Adenosine in Electrophysiology

An important drug you will come across in electrophysiology is ADENOSINE.
This article introduces uses of adenosine in electrophysiology. It does not cover indications/contraindications or dose, for which local/national guidelines should be consulted.

Adenosine is a naturally occuring compound that plays an important role in many biochemical processes. It inhibits calcium channels causing a decrease in the conduction velocity of the atrioventricular (AV) node. At sufficient dose this causes transient AV nodal block, an action that can be useful to the electrophysiologist.

Adenosine also slows the rate of firing of pacemaker cells, resulting in sinus bradycardia. Because it is rapidly metabolised these effects last ony seconds.

Because the depolarisation of cardiac muscle cells is less dependent on calcium channels, atrial/ventricular tissue is much less sensitive to adenosisne.

Accessory pathways including those responsible for Wolff Parkinson White syndrome are comprised of normal cardiac muscle cells so are not usually affected by adenosine.

Summary of the electrophysiological effects of adenosine:

• Profound effect on “pacemaker” cells

• At sufficient dose blocks the AV node

• Will terminate a re-entry circuit which involves the AV node

• Doesn’t affect most accessory pathways

• May terminate some focal atrial and focal ventricular tachycardias

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Use of Adenosine in Electrophysiology

Adenosine is used in two ways. Firstly, for non-invasive termination of tachycardias and second, in the EP lab to unmask accessory pathways or confirm their ablation. The effect of adenosine given in an attempt to terminate tachycardia can provide useful clues about the nature of the arrrythmia.

Therapeutic use: To terminate symptomatic tachycardias in an emergency room setting

Adenosine is often chosen to terminate tachycardias in particular narrow complex tachycardia because it blocks the AV node - an essential part of the re-entrant circuit for two very common arrhythmias - AV nodal re-entrant tachycardia (AVNRT) and AV re-entry tachycardia (AVRT). The very short half life is also useful.

Diagnostic information provided by adenosine

Termination of tachycardia by adenosine suggests involvement of the AV node in a re-entry circuit. The AV node is one limb of the re-entrant circuit in AVNRT and AVRT.

Failure to terminate indicates either that the dose was insufficient to cause AV nodal block or that the AV node is not a requisite structure for maintenance of the particular tachycardia.

The AV node is not essential for maintenance of atrial or ventricular tachycardia and so these arrythmias may continue in the presence of AV nodal block. I have stressed may continue because, to make things awkward some atrial and indeed some ventricular tachycardias are terminated by adenosine.

When atrial tachycardia is conducted to the ventricles in a 1:1 relationship the frequent QRS complexes and T waves can obscure the p waves and make diagnosis difficult or impossible. By introducing a higher degree of AV block adenosine allows p waves to be seen. Continuation of tachycardia with more p waves than QRS complexes is indicative of atrial tachycardia and the p waves morphology can be ascertained. Atrial flutter may present with 1:1 conduction (see fig 3). This is more common when the flutter rate is somewhat slower than usual or has been slowed by anti-arrhythmic medication.

Administration of adenosine often allows underlying flutter waves to be seen and a diagnosis to be made. Flutter is not terminated by adenosine but changing AV node conduction from 1:1 to 2:1 reveals the flutter waves in the inferior leads (see Fig 5).

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Use of Adenosine during EP and Ablation Procedures

Electrophysiologists use the ability of adenosine to selectively block the AV node to reveal “hidden” accessory pathways. A pathway may be hard to identify because it has conduction and refractory properties similar to the AV node. Sometimes during an ablation attempt an accessory pathway becomes difficult to detect because of damage it has sustained during energy application.

By blocking AV node conduction adenosine can reveal accessory pathway conduction and can help confirm successful pathway ablation.

Figure 5 shows the surface ECG during administration of adenosine in a patient with Wolff Parkinson White (WPW) following a number of energy applications. Although there is a suspicion of remaining pre-excitation even before adenosine (see V2), slowing/block in AV node conduction caused by adenosine reveals a more overt WPW appearance. Note also the slowing of the sinus rate also due to adenosine.

Intra-cardiac signals

Figure 6 documents the administration of adenosine. The first two QRS complexes on the ECG (bottom left) are narrow and appear normal. The last two are broad with a right bundle branch block appearance. Look at the middle ECG complex – the QRS morphology is a mixture of the other two – a fusion complex. As is often the case, the His electrogram is key to understand EP. The AH interval, which represents conduction through the AV node is normal for the first two beats but starts to lengthen on the third. On the last two beats the His spike apparently disappears (it has probably fused with the ventricular component labelled V).

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• Figure 7 Figure 7
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Now look at CS 11-12. There are two components for each beat – the first is sharp (the atrial component) and the second smaller and more rounded (the ventricular component). If you run your eye along the trace you notice that the interval between these left atrial and left ventricular components stays constant.

This patient has a left-sided accessory pathway yet there is little evidence of this on the surface ECG. Adenosine has caused progressive slowing of the AV node but pathway conduction remains constant. Consequently more and more of the ventricles are activated via than pathway, resulting in first a fused and then a pre-excited complex.
The previous examples document the use of adenosine to demonstrate anterograde (atrium to ventricle) accessory pathway function. However some accessory pathways, known as concealed pathways only conduct retrogradely (ventricle to atrium). For adenosine to be useful in determining the presence or absence of such pathways it must be administered during ventricular pacing instead of sinus rhythm. VA block demonstrates the absence of a concealed accessory pathway in the same way that AV block demonstrates absence of an anterograde pathway.

Figure 7 shows adenosine given at the end of an ablation to confirm procedural success. It is given during continuous ventricular pacing (note the surface ECG). The fourth V paced beat is not conducted to the atrium (there are no corresponding atrial signals) due to retrograde block in the AV node. (Note - the third beat is probably conducted via the slow AV nodal pathway).

Figure 8 In this case the retrograde activation sequence was very similar to that during normal AV node conduction because of the anatomical location of the pathway (right anterior/right antero-septal). Continuation of VA conduction despite anterograde AV block added to the evidence for an accessory pathway.

Adenosine is administered and V pacing initiated immediately anterograde AV block is observed. There is VA conduction at the onset of pacing and if the AV node is blocked this conduction must be taking a different route- over an accessory pathway.

Caution: Initiatiation of Atrial Fibrillation

By causing a shortening of the atrial refractory period adenosine can promote atrial fibrillation, which may initiate polymorphic VT or VF in some patients with WPW syndrome. Evidence of the pathway may not be present in tachycardia, which may have a narrow complex (orthodromic AVRT).