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ARRHYTHMIAS

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

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ARRHYTHMIAS

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  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

  20. 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

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