Adenosine ECG test

What it looks like on ECG

The effect of adenosine is visible on a long recording during bolus administration. In narrow-complex tachycardia mediated by AV nodal re-entry (AVNRT, AVRT), sudden termination of the tachycardia occurs — the last QRS complex is followed by a pause, sometimes with a single non-conducted P wave, after which sinus rhythm is restored.

In typical atrial flutter, adenosine induces transient AV block (usually a few seconds, exact duration is variable): some ventricular complexes drop out, revealing continuous regular F waves, especially in leads II, III, aVF, and V1, which were previously obscured by the QRS complex or T wave. The flutter itself usually persists — after AV conduction resumes, the tachycardia returns. In atrial tachycardia, the response is less predictable: AV block more frequently unmasks P waves without terminating the arrhythmia, but some focal atrial tachycardias, especially those related to triggered activity, are adenosine-sensitive and may terminate. Therefore, the mere fact of rhythm termination following administration does not prove that it is AVNRT or AVRT — it does not rule out atrial tachycardia either.

In sinus tachycardia, a gradual slowing of the sinus rate is observed, returning to the baseline heart rate after the drug wears off, without sudden termination.

In ventricular tachycardia (VT), the QRS complex remains unchanged in most cases, as the AV node is typically not part of the tachycardia circuit. However, specific forms of VT, notably certain ventricular outflow tract tachycardias, are adenosine-sensitive and may terminate. Therefore, neither the absence nor the presence of a response establishes the origin of the tachycardia by itself — assessment of QRS morphology and the clinical context is required.

Mechanism

Adenosine binds to A1 receptors of sinoatrial and atrioventricular node cells, activating potassium channels ($I_{K,ACh}$), which hyperpolarizes the cell membrane and suppresses the slow inward calcium current through nodal tissue. The result is a sharp, yet brief, slowing of conduction through the AV node (prolongation of the PQ interval up to complete block) and suppression of sinus node automaticity. The half-life of adenosine in the blood is measured in seconds, so the effect disappears quickly, making the test safe for diagnostic purposes when performed correctly, but requiring rapid bolus injection and immediate ECG recording.

Indications

• Differential diagnosis of regular narrow QRS complex tachycardia when the mechanism is unclear on a standard ECG
• Suspected 2:1 atrial flutter when flutter waves are not visible due to superimposition on the T wave
• Termination of AVNRT and orthodromic AVRT (as an alternative or adjunct to vagal maneuvers)
• As an adjunctive diagnostic tool in hemodynamically stable regular monomorphic wide QRS tachycardia without signs of pre-excitation when the mechanism is unclear — it does not replace VT/SVT differentiation algorithms with aberration (Brugada, Vereckei). In irregular wide-complex rhythms (particularly AF with pre-excitation), adenosine is not administered due to the risk of accelerated conduction via an accessory pathway; in hemodynamic instability, the maneuver is not performed, and immediate synchronized cardioversion is carried out instead

Contraindications and risks

• Active bronchospasm and severe bronchial asthma/severe chronic obstructive pulmonary disease — avoided per the drug's prescribing information due to the risk of exacerbating bronchospasm
• Known or suspected pre-excitation (WPW syndrome) in atrial fibrillation, as well as any irregular wide QRS tachycardia in the setting of pre-excitation — contraindicated: AV nodal blockade can enhance conduction down the accessory pathway and precipitate ventricular fibrillation
• Second- or third-degree AV block or sick sinus syndrome without a functioning pacemaker — contraindicated (risk of severe bradycardia or prolonged asystole), except under special conditions specified in the prescribing information
• Hemodynamic instability — performing the maneuver must not delay electrical cardioversion
• Dipyridamole use enhances the effect of adenosine, while caffeine and theophylline attenuate it
• Frequent transient side effects: flushing, chest discomfort, dyspnea, which resolve within seconds
• Transient AV block and a short pause (a few seconds) are expected pharmacological effects, but any prolonged asystole, marked bradycardia, hemodynamic deterioration, or failure of rapid spontaneous rhythm restoration requires immediate evaluation and readiness for resuscitation measures, especially in unrecognized sinus node dysfunction or AV conduction disturbances

Differential diagnosis

• 2:1 atrial flutter without a response to adenosine is sometimes mistaken for a complete lack of effect — in fact, one must carefully look for F waves during the AV block pause
• Failure of tachycardia termination in atrial tachycardia or flutter does not mean the test was ineffective — the goal here is diagnosis, not termination; meanwhile, rhythm termination following adenosine does not prove AVNRT or AVRT, as some atrial tachycardias and rare VTs are also sensitive to the drug
• VT with no changes in response to adenosine cannot be interpreted as "confirmed VT" based on this sign alone — Brugada and Vereckei criteria and the clinical context are required
• A short pause or transient AV block (a few seconds) with spontaneous and rapid rhythm restoration corresponds to the expected pharmacological effect, but not every asystole following adenosine is unconditionally benign — a prolonged pause, absence of rapid recovery, or hemodynamic deterioration requires immediate intervention and should not be prematurely dismissed as normal

Clinical significance and management

The test is performed only with continuous ECG monitoring, intravenous access, and readiness for cardiopulmonary resuscitation (defibrillator nearby). Before administration, the absence of contraindications is verified — active bronchospasm/severe bronchial asthma, second- to third-degree AV block or sinus node dysfunction without a pacemaker, pre-excitation in AF — and hemodynamic stability is assessed: in case of instability, the test is not performed, and immediate synchronized cardioversion is carried out. For wide-QRS tachycardia, the test is considered only in the case of a stable regular monomorphic form and the absence of signs of pre-excitation; in irregular wide-complex rhythms, adenosine is not administered. A long ECG strip is recorded continuously in two to three leads, the drug is administered as a rapid bolus with immediate saline flush through the same catheter, since the half-life is in seconds. The dosing regimen and the possibility of re-administration in an increased dose in the absence of an effect are determined by the instructions of the specific drug: regimens for adenosine and for ATP differ in doses and intervals, and the dosages of one drug cannot be transferred to another. Any prolonged pause, marked bradycardia, or hemodynamic deterioration after administration requires immediate assessment of the condition and readiness for resuscitation measures, regardless of the fact that the effect is considered pharmacologically expected. The result of the test is documented in the ECG report indicating the dose and rhythm response, which is important for subsequent management (referral for an electrophysiological study, choice of antiarrhythmic therapy).

Common interpretation errors

• Administration too slowly or into a small peripheral vein — the drug is degraded before reaching the heart, there is no effect, leading to a false conclusion that the test is "non-diagnostic"
• Absence of a long continuous ECG recording during administration — short-term changes simply are not captured
• Interpretation of transient slowing of sinus tachycardia as "an adenosine effect confirming AVNRT"
• Ignoring a history of bronchial asthma, severe AV block without a pacemaker, or WPW syndrome with AF before administration
• Attempting to use the test result (termination or absence of effect) as the sole criterion for the diagnosis of VT or atrial tachycardia without applying Brugada or Vereckei algorithms and the clinical context

Frequently asked questions

Related terms

More in the section "Criteria, Formulas, Algorithms"

Entire section

Sources

• Goldberger A. Clinical Electrocardiography
• Hampton J. The ECG in Practice
• Clinical Guidelines of the Russian Ministry of Health on Supraventricular Tachycardias
• Orlov V.N. Guide to Electrocardiography

Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.