ECG DIAGNOSIS OF ISCHEMIC VT

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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. - PowerPoint PPT Presentation

Transcript of ECG DIAGNOSIS OF ISCHEMIC VT

ECG DIAGNOSIS OF ISCHEMIC VT

BYSAID FAWZY

ASSISSTENT LECTURER OF CARDIOLOGYBENHA 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

ECG is very specific tool for localizing VT foci or reentry circuit

exit sites ?AGREE

DO NOT AGREE

IT DEPENDS

Clinical or inducible non clinical VT ?!

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

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

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.

Continue…Limitations

Effect of acute ischemia,drugs,and metabolic abnormalities on conduction.

Integrity of the His-Purkinje system.

Presence of increased myocardial mass

What we are searching for ? QRS initial forces

QRS amplitude

QRS width

QRS frontal plane axis

BBB pattern

Concordance

The presnece of QR complexes.

QRS initial forcesRapid initial forces>>> More likely arising

from normal myocardium

Slurred initial forces (pseudodelta wave )>>> More likely from a scar or from epicardium

QRS amplitude

Usually VTs arising from diseased myocardium have lower QRS amplitudes from those arising from normal myocardium

QRS widthFree wall VTs > Septal VTs

( assuming conduction in all directions is equal )

Epicardial VTs > Endocardial VTs

QRS frontal plane axisSuperior axis >>> apical site (septal

or lateral ) or inferior wall VTs

Inferior axis>>> basal , outflow tract,high septal or latral wall of LV.

ConcordancePositive concordance>>> Basal

sites

Negative concordance>>> Apical ( mainly apical septum and most commonly seen with anteroseptal infarctions )

BBB patternRBBBR pattern>>> VT certainly from

LV

LBBB pattern>>> VT from LV septum or the right side of the septum

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.

Just to rememeber

Basic roles in post MI VTsAlmost 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.

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

Inferior infarction VTActivation 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).

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

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

Endocadial or Epicardial VT ?

Can the ECG alone answer this Q ?

The answer is simply

NO

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

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.

Suggested ECG criteria

1-Total QRS duration

QRS more than 198 ms has 86% specificity and 69% sensitivity for epicardial origin of VT.

2-Pseudo delta wave Earliest

ventricular actiavation to the fastest delection an any precordial lead

Pdw >34 ms has 80% sensitivity and specificty

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.

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

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.

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.

7-Regional Q waves

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.

Post MI VTs from papillary muscles

When to suspect ?

ECG…nothing specific

Gadolinium enhanced MRI

BBR VTMore 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

Typical and Atypical BBR VT.

VT involving the left purkinje system

When to suspect ?

Conclusion Different VT mechanisms are involved in patients with IHD ECG, inspite of limitations, is a useful tool in localizing or at

least regionalizing the exit sites of VTs in post MI patients. ECG has poorer predictive value in patients with anterior

infarction than those with inferior MI Different ECG criteria can support epicarial focus or exit site

but this does not necessarily indicate the successful ablation site.

Finally,it is mapping and not the ECG that determine where you have to ablate

THANK YOU