Pulse	Heart rate (beats/min)	Possible nature of any arrhythmia
Arterial pulse
Regular	< 50	Sinus bradycardia
		Second or third degree block
		Atrial flutter with 3 : 1 or 4 : 1 block
		Idionodal rhythm (junctional escape), with or without
		sick sinus syndrome
	60-140	Probable sinus rhythm
	140-160	Sinus tachycardia or an arrhythmia
	150	Probable atrial flutter with 2 : 1 block
	140-170	Atrial tachycardia
		Atrioventricular re-entry tachycardia (AVRT)
		Atrioventricular nodal re-entry tachycardia (AVNRT;
		junctional (nodal) tachycardia)
		Ventricular tachycardia
	> 180	Probable ventricular tachycardia
	300	Atrial flutter with 1 : 1 conduction
Irregular		Marked sinus arrhythmia
		Extrasystoles (supraventricular or ventricular)
		Atrial fibrillation
		Atrial flutter with variable block
		Rhythm varying between sinus rhythm and any arrhythmia or conduction defect
Jugular venous pulse
More pulsations visible than heart rate		Second or third degree block
		Cannon waves – third degree block

MECHANISM OF TACHYCARDIAS

Electrophysiology is the process of recording the ECG from inside the heart, using electrodes inserted via a peripheral vein. This is a highly specialized area, and yields additional information to that obtained from a conventional 12-lead ECG.

The main purpose of electrophysiological studies is to identify the site of origin of an arrhythmia. Arrhythmias occur either because of an abnormality of focal depolarization of the heart, or because of re-entry circuits. If the origin can be localized, the arrhythmia may be prevented permanently by ablation. This technique uses local endocardial (or more rarely epicardial) cautery burns to abolish areas of abnormal cardiac electrical activity, or to interrupt re-entry circuits.

Before the advent of electrical (ablation) therapy, the cause of arrhythmias was a fairly esoteric subject. Now, however, it is essential to understand the underlying electrical mechanisms, because they form the basis of ablation therapy.

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. 3.1) resembles that of a slow ventricular tachycardia, and that is the old-fashioned name for this condition. This rhythm causes no symptoms, and should not be treated.

Fig 3.1 Accelerated idioventricular rhythm
Note

• After two sinus beats, there are four beats of ventricular origin with a rate of 75/min

• Sinus rhythm is then restored

If the junctional intrinsic frequency is increased to a point at which it approximates to that of the SA node, an ‘accelerated idionodal rhythm’ results. This may appear to ‘overtake’ the P waves ( Fig. 3.2). This rhythm used to be called a ‘wandering pacemaker’. The term ‘focal junctional tachycardia’ is used in the (probably rare) instances of a supraventricular tachycardia originating around the AV node, by mechanisms other than re-entry.

Fig. 3.2 Accelerated idionodal rhythm
Note

• After three sinus beats, the sinus rate slows slightly

• A nodal rhythm appears and ‘overtakes’ the P waves

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. 3.3).

Fig. 3.3 Right ventricular outflow tract ventricular tachycardia (RVOT-VT)
Note

• Broad complex tachycardia

• Left bundle branch block and right axis deviation, typical of RVOT-VT

ABNORMALITIES OF CARDIAC RHYTHM DUE TO RE-ENTRY

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 reentry tachycardia (AVRT) experienced by patients with the Wolff-Parkinson-White (WPW) syndrome or the Lown-Ganong-Levine (LGL) syndrome ( Fig. 3.4).

Fig. 3.4 Re-entry pathways in the pre-excitation syndromes
Note

• Broken lines indicate the potential re-entry pathways in AVRT

ATRIOVENTRICULAR RE-ENTRY TACHYCARDIA (AVRT)

In the pre-excitation syndromes, normal and accessory pathways between an atrium and a ventricle together form an anatomical circuit round which depolarization can reverberate, causing a ‘re-entry’ tachycardia ( Fig. 3.5). 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).

Fig. 3.5 Re-entry mechanisms causing tachycardia

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. 3.4). If forward conduction in the accessory pathway is blocked, depolarization can spread down the normal pathway and back (i.e. retrogradely) via the accessory pathway, to reactivate the atria. Recurrent activation of the circuit can cause a ‘circus movement’, resulting in a ‘reciprocating tachycardia’.

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. 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. When the re-entry tachycardia is associated with a narrow QRS complex (i.e. when it is orthodromic), the pattern resembles a junctional (AV nodal re-entry) tachycardia (see below) and the presence of a preexcitation syndrome may not be suspected ( Figs 3.6 and 3.7).

Fig. 3.6 Supraventricular tachycardia
Note

• Narrow complex tachycardia

• No P waves visible

• Some ST segment depression, suggesting ischaemia

Narrow complexes with ST segment depression in lead V₄

Fig. 3.7 Sinus rhythm, the Wolff–Parkinson–White syndrome, type A
Note

• Same patient as in Figure 3.6, after cardioversion

• Sinus rhythm

• Short PR interval

• Broad QRS complexes with delta wave

• Dominant R wave in lead V₁ shows the WPW syndrome type A

Short PR interval and delta wave in lead V₄

The broad complex (antidromic reciprocating) tachycardias which occur in patients with the WPW syndrome may resemble ventricular tachycardia ( Fig. 3.8). A very irregular broad complex tachycardia, as shown in the lower trace of Figure 3.8, will usually be due to the WPW syndrome with atrial fibrillation and antidromic conduction through the re-entry circuit. This rhythm can only be distinguished with certainty from atrial fibrillation and left bundle branch block if the appearance of the ECG in sinus rhythm is known. Superficially, the rhythm may resemble torsade de pointes ventricular tachycardia, but it lacks the characteristic ‘writhing’ of the QRS complexes that is associated with this arrhythmia.

Fig. 3.8 Tachycardias in the Wolff–Parkinson–White syndrome
Note

• The upper trace shows a narrow complex (orthodromic) tachycardia

• The lower trace shows a wide complex (antidromic) tachycardia

• In the lower trace the marked irregularity and variation of the complexes suggest that the rhythm is atrial fibrillation

• The underlying diagnosis of the WPW syndrome is not apparent from either trace

TACHYCARDIAS WITH SYMPTOMS

SINUS RHYTHM CAUSING SYMPTOMS

Sinus rhythm can be irregular (sinus arrhythmia) but the patient is never aware of this. The ECG of a patient with sinus arrhythmia ( Fig. 3.14) may suggest atrial extrasystoles – but in sinus rhythm, P wave morphology is constant while with atrial extrasystoles it varies.

Fig. 3.14 Sinus arrhythmia
Note

• Sinus rhythm

• All P waves identical

• Progressive shortening then lengthening of the R–R interval

Identical P waves and irregular R–R interval

Patients often complain of palpitations that are due to sinus tachycardia: the main causes are exercise, anxiety, thyrotoxicosis and the treatment of asthma with beta-adrenergic agonists, and other causes are summarized in Box 1.1 (p. 3). The ECG in Figure 3.15 shows sinus tachycardia due to an unusual cause – the habitual drinking of large quantities of cola.

Fig. 3.15 Sinus tachycardia

Sinus rhythm, rate 120/min

Nonspecific ST segment changes in leads III,VF,V₆

When sinus tachycardia results from anxiety, heart rates of up to 150/min are possible and the rhythm may be mistaken for an atrial tachycardia. Pressure on the carotid sinus will cause transient slowing of the heart rate and the P waves will become more obvious (see Fig. 3.53, p. 153).

Fig 3.53 CSP and sinus rhythm
Note

• Upper trace shows a broad complex tachycardia

• It is not obvious whether the deflection before the QRS complex represents a T wave, or a T wave followed by a P wave

• Lower trace shows that with CSP the rate falls, and Pwaves become obvious

EXTRASYSTOLES CAUSING SYMPTOMS

An ECG is necessary to differentiate between supraventricular and ventricular extrasystoles.

When extrasystoles have a supraventricular origin ( Fig. 3.16), 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.

Fig. 3.16 Supraventricular extrasystoles
Note

• Sinus rhythm with atrial and junctional extrasystoles

• Normal axis

• Normal QRS complexes

• Inverted T waves in leads III, VF

First beat: normal; second beat: atrial extrasystole, with abnormal P wave; third beat: AV nodal (junctional) extrasystole, with no P wave

Ventricular extrasystoles produce wide QRS complexes of abnormal shape, and the T wave is also usually abnormal. No P waves are present ( Fig. 3.17).

Fig. 3.17 Ventricular extrasystoles
Note

• Sinus rhythm with coupled ventricular extrasystoles

• Sinus beats show tall R waves and inverted T waves in leads V₅–V₆ (indicating left ventricular hypertrophy)

• Extrasystoles are of right bundle branch block (RBBB) configuration, and their T wave inversion has no other significance

Extrasystole with RBBB configuration in lead V₁

When a ventricular extrasystole appears on the upstroke of the preceding beat, the ‘R on T’ phenomenon is said to be present ( Fig. 3.18). This can initiate ventricular fibrillation, but usually it does not do so.

Fig. 3.18 R on T phenomenon
Note

• Ventricular extrasystoles occurring near the peak of the preceding T wave

NARROW COMPLEX TACHYCARDIAS CAUSING SYMPTOMS

A tachycardia can be described as ‘narrow complex’ if the QRS complex is of normal duration, i.e. < 120 ms. Although sinus, atrial and junctional arrhythmias are all supraventricular, the term ‘supraventricular tachycardia’ is often inappropriately used interchangeably with junctional or atrioventricular nodal re-entry tachycardia (AVNRT). All these supraventricular rhythms have QRS complexes of normal shape and width, and the T waves have the same shape as in the sinus beat.

Types of narrow complex tachycardias are listed in Box 3.1.

ATRIAL TACHYCARDIA

In atrial tachycardia ( Fig. 3.19), P waves are present but they have an abnormal shape. They are sometimes hidden in the T wave of the preceding beat.

Fig 3.19 Atrial tachycardia
Note

• Narrow complex tachycardia, heart rate 140/min

• Abnormally shaped P waves, one per QRS comple

• Short PR interval

• ECG otherwise normal

Abnormal P waves in lead II

The P wave rate is in the range 130-250/min. When the atrial rate exceeds about 180/min, physiological block will occur in the AV node, so that the ventricular rate becomes half that of the atria. Atrial tachycardia with 2 : 1 block is characteristic of (but not commonly seen with) digoxin toxicity.

ATRIAL FLUTTER

In atrial flutter, the atrial rate is 300/min 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. Figure 3.20 shows atrial flutter with 2 : 1 block, giving a ventricular rate of 150/min. The ECG in Figure 3.21 is from the same patient after reversion to sinus rhythm.

Fig. 3.20 Atrial flutter with 2:1 block
Note

• Regular narrow complex tachycardia

• ‘Sawtooth’ of atrial flutter most easily seen in lead II

Flutter waves in lead II

The ECG in Figure 3.22 shows atrial flutter with 4 : 1 block.

Fig 3.22 Atrial flutter with 4:1 block
Note

• With 4:1 block and a ventricular rate of 72/min, flutter waves can be seen in all leads

Flutter waves

The ECG in Figure 3.23 shows a narrow complex (and therefore supraventricular) rhythm with a rate of 300/min. This is almost certainly atrial flutter with 1 : 1 conduction.

Fig 3.23 Atrial flutter with 1:1 conduction
Note

• Narrow complex tachycardia at nearly 300/min

• No P waves visible

• Ventricular rate suggests that the underlying rhythm is atrial flutter

Narrow complex tachycardia at 300/min in lead II

If the ventricular rate is rapid and P waves cannot be seen, carotid sinus pressure will usually increase the block in the AV node and make the ‘sawtooth’ more obvious (see Fig. 3.54, p. 153).

Fig 3.54 CSP in atrial flutter
Note

• CSP increases the block at the AV node

• Ventricular activity is completely suppressed

• Flutter waves are obvious

ATRIOVENTRICULAR NODAL RE-ENTRY TACHYCARDIA (AVNRT) OR ‘JUNCTIONAL’ TACHYCARDIA

In AVNRT, no P waves can be seen ( Fig. 3.10, p. 110). Carotid sinus pressure either reverts the heart to sinus rhythm or has no effect (see Fig. 3.55, p. 153).

Fig 3.55 CSP in junctional tachycardia
Note

• CSP reverts junctional tachycardia to sinus rhythm, but in this case multifocal ventricular extrasystoles occurred

The ECG in Figure 3.24 shows a narrow complex tachycardia at 150/min, without any obvious P waves. After reversion to sinus rhythm ( Fig. 3.25), the shape of the QRS complexes does not change.