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VT IN NORMAL AND ABNORMAL HEARTS

VT IN NORMAL AND ABNORMAL HEARTS. Ventricular Tachycardia. Ventricular Tachycardia is Defined as Three or more consecutive PVC’s r ate i s usually Between 100-200 BPM Sustained VT Episodes last at least 30 seconds/ req intervention for termination Non-sustained VT

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VT IN NORMAL AND ABNORMAL HEARTS

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  1. VT IN NORMAL AND ABNORMAL HEARTS

  2. Ventricular Tachycardia Ventricular Tachycardia is Defined as Three or more consecutive PVC’s • rate is usually Between 100-200 BPM • Sustained VT • Episodes last at least 30 seconds/ req intervention for termination • Non-sustained VT • Episodes last at least 6 beats but < 30 seconds

  3. VENTRICULAR TACHYCARDIA • CLASSIFICATION ECG MORPHOLOGY DURATION MECHANISM ETIOLOGY

  4. 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)

  5. VT IN NORMAL HEART

  6. 10% with VT - no apparent SHD • Idiopathic ventricular tachycardia (VT)-SUBTYPES 1) QRS morphology 2) ventricular origin, and 3) response to pharmacologic agents • management and prognosis • DEF:-implies a structurally nl heart in young & middle aged subjects & a nl QT interval, although biopsy & MRI may detect subtle micro / macroscopic abnormalities

  7. Synd of idiopathic VT refers specifically to monomorphic VTs. • Polymorphic VTs and VF -structurally normal hearts differ from idiopathic VT -mechanistically and prognostically • Commonly- subgrouped as 1)outflow tract tachycardias, 2)idiopathic left VTs (ILVTs), and 3)automatic VTs.

  8. Outflow tract tachycardia • outflow tract region - RV region between the pulm and tricuspid valves, - Basal left ventricle- outflow tract under the AoV, the aortic cusps, and the basal LV epicardium. • A)repetitive monomorphic VT B)paroxysmal sustained VT

  9. Classification by symptoms

  10. delayed afterdepolarization(DAD)-mediated triggered activity - mechanism • DAD- mediated by intracellular calcium overload • Freq precip by catecholaminergic stimulation,↑ in intracellular cAMP and ca • rapid stimulation- isoproterenol infusion. • dependence on cAMP- sensitivity to β-blockade, CCB and adenosine

  11. RVOT VTs -75% - LBBB+ INF AXIS -QRS transition from V₃\V₄ (late) • Jadonath RL et al, localizing the origin of right ventricular outflow tract tachycardia. Am Heart J 1995 RVOT - 9 regions and used QRS morphology in leads I and aVL + R wave transition to diff ant from post RVOT sites • Anterior sites- Q wave (Q or qR) in lead I and a QS in lead aVL. • Posterior site- R wave in lead I and an early precordial transition( R to S) in V3 • Septal- taller, narrower monophasic R-inferior leads • Free wall RVOT VTs-notchiinf leads and later transition (>V3) • RVOT VT-Posterior- +ve in V1, ant- -ve in V1

  12. RVOT VT

  13. VT arising from the LVOT (1)a) RBBB + inf axis b) dominant R wave in V1 c) lack of precordial transition d)+_a late appearing S wave in V6 and V2 (2) a) LBBB+ inferior axis+ b)early precordial R wave transition (<V₂)

  14. Aortic cusps Dep on the s/o origin from the R/L cor cusp- RBBB or LBBB VT- LCC or aortomitral cont- terminal S wave in lead I Precordial transition-earlier in cusp VT (< V3) R duration & the R/S ratio V1 & V2 were > in cuspVT

  15. Lcc VT

  16. 9%–13% of idiopathic VT- originate from epicardial locations R amplitude was signif > inferior leads lead I had an S wave ( rS or QS pattern) Q wave ampli was >in aVLvsaVR (ratio >1.4) • LV epicardial grp- 1)R wave in V1 with a > amplitude than in the RV endocardial group 2)signif S waves in V1 (>1.2 mV) and V2

  17. Outflow tract VT - good prognosis- benign course • Polymorphic VT- unusually short–coupled RVOT VPCs- respond well to successful VPC ablation • Management of outflow tract VTs medical therapy or catheter ablation. • adenosine, verapamil, b-blockers, and carotid sinus massage-acutely • b-blockers and CCBs-c/c supp therapy (efficacy 67% typical RVOT VT) • Pats- breakthrough tachy on b-blocker or CCB, class I or class III antiarrhythmic therapy

  18. Catheter ablation - high success rate (>80%) in treating these arrhythmias • Long-term cure rates after a successful initial ablation are high • overall recurrence rate is approximately 10%

  19. Idiopathic left ventricular tachycardia • MC-ILVT is verapamil-sensitive tachycardia • 1st -Zipes and colleagues in1979 • Belhassen – demon verapamil sensitivity of the tachycardia (Response of recurrent sustained ventricular tachycardia to verapami , Br Heart J ;1981) triad: (1) induction with atrial pacing (2) RBBB morphology+ left axis deviation (3)no structural heart disease

  20. 15- 40 years old. • Typical symptoms palpitations, fatigue, and presyncope. Syncope and SCD are rare but described Incessant- tachycardia-induced cardiomyopathy Most episodes occur at rest( making exercise testing unreliable in assessment)

  21. Anatomic basis for ILVT is unclear • earliest site of activation -inferoposterior LV septum • originates from a false tendon - extending from the posteroinferior LV to the basal septum • localized reentry as the predmech in verapamil-sensitive ILVT.

  22. Fascicular VT - Circuit

  23. Fascicular VT – Anatomy and Physiology • Relatively narrow WCT • 90% originate from left posterior fascicle • Anatomic substrate: LV “false tendon” or postero-inferior fibromuscular band to basal septum • Diagnostically – may require isoprenaline to facilitate induction Purkinje Tissue running in false tendon

  24. baseline 12-lead ECG is normal in most patients. • ILVT-RBBB, left sup axis + rel narrow QRS duration(≤140 ms), RS int <80 ms -exit site near the area of the left posterior fascicle • ILVT-RB+ RAD –exit site near anterior fasicle

  25. Three Subtypes

  26. L post fascicle-RBBB+R SUP AXIS

  27. Fascicular VT – Rare mimics • Inter-fascicular VT • RBBB and right or leftward axis • Structurally abnormal heart: Previous anterior infracts and LAFB or LPFB • A subtype of BBR VT • Idiopathic mitral annular VT • RBBB and rightward axis • Variable verapamil-sensitivity • Ill-defined

  28. Long term prognosis good • A/c-iv verapamil, c/c-oral verapamil • RFA- severe symptoms, resistant or intolerant to med tpy • Long-term success after catheter ablation is >than 90%

  29. Automatic ventricular tachycardia • adrenergic or propranolol sensitive VT • automaticity from within the Purkinje fibers mediated by I f • result from adrenergically mediated automaticity • <50 yrs, ppt by exercise • Mc sites-mitral annulus,pappilarymus, RV in flo • ECG - RBBB or LBBB morph and may present as monomorphic or polymorphic VT • sensitive to b-blockers • unresponsive to CCBs • cannot be initiated with programmed stimulation

  30. VT IN ABNORMAL HEART

  31. CAD • Incidence of sustained, monomorphic VT after infarction -3%. • Modern therapy- > smaller infarcts and less aneurysm formation ---↓ incidence of VT to <1 % • electrophysiologic substrate - develops in the first 2 weeks • once established- remain indefinitely • Once sustained VT occurs, the risk for arrhythmia continues indefinitely • inducible VT signifies the presence of an anatomic VT substrate

  32. PATHOPHYSIOLOGY • In post MI -re-entry • Areas of slow conduction -substrate for re-entry • conduction is slow and discontinuous -abnormalities in gap junction distribution and function • anatomic characteristics - islands of relatively viable muscle alternating with areas of necrosis and later fibrosis • result in fragmentation of the propagating electromotive forces

  33. MI Scar-Related Sustained Monomorphic VT Circuit

  34. Sustained Ventricular Tachycardia:Role of the 12-lead Electrocardiogramin Localizing Site of OriginMARK E. JOSEPHSON, M.D., LEONARD N. HOROWITZ, CIRCULATION 1981 • QRS morphology of 41 morphologically distinct VT was correlated with their site of origin as determined by catheter and intraoperative mapping. • 12-lead ECG could not precisely identify the site of origin in patients with CAD • Could differentiate anterior from posterobasal regions, particularly in VT -LBBB. • ECG was less useful in localizing VT-RBBB because of overlapping patterns • General QRS patterns were useful in differentiating anterior from posterior regions of origin

  35. RBBB & LBBB VT- ANTERIOR

  36. RBBB & LBBB VT -POSTERIOR

  37. q wave in lead 1 and/or V6 - RBBB –anteriorly

  38. RBBB-FROM ANTEROLATERAL LEFT VENTRCLE

  39. R in leads L1 and V1 through V6, in RBBB specific for a posterior origin

  40. Electrocardiograrm During Ventricular Tachycardia with Left Bundle Branch Morphology

  41. LBBB pattern+Q waves in leads I and V6 -anteriorsuperior and leftward axis -inferior aspect of septum.

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