Atrioventricular Re-entrant Tachycardia

Presentation

Atrioventricular tachycardia (AVRT) is the commonest supraventricular arrhythmia in childhood accounting for approximately 33% of cases. It usually presents either in the fetus, neonate or infant but can occasionally present in the older child.

The fetus may have reduced movements or the fast heart rate may be picked up by the midwife or the sonographer during routine antenatal visits. Detailed cardiac ultrasound can usually identify the arrhythmia mechanism and allow treatment to be monitored. The neonatal and infant presentation is usually a rapid heart beat (usually 220 bpm or more) or cardiac failure (poor feeding and breathlessness).

The older child usually complains of intermittent palpitations. Characteristically these have a sudden onset with no obvious precipitating cause and they may also feel a little faint. Although the arrhythmia may spontaneously stop suddenly the patient notices only a gradual reduction in heart rate as it takes time for haemodynamic stability to return.

Mechanism

An accessory pathway (AP) is composed of atrial tissue and bridges the electrically isolating fibrous AV valve ring.

Typically the arrhythmia is orthodromic in nature with the impulse passing retrogradely though the AP. Tachycardia is initiated by either by a ventricular or atrial premature beat. When a ventricular premature beat is responsible then it must occur when the AP is excitable. The depolarisation then passes retrogradely through the AP to activate the atria and back to activate the ventricle again through the AV node initiating tachycardia. If an atrial premature beat triggers the tachycardia then the AP must be refractory and conduction passes anterograde through the AV node and provided the AP is now excitable, retrogradely through the AP to activate the atria again.

AVRT initiated by VE (file download time 15s)

AVRT initiated by PAC (file download time 15s)

Hover the mouse over the heart to see the animation

Much more rarely the tachycardia may be antidromic - the anterograde conduction is down the AP with retrograde AV node conduction. This tachycardia is broad complexed and the ECG can be difficult to distinguish from ventricular tachycardia..

ECG

There are two ECG patterns in sinus rhythm depending upon whether the accessory pathway can conduct anterograde as well as retrogradely. If anterograde conduction is possible then in sinus rhythm the ventricle will be activated prematurely giving a delta wave (blue arrow) and a short PR interval.

Delta wave

Hover the mouse over the heart to see the animation

This is the typical ECG pattern seen in Wolff Parkinson White Syndrome occurring in approximately 25% of all children with SVT. If the AP can only conduct retrogradely then in sinus rhythm the ECG is normal - the so called concealed accessory pathway (30% of patients with AVRT).

In tachycardia the rate is usually 220-240 bpm in the child although rates are often slower in the adult. It is a narrow complex tachycardia as activation is via the AV node and Purkinje system and the delta wave (if present in sinus rhythm) is lost.

AVRT in Tachycardia

The P wave is usually buried in the QRS complex and not visible. These are often know as short RP tachycardia because the distance from the R wave to P wave is shorter than the distance from the P wave to the R wave. This is in contrast to permanent junctional reciprocating tachycardia and atrial ectopic tachycardia.

Management

Acute Attack

The tachycardia may resolve by increasing vagal tone and increasing the AV node refractory period. Immersing a baby's face in cold water initiates the diving reflex and stimulates the vagus. In the older child rubbing the carotid sinus or initiating a valsalva maneuver (whistle trick) may convert the patient to sinus rhythm.

Forced expiration using the thumb as a "whistle"

Unfortunately the majority of patients fail to convert using vagal stimulation and drug treatment is necessary. Adenosine given by rapid intravenous injection (it is metabolised by erythrocytes within 30 seconds) is a very potent AV node blocker and usually terminates the arrhythmia with a non-conducted p wave (arrow). Exceptionally some patients may be haemodynamically compromised by the tachycardia to the extent that they are shocked. DC cardioversion may be required if adenosine fails to terminate the tachycardia.

Adenosine conversion

Most patients will then remain in sinus rhythm but others will revert into tachycardia. They may then require further antiarrhythmic therapy the choice of which will depend upon the age but may include digoxin, β blockers, flecainide or verapamil.

Recurrent Attacks

The necessity for treatment depends upon the frequency of attacks, their severity and the affect upon lifestyle. Those with brief, infrequent attacks do not require treatment. When treatment is required then the choice is between drug therapy or radiofrequency ablation and selected according to the patient's age, expected prognosis and family preference.

Prognosis

Those presenting in the fetal and neonatal period may only have a single episode of tachycardia or recurrences confined to the first year of life. Their prognosis is excellent however a small minority (10%) may have a recurrence in later childhood.

If presentation is later in childhood then the episodes of tachycardia tend to persist with periods of exacerbation and remission. Whilst these may be no more than "nuisance value" in adult life they can be life threatening if atrial fibrillation occurs in those with anterograde AP conduction (ie. those with a delta wave) as very fast ventricular rates can occur with an antidromic tachycardia. Digoxin therapy is contraindicated in these patients because it reduces the refractory period of the AP and thus encourage even higher ventricular rates.

This page was last edited 14/2/2004

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