Supraventricular arrhythmias

1. Supraventricular arrhythmias Jerry John July 29, 2009

2. Objectives • Supraventricular Arrhythmias • How do supraventricular arrhythmias manifest? • What are the common supraventricular arrhythmias? • What is the mechanism of atrioventricular arrhythmias? • Which drugs are used in the management of supraventricular arrhythmias? • Which patients should be offered catheter ablation? • Atrial Fibrillation and Atrial Flutter • What are the incidence and prevalence of atrial fibrillation? • What are the major sequelae of atrial fibrillation? • What are the risk factors for stroke in atrial fibrillation? • What are the treatment options for patients with atrial fibrillation?

3. History • F > M (2:1) – AVNRT • M >F AVRT • Posture • Menses • 3rd trimester pregnancy • Neck pulsations (“Frog sign”) • Age of onset (10 year difference AVNRT(39) vs. AVRT (26) • Thyroid symptoms • Acute precipiants (post op, PE, drug withdrawal, ischemia) JACC 2009; 53:2353-58

4. EKG • AV node dependent (Y/N) • Re-entrant circuit (Y/N) • Circuit (Macro/Micro) • Anatomic (e.g. previous ASD repair, CVTI) • Accessory pathway ( WPW, Mahaim, etc. ) • P wave • Rate • Morphology (Sinus/Retrograde/abnormal): look at the T waves and the psuedo R (V1) and psedo S (inferior leads) • Conduction (2:1; 3:1, etc.) • Response to AV Block • VA conduction (i.e. R-P relationship): (short/long) • Initiation (PAC or PVC) & Termination (P wave or QRS)

7. Anatomy & Physiology • SA node • 1 mm subendocardial near RSPV • AV node • Decremental conduction properties • His-Purkinje • Accessory pathways • No decremental conduction • AV conduction 10-20 ms

8. ORT AVNRT Non paraoxysmal junctional tach Atach (reentry or automaticity)

9. AV Node Depdendence (Y/N) AV nodal dependent arrhythmias • AVNRT (micro-reentrant circuit) • AVRT (macro-reentrant circuit): anti/orthodromic • JET (junctional ectopic tachycardia) - childhood and associated with congenital heart disease AV nodal independent arrhythmias • Atrial tachycardia • Inappropriate Sinus Tachycardia • Sinus Node Reentrant Tachycardia • Atrial flutter • Atrial fibrillation

10. RP relationship • Short “RP” Tachycardias: Typical AVNRT AVRT • Long “RP” Tachycardias: Atrial Tachycardia Atypical AVNRT AVRT with long retrograde conduction PJRT

11. Where’s the P wave • Valsalva • Carotid sinus massage • Slows SA nodal; and/or AV nodal conduction • Adenosine • Slows sinus rate • Increases AV nodal conduction delay • T ½ 5 seconds • 6 or 12 mg bolus • Effect blocked by theophylline, methylxanthines (caffeine); and potentiated by dipyridamole

13. P waves • Rate • Morphology (Sinus/Retrograde/abnormal) • Conduction (2:1; 3:1, etc.) • Response to AV Block • VA conduction (i.e. R-P relationship): (short/long)

15. P waves • (-) Inferior leads atrial activation from low to high: AVNRT, atypical AVNRT; AVRT • Right atrial focus: 1) (-/+) in aVL right atrium activated first and then left atrium) 2) (-) or biphasic in V1 • Left atrial focus: 1) (-) or isoelectric in aVL 2) (+) V1 suggests back to front

16. Tachycardia onset • Most SVTs triggered by a PAC • If the PAC conducts with a long PR, dual AV nodal physiology is suggested with the conduction being through the slow pathway • If a PVC initiates SVT, it is likely to be AV node dependent

17. Tachycardia termination • Ends with a P wave: suggests an AV nodal dependent arrhythmia because the generation of the P wave without a QRS suggests block in the AV node… this is more likely to be AVNRT or AVRT • AVNRT p waves however can be buried in the QRS if VA conduction is very short • Ends with a QRS : almost always atrial tachycardia (some rare AV node dependent tachycardias can terminate in this manner)

18. AVNRT • Most common cause of a regular narrow complex tachycardia • Involves a slow and a fast pathway in the region of the AV node • Turn around point appears above the bundle of His • 160-190 bpm but may exceed 200 bpm • Slow-fast form accounts for 90% of AVNRT • Fast-slow or slow-slow AVNRT accounts for 10% • Pseudo r’ in V1, pseudo S wave in 2,3,avf, and p wave absence help distinguish AVNRT from AVRT and atrial tachycardia

19. AVNRT • Initiation and termination by APDs, VPDs or atrial pacing during AVW • Dual AVN physiology • Initiation depends on critical A-H delay • Concentric retrograde atrial activation(V-A -42 to 70 msec) • Retrograde P wave within QRS with distortion of terminal portion of the QRS • Atrium, His bundle and ventricle not required , vagal maneuvers slow and then terminate SVT

21. Atypical AVNRT • Initiation and termination by APDs, VPDs, or ventricular pacing during retrograde AVW • Dual retrograde AVN physiology • Initiation dependent on critical H-A delay • Earliest retrograde activation at CS os • Retrograde P wave with long R-P interval • Atrium, His bundle, and ventricle not required, vagal , maneuvers slow and then terminate SVT, always in the retrograde slow pathway

22. AVNRT Treatment • Low threshold for catheter ablation given long term success rate > 90% and low risk of complications • AV nodal blocking agents (diagnosis/treatment) • Adenosine • BB/CCB • Digoxin • Anti-arrhythmics (third choice) • Procainamide • Amiodarone • Disopyramide • Flecainide/Propafenone

23. AVRT • Activation sequence is ventricle via atria; therefore P wave often in the ST or T • Left lateral AP: (+) Delta V1; (-) Delta I • Right sided AP: (-) Delta V1 {QS pattern}; (+) Delta I • Concealed AP implies only retrograde conduction; i.e. no pre-excitation and only orthodromic AVRT. • Rapidly conducted Afib occurs may occur for 2 reasons: 1) AP may have a short refractory period ; 2) AP does not exhibit decremental conduction properties like the AV node • Flecainide and Propafenone preferred as they prolong the effective refractory period

24. BBB on tachycardia • Interval development of BBB and increased tachycardia cycle length suggests contralateral AVRT • Pre-existing BBB • Rate related BBB: will look like a conventional BBB • Accessory pathway

27. AVRT • Use of Adenosine or Verapamil • There is a small risk (3-5%) of preferential conduction down the accessory pathway, and ibutilide or procainamide, or electric cardioversion should be immediately available

29. Asymptomatic WPW • 165 children (5-12 years) screened • 60 randomized, 3 withdrew: 20 ablation and 27 no ablation • 1 child in ablation group had arrhythmia (5%) and 12 of 27 in control group ( 44% ) • 2 children in control group had VF and one died Pappone et al; NEJM 2004;351:1197-05

30. AVRT Treatment • Low threshold for catheter ablation given long term success rate > 90% and low risk of complications • Posteroseptal pathways have less success rates • L sided • AV nodal blocking agents (diagnosis/treatment) • Adenosine • BB orCCB in conjunction with Flecainide or Propafenone

31. Atrial tachycardia • Older patients - related to atrial stretch or scarring • If conduction to the ventricle via the AV node, variable AV block may occur • A bystander (accessory) pathway may be used to conduct antegrade to the ventricles; i.e. the accessory pathway is not what is causing the atria to beat so fast • Tachycardia may be incessant: “the ventricle is a slave to the atrium” • Procainamide may be considered to achieve immediate control • AV nodal blocking agents and sotalol may be considered for chronic treatment

32. Irregular SVT • AV block • Wenckebach • Variable block (e.g. atrial tachycardias) • 2:1 with typical flutter; odd multiples with atypical flutter • Multifocal atrial tachycardia (MAT) • Atrial Fibrillation (with or w/o pre-excitation)

33. Focal Atrial Tachycardia • Incessant or paroxysmal atrial rhythms 120-250 bpm • Demographic profile similar to reentrant AT, but less likely to have cardiac surgery • Typically 1:1 conduction • P wave morphology different from sinus • Typically terminate or transiently suppress with adenosine • Centrifugal activation • Cannot be entrained

34. Focal Atrial Tachycardia Three Subgroups: • Cristal Tachycardia - Initiated and terminated with PES - Arise along crista - P wave similar to NSR - Terminates with adenosine • Repetitive monomorphic AT - Repetitive runs of nonsustained AT - Suppress with adenosine - Variable locations • Automatic AT - Incessant AT - Transient suppression with adenosine

37. Junctional Tachycardia • Nonparoxysmal Junctional Tachycardia • Junctional Ectopic Tachycardia • Congenital Automatic Junctional Tachycardia

38. Nonparoxysmal Junctional Tachycardia • 70-120 bpm • Generally regular with VA conduction • Seen with dig toxicity, ischemia, COPD, metabolic disturbances, carditis and after cardiac surgery • Mechanism is triggered activity due to DADs

39. Junctional Ectopic Tachycardia(JET) • Following surgery for congenital heart disease • 3% of VSD repairs, 10% of TGV, 7% of TOF and 2% of Fontan • Perinodal trauma • Procainamide and cooling, amiodarone

40. Congenital Automatic Junctional Tachycardia • < 1% of pediatric SVTs • Average HR 230 bpm (140-370) • Infants < 6 months old • High mortality. Less malignant older the child is • Triggered activity, enhanced automaticity • Amiodarone, ablation with PM

41. PJRT • Orthodromic reciprocating tachycardia • Earliest retrograde activation in proximal CS • Tachycardia terminates with adenosine with retrograde AP block • HIS refractory PVC advances atrial activation

43. Atrial Flutter • Typical or type I atrial flutter: Counter clockwise atrial activation manifested as - P waves in II,III,avf and + in VI with transition to - 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%)

47. Afib • What are the incidence and prevalence of atrial fibrillation? • What are the major sequelae of atrial fibrillation? • What are the risk factors for stroke in atrial fibrillation? • What are the treatment options for patients with atrial fibrillation?

48. Afib epidemiology • Age adjusted incidence has been increasing from 1980 to 2000: 3.2 million in 1980; 5.1 million in 2000 • The detection of Afib requires symptoms and asymptomatic PAF may go undetected.. Current estimates at the Mayo Clinic would suggest 2.3 million Americans. • Afib prevalence increases with age: 0.1% <55 years; at 9% in octogenerians. • At younger ages (<70), Afib has a greater prevalence among males (5.8%) than females (2.8%) based on data from CHS • The lifetime risk based on the Framingham cohort is 23-26% among 40 year olds. Circulation 2006; 114(2):119-125. ;Am J Cardiol 1994; 74:236-241).; JAMA 2004; 292:2471-2477; JACC 2007; 49:565-571).

49. Afib epidemiology • Age alone does not explain the increased incidence: an increase in obesity accounted for 60% of the age adjusted increase in AF incidence • HTN and Diastolic dysfunction • Obesity has been associated with new onset Afib in the Framingham and other cohorts • OSA, Etoh, Anger, ethnicity, and genetic influences have been reported to be associated with incident Afib. • Appropriately treated OSA reduces AFib recurrence after cardioversion • AA race is associated with less Afib than whites. • Afib and CAD are co-existent • Rheumatic heart disease and valvular heart disease Circulation 2006; 114(2):119-125. ;Am J Cardiol 1994; 74:236-241).; JAMA 2004; 292:2471-2477; JACC 2007; 49:565-571; Circ 2003; 107:2589-2594).

50. Afib categories • Lone atrial fibrillation: no structural heart disease (usually <60 years) • Paroxysmal : terminate spontaneously <7 days • Persistent: fails to self-terminate within 7 days. Episodes may eventually terminate spontaneously, or they can be terminated by cardioversion. • Permanent : > 1 year and CV not attempted or failed. ** Episodes > 30 seconds unrelated to a reversible cause (cardiac surgery, pericarditis, MI, hyperthyroidism, PE)