Enhanced automaticity and triggered activity

If the intrinsic frequency of depolarization of the atrial, junctional or ventricular conducting tissue is increased, an abnormal rhythm may occur. This phenomenon is called ‘enhanced automaticity’. Single early beats, or extrasystoles, may be due to enhanced automaticity arising from a myocardial focus. The most common example of a sustained rhythm due to enhanced automaticity is ‘accelerated idioventricular rhythm’, which is common after acute myocardial infarction. The ECG appearance (Fig. 4.1) resembles that of a slow ventricular tachycardia (VT). This rhythm causes no symptoms and should not be treated.

If the junctional intrinsic frequency is increased to a point at which it approximates to that of the sinoatrial node, an ‘accelerated idionodal rhythm’ results. This may appear to ‘overtake’ the P waves (Fig. 4.2). This rhythm used to be called a ‘wandering pacemaker’. Enhanced automaticity is also thought to be the mechanism causing some non-paroxysmal tachycardias, particularly those due to digoxin intoxication.

‘Triggered activity’ results from late depolarizations which occur after normal depolarization, during what would normally be a period of repolarization. Like enhanced automaticity, this can cause extrasystoles or a sustained arrhythmia, such as right ventricular outflow tract ventricular tachycardia (RVOT-VT) (Fig. 4.3).

Normal conduction results in the uniform spread of the depolarization wave front in a constant direction. Should the direction of depolarization be reversed in some part of the heart, such as in an accessory connection between the atria and ventricles, it becomes possible for a circular or ‘re-entry’ pathway to be set up. Activation travels round and round the circuit, causing a tachycardia such as the atrioventricular re-entry tachycardia (AVRT) experienced by patients with Wolff–Parkinson–White (WPW) syndrome or the atrioventricular nodal re-entry tachycardia (AVNRT) (Fig. 4.4).

Except in the case of the pre-excitation syndromes, there is no certain way of distinguishing from the surface ECG between a tachycardia due to enhanced automaticity and one due to re-entry. In general, however, tachycardias that follow or are terminated by extrasystoles, and those that can be initiated or inhibited by appropriately timed intracardiac pacing impulses, are likely to be due to re-entry (Figs 4.5 and 4.6).

Occasional extrasystoles are a normal variant (see Ch. 1, p. 5, Figs 1.7 and 1.9). However, some patients may experience associated symptoms. Extrasystoles may occur in clusters. When occurring every other beat this is termed bigeminy, and when occurring every third beat trigeminy. Very frequent ventricular extrasystoles are sometimes associated with structural or ischaemic heart disease. An ECG is necessary to differentiate between supraventricular and ventricular extrasystoles.

When extrasystoles have a supraventricular origin (Fig. 4.7), the QRS complex is narrow and both it and the T wave have the same configuration as in the sinus beat. Atrial extrasystoles have abnormal P waves. Junctional (AV nodal) extrasystoles either have a P wave very close to the QRS complex (in front of it or behind it) or have no visible P waves.

Ventricular extrasystoles produce wide QRS complexes of abnormal shape, and the T wave is also usually abnormal. No P waves are present (Fig. 4.8).

When a ventricular extrasystole appears on the upstroke of the preceding beat, the ‘R on T’ phenomenon is said to be present (Fig. 4.9). This can initiate ventricular fibrillation, but usually it does not do so.

The types of narrow complex tachycardias are listed in Box 4.1.

Atrioventricular re-entry tachycardia

In the pre-excitation syndromes, normal and accessory pathways between an atrium and a ventricle together form an anatomical circuit around which depolarization can reverberate, causing a ‘re-entry’ tachycardia (Fig. 4.10). Once established, a circular wave of depolarization will continue until some part of the pathway fails to conduct. Alternatively, the circular wave may be interrupted by the arrival of another depolarization wave, set up by an ectopic focus (e.g. an extrasystole).

In the WPW syndrome, the re-entry circuit comprises the normal AV node–His bundle connection between the atria and the ventricles, and an accessory pathway, the bundle of Kent, which also connects the atria and ventricles, bypassing the AV node (Fig. 4.4). If forward conduction in the accessory pathway is blocked (e.g. by an extrasystole causing the pathway to be transiently refractory to depolarization), conduction can spread down the normal pathway and back (i.e. retrogradely) via the accessory pathway (which by this time is no longer refractory), to reactivate the atria. Recurrent activation of the circuit can cause rapid cycling leading to a tachyarrhythmia.

The tachycardia is described as ‘orthodromic’ when conduction within the His bundle is in the normal direction: the ECG then has narrow QRS complexes, and sometimes P waves are visible just after each QRS complex. The pattern resembles an AV nodal re-entry tachycardia (see below), and the presence of a pre-excitation syndrome may not be suspected until sinus rhythm is restored (Figs 4.11 and 4.12) – except in ‘concealed cases’ where the sinus 12-lead ECG may be normal (see Ch. 2, pp 68–72)

Less commonly, depolarization passes down the accessory pathway and retrogradely up the His bundle, to cause an ‘antidromic reciprocating tachycardia’, in which the QRS complexes are broad and slurred, and P waves may or may not be seen.

This is described below in the section on broad complex tachycardias (see page 135)

AV nodal re-entry tachycardia (AVNRT)

AVNRT, or junctional tachycardia, originates in or very close to the AV node or His bundle. It may be facilitated by a congenital abnormality of the AV node, in which there are two (or sometimes more) electrically distinct pathways. These allow re-entry to start and be sustained within the node itself. In the absence of a tachycardia, the sinus ECG has no distinguishing features, so the potential for an AVNRT (as for a ‘concealed’ AVRT) cannot be detected from the baseline sinus ECG, unlike in cases of ‘manifest’ WPW. During AVNRT, atrial and ventricular activation are virtually simultaneous, so the P wave is hidden within the QRS complex (Figs 4.13 and 4.14). Carotid sinus pressure either reverts the heart to sinus rhythm or has no effect, but the circuit can usually be disrupted by administration of incremental doses of adenosine. The ECG in Fig. 4.14 shows a narrow complex tachycardia at 150 bpm, without any obvious P waves. After reversion to sinus rhythm (Fig. 4.15), the shape of the QRS complexes does not change.

Atrial tachycardia

Re-entry within the atrial muscle causes a tachycardia characterized by P waves with a different shape to those occurring with normal sinus beats. Atrial tachycardia can also result from enhanced automaticity. In atrial tachycardia (Fig. 4.16), P waves are present but they have an abnormal shape. They are sometimes hidden in the T wave of the preceding beat.

The P wave rate is in the range 130–250 bpm. When the atrial rate exceeds about 180 bpm, physiological block will occur in the AV node, so that the ventricular rate becomes half that of the atria.

Atrial flutter

Atrial flutter depends on a variety of re-entry circuits, which often occupy large areas of the atrium and are known as ‘macro-re-entrant’ circuits. The most common type of flutter, ‘isthmus-dependent’ flutter, involves circuits utilizing the cavotricuspid isthmus. The involvement of this defined isthmus is important in considering ablation therapy (see p. 139 and Fig. 4.48). In atrial flutter, the atrial rate is around 300 bpm and the P waves form a continuous ‘sawtooth’ pattern. As the AV node usually fails to conduct all the P waves, the relationship between P waves and QRS complexes is usually 2 : 1, 3 : 1 or 4 : 1. Fig. 4.17 shows atrial flutter with 2 : 1 block, giving a ventricular rate of 150 bpm. The ECG in Fig. 4.18 is from the same patient after reversion to sinus rhythm.

The ECG in Fig. 4.19 shows atrial flutter with 4 : 1 block.

The ECG in Fig. 4.20 shows a narrow complex (and therefore supraventricular) rhythm with a rate of 300 bpm. This is almost certainly atrial flutter with 1 : 1 conduction.