCEP.111.965947

Pitcher D, Nolan J. (2015) Peri-arrest arrhythmias. London: Resuscitation Council UK

Viskin, S., Fish, R., Glick, A., Glikson, M., Eldar, M. & Belhassen, B. (2001) The adenosine triphosphate test: a bedside diagnostic tool for identifying the mechanism of supraventricular tachycardia in patients with palpitations Journal of the American College of Cardiology 38 1 pp173-177 https://www.sciencedirect.com/science/article/pii/S0735109701013365?via%3Dihub

Whinnet, Z.I., Sohaib, S.A. & Davies, D.W. (2012) Diagnosis and management of supraventricular tachycardia. British Medical Journal 345 pp7639

This guideline has been registered with the Trust. However, clinical guidelines are guidelines only. The interpretation and application of clinical guidelines will remain the responsibility of the individual clinician. If in doubt, contact a senior colleague or expert. Caution is advised when using guidelines after the review date.
This guideline is for use in Frimley Health NHS Foundation Trust hospitals only. Any use outside this location will not be supported by the Trust and will be at the risk of the individual using it.

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