• PR interval. The PR interval (Fig. 12.1 and Box 12.1) is measured from the start of the P wave to the start of the QRS complex. It is the time taken for electrical activity beginning in the sinus node to pass through to the ventricles.

• ST segment. The ST segment begins at the end of the QRS complex and, together with the T wave, represents ventricular repolarization.

• QT interval. The QT interval is measured from the start of the QRS complex to the end of the T wave and divided by the square root of the R–R interval to correct for the heart rate. It is the time taken for ventricular depolarization and repolarization; if prolonged, it may predispose to ventricular arrhythmias.

• QRS. In the frontal plane, the mean QRS axis ranges from −30° to +100°. Hence, the normal QRS pattern is very variable in the limb leads. Left axis deviation is when the axis is more negative than −30° and right axis deviation is when the axis is more positive than +100°. Left axis deviation may be a normal variant or due to LV hypertrophy, left anterior hemiblock or inferior myocardial infarction. Right axis deviation may be a normal variant or due to right ventricular strain, left posterior hemiblock or lateral myocardial infarction.

Box 12.1 Normal ECG intervals

P wave duration	120 ms or less
PR interval	120–200 ms
QRS duration	100 ms or less
Corrected QT interval	440 ms or less in males
	460 ms or less in females

Action	Measurements	Note
Sinus rhythm	Basic intervals (PA, AH, His duration, HV, QRS and corrected QT)	Is there pre-excitation or evidence for slowed conduction?
Single ventricular extra-stimulus testing	Retrograde AV node effective refractory period (AVNERP)	Is there VA conduction? If so, is it via the AV node and decremental, or an accessory pathway?
Incremental ventricular pacing	Retrograde Wenckebach cycle length (WCL)
Single atrial extra-stimulus testing	Anterograde AVNERP	Is there AV conduction? If so, is it via the AV node and decremental, or an accessory pathway? Is there evidence for dual AV node physiology?
Incremental atrial pacing	Anterograde WCL
Arrhythmia induction pacing from the atrium	Atrial effective refractory period (AERP) Coupling interval(s) for arrhythmia induction	Extra-stimulus testing with 2 or more extra-stimuli, burst pacing and 2 or more premature beats during sinus rhythm
Wellen’s protocol	Ventricular effective refractory period (VERP) Coupling interval(s) for arrhythmia induction	Used to induce ventricular tachycardia. Ventricular extra-stimulus testing with up to 3 extra-stimuli

Pathophysiology of arrhythmias

• Normal electrical activation. The heart contains specialized conduction tissue that can generate rhythmic electrical pulses spontaneously. This is due to cyclical variations in the permeability of cell membranes to potassium, sodium and calcium ions. The activity of the specialized conduction tissue is modulated by the autonomic nervous system. Electrical pulses are rapidly conducted to the mass of cardiac myocytes, producing the mechanical events of each cardiac cycle. Usually, the cells of the sinus node generate electrical pulses most rapidly and are the physiological pacemaker. Cardiac myocyte activation can be divided into four stages (Fig. 12.2). Abnormalities during any of these stages can result in both bradyarrhythmias and tachyarrhythmias.

• Enhanced automaticity. Any cardiac myocytes depolarizing faster than the sinus node can override it and cause arrhythmias. These foci of abnormal cells typically occur at the ostia of the caval or pulmonary veins, along the crista terminalis in the right atrium, within the coronary sinus, close to the AV node, around the insertions of both AV valves and within the ventricular outflow tracts.

• Triggered activity. Oscillations in the membrane potential during stage 3 or 4 of the action potential are called early and late after-depolarizations respectively. If they achieve the threshold potential, premature action potentials may be triggered, causing arrhythmias. Myocardial ischaemia, electrolyte disturbances, pacing, catecholamines and certain drugs are potential causes. Torsades de pointes from QT interval prolongation and arrhythmias due to digoxin toxicity are examples.

• Re-entry. This causes the majority of clinical tachyarrhythmias. It is due to the rotation of electrical activity around a region of conduction block that is either fixed, e.g. scar, or functional. The initiating event is usually an ectopic beat that is conducted around the region of conduction block in one direction only due to differences in conduction velocity and refractoriness. As long as the head of the rotating electrical wavefront meets excitable myocardium, a stable re-entry circuit is established.

• Suppressed automaticity and conduction block. If depolarization of the sinus node is slowed by either excessive vagal tone or drugs such as β-blockers, sinus bradycardia results. Bradyarrhythmias also occur if conduction through the AV node is slowed or blocked by excessive vagal tone, drugs or disease. Other parts of the specialized conduction system may assume the role of cardiac pacemaker, producing an escape rhythm.

Fig. 12.2 The cardiac myocyte action potential.

Mechanisms and diagnosis of bradyarrhythmias

Sinus node-dependent arrhythmias

These include sinus bradycardia and sinus pauses with or without an escape rhythm.

Sinus bradycardia

Sinus bradycardia is a heart rate of < 60 bpm during sinus rhythm, with every P wave associated with a QRS complex. The causes of sinus bradycardia can be:

• Cardiac, e.g. sinus node ischaemia/infarction, sinus node and atrial fibrosis, myocarditis and cardiomyopathies

• Systemic, e.g. hypothermia, hypothyroidism, cholestatic jaundice, raised intracranial pressure, carotid sinus hypersensitivity and vasovagal syncope. Drugs include β-blockers, calcium channel blockers, amiodarone, digoxin and disopyramide.

Treatment of sinus bradycardia involves identifying and excluding specific causes, if possible. Specific measures are summarized in Box 12.2.

Sinus pauses

Sinus pauses can be due to either sinus node exit block or sinus arrest. Exit block is when an electrical impulse generated within the sinus node fails to conduct into the atria. Sinus arrest is when the sinus node fails to generate electrical impulses. In either case there is an absent P wave on the ECG; if the pause is prolonged, an escape rhythm may occur.

Sick sinus syndrome

Sick sinus syndrome encompasses sinus bradycardia, sinus pauses, permanent atrial fibrillation with bradycardia and tachycardia-bradycardia syndrome. The latter is a failure of stable sinus rhythm to establish following termination of a tachycardia such as atrial fibrillation and flutter, focal atrial tachycardia, junctional tachycardia and AV node re-entry tachycardia. Many patients also exhibit AV conduction abnormalities and bundle branch blocks.

Atrio-ventricular node-dependent arrhythmias

First-degree AV block

This is when every atrial electrical impulse is conducted slowly to the ventricles. Hence, each P wave is associated with a QRS complex but the PR interval is > 200 ms.

Second-degree block

This is when one or more, but not all, atrial electrical impulses fail to conduct to the ventricles. This encompasses both physiological and pathological variations in AV node conduction. The normal AV node exhibits the property of decrementation, which prevents excessive ventricular rates. Hence, increasingly premature atrial electrical impulses either are conducted to the ventricles more slowly or are blocked. This is due to the refractory properties of the AV node and is associated with changes in the PR intervals.

• Wenckebach AV block (Mobitz type 1 block). This is a benign form of second-degree block in which the PR interval progressively lengthens until an atrial electrical impulse fails to conduct to the ventricles (Fig. 12.3). However, successive PR intervals change in smaller increments, producing a progressive decrease in the RR intervals. The longest RR interval during Wenckebach periodicity incorporates the non-conducted P wave. Anatomically, this usually occurs at the level of the AV node. Patients are usually just monitored. If symptomatic, give atropine 0.5 mg IV every 2 mins, maximum dose 0.04 mg/kg.

• Mobitz type 2 block. Atrial electrical impulses failing to reach the ventricles despite a normal PR interval usually indicate a pathological process and may be associated with bundle branch block. Anatomically, the block is usually at the infra-nodal level of the His bundle and the ratio of non-conducted to conducted P waves is variable. The risk of progression to heart block is greater than Wenckebach AV block, and cardiac pacing is usually indicated. Atropine is not used and may in fact worsen the block.

Fig. 12.3 Rhythm strip ECG showing Wenckebach AV block with progressive PR prolongation, as marked out by the arrows, followed by a non-conducted P wave.

Third-degree or complete block (AV dissociation)

This is when no atrial electrical impulses are conducted to the ventricles. Hence, there is a continuously changing relationship between the P waves and QRS complexes (Fig. 12.4). Usually, there is a regular escape rhythm that arises below the level of block. A narrow QRS complex (< 125 ms) escape rhythm is from the His bundle and more stable than a broad QRS complex (> 125 ms), ventricular escape rhythm.

• Causes of third-degree block include ischaemic heart disease (e.g. acute myocardial infarction), post-cardiac operations/ablation, congenital abnormalities, autoimmune rheumatic disorders (e.g. SLE, rheumatoid arthritis, systemic sclerosis), infiltrative disorders (e.g. amyloid, sarcoid), haemochromatosis, infections and drugs.

• Treatment depends on aetiology. Recent-onset narrow-complex AV block may respond to IV atropine 600 mcg boluses but temporary pacing may be required. Chronic block will require permanent (dual chamber) pacing (p. 410). Broad-complex AV block presenting with a slow (15–40 bpm) rhythm, dizziness and blackouts (Stokes–Adams, p. 385) is treated with temporary, followed by permanent, pacing, which reduces the mortality. As ventricular arrhythmias are not uncommon, an implantable cardioverter-defibrillator (ICD) may be required.

Fig. 12.4 Complete heart block. The P waves and QRS complexes are completely dissociated from each other, with different PP and RR intervals.

Bundle branch blocks and hemiblocks

These are due to delayed conduction within the His–Purkinje system, producing QRS complex durations > 120 ms. Causes include ischaemic heart disease, idiopathic fibrosis of the conduction system, cardiomyopathies, aortic stenosis, hypertensive heart disease, recurrent pulmonary emboli, cor pulmonale, congenital lesions, infective endocarditis and myotonic dystrophy.

• Left bundle branch block (LBBB). In LBBB depolarization of the left ventricle is delayed, giving a deep QS pattern in lead V1 and tall R waves in leads 1 and V6 (Fig. 12.5). This is usually associated with heart disease and causes a reverse split of the second heart sound. In some patients with poor LV function this can result in dyssynchronous ventricular contraction that requires biventricular pacing.

• Right bundle branch block (RBBB). In RBBB depolarization of the right ventricle is delayed, giving an RSR complex in lead V1 and deep S waves in leads 1 and V6. This may be a normal finding in 1% of young adults and in 5% of the elderly population.

• Hemiblock and bifascicular blocks. The left bundle has anterior and posterior divisions, also known as fascicles. Conduction block may also occur at this level, producing the hemiblocks. Left anterior hemiblock causes left axis deviation, and left posterior hemiblock causes right axis deviation. Either hemiblock together with an RBBB is called a bifascicular block. In this situation, conduction block within the remaining fascicle will produce complete heart block.

Fig. 12.5 Part of a 12-lead ECG showing typical left bundle branch block with a broad, negative QRS complex in lead V1.

Mechanisms and diagnosis of tachyarrhythmias

Atrial origin

Sinus node tachycardias

These are sinus rhythms with a heart rate > 100 bpm. Causes are cardiac or systemic. Cardiac causes include acute myocardial ischaemia, acute heart failure, sinus node re-entry or enhanced sinus node automaticity. Systemically, it is found normally in children, exercise and pregnancy. Anaemia, hypovolaemia, acute hypoxia, thyrotoxicosis, pyrexia, catecholamine excess and drugs also cause sinus tachycardia.

• Specific treatment is directed against the potential causes, together with rate-slowing drugs such as β-blockers and calcium channel blockers. Enhanced sinus node automaticity or sinus node re-entry may require catheter ablation with or without permanent pacemaker implantation.

Focal tachycardias

These are uncommon tachycardias, caused by atrial foci that exhibit enhanced automaticity, triggered activity or micro re-entry. Typical causes include myocardial infarction, myocarditis, digoxin toxicity, chronic lung diseases, alcohol, hypokalaemia and catecholamine release. Foci can occur anywhere within the atria and at the junctions with their respective veins. They are usually conducted to the ventricles with varying degrees of AV block. Automatic foci usually exhibit gradual acceleration and deceleration. They also cause incessant tachycardias with a subsequent tachycardia cardiomyopathy.

The morphology of the P waves during tachycardia is highly variable, depending on the site of the tachycardia focus. If the focus is close to the sinus node, typical P waves may be seen. P wave morphologies may give some indication as to the site of the tachycardia focus (Table 12.2).

• Treatment. Some focal atrial tachycardias respond to adenosine IV up to 0.25 mg/kg and are subsequently treated pharmacologically or by catheter ablation.

Table 12.2 P wave morphologies in different ECG leads for focal atrial tachycardias

Flutters

These are caused by atrial macro re-entry circuits that rotate around anatomical structures and scars. They are associated with a slightly increased risk of embolic stroke and may compromise ventricular filling causing breathlessness.

Typical atrial flutter usually, but not always, has negative sawtooth-like flutter waves in the inferior ECG leads and positive flutter waves in lead V1 (Fig. 12.6). Frequently, typical atrial flutter is conducted with a 2-to-1 AV block, giving a heart rate of 150 bpm. The re-entry circuit is well characterized, and the zone of slow conduction critical to sustaining the circuit is the cavo-tricuspid isthmus.

• Treatment. Patients should be given warfarin and either rate control with digoxin and β-blockers, or rhythm control. Some patients also benefit from DC cardioversion. Catheter ablation of the cavo-tricuspid isthmus can successfully terminate and prevent recurrence of typical atrial flutter with minimal risk in 95% of patients. It is used for all patients with recurrent or haemodynamically significant atrial flutter.

Fig. 12.6 Atrial flutter. Flutter waves are marked with an F with a frequency of 240/min. Every fourth flutter wave is transmitted to the ventricles with a ventricular rate of 60/min.

Atrial fibrillation (AF)

AF is the commonest arrhythmia globally, with a prevalence of 0.5–1% of the general population and 5–10% of the population over 65 years. It is characterized by rapid (300–600 bpm), irregularly irregular contractions of the atria. The 12-lead ECG shows no regular atrial activity (Fig. 12.7) and the ventricles beat in an irregularly irregular fashion at rates of up to 150–200 bpm. The mechanisms underlying AF are thought to be a combination of triggering atrial ectopics usually originating within the pulmonary veins, and progressive electrical changes within the atrial myocardium (remodelling) that allow it to be sustained. AF is a consequence of a wide range of pathologies but it can exist independently in a structurally normal heart (lone AF).

Fig. 12.7 A 12-lead ECG showing atrial fibrillation. There are no P waves but in leads V1 and V2 there is a rapid undulation of the baseline between the QRS complexes, demonstrating the fibrillatory activity. The RR intervals are continuously changing, resulting in an irregularly irregular pulse that is characteristic.

Clinically, patients either are asymptomatic or complain of palpitations, breathlessness, dizziness and, less commonly, syncope. AF is a spectrum ranging from infrequent episodes (paroxysmal), to those requiring termination with drugs or DC cardioversion (persistent), to permanent AF.

Management of AF consists of either restoring rate and rhythm or, if this is not possible in the long term, controlling rate and preventing complications.

• Acute AF

• AF that is a complication of an acute illness, e.g. a respiratory infection or alcohol toxicity, often reverts to sinus rhythm when the infection/cause is treated and resolves.

• Acute symptomatic AF, if documented < 48-hour duration, can be treated with synchronized DC cardioversion following immediate heparinization. This is successful in over 75% of cases but can recur.

• If AF lasts for > 48 hours, patients should be anticoagulated with warfarin (INR 2–3) for 3 weeks prior to cardioversion. The anticoagulation should be continued after successful cardioversion for at least 4 weeks, or longer if there are high risk factors for strokes. Alternatively, a transoesophageal echocardiogram (TOE) can be performed to rule out thrombosis in the left atrial appendage, obviating the need for anticoagulation prior to DC shock.

• Chemical cardioversion can alternatively be achieved by using an IV infusion of flecainide 2 mg/kg over 30 mins, maximum dose 150 mg or amiodarone IV infusion via a central venous catheter, initially 5 mg/kg over 20–120 mins with ECG monitoring. Patients again should be warfarinized prior to treatment

• If cardioversion fails (or the AF recurs), give amiodarone 300 mg over 1 hour before a further attempt at cardioversion. A second dose of amiodarone can be administered if necessary. Biphasic waveforms for cardioversion require less energy and have a higher efficacy than monophasic waves. The aims are as follows.

• Chronic AF

• Maintain sinus rhythm following DC conversion with anti-arrhythmic drugs (class 1c, e.g. flecainide, propafenone; or class III, e.g. amiodarone, sotalol — see p. 411).

• Control rate with a combination of digoxin, β-blockers or verapamil or diltiazem. The heart rate should be between 60 and 80 bpm at rest. Anticoagulant therapy should be continued. Dabigatran 220 mg oral daily, a direct thrombin inhibitor, is now being used instead of the more traditional warfarin (p. 245) as monitoring is not required.

• If rate control is poor despite optimal medical therapy patients should be considered for AV node ablation and pacemaker implantation (‘ablate and pace strategy’) but will require lifelong anticoagulation therapy.

• Catheter ablation should be offered to patients who remain symptomatic despite drug therapy with two different agents.

• For paroxysmal AF the pulmonary veins are electrically isolated, thereby eliminating the triggers. Success rates are between 80 and 85%.

• In persistent AF additional linear ablation is undertaken to compartmentalize the left atrium (catheter maze). This aims to prevent the formation of multiple re-entry circuits that sustain the AF. The success rate for permanent AF is 60–70% after one procedure. The ablation is a complex procedure, usually requiring an advanced mapping system, which can last up to 4 or 5 hours. The main risks include cardiac tamponade (1%), stroke (1–2%) and pulmonary vein stenosis (1%). Patients with structurally abnormal hearts and those over 65 years have an increased risk for embolic strokes (up to 5% per year) and should be anticoagulated with warfarin or dabigatran, even after ablation.

Atrio-ventricular junction origin

Atrio-ventricular node re-entry tachycardia (AVNRT)

This is one of the commonest causes of a paroxysmal supraventricular tachycardia, occurring in up to 60% of cases. It is more frequently found in females and most patients have structurally normal hearts.

• Clinical features. Typical symptoms include palpitations, dizziness, neck pulsations, chest discomfort and a polyuria that follows the termination of an episode. Syncope may occur in patients with impaired ventricular function and following termination from tachycardia-induced sinus arrest. AVNRT usually has an abrupt onset and termination, and can last from seconds to days. Patients usually have two functional and anatomically different pathways within the AV node — a fast conducting pathway and a slow pathway. The slow pathway repolarizes faster than the fast pathway. During sinus rhythm, antegrade conduction usually occurs via the fast pathway. If an atrial impulse occurs early, e.g. a premature beat when the fast pathway is refractory, antegrade conduction proceeds via the slow pathway in propagating the atrial impulses to the ventricles. Not all patients with dual AV node physiology develop AVNRT.

• Investigations. AVNRT can only occur if a stable micro re-entrant circuit can be established within the AV node between the fast and slow pathways. Usually, an atrial premature beat initiates the tachycardia. Less frequently, the initiation is from a ventricular premature beat.

• In typical AVNRT, the antegrade limb of the circuit is the slow pathway, with retrograde conduction up the fast pathway. Consequently, the atria and ventricles are depolarized almost simultaneously. This produces a narrow complex tachycardia (QRS < 0.125 sec) with rates between 150 and 240 bpm. The P wave resulting from retrograde conduction up the fast pathway is usually fused with the QRS complex. Sometimes, its terminal portion may be seen as a small positive deflection at the end of the QRS complex in lead V1 (Fig. 12.8).

• In atypical AVNRT, the antegrade limb is the fast pathway. Hence, atrial depolarization follows that of the ventricles, producing a distinct retrograde P wave and a long RP tachycardia.

• Treatment. AVNRT can be terminated using vagal manœuvres, e.g. Valsalva manœuvre, and drugs, e.g. IV adenosine, calcium channel blockers, e.g. verapamil, and β-blockers, e.g. propranolol. Prophylaxis with calcium channel blockers and β-blockers, flecainide and propafenone is used, but symptomatic AVNRT should be referred for catheter ablation, which has a low complication rate and is curative in 95% of cases.

Fig. 12.8 Typical atrio-ventricular node re-entry tachycardia. The ECG shows a regular narrow-complex tachycardia with retrograde P waves that are fused with the QRS complexes and appear as small ‘pseudo-R waves’ in V1 and ‘pseudo-S waves’ in the inferior leads, as marked by the blue arrows. These deflections are absent in the sinus rhythm QRS complexes.

Junctional tachycardia

This is caused by an automatic focus in the AV node. The commonest cause of this is digoxin toxicity, which produces a tachycardia with a Wenckebach-type AV block. Other causes include acute myocardial infarction, cardiac surgery, chronic obstructive pulmonary disease, rheumatic fever and hypokalaemia. The ECG usually shows a narrow-complex tachycardia with retrograde P waves that may be fused with the QRS complex or occur either side of it.

• Treatment is directed at the underlying cause.

Accessory pathway-dependent tachycardias

Accessory pathways (APs) are myocardial bundles that electrically couple the atria and ventricles, at one or several points across the AV junction, in addition to the AV node and His–Purkinje system. Most APs do not exhibit decremental conduction and are therefore able to conduct rapidly between atria and ventricles. APs may conduct both antegradely and retrogradely, or only retrogradely. The former are seen in the Wolff–Parkinson–White syndrome and the latter are known as concealed APs. A rare form of AP is the atrio-fascicular or Mahaim connection between the right atrium and the right bundle branch. These APs usually conduct in the antegrade direction only and exhibit decrementation.

• Wolff–Parkinson–White syndrome (WPW) has a prevalence of 0.1–0.4% and typically presents during infancy or in the second and third decades. Antegrade conduction via the AP causes ventricular pre-excitation, characterized by a PR interval of < 0.12 secs and a slurred initiation to the QRS complex called a delta wave (Fig. 12.9). During sinus rhythm, the extent of pre-excitation is determined by the relative conductions through the AP and the AV node–His–Purkinje system. AP conductivity and location, as well as the effects of autonomic tone on AV nodal conduction, are significant factors. Several detailed ECG algorithms have been devised for identifying AP location. Orthodromic AV re-entry tachycardia (AVRT) is seen in 84% of cases of WPW, AF in 51%, antidromic AVRT in 10% and ventricular fibrillation in less than 1%.

• Orthodromic AVRT is usually initiated by a premature ventricular or atrial beat establishing the macro re-entry circuit shown in Fig. 12.10a. The 12-lead ECG shows regular, narrow QRS complexes with retrograde P waves (Fig. 12.10b). However, functional delay in one of the bundle branches can produce broad QRS complexes. Orthodromic AVRT usually terminates with block in the AV node, although any limb of the circuit may be responsible. This is also the re-entry circuit seen with concealed AP tachycardias.

• Antidromic AVRT has a re-entry circuit that is the reverse of that for orthodromic AVRT (Fig. 12.11a). The ventricles are fully pre-excited and the 12-lead ECG demonstrates regular, broad QRS complexes similar to those in ventricular tachycardia (Fig. 12.11b). Antidromic AVRT usually terminates with block in the AV node. Atrio-fascicular or Mahaim APs produce a characteristic antidromic AVRT with LBBB morphology and left axis deviation.

• Atrial fibrillation in WPW has the greatest risk of causing haemodynamic compromise and ventricular fibrillation. The initiation is thought to be secondary to orthodromic and conducted ventricular ectopics AVRT, and the 12-lead ECG demonstrates a variably pre-excited, rapid, irregularly irregular broad QRS complex tachycardia (Fig. 12.12). However, there may be occasional normal QRS complexes due to dominant anterograde conduction down the AV node–His–Purkinje system.

• Treatment. Haemodynamically unstable patients should be treated by DC cardioversion. Drug therapy is targeted at the AV node, accessory pathway or both (Box 12.3).

• Orthodromic AVRT is usually terminated with IV AV nodal-blocking drugs such as adenosine, verapamil or diltiazem. If this fails, IV procainamide is administered with BP monitoring (Fig. 12.13). Chronic drug prophylaxis can be with either AV node-blocking drugs or those affecting the accessory pathway.

• Antidromic AVRT and pre-excited AF are treated with procainamide as first-line therapy, since AV nodal-blocking drugs may accelerate the tachycardia and cause ventricular fibrillation. Chronic drug prophylaxis is usually with flecainide and propafenone, which suppress conduction via the AP and AV node. Alternative drugs include procainamide, quinidine and disopyramide. Amiodarone is used only if other drugs are ineffective, due to its potential side-effects.

Fig. 12.9 Wolff–Parkinson–White syndrome. The ECG shows sinus rhythm with pre-excitation, as demonstrated by a short PR interval (marked in V5 by the blue lines) and a slurred upstroke to the QRS complex or ‘delta wave’ (marked in V5 by blue arrows).

Fig. 12.10 (a) Orthodromic AV re-entry. This circuit involves four sequential anatomical components — the left (or right) atrium, the AV node and His–Purkinje system, the left (or right) ventricle and the accessory pathway. The ventricles are activated via the AV node and His–Purkinje system. The atria are activated retrogradely via the accessory pathway. RA, right atrium; LA, left atrium; RV, right ventricle; LV, left ventricle. (b) Orthodromic AV re-entry tachycardia. The ECG complex shows a regular narrow-complex tachycardia with no pre-excitation. There are retrograde P waves that are shown in leads III and aVF by the blue arrows.

Fig. 12.11 (a) Antidromic AV re-entry. This circuit has four sequential anatomical components — the left (or right) atrium, the AV node and His–Purkinje system, the left (or right) ventricle and the accessory pathway. The ventricles are pre-excited via the accessory pathway. The atria are activated retrogradely via the AV node. RA, right atrium; LA, left atrium; RV, right ventricle; LV, left ventricle.(b) Antidromic AV re-entry tachycardia. The ECG shows a regular broad-complex tachycardia with full pre-excitation. There are delta waves in each QRS complex that are marked in leads V1 and V4 by the blue arrows.

Fig. 12.12 Atrial fibrillation in Wolff–Parkinson–White syndrome. Note tachycardia with broad QRS complexes and fast and irregular ventricular rate.

Fig. 12.13 Management strategy for tachycardias in Wolff–Parkinson–White syndrome. AAVRT, antidromic AV re-entry tachycardia; AF, atrial fibrillation; DCC, DC cardioversion; OAVRT, orthodromic AV re-entry tachycardia

(Modified from Dhinoja & Lambiase 2005, with permission).

All patients with symptomatic WPW should be assessed for curative catheter ablation of the AP. This can be performed safely and has a success rate of 95%.

Long RP tachycardias

This is a special group of supraventricular tachycardias whose RP interval is > 50% of the RR interval (Fig. 12.14). The possible causes include focal atrial tachycardia, atypical AVNRT and orthodromic AVRT.

• Atypical AVNRT involves antegrade conduction via the fast pathway and retrograde conduction over the slow pathway. The retrograde P waves are therefore clearly visible after their associated QRS complexes.

• Orthodromic AVRT, also known as permanent junctional reciprocating tachycardia (PJRT), a type of AVRT, usually involves a concealed posteroseptal accessory pathway. The latter usually conducts slowly and may have decremental properties. The tachycardia is often incessant, causing a tachycardia-mediated cardiomyopathy that resolves following successful ablation of the accessory pathway.

Fig. 12.14 Long RP tachycardia. The ECG shows a regular narrow-complex tachycardia. There is a long RP interval and the retrograde P waves are marked by the blue arrows in lead III. The cause in this patient was an atypical AVNRT.

Ventricular origin

Ventricular tachycardia (VT)

This tachyarrhythmia originates from the ventricles and is usually a broad-complex tachycardia (QRS > 140 msec) with rates between 150 and 200 bpm, which can cause haemodynamic compromise. In monomorphic VT the QRS complexes are identical, whereas they vary in polymorphic VT. There is frequently underlying heart disease, most commonly ischaemic heart disease with previous myocardial infarction. Other pathologies include cardiomyopathies, ion channel disorders and congenital heart disease. Rarely, VT occurs in structurally normal hearts.

Typical symptoms of VT include palpitations, chest pain, dizziness, syncope and breathlessness. In some patients the presentation is with sudden death.

• Monomorphic VT is usually a re-entrant tachyarrhythmia. It is initiated by a premature ventricular beat that establishes a macro re-entry circuit around a region of scarring. The re-entry wavefront may traverse the scar through several different channels, occasionally producing a variable RR interval. Table 12.3 shows the ECG features that distinguish VT from an aberrantly conducted supraventricular tachycardia (SVT) and a pre-excited tachycardia. Fig 12.15 shows the Resuscitation Council (UK) management for tachycardias in adults.

• Bundle branch re-entry VT (BBR VT) is a re-entrant tachyarrhythmia in which the circuit involves the His bundle, both bundle branches and interventricular septal myocardium. As with other macro re-entry circuits, a zone of slow conduction is necessary to sustain the tachycardia. This is the LBB in the common form of BBR VT, which is the retrograde limb and gives an LBBB pattern on the ECG. However, since antegrade conduction is via the His–Purkinje system, the QRS complexes are similar to those for an SVT with aberrant conduction. There is usually underlying heart disease, particularly dilated cardiomyopathy.

• Idiopathic VT occurs in structurally normal hearts and can arise from either ventricle. Patients usually present with palpitations or syncope and the prognosis is good. The QRS duration is relatively short at 0.13–0.16 secs and VT may be misdiagnosed as SVT with aberrant conduction.

• The left ventricular type (also known as fascicular VT) is a re-entrant arrhythmia that responds to verapamil. The 12-lead ECG shows an RBBB monomorphic VT with left axis deviation.

• The right ventricular type, which is adenosine-sensitive, usually originates from the right ventricular outflow tract and is thought to be caused by triggered activity; it may, however, also arise from the LV outflow tract and aortic cusps. The 12-lead ECG usually shows LBBB with an inferior axis.

Table 12.3 ECG features distinguishing ventricular tachycardia from supraventricular tachycardia with aberrant conduction

ECG criterion	VT	SVT with aberrant conduction
AV relationship	Usually dissociated	Usually associated
Capture and fusion beats	Present	Absent
QRS duration	> 140 msec with RBBB morphology > 160 msec with LBBB morphology	≤ 140 msec ≤ 160 msec
Mean frontal plane axis	−90 to ±180°	Similar to sinus rhythm
QRS transition across chest leads	Usually positive or negative concordance, i.e. no transition	Similar to sinus rhythm

LBBB/RBBB, left/right bundle branch block.

Fig. 12.15 Adult tachycardia algorithm (with pulse).

(Reproduced with permission from the Resuscitation Council (http://www.resus.org.uk/siteindex.htm.)

•Investigations

• Patients should have transthoracic echocardiography.

• Some require further investigations with contrast echocardiography, cardiac MR scan, ajmaline testing and signal-averaged ECG.

• Certain patients may benefit from further risk stratification by VT stimulation testing. This especially applies to people with ischaemic heart disease and Brugada syndrome.

• Idiopathic and bundle branch re-entry VTs are referred for electrophysiology studies and possible curative ablation.

•Treatment

• Haemodynamically compromising VT requires immediate DC cardioversion.

• Drug therapy is usually with β-blockers and amiodarone.

• Fascicular VT is especially sensitive to verapamil.

• All patients with impaired LV function should also have optimal heart failure drug therapy (p. 419).

• Most other patients with symptomatic VT should have an ICD fitted (p. 410).

The only treatments to improve prognosis are β-blockers and ICDs. N.B. In patients with LV impairment, flecainide and propafenone increase mortality and should not be used.

Ventricular fibrillation (VF)

This is a cardiac arrest rhythm requiring immediate electrical defibrillation. There are advanced life support treatment algorithms that should be applied (p. 705). The underlying causes are similar to those of VT; the commonest is ischaemic heart disease with previous or acute myocardial infarction. The ECG shows disorganized electrical activity (Fig. 12.16) that is usually sustained. Unless there is an obvious reversible cause, such as acute myocardial ischaemia, all patients require ICD implantation.