1. CHAIRPERSON : DR.M.M GUPTA SPEAKER : DR.MANISH VINAYAK 1

2. A normal heart beat 2 3. Define arrhythmia Any disturbance in the normal sequence of impulse generation & conduction in the heart Arrhythmias may occur with or without underlying heart disease. 3 4. 4 5. Supraventricular Tachycardia Includes any tachycardia with signal originating above the ventricles. TYPES OF SVT : Premature atrial contractions (PACs) Paroxysmal supraventricular tachycardia (PSVT) Accessory pathway tachycardia (such as Wolff- Parkinson-White syndrome) Atrial tachycardia Atrial fibrillation Atrial flutter 5 6. Premature Atrial Complex (PAC) 6 NonCompensatory PauseP Timing of Expected P P P 7. Non-Conducted PAC 7 P Note deformation of T wave by the PAC 8. 3 most common types of PSVT PSVT is defined as conduction of supraventricular impulses at a rate of more than 100 bpm with narrow QRS, regular R-R intervals and without an evidence of pre-excitation. Atrioventricular node reentrant tachycardia (AVNRT) Atrioventricular reentrant tachycardia (AVRT) Atrial tachycardia 8 9. AVNRT AV nodal re-entrant tachycardia is the most common form of paroxysmal SVT. The initial presentation of AV node re-entry occurs most often in the fourth and fifth decades, although it can manifest at any age. It is more common in women than in men. AVNRT occurs mostly in patients with no structural heart disease. 9 10. AVNRT CIRCUIT 10 11. Initiation of AV Nodal Reentrant Tachycardia 11 12. Sustainment of AV Nodal Reentrant Tachycardia 12 13. Sustained AV Nodal Reentrant Tachycardia 13 P P P P Note fixed, short RP interval mimicking r deflection of QRS V1 14. AVRT This is less common form of PSVT. It uses macroentry circuit through accessory pathway(bundle of kent). ORTHODROMIC AVRT Most common symptomatic arrhythmia associated with accessory pathway (90% of arrhythmias in pts with WPW syndrome). Antegrade limb is AV node & normal His-Purkinje system, and an accessory pathway that conducts retrograde. Either PAC or PVC can incite this tachycardia. 14 15. ORTHODROMIC AVRT 15 APRetrograde conduction via accessory pathway (AP) 16. Orthodromic AV Reentrant Tachycardia 16 Note retrograde P waves in the ST segment 17. Antidromic AVRT Antegrade limb of this circuit is accessory pathway. This is rare tachycardia. B/c earliest site of ventricular activation is ventricular myocardium instead of normal conduction system, the QRS complex is wide, bizarre and maximally preexcited simulating ventricular tachycardia. Drugs that inhibit AV nodal conduction & vagal maneuvers with terminate this tachycardia also. 17 18. 18 19. Atrial Tachycardia Arises from atria OUTSIDE the SA Node. P wave morphology pattern depends on exact site of origin. Automatic AT usually presents with long RP tachycardia. Can be due to Digitalis toxicity. AV nodal blocking agents slows the ventricular rate but do not terminate the tachycardia. 19 20. MULTIFOCAL ATRIAL TACHYCARDIA Ectopic SVT that originates from three or more atrial foci. It has rate of 100-150 bpm. If rate is less than 100 bpm then called as wandering atrial pacemaker. Commonly due to hypoxaemia due to pulmonary diseases, CHF & due to theophylline. ECG shows irregular HR & three or more P wave configurations with narrow QRS complexes. 20 21. RP Interval 21 22. RP Short RP tachycardia indicates relatively fast retrograde activation of atrium (orthodromic AVRT) or near simultaneous activation of atrium & ventricle (AVNRT & junctional tachycardias) Similar to sinus tachycardia, AT has long RP interval b/c there is no retrograde activation of atrium from ventricle. Once P wave is noted, if it occurs within 1st half of RR interval (short RP interval), AVNRT & orthodromic AVRT should be considered If PR interval is shorter than RP interval, AT is likely. 22 23. Differential diagnosis of narrow complex tachycardia 23 24. 24 25. Carotid Sinus Massage Stimulation of carotid sinus triggers baroreceptor reflex and increased vagal tone, affecting SA and AV nodes 25 26. SVT Responses to AV Nodal Depressant Maneuvers SVT termination AV nodal reentrant tachycardia Orthodromic AV reentrant tachycardia No SVT termination (despite maximal attempts) Sinus tachycardia Atrial flutter or fibrillation Most atrial tachycardias (a minority are adenosine- sensitive) 26 27. 27 28. SVT refractory to previous drugs or SVT /AF with preexcitation Think again about the diagnosis DC cardioversion Flecainide - 2 mg/kg iv over 10 min Side effects : Hypotension QRS widening Torsades de pointes 28 29. Atrial Flutter 29 Reentrant mechanism 30. Atrial Flutter Typical or type I atrial flutter: Counter clockwise atrial activation manifested as -ve P waves in II, III, avf and +ve in V1 with transition to -ve P in V6 Clockwise with reverse activation Atypical or type II atrial flutter Also called as fib flutter In the absence of AFib symptomatic Aflutter is often amenable to ablation (success rates >90%) 30 31. Atrial Flutter Classic inverted sawtooth flutter waves at 300 min-1 (best seen in II, III and AVF) 31 Note variable ventricular response 4:1 2:1 32. Atrial flutter Atrial flutter is much more difficult to rate control than Atrial Fibrillation. Digitalis often converts flutter into fib by shortening atrial refractory period & this can revert to sinus rhythm on digitalis withdrawl. Class 1 or 3 drugs should not be used unless vent rate has been slowed by rate controlling drugs because Class Ic drugs may lead to 1:1 conduction by slowing the atrial rate If > 48 h , cardioversion should be avoided without TEE 32 33. Atrial Fibrillation Focal firing or Multiple wavelets Chaotic, rapid atrial rate at 400-600 beats per min 33 34. Atrial Fibrillation: Characteristic Irregularly Irregular Ventricular Response 34 II 35. Atrial Fibrillation 35 Rapid, undulating baseline (best seen in V1) 36. RECOMMENDATIONS FOR ANTITHROMBOTIC THERAPY IN AF Prior H/O stroke or TIA. Valvular heart disease. Hypertension Diabetes Age > 65 yrs Left atrial enlargement > 2.5 cm/m2 & LVD CAD CHF Anticoagulation with WARFARIN with INR between 2-3 36 37. Anticoagulation during reversion to NSR Risk of embolism after cardioversion is 0-7% & is independent of method of cardioversion AF >48 hrs or unknown Anticoagulate for >3 weeks, INR 2-3 Or, TEE to eval for clots in LA Appendage if no clots convert. After, anticoagulate for 4 weeks with warfarin stunned atrium Anticoag with heparin has been recommended for emergency cardioversion. 37 38. ACUTE MANAGEMENT OF AF If sudden onset of AF results in cardiovascular decompensation, ELECTRICAL CARDIOVERSION is treatment of choice. For pt who donot require emergent cardioversion, chemical cardioversion is effective in 35-75% pts. I.V Flecanide has good results (200 -300 mg po or 2mg/kg iv over 10 min) I.V Amiodarone appears to be less effective with no difference in conversion rate from placebo. In absence of decompensation, treat with digitalis, beta blocker or calcium antagonists. 38 39. LONG TERM MANAGEMENT (RATE vs RHYTHM CONTROL) No clear benefit has been ascribed to one treatment strategy over the other. Treatment should be individualized based on whether pts are symptomatic from uncontrolled vent rates or from AF itself. Rate control- Digitalis, beta blocker or calcium antagonists Radio frequency ablation or Atrial or Dual Chamber Pacing if rate not controlled by drugs 39 40. RHYTHM CONTROL For pt without structural heart disease CLASS 1c (Flecanide or Propafenone) are first line agents. For pt with structural heart disease CLASS 3 (Amiodarone, Dofetilide or sotalol) are preferred Strategy of maintaining sinus rhythm alone is insufficient to prevent thromboembolism. 40 41. Ventricular Tachyarrhythmias 41 42. Premature Ventricular Complex (PVC) 42 Compensatory Pause 43. PVCs: Bigeminal Pattern 43 Regularly Irregular Rhythm 44. SIGNIFICANCE OF VPC VPC are always significant if associated with heart ailment. Polymorphic VPC & VPC occuring in couplets are always abnormal. Monomorphic VPC are indicative of heart disease if: a) They occur frequently (>10/min). b) Follow bigeminal pattern or show R on T phenomenon. c) Are precipitated by exercise d) Occur in pt above 40 yrs of age. 44 45. Ventricular Tachycardia (VT) 45 Non-sustained or sustained P waves often dissociated (as seen here) 46. SVT vs VT ECG criteria A fundamentally simple approach: If WCT is due to SVT with aberration, the QRS must be compatible with some form of BBB or FB. -QRS duration:70% of VTs have QRS duration >140, but no SVT has it. The more leftward the axis , the more probable VT. The quadrant between -90 and 180 (northwest )cant be achieved with any combination of FB or BBB. Concordant pattern in precordial leads is uncommon in SVT Presence of capture & fusion beats favor VT. Wide QRS preceded by P waves favour SVT. 46 47. Ventricular Flutter 47 VT 250 beats/min, without clear isoelectric line Note sine wave-like appearance 48. Ventricular Fibrillation (VF) 48 Totally chaotic rapid ventricular rhythm Often precipitated by VT Fatal unless promptly terminated (DC shock) 49. Sustained VT: Degeneration to VF 49 50. Management of wide QRS complex tachycardia Haemodynamically unstable DC cardioversion Haemodynamically stable IV amiodarone ( Initial loading dose of 15mg/min given over 10 min..followed by infusion of 1 mg/min for 6 hrs and then maintenance dose of 0.5 mg/min for next 18 hrs and for next days if necessary.) 50 51. 51