Atrial Tachycardia

Firstly there is disagreement about how the term atrial tachycardia should be used. A strict definition would be all fast rhythms which originate in the atria and that not require other tissue to sustain. This would of course include typical atrial flutter and atrial fibrillation (AF). We can exclude AF however as atrial tachycardias must be (fairly) regular.

Focal verses re-entrant mechanisms

In practice electrophysiologists tend to use this term to refer to focal atrial tachycardias. Re-entrant tachycardias are referred to as macro re-entrant atrial tachycardia or atrial flutters. Sometimes distinction between focal and re-entrant cannot be made on the basis of the surface ECG, particularly if there is atrial disease or previous surgery/ablation. For example both focal and re-entrant atrial tachycardias are reported as a complication after AF ablation and in these patients a diagnosis of the underlying mechanism may only be possible at an EP study.

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A focal tachycardia originates from a point source with activation spreading concentrically to activate surrounding tissue. The rate of firing of the focus drives the tachycardia rate – sinus tachycardia for example is a focal atrial tachycardia. In contrast re-entrant rhythms occur due to the existence of an “endless loop” of activation with an impulse travelling in a circuit formed by obstacles to conduction – an analogy is a Mexican wave. The time taken for one revolution of the circuit (the cycle length) determines the rate of tachycardia. Focal tachycardias are ablated by identifying the site of earliest activation - in atrial tachycardias this occurs before the onset of the p wave on the surface ECG. Re-entrant tachycardias are ablated by defining the tachycardia circuit and ablating a critical isthmus (narrow region) of slow conduction without which the circuit cannot sustain.

In focal tachycardias there is often (but not always) an iso-electric baseline between p waves, as is seen in sinus tachycardia. If this is evident in all 12 leads the rhythm is likely to be focal. Unfortunately the preceding T wave can interfere with this determination during one to one conduction. An iso-electric interval occurs because atrial activation occurs in a shorter period of time than the tachycardia cycle length, leaving an interlude between the latest atrial activation and the next depolarisation of the focus. However, where there is slow atrial conduction away from the focus and/or the tachycardia is particularly rapid the iso-electric line can be absent. In macro re-entrant atrial tachycardia (atrial flutters) there must be continuous activation in the re-entrant circuit from one cycle to the next (see fig 4). This manifests as “flutter” or “f” waves on the surface ECG rather than distinct p waves. Re-entrant atrial rhythms occur in patients with atrial pathology, previous atrial surgery or extensive ablation for AF.

At EP study mode of initiation and termination, reliance on isoprenaline for induction, warm-up/cool down and responses to entrainment contribute to an understanding of the mechanism, which is critical for the adoption of an appropriate ablation strategy.

Diagnosis

In the absence of bundle branch block or an accessory pathway atrial tachycardias present as a regular narrow complex tachycardia. The differential diagnosis is AV nodal re-entrant tachycardia (AVNRT), A-V re-entrant tachycardia (AVRT) atrial tachycardia or atrial flutter. Atrial tachycardia can sustain without the participation of the ventricles or the AV node. The diagnosis is therefore self evident where there is a high degree of A-V block (see fig 4). When atrial tachycardias are conducted to the ventricle in a one to one relationship the diagnosis may be more difficult. Adenosine can be used to induce transient high grade AV block – if the tachycardia can sustain despite loss of AV conduction it is atrial tachycardia. Unfortunately some atrial tachycardias are terminated by adenosine (adenosine sensitive) and so termination, though suggesting AV nodal involvement in a circuit (i.e. AVNRT, AVRT) cannot rule out atrial tachycardia.

In some cases the p wave morphology can be seen to be inconsistent with retrograde atrial activation. In AVNRT and AVRT the atrial activation must be retrograde –it must begin somewhere on the A-V ring. A p wave axis or intra-cardiac signal sequence not consistent with retrograde atrial activation strongly supports a diagnosis of atrial tachycardia. This is seen in figures 1 and 2 showing tachycardia from the superior crista terminalis. The p wave is similar to a sinus p wave with activation from superior to inferior (“high to low”). On the intracardiac signals the high right atrial (HRA) signal is much earlier than the annular signals (CS and His catheter) – inconsistent with retrograde activation. When the atrial sequence is consistent with retrograde activation, particularly when compatible with atypical AVNRT, the diagnosis is more difficult.

Pacing manoeuvres can be used to facilitate a diagnosis. One technique involves entraining the tachycardia from the ventricle and observing the A-V relationship on cessation of pacing (see fig 7) An A-A-V response (in contrast to an A-V response) upon cessation of ventricular pacing associated with 1:1 ventriculo-atrial conduction is highly sensitive and specific for distinguishing atrial tachycardia.

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• Figure 7 Figure 7
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Focal atrial tachycardia

Focal atrial tachycardia (AT) is a relatively uncommon form of supra-ventricular tachycardia (10%) often in the absence of structural heart disease. It is usually located to one of a number of specific anatomical “hot spots”. The pulmonary veins have received an enormous amount of publicity in recent years due to their importance in atrial fibrillation. However, 75% of patients presenting for ablation of regular focal atrial tachycardias (in patients who have not had previous AF ablation) have a right atrial source. The crista terminalis accounts for some 60% of right atrial tachycardias whilst the pulmonary veins are the site of origin of half of all left atrial tachycardias. The cellular mechanism underlying focal atrial tachycardias is abnormal automaticity or triggered activity. Automatic tachycardias may exhibit “warm up” and “cool down” behaviour on initiation and termination.

Ablation of focal atrial tachycardia

Ablation is achieved by targeting sites of earliest atrial activation that precede the p wave during tachycardia (see fig 8). Potential complications are related to the anatomical location of the focus. The crista terminalis is close to the sinus node and the phrenic nerve, so there is a potential for damage to these structures. Sinus node damage is rare but its location can be mapped used 3D mapping systems and the timing of the ablation electrogram should not be the earliest recordable signal in sinus rhythm. Proximity to the phrenic nerve can be checked phrenic nerve stimulation by high output pacing from the ablation catheter. There is a risk AV block complicating ablation of Triangle of Koch foci due to their proximity to the AV node. Cryoablation may be used to maximise safety. Left atrial locations necessitate transeptal puncture with its associated risks.

References/further reading

• Kistler PM, Roberts-Thomson KC, Haqqani HM, Fynn SP, Singarayar S, Vohra JK, Morton JB, Sparks PB, Kalman JM
  P-Wave Morphology in Focal Atrial Tachycardia: Development of an Algorithm to Predict the Anatomic Site of Origin
  Journal of the American College of Cardiology Vol. 48, No. 5, 2006

• Knight BP, Adam Zivin A, Souza J, Flemming M, Pelosi F, Goyal R, Ching Man K, Strickberger A, Morady F
  A Technique for the Rapid Diagnosis of Atrial Tachycardia in the Electrophysiology Laboratory
  Journal of the American College of Cardiology Vol. 33, No. 3, 1999