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Overview of Arrhythmias

by | 20 May, 2020

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Introduction

A cardiac arrhythmia is a disturbance in the electrical rhythm of the heart, producing an abnormal rhythm. They are usually a manifestation of structural heart disease (e.g. valve pathology) but may also occur because of abnormal conduction or depolarisation.

Classification

By heart rate

The normal heart rate is 60-100 beats per minute. Abnormal rates can be:
  1. Tachycardia/Tachyarrhythmias: >100 beats per minute
  2. Bradycardia/Bradyarrhythmias: <60 beats per minute

By site

  1. Supraventricular tachycardia (SVT): sinus, atrial or junctional origins
  2. Ventricular tachycardia (VT)

Causes

  1. Myocardial infarction
  2. Drugs
  3. Myocarditis
  4. Thyrotoxicosis
  5. Electrolyte imbalance e.g. potassium, magnesium
  6. Cardiomyopathy
  7. Cardiac dilation
  8. Congenital conduction defects e.g. Wolff-Parkinson-White syndrome

Pathophysiology

Tachyarrhythmias

There are 3 main mechanisms:
  1. Increased automacity: spontaneous depolarisation from ectopic focus, often in response to catecholamines
  2. Re-entry: initiated by ectopic beats and sustained by re-entry circuits
  3. Triggered activity: secondary depolarisation from an incompletely repolarised (after depolarisation) cell. Usually seen in coronary heart disease.

Bradyarrhythmias

There are 2 main mechanisms:
  1. Reduced automacity e.g. sinus bradycardia, sick sinus syndrome
  2. Blocked or abnormally slow conduction: atrioventricular conduction block, bundle branch blocks

Clinical features

May be asymptomatic or present with:
  1. Palpitations
  2. Haemodynamic disruption: dyspnoea, chest pain, syncope

Investigations

  1. ECG
  2. 24-/48-/72-hour tapes if arrhythmia suspected despite normal ECG
  3. Blood tests: FBC, U&E, thyroid function, glucose, cardiac enzymes (e.g. troponin I/T)
  4. Chest x-ray
  5. Echocardiogram

Management

There are several treatments available for arrhythmias, including:
  • Conservative – correct electrolyte imbalances, vagal manoeuvres
  • Drug therapies
  • Catheter ablation
  • Pacing
  • Defibrillation

Management by arrhythmia type

Bradycardia:
  1. Drugs e.g. atropine
  2. Pacing, which can be temporary or permanent
Supraventricular tachycardia:
  1. Vagal manoeuvres
  2. Antiarrhythmic drugs
  3. Electrical cardioversion
  4. Catheter ablation
Ventricular tachycardia:
  1. Antiarrhythmic drugs
  2. Electrical cardioversion
  3. Implantable cardioverter-defibrillator (ICD) device

Vagal manoeuvres

Used in supraventricular tachycardia. Includes:
  • Valsalva manoeuvre
  • Carotid sinus massage (avoid in elderly as may dislodge carotid clots)
  • Coughing
  • Gagging
  • Plunging face in cold water

Drug therapy – Vaughan-Williams classification

  • I (sodium channel blockers):
    • Ia (prolong action potential): quinidine, disopyramide
    • Ib (shorten action potential): lidocaine, mexiletine
    • Ic (no effect on action potential duration): flecainide, propafenone
  • II (beta-blockers): atenolol, bisoprolol, metoprolol
  • III (action potential prolonging drugs): amiodarone, sotalol
  • IV (non-dihydropyridine calcium channel blockers): verapamil, diltiazem
Others: adenosine, atropine, digoxin Note that all the above drugs also have proarrhythmic effects, so their clinical response should be monitored.

Catheter ablation

The treatment of choice for SVTs and atrial flutter. It is also used in atrial fibrillation and ventricular fibrillation. This technique involves inserting catheters into the heart via the venous system and recording electrical activity. The focus and/or circuit of the arrhythmia is identified and the catheters are used to ablate the aberrant regions, either through cryoablation or radiofrequency ablation.

Cardioversion and defibrillation

Cardioversion is used in tachycardias to attempt to restore a normal rhythm. It may be performed chemically or electrically. Chemical cardioversion can be attempted with amiodarone, flecainide and calcium channel blockers. Electrical cardioversion involves passing a large current from an external source through the heart to completely depolarise it, creating a period of asystole that aims to disrupt the arrhythmia. Defibrillators deliver a high-energy, short duration shock via 2 large electrodes placed over the right sternal edge and apex.  Synchronised cardioversion is used in stable patients under general anaesthesia. Haemodynamically unstable patients should receive unsynchronised cardioversion.

Implantable cardioverter-defibrillator (ICD) device

A medical device that is implanted to defibrillate the heart when tachycardias occur. It is primarily used in ventricular arrhythmias to prevent sudden cardiac death. Some devices can also act as pacemakers.

Pacemakers

Temporary and permanent pacemakers are available for bradycardias. They are used for treating bradyarrhythmias by introducing an electrical signal that initiates depolarisation. Complications of pacemaker insertion include pneumothorax and brachial plexus injury. Permanent pacemakers can be single chamber (right atrium), dual chamber (right atrium and right ventricle) or biventricular (referred to as cardiac resynchronisation therapy; usually also paces the right atrium) Permanent pacemakers can be programmed and have 4 pacing codes:
  1. First letter = Paced chamber(s). Can be A (atrial), V (ventricle) or D (dual)
  2. Second letter = Sensed chamber(s). Can be O (none), A (atrial), V (ventricle) or D (dual)
  3. Third letter = Response to sensed activity. Can be O (none), I (inhibit), T (triggered), D (dual)
  4. Fourth letter (usually not used if O) = Rate modulation. Can be O (none) or R (rate modulated)
For example, VVI means that the ventricle is being paced and sensed, with pacing being inhibited if an intrinsic signal is sensed.

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