1 / 55

ECG DIAGNOSIS OF ISCHEMIC VT

ECG DIAGNOSIS OF ISCHEMIC VT . BY SAID FAWZY ASSISSTENT LECTURER OF CARDIOLOGY BENHA UNIVERSITY. Disclosures. None. Do you think that it is important to have a 12 lead ECG recording of VT before starting VT ablation procedure ?. YES NO IT DEPENDS.

abiba
Télécharger la présentation

ECG DIAGNOSIS OF ISCHEMIC VT

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. ECG DIAGNOSIS OF ISCHEMIC VT BY SAID FAWZY ASSISSTENT LECTURER OF CARDIOLOGY BENHA UNIVERSITY

  2. Disclosures None

  3. Do you think that it is important to have a 12 lead ECG recording of VT before starting VT ablation procedure ? • YES • NO • IT DEPENDS

  4. ECG is very specific tool for localizing VT foci or reentry circuit exit sites ? • AGREE • DO NOT AGREE • IT DEPENDS

  5. Clinical or inducible non clinical VT ?!

  6. Possible VT mechanisms in ischemic patients • Scar related reentrant VTs (most common). • Focal VTs (including those originating from the papillary muscles). • Fascicular VTs (inter-fascicular) • BBR VT

  7. What do we expect from the ECG ? • Localize or at least Regionalize the focus or the exit site. • The possible mechanism of the tachycardia. • Is it endocardial or Epicardial

  8. Limitations of the ECG as a mapping tool • The presence and the extent of infarction. • The degree of intra-myocardial fibrosis. • The shape of the heart and its position in the chest . • Influence of non-uniform anisotropy in affecting propagation from tachy site.

  9. Continue…Limitations • Effect of acute ischemia,drugs,and metabolic abnormalities on conduction. • Integrity of the His-Purkinje system. • Presence of increased myocardial mass

  10. What we are searching for ? • QRS initial forces • QRS amplitude • QRS width • QRS frontal plane axis • BBB pattern • Concordance • The presnece of QR complexes.

  11. QRS initial forces • Rapid initial forces>>> More likely arising from normal myocardium • Slurred initial forces (pseudodelta wave )>>> More likely from a scar or from epicardium

  12. QRS amplitude • Usually VTs arising from diseased myocardium have lower QRS amplitudes from those arising from normal myocardium

  13. QRS width • Free wall VTs > Septal VTs ( assuming conduction in all directions is equal ) • Epicardial VTs > Endocardial VTs

  14. QRS frontal plane axis • Superior axis >>> apical site (septal or lateral ) or inferior wall VTs • Inferior axis>>> basal , outflow tract,high septal or latral wall of LV.

  15. Concordance • Positive concordance>>> Basal sites • Negative concordance>>> Apical ( mainly apical septum and most commonly seen with anteroseptal infarctions )

  16. BBB pattern • RBBBR pattern>>> VT certainly from LV • LBBB pattern>>> VT from LV septum or the right side of the septum

  17. Presence of QS complexes • QS complexes in the inferior leads>>> Activation start at the inferior wall ! • QS complexes in precordial leads>>> Activation is going away from the anterior wall.

  18. Just to rememeber

  19. Basic roles in post MI VTs • Almost all VTs arise in the LV or IVS • ECG looses a lot of its ability to precisely localize VT origin or exit sites • Accuracy of the ECG in anterior MI (greater myocardial damage)patients is much less than in inferior MI.

  20. Continue…Basic roles • It is extremely rare for an inferior MI dependent VT to have an exit site at the higher septum close to the aortic valve • QS complexes in the lateral leads (V4-V6) reflect origin near the apex ( septal or lateral ) • Almost impossible to distinguish VTs coming from apical septum and apical free wall based on ECG alone

  21. Inferior infarction VT • Activation goes from back to front>> large R wave in the precordial leads starting from V2 • LBBB VT in inferior MI >> mainly basal septum (inferobasal septum with left axis and higher septal with normal axis).

  22. Anterior infarction VT • The situation becomes more complicated with less accuracy of the ECG (more myocardial damage). • LBBB VT or RBBB VT can occur • LBBB VT and LAD is associated usually with inferoapical septal region.It can present with negative concordance and always associated with Q wave in I and aVL

  23. R wave in V1 and Q in aVL indicates more posterior position on the septum • RBBB VT usually shows superior axis. V1 can show monophasic R or qR pattern with QS from V2-V4 or up to V6

  24. Endocadial or Epicardial VT ? Can the ECG alone answer this Q ?

  25. The answer is simply NO

  26. What is epicardial VT ? • VTs in which the origin or the critical sites of the reentrant circuit are located in the subepicardial tissue as suggested by entrainment maneuvers and/or termination withen 10 seconds of standard RF pulses. • Critical epicardial sites may be entained or interrupted from both the epicardial and endocardial surfaces making it difficult to demonstrate the presence of a truly epicardial circuit in a given case

  27. Limitations • Most of the adopted ECG criteria to predict Epicardial foci or exit sites have been described in patients with NICM and idiopathic VTs . • Even VTs with presumed epicardial exit sites can be still ablated from the endocardial approach (The entrance or the central isthmus). • No ECG features distinguished outflow tract epicardial exit sites. • Poor sensitivity and specificty.

  28. Suggested ECG criteria

  29. 1-Total QRS duration • QRS more than 198 ms has 86% specificity and 69% sensitivity for epicardial origin of VT.

  30. 2-Pseudo delta wave • Earliest ventricular actiavation to the fastest delection an any precordial lead • Pdw >34 ms has 80% sensitivity and specificty

  31. 3-Intrinscoid deflection time • ID from the earlist ventricular activation to the nadir of the first S wave in any precordial lead . • ID more than 97 ms has 80% specificity and 50% sensitivity for epicardial VT origin.

  32. 4-RS duration • RS from the earliest ventricular activation to the peak of R wave in lead V2 • RS >121 ms is 82% specific and 57% sensitive for epicardial VT

  33. 5-Maximum Deflection Index( MDI) • It is defined as the shortest time to maximum positive or negative deflection in any precordial lead divided by the QRS duration. • A cut-off value of 0.55 has high sensitivity (100%) and specificity (98%) for epicardial VT. • This was mainly adopted for epicardial VTs arising from sinuses of Valsalva.

  34. 6-Precordial pattern break (R wave regression progression) • This was mainly described by Marchilinski group in Pheladelphia and was in the context of idiopathic VTs (but may still work). • There is a brupt loss of R wave in V2 followed by a resumption in R waves from V3 to V6. • Unkown predictive value.

  35. 7-Regional Q waves

  36. Again….Remember • Even with the presence of all of the above mentioned criteria, the ECG is not predictive for epicardial access and mapping . • Endocardial mapping should be commenced at first for all cases • The role of the above mentioned criteria in post MI patients has no strong evidence.

  37. Post MI VTs from papillary muscles When to suspect ?

  38. ECG…nothing specific

  39. Gadolinium enhanced MRI

  40. BBR VT • More common in patients with NIDCM. • Its incidence is propably underestimated. • Should be considered in DD specially if there is ECG evidence of His Purkinje disease

  41. Typical and Atypical BBR VT.

More Related