Anti-arrhythmic Drugs

Arrhythmias are due to a disturbance of the electrical impulses which regulate the heart. The heart may beat too slowly (bradycardia), too quickly (tachycardia) or in an irregular way. The normal heart rate is between 60-100 beats per minute for adults.

• Management of an arrhythmia requires precise diagnosis of the type of arrhythmia, and electrocardiography is essential.
• Underlying causes (e.g. myocardial infarction, heart failure, thyrotoxicosis, alcohol abuse) require appropriate treatment.

Anti-arrhythmic drugs can be classified clinically into:

• Those that act on supraventricular arrhythmias, e.g. adenosine, verapamil, cardiac glycosides and beta-blockers.
• Those that act on both supraventricular and ventricular arrhythmias, e.g. amiodarone, beta-blockers, disopyramide, flecainide, procainamide, propafenone and quinidine.
• Those that act on ventricular arrhythmias e.g. lidocaine (lignocaine) and moracizine.

Anti-arrhythmic drugs can also be classified according to their effects on the electrical behaviour of myocardial cells during activity but this classification is of less clinical use. The Vaughan Williams classification is based on the movement of ions (sodium, potassium, calcium) into heart cells:

• Class I: Membrane-stabilizing (Ia) quinidine, (Ib) lidocaine, (Ic) flecainide
• Class II: Reduce adrenergic input, beta blockers
• Class III: Potassium blocker, e.g. amiodarone, sotalol
• Class IV: Calcium influx blocker, e.g. verapamil (but not dihydropyridines)

Sotalol has both Class II and Class III actions. Digoxin does not fit into this classification.

• Arrhythmias can present as palpitations or with the symptoms of reduced cardiac outflow: chest pain, dyspnoea, dizziness or blackouts (typically with a rapid recovery).
• The history from an observer can be invaluable in distinguishing an arrhythmia from a cerebral event or convulsion.
• Arrhythmias, range in severity from a minor inconvenience to a potentially fatal problem. They are common, particularly in the elderly. They can have a profound effect on quality of life.¹ Appropriate information and support can relieve psychological as well as physical problems.

• Bradycardia
• Extrasystoles
• Supraventricular tachycardias
• Wolff-Parkinson-White syndrome
• Atrial fibrillation
• Atrial flutter
• Ventricular tachycardia
• Torsades de Pointes
• Ventricular fibrillation

• Accurate diagnosis of a suspected arrhythmia, requires a prompt recording and archiving of a 12-lead ECG. Even if symptoms have subsided, this improves the chance of accurate diagnosis and treatment:
• High resolution ECG averages signals to reduce background noise and can reveal areas of slow conduction.
• Supra-ventricular (atrial and A-V node initiated) fast rhythms which are transmitted by the normal conducting pathway are generally narrow complex tachycardias.
• Tachyarrhythmias that either originate from the ventricle, or are atrial rhythms but are aberrantly propagated through the ventricular muscle rather than completely through the conducting pathway, have wider QRS complexes and are called broad complex tachycardias.
• Ambulatory ECG monitoring over 24-48 hours allows analysis of heart rate variability and matching of arrhythmia to symptoms. More detailed electro-physiological studies require cardiac catheterisation.
• All causes and effects of any arrhythmia must be thoroughly evaluated. This will depend on the particular arrhythmia and clinical context but may include blood tests (e.g. renal function, electrolytes, thyroid function tests), echocardiogram (structural and function heart abnormalities, detection of intracardiac thrombus) and exercise tolerance testing.

• Deciding on appropriate therapy depends on distinguishing between supraventricular from ventricular rhythms. This is not always easy and expert advice should be sought if there is any doubt.
• All anti-arrhythmic drugs have potentially serious side effects. They may worsen or provoke arrhythmias in certain circumstances, such as hypokalaemia. Close monitoring is therefore essential.
  The dangers became apparent after the CAST (Cardiac Arrhythmia Suppression Trial) study which surprisingly showed that suppression of ventricular ectopics with flecainide actually worsened survival, and CAST II in 1992, which was terminated prematurely as moracizine was found to cause increased cardiac mortality.²
• The negative inotropic effects of anti-arrhythmic drugs tend to be additive when more than one drug is required. Therefore special care should be taken if two or more are used, especially if myocardial function is impaired. A combination of one drug plus an implantable device or an ablation procedure may in some situations be more appropriate.
• Ablation therapy provides an alternative for treating certain cardiac arrhythmias.