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Management of Supraventricular Tachycardias

Management of Supraventricular Tachycardias. Sandeep K. Jain, M.D. Cardiac Electrophysiology. May 31, 2008. History. Pattern of symptoms / palpitations Triggers Caffeine, tobacco, alcohol Nasal decongestants Emotional events Syncope. Physical Exam. AV dissociation Split S2

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Management of Supraventricular Tachycardias

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

  2. History • Pattern of symptoms / palpitations • Triggers • 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 ?

  6. 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

  7. 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

  8. 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

  9. 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 250-350 beats/min • Ventricular rate of 150 – look out for 2:1 flutter

  10. Counterclockwise Clockwise

  11. Diagnostic maneuvers - Adenosine

  12. 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

  13. 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

  14. Flecainide administration

  15. 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

  16. 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

  17. Atrial Fibrillation • Rate vs Rhythm Control • 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

  18. Atrial Fibrillation • Rate Control • 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

  19. Atrial Tachycardia • Rapid, focal discharge in the atrium • Rate generally 150-200 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

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

  21. 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

  22. AV Node Reentry Tachycardia • Regular, sudden onset and termination at rates between 150-250 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

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

  24. Baseline

  25. AV Node Reentry Tachycardia

  26. AVNRT 2:1

  27. 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)

  28. 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

  29. 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

  30. 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

  31. Accessory Pathways

  32. Accessory Pathways

  33. 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

  34. 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

  35. 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

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

  37. Pre-excitation syndromes

  38. 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

  39. Pre-excitation syndromes

  40. Pre-excitation syndromes

  41. 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

  42. 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

  43. 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

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