Twelve-lead electrocardiogram (ECG)

This test provides a three-dimensional snapshot of the electrical activity of the heart and is a useful screening tool. The sum of the depolarization (activation) and repolarization (recovery) potentials of the atrial and ventricular myocardium gives rise to the ECG waveform (Fig. 12.1).

Fig. 12.1 The waves and elaboration of the normal ECG.

Potentials are recorded in the frontal or coronal plane by the six limb leads and in the transverse plane by the six chest leads. Deflections on the ECG are positive if the depolarization wavefront spreads towards the positive pole of a lead. The converse is true if the wavefront spreads towards the negative pole. If the wavefront is orthogonal to the lead’s axis, the deflection will be equally positive and negative, i.e. biphasic.

Atrial depolarization spreads from the sinus node inferiorly and to the left, producing a P wave that is usually positive in lead II and negative in aVR. Ventricular activation begins with depolarization of the interventricular septum from left to right, producing a small, positive R wave in lead V1 and a small, negative Q wave in lead V6. Depolarization of the remaining ventricular mass is usually dominated by the more massive left ventricle and therefore directed to the left and posteriorly. This results in a negative S wave in lead V1 and a positive R wave in lead V6. The normal transition from leads V1 to V6 is marked by a progressive increase in R wave amplitude and a simultaneous decrease in S wave amplitude. QRS duration is usually 100 ms or less. Ventricular repolarization usually proceeds in the reverse direction to depolarization, i.e. apex to base and epicardium to endocardium, producing a deflection of similar polarity called the T wave. See Fig. 12.1 and Box 12.1.

Ambulatory ECG (Holter recordings)

These lightweight, battery-powered ECG recorders can be worn continuously for one or more days during routine activities. There is usually an internal clock and a manual symptom indicator that should be correlated to a patient’s symptom diary. This allows the patient’s symptoms to be correlated with any arrhythmias or changes in heart rate. Two leads are recorded and these are usually modifications of leads V1 and V5, which allow easy recognition of P waves and bundle branch blocks. The data is downloaded on to a computer and analysed, providing quantification of heart rate, premature atrial and ventricular complexes, and episodes of tachycardia and bradycardia. Holter monitoring is useful for detection of suspected arrhythmias, for the assessment of the efficacy of drug or ablation treatments and for risk stratification.

Patient-activated recorders

Some arrhythmias occur so infrequently that the diagnostic yield from Holter recorders is low. Hence, recorders that can be activated automatically by arrhythmias or manually by the patient are more useful. They can record at least 30 secs of information that can be retrieved subsequently. However, such devices are only useful in symptomatic arrhythmias that are of sufficient duration to allow their activation.

Implantable loop recorders

Asymptomatic arrhythmias or those causing significant incapacitation are best detected by loop recorders. These devices can be activated manually or automatically and record a 5-min loop that includes the rhythm prior to the recorder’s activation. They are surgically implanted in a subcutaneous pocket and remain in situ for up to 18 months. Such devices are easy to implant with minimal risk and permit prolonged recording periods (up to 40 mins of prior ECG data when activated by a symptomatic patient) without the inconvenience of ECG cables. Following diagnosis of the arrhythmia or when the battery is drained, the device is easily explanted.

Electrophysiology study (EPS)

This is an invasive test used to detect suspected arrhythmias when the above techniques are equivocal. Electrode catheters are advanced, usually from the femoral veins, and placed at specific locations within the heart under fluoroscopic guidance. Intracardiac electrograms from each location are recorded and displayed simultaneously on a monitor, together with the surface ECG. Each electrode catheter can also be used to pace the heart from different locations. This permits the analysis of the electrical activation of the heart during both sinus rhythm and a tachyarrhythmia.

Table 12.1 The basic electrophysiology study

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:

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.

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.

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.

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

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.

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).

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.

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.

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.

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.

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.

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.

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 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.

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

Fig. 12.15 Adult tachycardia algorithm (with pulse).

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

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.

Fig. 12.16 Ventricular fibrillation. Four beats of sinus rhythm are followed by a ventricular ectopic beat that initiates ventricular fibrillation. The ST segment during sinus rhythm is elevated owing to acute myocardial infarction in this case.

Brugada syndrome

This is an inherited cause of idiopathic VF. It is commonest in young males from South-East Asia and classically presents with sudden death during sleep. Other symptoms include dizziness and syncope; some patients remain asymptomatic. In 20% of cases there is a sodium channel mutation (SCN5A) that causes characteristic coved ST segment elevation in ECG leads V1–V3. These changes either are present at baseline or may be provoked by drugs such as flecainide or ajmaline. In the absence of symptoms or documented ventricular arrhythmias, the presence of ECG changes is not associated with an increased risk of SCD. Patients with syncope or documented ventricular arrhythmias usually require ICD implantation, which improves prognosis.

Long QT syndrome (LQTS)

This is another cause of potentially lethal ventricular arrhythmias in structurally normal hearts and presents with sudden death or syncope. It is characterized by prolongation of the QT interval > 440 msec due to abnormal myocardial repolarization. The underlying causes may be ion channel mutations, certain drugs and electrolyte disturbances. The prevalence is around 1 in 4000, although it is probably under-diagnosed.

Two major forms of inherited LQTS have been described. They are the Romano–Ward and Jervell–Lange–Nielson (JLN) syndromes, which have ion channel mutations. These mutations affect currents generated by sodium or potassium ions. QT prolongation is the result of overloading cells with positive ions during repolarization. They each cause variations in T wave morphology. Some have a normal corrected QT interval (15%) but QT interval prolongation during exercise testing at faster heart rates. Ventricular arrhythmias are usually caused by adrenergic stimuli such as exercise, emotion and loud noises.

The classical VT in LQTS is torsades de pointes. This is a polymorphic VT in which the amplitude of the QRS complexes constantly changes around the isoelectric line (Fig. 12.17). This causes palpitations or syncope. Most episodes are self-terminating but SCD results from degeneration into VF.

Fig. 12.17 Supraventricular rhythm with a long QT interval giving way to atypical ventricular tachycardia (torsades de pointes). The tachycardia is short-lived and is followed by a brief period of idioventricular rhythm.

Cardiomyopathies

SCD is uncommon in hypertrophic cardiomyopathy but is the commonest cause of SCD in young adults (p. 408).