If physical manoeuvres have not been successful, intravnous adenosine (up to 0.25 mg kg-I) may be tried. This is a very short-acting (half-life < 10 s) naturally occurring purine nucleoside that causes complete heart block for a fraction of a second following intravenous admllllstratlOn (Usual dose in adUIt 3 mg; maximum 12 mg). It IS hjgb.1y effective at terminating junctional tach cardias or reveing atrial tac ycar ias. It rarely affects ventricular tachycardia. The side-effects of adenosine are very brief but include bro~pasm, che~ain and heaviness of the limbs. An alernative treatment is verapaniirIO mg i.v. over 5-10 min . It is important not to give verapamil if”p–blockers have been previously administeres or if the tachycardia presents with broad (>0.14 s) QRS complexes.
Rarely, medical therapy fails to terminate a tachycardia and rapid atrial pacing (directly or via the oesophagus) or DC-cardioverslOn may be considered., Prophylaxis To prevent recurrences, drugs may be used to impair AV nodal conduction (classes II and IV and digoxin), impair abnormal connEction conJuctio;(dasses a and III) or suppress the ectopic beats that initiate the arrhYthmia (classes I, II and III). In most cases, however, AV nodal- mociihcation, by a radiofrequency ablation technique, is used to destroy the tachycardia circuit and prevent recurrences.
Wolff-Parkinson-White (wpw) syndrome
This is a congenital condition caused by an abnormal myocardial connectio~between atrium and ventricle (bundle of kent). During sinus rhythm the electrical impulse can conduct quickly over this.abnormal connection to depolarize the ventricles abnormally. This results in the typical ECG pattern of WPW syndrome-a short PR interval and a wide QRS complex that begins as a slurred part known as the Il wave (see Fig. llAl). About half of those with WPW pattern on the ECG have tachycardias. The tachycardias are of two sorts:
ATRIOVENTRICULAR RE-ENTRY. This is a circus movement tachycardia in which a depolarization wave travels from the atrium to the ventricle, usually through the AV node, and from the ventricle to the atrium through the abnormal pathway. Intravenous verapamil will terminate most of these tachycardias. ATRIAL FIBRILLATION. During atrial fibrillation the ventricles may be depolarized by impulses travelling over both the abnormal and the normal pathways. The conduction ability of the abnormal pathway is depressed by drugs that affect the atrium (e.g. disopyramide and amiodarone) but not by verapamil and digoxin, which, paradoxically, may improve conduction over the abnormal pathway. Therefore, neither verapamil nor digoxin should be used to treat atrial fibrillation associated with the WPW syndrome.
Symptomatic patients should be treated by radiofrequency ablation of the abnormal pathway. Drugs, such as class Ia, Ie and III, may be used if ablation is (rarely) unsuccessful or not wanted.
There are four main types of ventricular tachyarrhythmia:
1 Ventricular premature beats
2 Ventricular tachycardia
3 Ventricular fibrillation
4 Torsades de pointes (twisting of points)
Except for torsades de pointes, most ventricular arrhythmias are caused by coronary heart disease, hypertension or cardiomyopathy. Torsades de pointes arises when ventricular repolarization is greatly prolonged (long QT interval). The causes of QT prolongation and torsades de pointes are listed. Congenital QT prolongation may be associated with syncope, and torsades de pointes which may cause sudden death. Congenital QT prolongation may (Jervell-Lange-Nielsen syndrome) or may not (Romano-Ward syndrome) be associated with congenital deafuess.
Ventricular premature beats
These may be uncomfortable, especially when frequent. The patient may complain of extra beats, missed beats or heavy beats because it may be the premature beat, the post-ectopic pause or the next sinus beat that is noticed by the patient. The pulse is irregular owing to the prema- (b) ture beats. Some early beats may not be felt at the wrist. When a premature beat occurs regularly after every normal beat, ‘pulsus bigeminus’ may occur.
On the ECG the premature beat has a broad (>0.12 s) and bizarre QRS complex because it arises from an abnormal (ectopic) site in the ventricular myocardium. Following the premature beat there is usually a complete compensatory pause because the timing of sinus rhythm is not influenced by the premature beat. Ventricular premature beats have been graded in order of severity. The ‘Lown Classification’ is designed for premature beats occurring in the setting of acute myocardial infarction, but has been wrongly applied to other situations. This is particularly true of R-on- T ventricular’ premature beats (occurring simultaneously with the upstroke or peak of the T wave of the previous beat). Following myocardial infarction, such premature beats may induce ventricular fibrillation. This is extremely uncommon in other circumstances.
Treatment of ventricular ectopics may be advised because of symptoms or because they may provoke or threaten to provoke more serious arrhythmias. If structural heart disease is present and premature beats are frequent or run together (three or more beats at a time), treatment is offered. Drugs from classes I, II or III are used. In the absence of heart disease, ventricular premature beats may safely be ignored.