1. Management of Supraventricular Tachycardias
May 31, 2008
Sandeep K. Jain, M.D.
Cardiac Electrophysiology

2. History Pattern of symptoms / palpitations Triggers Syncope
Caffeine, tobacco, alcohol
Nasal decongestants
Emotional events
Syncope

3. Physical Exam AV dissociation Split S2
More than one arrhythmia can yield similar exam findings so not as useful for making a diagnosis

4. SVT mechanisms Sinus tachycardia Atrial flutter Atrial fibrillation
Junctional tachycardia
Atrial tachycardia
AV node reentry tachycardia (AVNRT)
Accessory pathway mediated tachycardia (AVRT)

5. ECG Are P-waves present?
What are atrial and ventricular rates and are they the same ?
Regular or Irregular ?
Is the PR or RP constant ?

7. Carotid Sinus Massage Increases vagal tone
Sinus slowing and prolongs AV nodal refractoriness
Sinus tach – gradually slows then returns to rate prior to massage
AVNRT or AVRT can terminate
AT, AF and AFL ventricular response slows

8. Sinus Tachycardia Gradual change in heart rate Normal P-wave contour
Constant PR interval before each QRS unless there is AV block (long RP)
Carotid massage or Valsalva will gradually slow rate and then resume to original rate

9. Almost always secondary
Management is to treat underlying cause
Rarely, inappropriate sinus tachycardia in which case beta-blockers, Ca-blockers can be utilized
Sinus node reentry tachycardia is abrupt in onset, anxiety related and can be treated with RF ablation

10. Atrial Flutter Macro-reentrant rhythm in the atria
Usually associated with underlying heart disease
Typical flutter is in the right atrium and can travel in counterclockwise and clockwise directions
Incisional scars from prior cardiac surgery / congenital abnormalities
Atrial rate is typically beats/min
Ventricular rate of 150 – look out for 2:1 flutter

11. Counterclockwise
Clockwise

13. Diagnostic maneuvers - Adenosine

14. Atrial Flutter - Management
Rate control / anticoagulation
Beta-blocker, Ca-blocker, Digoxin
Stroke risk likely not much different than atrial fibrillation
Cardioversion
DCCV with low energies possible (50-100J)
Ibutilide successful in 60-90%
Prolongs QT and need to be monitored 4-6 hours
post administration
Overdrive atrial pacing if available

15. Atrial Flutter - Management
Antiarrhythmics
Class Ia and Ic agents – convert and maintain sinus rhythm
Class III – amiodarone, sotalol, dofetilide
Need to have AV nodal agent on board to prevent 1:1 flutter
Flutter rate slows and allows 1:1 conduction
Class IA agents also have a vagolytic effect

16. Flecainide administration

17. Atrial Flutter - Management
Radiofrequency Ablation
High success rates for typical flutter
Atypical circuits can be approached percutaneously with advanced mapping systems
Significant proportion of patients eventually develop atrial fibrillation indicating underlying substrate is the issue

18. Atrial Fibrillation
Multiple wavelets propagating in different directions
No effective atrial contraction
Most common arrhythmia
1% of those older than 60
5% of those older than 69
Mutliple causes – consider mechanical such as from an RA catheter

19. Atrial Fibrillation Rate vs Rhythm Control Anticoagulation
No benefit of either if asymptomatic
Anticoagulation
Congestive Heart Failure
Hypertension
Age > 65
Diabetes
Stroke
Maintenance of sinus rhythm does not necessarily eliminate stroke risk

20. Atrial Fibrillation Rate Control Conversion
Ca-blocker, Beta-blocker, digoxin
Conversion
DCCV
Class I : Procainamide, Flecainide, Propafenone
Class III: Amiodarone, Sotalol (both poor as converting agents), ibutilide
Maintenance of sinus rhythm
Same as above + dofetilide
50-70% efficacy at 1 year
RF ablation is an emerging tool

21. Atrial Tachycardia Rapid, focal discharge in the atrium
Rate generally bpm
P-wave contour different from sinus
P-waves generally found in second half of tachycardia cycle (long RP / short PR)
Most commonly in those with structural heart disease but also seen in those without any cardiac abnormality

22. Atrial Tachycardia Adenosine Response
Terminates tachycardia with an ‘R’ wave OR
Tachycardia persists with AV Block

24. Atrial Tachycardia - Management
Beta- and Ca- blockers
Class I antiarrhythmics in normal hearts
Class III antiarrhythmics in abnormal hearts
Radiofrequency ablation for those who are refractory / intolerant to medications

25. AV Node Reentry Tachycardia
Regular, sudden onset and termination at rates between bpm
QRS usually normal unless aberrancy is present
Reentry within the AV node
P-wave seen just prior to or just after the QRS complex (Short RP tachycardia)
Usually occurs without any structural heart disease

26. AV Node Reentry Tachycardia
Antegrade limb is the slow pathway
Retrograde limb is the fast pathway

28. Baseline

29. AV Node Reentry Tachycardia

30. AVNRT 2:1

31. AV Node Reentry - Management
IV adenosine, vagal maneuvers, carotid massage
Ca, Beta-blockers, rarely antiarrhythmics
Overdrive atrial or ventricular pacing
RF ablation is usually treatment of choice for chronic management – cost-effective and high success rate (~1% incidence of AV block requiring permanent pacemaker)

32. Accessory Pathways
Muscular connections outside of the specialized conduction system connecting the atrium and ventricle while bypassing the AV node
Can be manifest (WPW) or concealed (retrograde only conduction)
Concealed pathways not apparent on ECG
Manifest pathways have a delta wave representing pre-excitation of ventricular tissue prior to activation via the His-purkinje system

33. Concealed Accessory Pathways
30% of people with SVT referred for EP evaluation
Can present with syncope
Normal baseline 12-lead ECG
Orthodromic atrioventricular reentry tachycardia is the mechanism of SVT (down the AV node and up the accessory pathway)
Will often see a retrograde P-wave during SVT – short RP unless slowly conducting pathway

34. Orthodromic AV reentry tachycardia
Most common arrhythmia with presence
of an accessory pathway
Macro-reentrant circuit in which the
impulse travels down the AV node and
up the accessory pathway
Narrow QRS interval

35. Accessory Pathways

36. Accessory Pathways

37. Response to BBB Aberration
Does VA interval increase with development of BBB?
An increase in VA interval indicates the presence and participation of a bypass tract on the side of the blocked bundle

39. Concealed Accessory Pathways
Same management as for AV node reentry
RF ablation should be considered early in symptomatic patients
Atrial fibrillation in conjunction with a concealed pathway does not pose a risk of sudden death and IV Ca-blocker not contraindicated as the pathway does not conduct antegrade

40. Pre-excitation syndrome - WPW
WPW syndrome is when tachycardia is associated with the finding of a delta wave on the ECG
Incidence is 1.5 per thousand
Ebstein’s anomaly associated with multiple bypass tracts
Baseline ECG findings
PR interval < 120ms
QRS > 120ms with a slurred, slowly rising onset (delta wave) and usually normal terminal portion of QRS
Secondary ST-T changes in opposite direction of delta wave

41. Accessory pathways
Left free wall most common, then posteroseptal, right free wall and anteroseptal

42. Pre-excitation syndromes

44. Pre-excitation syndrome - WPW
Most common tachycardia is Orthodromic AVRT as seen in concealed bypass tracts
Major difference is the capacity for anterograde conduction over the pathway during atrial fibrillation (15-30%) or atrial flutter (5%) and thus the rare incidence of sudden cardiac death
Some children lose conduction in the pathway but usually persists if present at age 5

46. Pre-excitation syndromes

47. Pre-excitation syndromes

48. WPW - Treatment
ECG abnormality only without arrhythmias may not require EP evaluation
Symptomatic patients should receive treatment
Ablation – Electrical or Surgical
Good success rates but with procedural risks
Pharmacologic
Drugs prolong conduction and/or refractoriness in the AV node, accessory pathway, or both
Some agents can suppress premature atrial contractions which can induce arrhythmias

49. WPW - Treatment Prolong conduction time and refractoriness in AV node:
Adenosine, verapamil, beta-blockers, digoxin
Prolong refractory period in accessory pathway:
Class IA and IC drugs
Affect both AP and AV node:
Class IC drugs, amiodarone, and sotalol

50. WPW – Acute Episode
Normal QRS, regular R-R intervals, retrograde p-waves
Approach same as AVNRT – vagal maneuvers, adenosine, IV Ca-blocker
Note, atrial fibrillation can occur after drug administration, so external defibrillator back-up should be ready
Atrial Fibrillation or Flutter with irregular R-R intervals and abnormal QRS complexes
Agents which affect AV node and pathway (procainamide with beta blocker)
Any signs of hemodynamic impairment – electrical cardioversion is initial treatment of choice

52. WPW - Treatment DRUGS NOT TO USE in AF/AFL with WPW:
Digoxin has varying effects on the accessory pathway and can shorten refractoriness and speed ventricular response to atrial fibrillation
IV Lidocaine can also increase ventricular response rate
IV Verapamil can precipitate ventricular fibrillation in this circumstance (may not happen with oral)
Catecholamines

53. Supraventricular Tachycardias
Short RP / Long PR
AV node reentry
AV reentry
Long RP / Short PR
Atrial tachycardia
Sinus node reentry
Atypical AV node reentry
AV reentry with a slowly conducting pathway