1 / 44

Ventricular Tachyarrhythmias

Ventricular Tachyarrhythmias. An Electrophysiologic Overview. Module Objectives – Ventricular Tachyarrhythmias. After completion of this module, the participant should be able to:. Identify the mechanisms for ventricular tachycardias

zudora
Télécharger la présentation

Ventricular Tachyarrhythmias

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Ventricular Tachyarrhythmias An Electrophysiologic Overview

  2. Module Objectives – Ventricular Tachyarrhythmias After completion of this module, the participant should be able to: • Identify the mechanisms for ventricular tachycardias • Differentiate types of ventricular tachycardias using ECG and intracardiac electrogram recordings • Discuss treatment options for ventricular tachycardias

  3. Module Outline – Ventricular Tachyarrhythmias • Description • Characteristics • Mechanisms • Sustained vs. nonsustained • Premature ventricular contractions

  4. Module Outline – Ventricular Tachyarrhythmias • Classification • Monomorphic • Idiopathic • Description • ECG recognition • Treatment – ablation • Bundle branch • Description • ECG recognition • Treatment –ablation

  5. Module Outline – Ventricular Tachyarrhythmias • Classifications - continued • Ventricular flutter • ECG recognition • Ventricular fibrillation • ECG recognition • Polymorphic • Torsades de pointes • Description • ECG recognition • Treatment • Summary

  6. Ventricular Tachycardia (VT) • Originates in the ventricles • Can be life threatening • Most patients have significant heart disease • Coronary artery disease • A previous myocardial infarction • Cardiomyopathy

  7. Mechanisms of VT • Reentrant • Reentry circuit (fast and slow pathway) is confined to the ventricles and/or bundle branches • Automatic • Automatic focus occurs within the ventricles • Triggered activity • Early afterdepolarizations (phase 3) • Delayed afterdepolarizations (phase 4)

  8. Reentrant • Reentrant ventricular arrhythmias • Premature ventricular complexes • Idiopathic left ventricular tachycardia • Bundle branch reentry • Ventricular tachycardia and fibrillation when associated with chronic heart disease: • Previous myocardial infarction • Cardiomyopathy

  9. Automatic • Automatic ventricular arrhythmias • Premature ventricular complexes • Ischemic ventricular tachycardia • Ventricular tachycardia and fibrillation when associated with acute medical conditions: • Acute myocardial infarction or ischemia • Electrolyte and acid-base disturbances, hypoxemia • Increased sympathetic tone

  10. Abnormal Acceleration of Phase 4 Automaticity Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 16.

  11. Triggered • Triggered activity ventricular arrhythmias • Pause-dependent triggered activity • Early afterdepolarization (phase 3) • Polymorphic ventricular tachycardia • Catechol-dependent triggered activity • Late afterdepolarizations (phase 4) • Idiopathic right ventricular tachycardia

  12. Triggered Fogoros: Electrophysiologic Testing. 3rd ed. Blackwell Scientific 1999; 158.

  13. Sustained vs. Nonsustained • Sustained VT • Episodes last at least 30 seconds • Commonly seen in adults with prior: • Myocardial infarction • Chronic coronary artery disease • Dilated cardiomyopathy • Non-sustained VT • Episodes last at least 6 beats but < 30 seconds

  14. Premature Ventricular Contraction • PVC • Ectopic beat in the ventricle that can occur singly or in clusters • Caused by electrical irritability • Factors influencing electrical irritability • Ischemia • Electrolyte imbalances • Drug intoxication

  15. Classification • Ventricular Tachycardia • Monomorphic • Idiopathic VT • Bundle branch reentry tachycardia • Ventricular flutter • Ventricular fibrillation • Polymorphic • Torsades de pointes (TdP)

  16. Monomorphic VTs

  17. Monomorphic VT • Heart rate: 100 bpm or greater • Rhythm: Regular • Mechanism • Reentry • Abnormal automaticity • Triggered activity • Recognition • Broad QRS • Stable and uniform beat-to-beat appearance

  18. ECG Recognition ECG used with permission of Dr. Brian Olshansky.

  19. Intracardiac Recording of VT EGM used with permission of Texas Cardiac Arrhythmia, P.A.

  20. Idiopathic Right Ventricular Tachycardia • Right ventricular idiopathic VT • Focus originates within the right ventricular outflow tract • Ventricular function is usually normal • Usually LBBB, inferior axis • Treatment options: • Pharmacologic therapy (beta blockers, verapamil) • RF ablation

  21. ECG Recognition Kay NG. Am J Med 1996; 100: 344-356.

  22. Case History: Idiopathic VT 39 y.o. female with no prior cardiac history • First episode • 9 hours of palpitations • In ER, found to be in wide-complex tachycardia of LBBB, inferior axis, at 205 bpm • Converted with IV lidocaine; placed on tenormin • Second episode • While on tenormin, patient had onset of palpitations at airport • In ER, converted with IV lidocaine • Patient underwent EP study

  23. Case History: Idiopathic VT

  24. Case History: Idiopathic VT • At EP study, tachycardia focus was mapped and localized to right ventricular outflow tract • The focus was successfully ablatedusing radiofrequency energy, with no subsequent inducible or clinical VT

  25. Endocardial Activation Mapping • Using an ablation catheter, map the area around and inside of the right ventricular outflow tract • Find the electrograms that precede the onset of the QRS complex during tachycardia • This area identifies the site of earliest activation, and possibly the “site of origin” of the arrhythmia

  26. Pace Mapping • Pace mapping helps to localize the “site of origin” after endocardial mapping has been performed • If the heart is paced from this region, the resulting ECG should be identical to the ECG taken during tachycardia • Delivering RF energy to this site usually eliminates ventricular tachycardia

  27. Idiopathic VT Ablation in RVOT RAO RAO

  28. Idiopathic Left Ventricular Tachycardia • RBBB/LAFB • Involves the Purkinje network • Treatment options: • RF ablation • Pharmacologic therapy (verapamil, beta blockers)

  29. ECG Recognition ECG used with permission of Kay NG.

  30. Bundle Branch Reentry • Reentry circuit is confined to the left and right bundle branches • Usually LBBB, during sinus rhythm • Presents with: • Syncope • Palpitations • Sudden cardiac death • Treatment: RF ablation of right bundle

  31. VT Due to Bundle Branch Reentry

  32. Catheter Ablation of Right Bundle Branch I II V1 RA Current Voltage Courtesy of Dr. Warren Jackman

  33. Ventricular Flutter • Heart rate: 300 bpm • Rhythm: Regular and uniform • Mechanism: Reentry • Recognition: • No isoelectric interval • No visible T wave • Degenerates to ventricular fibrillation • Treatment: Cardioversion

  34. Ventricular Fibrillation • Heart rate: Chaotic, random and asynchronous • Rhythm: Irregular • Mechanism: Multiple wavelets of reentry • Recognition: • No discrete QRS complexes • Treatment: • Defibrillation

  35. P waves and QRS complexes not present Heart rhythm highly irregular Heart rate not defined ECG Recognition

  36. Polymorphic VT

  37. Polymorphic VT • Heart rate: Variable • Rhythm: Irregular • Mechanism: • Reentry • Triggered activity • Recognition: • Wide QRS with phasic variation • Torsades de pointes

  38. ECG Recognition EGM used with permission of Texas Cardiac Arrhythmia, P.A.

  39. Torsades de Pointes (TdP) • Heart rate: 200 - 250 bpm • Rhythm: Irregular • Recognition: • Long QT interval • Wide QRS • Continuously changing QRS morphology

  40. Mechanism • Events leading to TdP are: • Hypokalemia • Prolongation of the action potential duration • Early afterdepolarizations • Critically slow conduction that contributes to reentry

  41. QRS morphology continuously changes Complexes alternates from positive to negative ECG Recognition

  42. Possible Causes • Drugs that lengthen the QT: • Quinidine • Procainamide • Sotalol • Ibutilide • Physical • Ischemia • Electrolyte abnormalities

  43. Treatment • Pharmacologic therapy: • Potassium • Magnesium • Isoproterenol • Possibly class Ib drugs (lidocaine) to decrease refractoriness/shorten length of action potential • Overdrive ventricular pacing • Cardioversion

  44. Summary • VT ablation is not an FDA-approved indication • RF catheter ablation can be a useful technique in patients with ventricular tachycardia • Success largely depends on the etiology of the arrhythmia • Unstable sustained VT, polymorphic VT and ventricular fibrillation are not ablatable • Improved catheters and imaging techniques may change this in the future

More Related