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).

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).

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.

ATRIAL TACHYCARDIA

Re-entry within the atrial muscle causes a tachycardia characterized by P waves with a shape different from that of those related to sinus rhythm. The PR interval is usually short ( Fig. 3.9). Atrial tachycardia can also result from enhanced automaticity.

ATRIAL FLUTTER

Atrial flutter is an organized atrial rhythm with a rate of 250-350/min. This rhythm 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 a defined isthmus is important in considering ablation therapy (see p. 157).

AV NODAL RE-ENTRY TACHYCARDIA (AVNRT)

Atrioventricular nodal re-entry tachycardia (AVNRT), also known as atrioventricular nodal reciprocating tachycardia, originates in 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 ECG has no distinguishing features, so the potential for an AVNRT cannot be detected from the ECG, unlike in cases of the WPW and LGL syndromes. During AVNRT, atrial and ventricular activation are virtually simultaneous, so the P wave is hidden within the QRS complex ( Fig. 3.10). AVNRT used to be called ‘junctional tachycardia’.

VENTRICULAR TACHYCARDIA

Ventricular tachycardia may be due to re-entry through circuits within the ventricles (for example around areas of scar tissue following myocardial infarction), or may result from enhanced automaticity or triggered activity. The broad QRS complexes are of a constant configuration and are fairly regular if the re-entry pathway is constant ( Fig. 3.11).

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.

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.

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

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.

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).

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).

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.

The ECG in Figure 3.6 (p. 106) shows what appears to be a straightforward AVNRT, but on return to sinus rhythm ( Fig. 3.6) it shows the Wolff-Parkinson-White type A pattern. The tachycardia was therefore orthodromic, with the re-entry circuit involving anterograde (normal) conduction down the AV node and His bundle (see Fig. 3.5, p. 107).

ATRIAL FIBRILLATION

In atrial fibrillation, disorganized atrial activity causes the P waves to disappear and the ECG baseline becomes totally irregular ( Fig. 3.26). At times atrial activity may become sufficiently synchronized for a ‘flutter-like’ pattern to appear, but this rapidly breaks up ( Fig. 3.27). In atrial fibrillation, as opposed to atrial flutter, the frequency of the QRS complexes is totally irregular.

Some causes of atrial fibrillation are summarized in Box 3.2.

1. The presence of P waves. If there is one P wave per QRS complex, it must be sinus rhythm with bundle branch block. If P waves can be seen at a slower rate than the QRS complexes, it must be VT.

2. QRS complex duration. If longer than 160 ms, it is probably VT.

3. QRS complex regularity. VT is usually regular. An irregular broad complex tachycardia usually means atrial fibrillation with abnormal conduction.

4. The cardiac axis. VT is usually associated with left axis deviation.

5. QRS complex configuration. If the QRS complexes in the V leads all point either upwards or downwards (‘concordance’) it is probably VT.

6. When the QRS complex shows a right bundle branch block pattern, a supraventricular tachycardia with abnormal conduction is more likely if the second R peak is higher than the first. VT is likely if the first R peak is higher.

7. The presence of fusion and capture beats indicates that the broad complexes are due to VT (see p. 142).

P WAVES

The ECG in Figure 3.29 is from a patient with an acute infarction, and shows a broad complex rhythm at about 110/min. One P wave per QRS complex can clearly be seen, and this is obviously sinus rhythm with left bundle branch block (LBBB).

The ECG in Figure 3.30 shows a very irregular broad complex rhythm with no obvious P waves. There is an obvious LBBB pattern in leads V₅ and V₆. Whether the R-R interval is short or long, the appearance of the QRS complex is the same. The irregularity is the key to the diagnosis of atrial fibrillation with LBBB.

The ECG in Figure 3.31 is also an example of atrial fibrillation and LBBB, but this is not quite as obvious as in Figure 3.30. The QRS complexes at first sight may appear regular, but on close inspection they are not. The LBBB is also not so obvious, but can be seen in lead I.

Occasionally it may be possible to identify P waves with a slower rate than the QRS complexes, indicating that the QRS complexes must be ventricular in origin. A 12-lead ECG during the tachycardia is important for this, because P waves may be visible in some leads but not in others ( Fig. 3.32).

THE QRS COMPLEX

The ECG in Figure 3.33 shows a broad complex tachycardia recorded from a patient with an acute infarction, and there is no question that this represents VT.

The important features are:

The ECG in Figure 3.34 shows an ECG from another patient with an acute infarction. The shape of the QRS complexes is different from that in Figure 3.33, but the principles are the same:

The ECG in Figure 3.35 shows another example of VT, but this time the axis is normal. Unfortunately the ‘rules’ for diagnosing VT are not absolute and one or more of the features above may not be present.

The ECG in Figure 3.36 shows atrial fibrillation with an abnormal QRS complex, the duration of which (116 ms) is just within the normal range. The RSR¹ pattern, most obviously seen in lead V₂, and the slurred S wave in lead V₆, show that this is partial right bundle branch block (RBBB). Note that the second R peak of the QRS complex (R¹) is higher than first peak. This is characteristic of RBBB. These features show that this is a supraventricular rhythm.

The ECG in Figure 3.37 shows a regular tachycardia with no P waves and a QRS complex showing an RBBB pattern. The duration of the QRS complex is at the upper limit of normal, at 120 ms. This might be a supraventricular tachycardia (probably AVNRT) with RBBB conduction, or it might be a fascicular tachycardia. A fascicular tachycardia usually arises in the posterior fascicle of the left bundle branch. Typically there is left axis deviation (not present here). Fascicular tachycardia is an unusual rhythm with a benign prognosis, and it typically responds to verapamil.

The ECG in Figure 3.38 shows how difficult differentiation between supraventricular and ventricular rhythms can be. Some features suggest a supraventricular, and some a ventricular, origin of the rhythm.

Often only a comparison of the patient′s ECGs taken in sinus rhythm and when the tachycardia is present will establish the nature of the tachycardia. In the case of any patient with a tachycardia it is essential to look through the old notes, to see if any ECGs have been recorded previously. The ECG in Figure 3.39 shows the broad complex tachycardia of a patient who was in pain and was hypotensive. He was cardioverted, and Figure 3.40 shows the post-cardioversion record. The QRS complexes are narrow, so the arrhythmia must have been VT.

Figure 3.41 shows the ECG from a patient admitted to hospital with an inferior myocardial infarction, initially with atrial fibrillation. The patient then developed a broad complex tachycardia ( Fig. 3.42). In the context of an acute infarction this would almost certainly be VT. A comparison of Figures 3.41 and 3.42 shows the development of a different, indeterminate, axis and of RBBB. The change of axis is a strong pointer to a ventricular origin of the rhythm.

FUSION BEATS AND CAPTURE BEATS

If an early beat can be found with a narrow QRS complex, it can be assumed that a wide complex tachycardia is ventricular in origin. The narrow early beat demonstrates that the bundle branches will conduct supraventricular beats normally, even at high heart rates.

A ‘fusion beat’ is said to occur when the ventricles are activated simultaneously by a supraventricular and a ventricular impulse, so that a QRS complex with an intermediate pattern is seen ( Fig. 3.43). The appearance of fusion beats is variable.

A ‘capture beat’ occurs when the ventricles are activated by an impulse of supraventricular origin during a run of VT (also shown in Fig. 3.43), and so capture beats have a QRS complex like those seen in a supraventricular rhythm. Figure 3.44 shows another example of a capture beat, indicating that the broad complex tachycardia is VT.

DIFFERENTIATION OF BROAD COMPLEX TACHYCARDIAS

Box 3.5 summarizes some distinguishing features of broad complex tachycardias.

RIGHT VENTRICULAR OUTFLOW TRACT TACHYCARDIA (RVOT-VT)

This is usually an exercise-induced tachycardia, which originates in the right ventricular outflow tract. It is recognizable because the broad complex tachycardia shows a combination of right axis deviation and left bundle branch block ( Fig. 3.45). RVOT-VT can be treated by ablation.

1. Consider possible underlying diagnoses.

2. Simple investigations:

3. Ambulatory ECG: 24-h recording if symptoms are frequent, or event recording when symptoms are infrequent.

4. Echocardiography, to aid diagnosis when any sort of structural heart disease seems possible (e.g. valve disease with atrial fibrillation, or cardiomyopathy with syncope).

5. Tilt testing, when neurocardiogenic syncope or orthostatic hypotension (rather than an arrhythmia) is suspected.

PRECIPITATION OF ARRHYTHMIAS

Arrhythmias are sometimes precipitated by exercise ( Fig. 3.51), and if the patient′s history suggests that this is so, then treadmill testing may be helpful. Attempts to provoke an arrhythmia by exercise should, however, only be made when full resuscitation facilities are available.

If the patient complains of syncopal attacks, particularly on movement of the head, it is worth pressing the carotid sinus in the neck to see if the patient has carotid sinus hypersensitivity. Complete SA node inhibition may be induced, sometimes with unpleasant effects ( Fig. 3.52).

• Does the arrhythmia need treating as an emergency?

• Does the arrhythmia have an obvious cause?

• Some possible causes of palpitations are listed in Box 3.7.

• Consider the principles of arrhythmia management:

CAROTID SINUS PRESSURE IN THE MANAGEMENT OF TACHYCARDIAS

The first step in the management of any tachycardia is to try carotid sinus pressure (CSP).

In sinus rhythm, CSP will cause transient slowing of the heart rate. This may be useful in identifying the true origin of the rhythm when there is doubt ( Fig. 3.53).

In atrial flutter, AV conduction is blocked so the ventricular rate falls. The atrial activity becomes obvious, which helps to identify the rhythm ( Fig. 3.54). CSP seldom converts atrial flutter to sinus rhythm.

In atrial tachycardia and junctional tachycardia, CSP may restore sinus rhythm ( Fig. 3.55).

In atrial fibrillation and ventricular tachycardia, CSP has no effect.

• Supraventricular: no treatment. If the patient has symptoms, explanation and reassurance. Advise to discontinue smoking and avoid coffee and alcohol.

• Ventricular: usually no treatment, though treatment may be considered:

• Three ventricular extrasystoles together (a ‘salvo’) should be treated as a ventricular tachycardia.

1. Carotid sinus massage.

2. Adenosine 3 mg i.v. bolus, followed if necessary after 2 min by a further 6 mg adenosine and, if necessary after a further 2 min, by a further 12 mg adenosine. Unwanted but transient effects include asthma, flushing, chest tightness and dizziness.

3. Verapamil 2.5-5 mg i.v. or atenolol 2.5 mg i.v., repeated at 5 min intervals to a total of 10 mg. Note: These drugs should not be administered together, and verapamil should not be given to patients receiving a beta-blocker.

4. DC shock.

• have had atrial fibrillation for more than a year

• have cardiac enlargement

• have any form of structural abnormality in the heart.

• i.v. amiodarone

• i.v. verapamil

• i.v. beta-blocker

• i.v. digoxin 250 |g by slow injection, repeated at 30 min intervals to a total of 1 mg,

PREVENTION OF PAROXYSMAL ATRIAL FIBRILLATION

Atrial fibrillation is called ‘paroxysmal’ if there are attacks that revert spontaneously; ‘persistent’ if the rhythm is continuous but cardioversion has not been attempted; and ‘permanent’ if cardioversion has failed.

Digoxin will probably not prevent attacks of atrial fibrillation, but the prophylactic use of some drugs may prevent attacks for months, or possibly years:

These drugs can be used after DC cardioversion, but at best only about 40% of patients will still be in sinus rhythm after a year.

Electrophysiological ablation is an option (see below) and in very resistant cases, electrical ablation of the AV node can be used to cause complete heart block, and a permanent pacemaker inserted.

• Lidocaine 100 mg i.v., repeated twice at 5 min intervals, followed by a lidocaine infusion at 2–3 mg/min.

• Amiodarone 300 mg i.v. over 30 min then 900 mg over 24 h, followed by 200 mg t.d.s. by mouth for 1 week, 200 mg b.d. for 1 week and 200 mg daily thereafter.

• Atenolol 2.5 mg i.v., repeated at 5 min intervals to 10 mg.

• Flecainide 50–100 mg i.v., or 100 mg b.d. by mouth – but avoid in patients with coronary disease.

• Magnesium 8 mmol i.v. over 15 min, followed by 64 mmol over 24 h.

• atenolol

• flecainide

• amiodarone.

ATRIAL FLUTTER

Typical atrial flutter results from a re-entry circuit within the atria. This can be abolished by ablating an area known as the right atrial isthmus, which prevents re-entry from occurring ( Fig. 3.58).

ATRIAL FIBRILLATION

There is increasing evidence that in a high proportion of patients atrial fibrillation is initiated either by enhanced atrial automaticity or by triggered activity arising in the vicinity of the pulmonary veins, probably in atrial tissue extending into the pulmonary venous ostia and in the atrial area immediately outside the venous ostia. Ablation ( Fig. 3.59) can isolate the atrial tissue within the pulmonary veins from the rest of the atrium, and hence can suppress the initiation of paroxysmal atrial fibrillation and also reduce relapse after the cardioversion of permanent atrial fibrillation.

The ablation treatment of atrial fibrillation is more difficult than that of atrial flutter, because the left atrium has to be entered through the inter-atrial septum, involving trans-septal puncture through the foramen ovale, and more burns are needed. It is usually initially performed with a wide-area circumferential ablation (WACA, denoted by red dots in Fig. 3.59). Further segmental ablation, guided by pacing from a coronary sinus electrode, may be required to eliminate persisting areas of conduction until the pulmonary veins are electrically silent. At present this technique is usually regarded as a second-line option, limited to patients with symptoms refractory to conventional medical therapy, although its wider application is the subject of ongoing study.

AV NODE ABLATION

Patients with atrial-driven tachyarrhythmias, especially atrial fibrillation (whether paroxysmal or permanent), which cannot be controlled by pharmacological means, may undergo catheter ablation of the AV node. This leads to complete AV block, and brady-cardia is prevented by the implantation of a permanent pacemaker (‘ablate and pace’).

PATHWAY ABLATION

Atrioventricular re-entry tachycardias, such as in the Wolff-Parkinson-White syndrome, can be treated by ablation of the accessory pathway, as described above. This prevents re-entry and eliminates pre-excitation and episodes of supraventricular tachycardia. The ablation of pathways close to the AV node, including those involved in atrioventricular nodal re-entry tachycardia (AVNRT), can be attempted. The aim of ablation is to modify the slow pathway, and so prevent AVNRT, without damaging the fast pathway, which would lead to AV block and necessitate a permanent pacemaker.

VENTRICULAR TACHYCARDIA

Some forms of ventricular tachycardia (VT) are amenable to catheter radiofrequency ablation treatment. These include right ventricular outflow tract VT, where triggered activity is the cause, and also VT in some patients with surgically corrected congenital heart disease, if a simple ventricular re-entry circuit can be demonstrated. Ischaemic VT is not usually amenable to electrophysiological ablation, because often there are multiple potential foci of increased automaticity and potential re-entry circuits, due to areas of myocardial scarring. More sophisticated ventricular mapping tools are becoming available which potentially enable ablation treatment even for ischaemic VT.

• Airway

• Breathing

• Circulation.

• Begin cardiopulmonary resuscitation (CPR). Ventilation and chest compression should be given in a ratio of 2 breaths to every 30 compressions.

• Defibrillate in cases of ventricular fibrillation and pulseless ventricular tachycardia as soon as possible.

• Intubate as soon as possible.

• Gain or verify IV access.

1. Precordial thump (especially useful in VT).

2. Defibrillate at 200 J.

3. 2 min of CPR.

4. If unsuccessful, defibrillate at 360 J.

5. If unsuccessful, give adrenaline (epinephrine) 1 mg i.v.

6. Defibrillate at 360 J.

7. 2 min of CPR.

8. If VF/pulseless VT persists, give amiodarone 300 mg i.v.

9. Give further shocks after 2-min periods of CPR.

10. Give adrenaline (epinephrine) 1 mg i.v. immediately before alternate shocks.

11. For refractory VF, give magnesium sulfate 2 g i.v. bolus (8 mmol).

NON-SHOCKABLE RHYTHMS – ASYSTOLE AND PULSELESS ELECTRICAL ACTIVITY (PEA)

The term ‘PEA’ has replaced ‘electromechanical dissociation’ (EMD) because some pulseless patients have weak myocardial contractions, although insufficient to generate a cardiac output. In cases of PEA, think about the underlying causes. Actions:

• Hypoxia.

• Hypovolaemia.

• Hyperkalaemia, hypokalaemia, hypocalcaemia, acidosis, hypoglycaemia.

• Hypothermia.

• Tension pneumothorax.

• Tamponade.

• Toxic substances, or therapeutic substances in overdose.

• Thromboembolic or mechanical obstruction (e.g. pulmonary embolus).

• Arterial blood gases – if the pH is < 7.1 or if arrest is associated with tricyclic overdose, give bicarbonate 50 mmol.

• Electrolytes.

• ECG.

• Chest X-ray – principally to exclude a pneumothorax caused by the resuscitation.

• pacemaker

• defibrillator

• control of ventricular tachycardia.

PACEMAKER FUNCTION

ICD devices have the same functions as a conventional pacemaker (see Ch. 4) . They can be single or dual chamber, or biventricular (CRTD). In patients who do not require the pacing function, the ICD will usually be a single-chamber system, programmed as a backup VVI. The device will then be in continuous sensing mode.

DEFIBRILLATOR FUNCTION

The chest X-ray appearances of ICD devices are similar to those of conventional pacemakers. However, devices with a defibrillating function are bigger, incorporating more battery power for the delivery of shocks. In addition, the right ventricular lead contains the two poles of the shocking coil and so is thicker than a conventional lead ( Fig. 3.62).

In addition to the normal sensing functions of a pacemaker, an ICD can sense high rates of ventricular activity. If a predetermined ventricular rate is exceeded, an electrical shock discharges between the two poles of the defibrillator coil in the ventricular lead, with the aim of cardioverting a life-threatening ventricular arrhythmia ( Fig. 3.63). If the ventricular rate does not fall below the threshold following one shock, then further shocks may be delivered.

ANTI-TACHYCARDIA PACING

The device may also attempt to control ventricular tachycardia by ‘overdrive pacing’. If ventricular activity is detected within a certain range (usually significantly above normal cardiac rates but below the threshold set for defibrillation), the ICD will attempt to pace the ventricle at a high rate before reducing the rate of pacing. Ventricular capture with rapid pacing can sometimes terminate ventricular tachycardia. If anti-tachycardia pacing in this way is unsuccessful after a set number of attempts, the ICD will then usually default to defibrillation.

INDICATIONS FOR ICD DEVICES

These are summarized in Box 3.9.

ECG APPEARANCE

ECGs from patients with ICDs are the same as those from patients with conventional pacemakers, except when a ventricular arrhythmia is detected.

ABNORMAL ICD FUNCTION

Either the pacing function or the defibrillator function of an ICD device may fail. The defibrillator function may either fail appropriately to initiate ventricular arrhythmia therapy, or may deliver inappropriate shocks. This will require specialist input and analysis. In the event of inappropriate repeated shock delivery, an ICD can be inactivated in a monitored patient by the application of a magnet.

ICDs should always be interrogated shortly after shock delivery, even if this was appropriate, to check device function and battery life. The presence of pacemakers or ICDs in no way precludes external defibrillation, provided that the paddles are not applied directly over the device.