ARRHYTHMIAS Jamil Mayet

Arrhythmias - learning objectives –Mechanisms of action of antiarrhythmic drugs –Diagnosis To differentiate the different types of SVTs on the ECG To diagnose ventricular tachyarrhythmias from the ECG To differentiate different bradyarrhythmias from the ECG –Treatment Understand different options; drugs versus ablation; pacing Importance of anticoagulation in atrial fibrillation Appreciate increasing use of ICDs

Tachyarrhythmias Antiarrhythmic drugs –Vaughn-Williams Classification –Drugs divided according to EP effects on cells –All are negatively inotropic –Can also be pro-arrhythmic

Tachyarrhythmias Class I –Impede Na transport across cell membrane –Ia increase AP duration eg quinidine, disopyramide, procainamide –Ib shorten AP duration eg lignocaine, mexilitene, propafenone –Ic little effect on AP eg flecainide

Tachyarrhythmias Class II –Interfere with effects of SNS on the heart eg beta blockers Class III –Prolong AP duration but do not effect initial Na dependent phase eg sotalol, amiodarone Class IV –Antagonise Ca transport across cell membrane –SA and AV node particularly susceptible eg verapamil, diltiazem

Supraventricular arrhythmias Atrial fibrillation –Rapid atrial discharge ( /min) –AV node cannot conduct all impulses –Cardioversion (electrical or drugs) can restore SR –Class Ia, Ic, III drugs may maintain SR –Px often rate control and stroke prevention –Rate control with digoxin, class II, III, IV drugs –Anticoagulation with warfarin in most cases –Causes include ht, ischaemia, rheumatic hd, alcohol, thyrotoxicosis, cardiomyopathy, PTE, thoracotomy, idiopathic (“lone”)

Atrial fibrillation

Supraventricular arrhythmias Atrial flutter –Rapid atrial discharge ( /min) –Occasional 1:1 conduction –More often 2:1, 3:1, 4:1 conduction –Diagnosis aided by increasing block eg CSM, adenosine –Cardioversion (electrical or drugs) can restore SR –Class Ia, Ic, III drugs may maintain SR –Rate control with digoxin, class II, III, IV drugs –?Anticoagulation –Similar causes to atrial fibrillation

Atrial flutter

Atrial flutter with 2:1 block

Supraventricular arrhythmias Atrial tachycardia –Atrial discharge slower ( /min) –Occasional 1:1 AV node conduction –More usually 2:1 conduction –With AV block often due to digitoxicity –Cardioversion (electrical or drug) can restore SR –Overdrive pacing is an alternative

Atrial tachycardia

Supraventricular arrhythmias AV nodal re-entry tachycardia –Re-entry circuit within AV node –Rate usually /min –CSM or adenosine may terminate arrhythmia –Alternatives include cardioversion (electrical or drug) and overdrive pacing –Prophylaxis with class II, IV, III, Ia, Ic drugs

AV nodal re-entry tachycardia

Supraventricular arrhythmias Pre-excitation syndromes –WPW syndrome due to accessory pathway (bundle of Kent) –0.15% of population –Accessory pathway allows rapid conduction –Resting ECG shows short PR and delta wave –May cause AV re-entry tachycardia –A fib may be dangerous due to rapid conduction

Supraventricular arrhythmias Pre-excitation syndromes –Digoxin/verapamil may increase conduction in bundle of Kent and should be avoided –Class Ia, Ic and III drugs slow ventricular rate and may cardiovert to SR –Electrical cardioversion especially in fast A fib –Lown-Ganong-Levine syndrome: connection between atria and His bundle; short PR; no delta wave

WPW syndrome

Ventricular arrhythmias Ventricular tachycardia –Broad complex tachycardia –Independent atrial activity –Capture/fusion beats –Risk of degeneration to ventricular fibrillation –Cardioversion (electrical or drug) can restore SR –Overdrive pacing is an alternative –Idioventricular tachycardia; rate<120/min; often related to reperfusion in AMI; Px often unnecessary

Ventricular tachycardia

Ventricular arrhythmias Torsades de pointes –Twisting pattern –Precipitated by prolonged QT –May be congenital, metabolic or drug induced Ventricular fibrillation –Death –Electrical cardioversion

Torsades de Pointes

Rhythm Strip During Episode of Sudden Death

VT versus SVT with aberrant conduction History of IHD (VT) Age>60 (VT) Independent P wave activity (VT) Very broad QRS (>140ms) (VT) Resting BBB of same morphology (SVT) Concordant QRS direction (V1-V6) (VT) If in doubt assume VT

EP studies and ablation therapy Diagnosis and curative treatment of AVNRT, AVRT (eg WPW) atrial tachy and atrial flutter Potential curative treatment of VT Stratification of risk in patients with VT –Guide need for implantable defibrillator insertion –Guide antiarrhythmic drug treatment Potential for treatment of A fib

Implanatable defibrillators

Implanatable defibrillator in-situ

Bradyarrhythmias Sinus node disease –Bradycardias usually caused by idiopathic fibrosis, ischaemia or drugs Tachy-brady syndrome –Combination of tachycardic and bradycardic episodes

Sinus node disease

Bradyarrhythmias AV node disease –1st degree; prolonged PR interval –2nd degree; Mobitz type I (Wenckebach); increasing PR interval then non-conducted P wave –2nd degree; Mobitz type II; non-conducted P waves –2nd degree; 2:1 or 3:1 AV node block –3rd degree; complete heart block AV block usually caused by idiopathic fibrosis; other causes include MI, drugs and congenital block

AV node disease 1st degree heart block 2nd degree heart block (2:1)

AV node disease Complete (3rd degree) heart block

Bradyarrhythmias Treatment of symptomatic bradyarrhythmias often consists of pacing In the short-term drugs may be used to augment conduction eg atropine, isoprenaline