1. ARRHYTHMIAS Jamil Mayet

2. 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

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

4. 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

5. 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

6. Supraventricular arrhythmias Atrial fibrillation –Rapid atrial discharge (350-600/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”)

7. Atrial fibrillation

8. Supraventricular arrhythmias Atrial flutter –Rapid atrial discharge (250-350/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

9. Atrial flutter

10. Atrial flutter with 2:1 block

11. Supraventricular arrhythmias Atrial tachycardia –Atrial discharge slower (120-250/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

12. Atrial tachycardia

13. Supraventricular arrhythmias AV nodal re-entry tachycardia –Re-entry circuit within AV node –Rate usually 130-250/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

14. AV nodal re-entry tachycardia

15. 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

16. 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

17. WPW syndrome

18. 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

19. Ventricular tachycardia

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

22. Torsades de Pointes

23. Rhythm Strip During Episode of Sudden Death

24. 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

25. 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

26. Implanatable defibrillators

27. Implanatable defibrillator in-situ

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

29. Sinus node disease

30. 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

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

32. AV node disease Complete (3rd degree) heart block

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