Abnormal cardiac rhythms can begin in one of three places ( Fig. 3.2): the atrial muscle; the region around the atrioventricular (AV) node (this is called ‘nodal’ or, more properly, junctional′); or the ventricular muscle. Although Figure 3.2 suggests that electrical activation might begin at specific points within the atrial and ventricular muscles, abnormal rhythms can begin anywhere within the atria or ventricles.

Fig. 3.2 Points where cardiac rhythms can begin

Sinus rhythm, atrial rhythm and junctional rhythm together constitute the ‘supraventricular’ rhythms ( Fig. 3.3). In the supraventricular rhythms, the depolarization wave spreads to the ventricles in the normal way via the His bundle and its branches ( Fig. 3.4). The QRS complex is therefore normal, and is the same whether depolarization was initiated by the SA node, the atrial muscle, or the junctional region.

Fig. 3.3 Division of abnormal rhythms into supraventricular and ventricular

Fig. 3.4 Spread of the depolarization wave in supraventricular rhythms

In ventricular rhythms, on the other hand, the depolarization wave spreads through the ventricles by an abnormal and slower pathway, via the Purkinje fibres ( Fig. 3.5). The QRS complex is therefore wide and is abnormally shaped. Repolarization is also abnormal, so the T wave is also of abnormal shape. Remember:

Fig. 3.5 Spread of the depolarization wave in ventricular rhythm

• Supraventricular rhythms have narrow QRS complexes.

• Ventricular rhythms have wide QRS complexes.

• The only exception to this rule occurs when there is a supraventricular rhythm with right or left bundle branch block, or the Wolff-Parkinson-White (WPW) syndrome, when the QRS complex will be wide (see p. 79).

Abnormal rhythms arising in the atrial muscle, the junctional region or the ventricular muscle can be categorized as:

• bradycardias – slow and sustained

• extrasystoles – occur as early single beats

• tachycardias – fast and sustained

• fibrillation – activation of the atria or ventricles is totally disorganized.

THE BRADYCARDIAS – THE SLOW RHYTHMS

It is clearly advantageous if different parts of the heart are able to initiate the depolarization sequence, because this gives the heart a series of failsafe mechanisms that will keep it going if the SA node fails to depolarize, or if conduction of the depolarization wave is blocked. However, the protective mechanisms must normally be inactive if competition between normal and abnormal sites of spontaneous depolarization is to be avoided. This is achieved by the secondary sites having a lower intrinsic frequency of depolarization than the SA node.

The heart is controlled by whichever site is spontaneously depolarizing most frequently: normally this is the SA node, and it gives a normal heart rate of about 70/min. If the SA node fails to depolarize, control will be assumed by a focus either in the atrial muscle or in the region around the AV node (the junctional region), both of which have spontaneous depolarization frequencies of about 50/min. If these fail, or if conduction through the His bundle is blocked, a ventricular focus will take over and give a ventricular rate of about 30/min.

These slow and protective rhythms are called ‘escape rhythms’, because they occur when secondary sites for initiating depolarization escape from their normal inhibition by the more active SA node.

Escape rhythms are not primary disorders, but are the response to problems higher in the conducting pathway. They are commonly seen in the acute phase of a heart attack, when they may be associated with sinus bradycardia. It is important not to try to suppress an escape rhythm, because without it the heart might stop altogether.

The rhythm of the heart can occasionally be controlled by a ventricular focus with an intrinsic frequency of discharge faster than that seen in complete heart block. This rhythm is called ‘accelerated idioventricular rhythm’ ( Fig. 3.10), and is often associated with acute myocardial infarction. Although the appearance of the ECG is similar to that of ventricular tachycardia (described later), accelerated idioventricular rhythm is benign and should not be treated. Ventricular tachycardia should not be diagnosed unless the heart rate exceeds 120/min.

Fig. 3.10 Accelerated idioventricular rhythm
Note

• After three sinus beats, the SA node fails to depolarize

• An escape focus in the ventricle takes over, causing a regular rhythm of 75/min with wide QRS complexes and abnormal T waves

EXTRASYSTOLES

Any part of the heart can depolarize earlier than it should, and the accompanying heartbeat is called an extrasystole. The term ‘ectopic’ is sometimes used to indicate that depolarization originated in an abnormal location, and the term ‘premature contraction’ means the same thing.

The ECG appearance of an extrasystole arising in the atrial muscle, the junctional or nodal region, or the ventricular muscle, is the same as that of the corresponding escape beat – the difference is that an extrasystole comes early and an escape beat comes late.

Atrial extrasystoles have abnormal P waves ( Fig. 3.11). In a junctional extrasystole there is no P wave at all, or the P wave appears immediately before or immediately after the QRS complex ( Fig. 3.11). The QRS complexes of atrial and junctional extrasystoles are, of course, the same as those of sinus rhythm.

Fig. 3.11 Atrial and junctional (nodal) extrasystoles
Note

• This record shows sinus rhythm with junctional and atrial extrasystoles

• A junctional extrasystole has no P wave

• An atrial extrasystole has an abnormally shaped P wave

• Sinus, junctional and atrial beats have identical QRS complexes – conduction in and beyond the His bundle is normal

Ventricular extrasystoles, however, have abnormal QRS complexes, which are typically wide and can be of almost any shape ( Fig. 3.12).

Fig. 3.12 Ventricular extrasystole
Note

• The upper trace shows five sinus beats, then an early beat with a wide QRS complex and an abnormal T wave: this is a ventricular extrasystole (arrowed)

• In the lower trace, the ventricular extrasystoles occur (arrowed) at the peak of the T waves of the preceding sinus beats: this is the ‘R on T’ phenomenon

Ventricular extrasystoles are common, and are usually of no importance. However, when they occur early in the T wave of a preceding beat they can induce ventricular fibrillation (see p. 79), and are thus potentially dangerous.

It may, however, not be as easy as this, particularly if a beat of supraventricular origin is conducted abnormally to the ventricles (bundle branch block, see Ch. 2). It is advisable to get into the habit of asking five questions every time an ECG is being analysed:

1. Does an early QRS complex follow an early P wave? If so, it must be an atrial extrasystole.

2. Can a P wave be seen anywhere? A junctional extrasystole may cause the appearance of a P wave very close to, and even after, the QRS complex because excitation is conducted both to the atria and to the ventricles.

3. Is the QRS complex the same shape throughout (i.e. has it the same initial direction of deflection as the normal beat, and has it the same duration)? Supraventricular beats look the same as each other; ventricular beats may look different from each other.

4. Is the T wave the same way up as in the normal beat? In supraventricular beats, it is the same way up; in ventricular beats, it is inverted.

5. Does the next P wave after the extrasystole appear at an expected time? In both supraventricular and ventricular extrasystoles there is a (‘compensatory’) pause before the next heartbeat, but a supraventricular extrasystole usually upsets the normal periodicity of the SA node, so that the next SA node discharge (and P wave) comes late.

The effects of both supraventricular and ventricular extrasystoles on the following P wave are as follows:

• A supraventricular extrasystole resets the P wave cycle ( Fig. 3.13).

Fig. 3.13 Supraventricular extrasystol
Note

• Three sinus beats are followed by a junctional extrasystole

• No P wave is seen at the expected time, and the next P wave is late

• A ventricular extrasystole, on the other hand, does not affect the SA node, so the next P wave appears at the predicted time ( Fig. 3.14).

Fig. 3.14 Ventricular extrasystole
Note

• Three sinus beats are followed by a ventricular extrasystole

• No P wave is seen after this beat, but the next P wave arrives on time

THE TACHYCARDIAS – THE FAST RHYTHMS

Foci in the atria, the junctional (AV nodal) region, and the ventricles may depolarize repeatedly, causing a sustained tachycardia. The criteria already described can be used to decide the origin of the arrhythmia, and as before the most important thing is to try to identify a P wave. When a tachycardia occurs intermittently, it is called ‘paroxysmal’: this is a clinical description, and is not related to any specific ECG pattern.

SUPRAVENTRICULAR TACHYCARDIAS

Atrial tachycardia (abnormal focus in the atrium)

In atrial tachycardia, the atria depolarize faster than 150/min ( Fig. 3.15).

Fig. 3.15 Atrial tachycardia
Note

• After three sinus beats, atrial tachycardia develops at a rate of 150/min

• P waves can be seen superimposed on the T waves of the preceding beats

• The QRS complexes have the same shape as those of the sinus beats

The AV node cannot conduct atrial rates of discharge greater than about 200/min. If the atrial rate is faster than this, ‘atrioventricular block’ occurs, with some P waves not followed by QRS complexes. The difference between this sort of atrioventricular block and second degree heart block is that in atrioventricular block associated with tachycardia the AV node is functioning properly – it is preventing the ventricles from being activated at a fast (and therefore inefficient) rate. In first, second or third degree block associated with sinus rhythm, the AV node and/or the His bundle are not conducting normally.

Atrial flutter

When the atrial rate is greater than 250/min, and there is no flat baseline between the P waves, ‘atrial flutter’ is present ( Fig. 3.16).

Fig. 3.16 Atrial flutter
Note

• P waves can be seen at a rate of 300/min, giving a ‘sawtooth’ appearance

• There are four P waves per QRS complex (arrowed)

• Ventricular activation is perfectly regular at 75/min

When atrial tachycardia or atrial flutter is associated with 2:1 block, you need to look carefully to recognize the extra P waves ( Fig. 3.17). A narrow complex tachycardia with a ventricular rate of about 125-150/min should always alert you to the possibility of atrial flutter with 2:1 block.

Fig. 3.17 Atrial flutter with 2:1 block
Note

• Atrial flutter with an atrial rate of 250/min is present, and there is 2:1 block, giving a ventricular rate of 125/min

• The first of the two P waves associated with each QRS complex can be mistaken for the T wave of the preceding beat, but P waves can be identified by their regularity

• In this trace, T waves cannot be clearly identified

Any arrhythmia should be identified from the lead in which P waves can most easily be seen. In the record in Figure 3.18, atrial flutter is most easily seen in lead II, but it is also obvious in leads VR and VF.

Fig. 3.18 Atrial flutter with 2:1 block
Note

• P waves at just over 300/min (most easily seen in leads II and VR)

• Regular QRS complexes, rate 160/min

• Narrow QRS complexes of normal shape

• Normal T waves (best seen in the V leads; in the limb leads it is difficult to distinguish between T and P waves

Junctional (nodal) tachycardia

If the area around the AV node depolarizes frequently, the P waves may be seen very close to the QRS complexes, or may not be seen at all ( Fig. 3.19). The QRS complex is of normal shape because, as with the other supraventricular arrhythmias, the ventricles are activated via the His bundle in the normal way.

Fig. 3.19 Junctional (nodal) tachycardia
Note

• In the upper trace there are no P waves, and the QRS complexes are completely regular

• The lower trace is from the same patient, in sinus rhythm. The QRS complexes have essentially the same shape as those of the junctional tachycardia

The 12-lead ECG in Figure 3.20 shows that in junctional tachycardia no P waves can be seen in any lead.

Fig. 3.20 Junctional tachycardia
Note

• No P waves

• Regular QRS complexes, rate 200/min

• Narrow QRS complexes of normal shape

• Normal T waves

Carotid sinus pressure

Carotid sinus pressure may have a useful therapeutic effect on supraventricular tachycardias, and is always worth trying because it may make the nature of the arrhythmia more obvious ( Fig. 3.21). Carotid sinus pressure activates a reflex that leads to vagal stimulation of the SA and AV nodes. This causes a reduction in the frequency of discharge of the SA node, and an increase in the delay of conduction in the AV node. It is the latter which is important in the diagnosis and treatment of arrhythmias. Carotid sinus pressure completely abolishes some supraventricular arrhythmias, and slows the ventricular rate in others, but it has no effect on ventricular arrhythmias.

Fig. 3.21 Atrial flutter with carotid sinus pressure (CSP)
Note

• In this case, carotid sinus pressure (applied during the period indicated by the arrows) has increased the block between the atria and the ventricles, and has made it obvious that the underlying rhythm is atrial flutter

VENTRICULAR TACHYCARDIAS

If a focus in the ventricular muscle depolarizes with a high frequency (causing, in effect, rapidly repeated ventricular extrasystoles), the rhythm is called ‘ventricular tachycardia’ ( Fig. 3.22).

Fig. 3.22 Ventricular tachycardia
Note

• After two sinus beats, the rate increases to 200/min

• The QRS complexes become broad, and the T waves are difficult to identify

• The final beat shows a return to sinus rhythm

Excitation has to spread by an abnormal path through the ventricular muscle, and the QRS complex is therefore wide and abnormal.

Wide and abnormal complexes are seen in all 12 leads of the standard ECG ( Fig. 3.23).

Fig. 3.23 Ventricular tachycardia
Note

• No P waves

• Regular QRS complexes, rate 200/min

• Broad QRS complexes, duration 280 ms, with a very abnormal shape

• No identifiable T waves

Remember that wide and abnormal complexes are also seen with bundle branch block ( Fig. 3.24).

Fig. 3.24 Sinus rhythm with left bundle branch block
Note

• Sinus rhythm: each QRS complex is preceded by a P wave, with a constant PR interval

• The QRS complexes are wide and the T waves are inverted

• This trace was recorded from lead V₆, and the M pattern and inverted T wave characteristic of left bundle branch block are easily identifiable

For more on broad complex tachycardias, see p. 126

HOW TO DISTINGUISH BETWEEN VENTRICULAR TACHYCARDIA AND SUPRAVENTRICULAR TACHYCARDIA WITH BUNDLE BRANCH BLOCK

It is essential to remember that the patient′s clinical state – whether good or bad – does not help to differentiate between the two possible causes of a tachycardia with broad QRS complexes. If a patient with an acute myocardial infarction has broad complex tachycardia it will almost always be ventricular tachycardia. However, a patient with episodes of broad complex tachycardia but without an infarction could have ventricular tachycardia, or supraventricular tachycardia with bundle branch block or the Wolff-Parkinson-White syndrome (see p. 79). Under such circumstances the following points may be helpful:

1. Finding P waves and seeing how they relate to the QRS complexes is always the key to identifying arrhythmias. Always look carefully at a full 12-lead ECG.

2. If possible, compare the QRS complex during the tachycardia with that during sinus rhythm. If the patient has bundle branch block when in sinus rhythm, the QRS complex during the tachycardia will have the same shape as during normal rhythm.

3. If the QRS complex is wider than four small squares (160 ms), the rhythm will probably be ventricular in origin.

4. Left axis deviation during the tachycardia usually indicates a ventricular origin, as does any change of axis compared with a record taken during sinus rhythm.

5. If during the tachycardia the QRS complex is very irregular, the rhythm is probably atrial fibrillation with bundle branch block (see below).

FIBRILLATION

All the arrhythmias discussed so far have involved the synchronous contraction of all the muscle fibres of the atria or of the ventricles, albeit at abnormal speeds. When individual muscle fibres contract independently, they are said to be ‘fibrillating’. Fibrillation can occur in the atrial or ventricular muscle.

ATRIAL FIBRILLATION

When the atrial muscle fibres contract independently there are no P waves on the ECG, only an irregular line ( Fig. 3.25). At times there may be flutter-like waves for 2–3 s. The AV node is continuously bombarded with depolarization waves of varying strength, and depolarization spreads at irregular intervals down the His bundle. The AV node conducts in an ‘all or none’ fashion, so that the depolarization waves passing into the His bundle are of constant intensity. However, these waves are irregular, and the ventricles therefore contract irregularly. Because conduction into and through the ventricles is by the normal route, each QRS complex is of normal shape.