1. Management of Atrial Fibrillation

2. Definition A supraventricular tachyarrhythmia Characterized by
Uncoordinated atrial activation
Deterioration of atrial mechanical function

3. ECG No consistent P waves
Rapid oscillations or fibrillatory waves that vary in size, shape, and timing,
Irregular, frequently rapid ventricular response when AV conduction is intact.

4. Ventricular Response Electrophysiological properties of the AV node
depends on
Electrophysiological properties of the AV node
The level of vagal and sympathetic tone
The action of drugs

5. Variation
Regular RR intervals are possible in the presence of AV block or interference due to ventricular or junctional tachycardia

6. Special Situation
In patients with electronic pacemakers, diagnosis of AF may require temporary inhibition of the pacemaker to expose atrial fibrillatory activity

7. Special Situation
A rapid, irregular, sustained, wide-QRS-complex tachycardia strongly suggests AF with conduction over an accessory pathway or AF with underlying bundle-branch block.
Extremely rapid rates (over 200 bpm) suggest the presence of an accessory pathway.

8. Related Arrhythmias Atrial flutter or atrial tachycardia
Other atrial tachycardias
AV reentrant tachycardias
AV nodal reentrant tachycardias

9. Atrial Flutter May arise during treatment AF May degenerate into AF
May be initiated by AF
ECG pattern may alternate between atrial flutter and AF

10. Atrial Flutter More organized arrhythmia
Saw-tooth pattern of regular atrial activation, particularly in leads II, III, and aVF
Without an isoelectric baseline between deflections

11. Untreated Atrial Flutter
Typical atrial rate bpm
ƒ waves
Inverted in ECG leads II, III, and aVF
Upright in lead V1
Wave of activation in the right atrium may be reversed

12. Ventrivular Response of Atrial Flutter
Commonly occurs with 2:1 AV block
Resulting in a ventricular rate of bpm
Most characteristically about 150 bpm

13. A unique type of atrial tachycardia has recently been identified that commonly originates in the pulmonary veins but may arise elsewhere, is rapid (typically faster than 250 bpm), and often degenerates into AF.

14. Clinical Evaluation Minimum Evaluation Additional Investigation
Clinical History and Physical Examination
Investigations
Additional Investigation
Holter Monitoring and Exercise Testing
Transesophageal Echocardiography
Electrophysiological Study

15. Proposed Management Strategies

16. Newly Discovered AF

17. Recurrent Paroxysmal AF

18. Recurrent Paroxysmal AF

19. Recurrent Persistent AF & Permanent AF

20. Agents With Proven Efficacy
Amiodarone
Dofetilide
Flecainide
Ibutilide
Propafenone
Quinidine

21. Less Effective or Incompletely Studied Agents
Beta-Blockers
Calcium Channel Antagonists
Digoxin
Disopyramide
Procainamide
Sotalol