Ventricular Tachycardia in the Ischemic Heart

Ray Cutro, M.D.

USF Pseudo EP Fellow

Ventricular Tachycardia

Electrocardiographically can be difficult to identify

Following a few basic principles can help guide you

Well established criteria to assist diagnosis

Dr. Vinod Patel’s VT Algorithm

VT Definition

Defined by Duration and Morphology

Morphology Monomorphic Polymorphic

Duration Non Sustained Sustained

Arbitrarily defined as lasting greater than 15s to 30s unless not tolerated hemodynamically

In the Ischemic Heart….

Sustained monomorphic VT most commonly seen

Non sustained monomorphic VT can be seen in all hearts…regardless of presence or absence of structural heart disease

Can see PMVT….but less frequently observed

Mechanism of Arrhythmias

Re-entry Most common in Ischemics

Need two “limbs” for re-entry

Scar serves as a nice substrate as conduction through infarct and peri-infarct myocardium slowed

Triggered EAD’s – Typically in patients with long QT

DAD’s – Digitalis associated VT (bidirectional) Calcium dependent

Enhanced Automaticity Can be important clinically in post MI patients

“Reperfusion arrhythmia” – AIVR

Seen in diseased or ischemic tissue in which myocardial fibers develop phase 4 depolarization

What is required for re-entry?

Substrate Usually Scar Area of slowed conduction

Surrounded by area of normal conduction

Microscopy of Scar

Myocardial Activation in Ischemic VT

Initial activation eminates from exit site of scar

ECG Recognition of VT

Several well established criteria

Helps to define etiology of WCT SVT with aberrancy VT

Brugada Criteria

Study done in 1993 to establish set criteria to delineate WCT’s

SVT

VT

Brugada Criteria…Cont’ Precordial Leads Criteria

V1, V2 and V6 94% specific

Ventricular Concordance Absence of an RS complex in precordial leads 99% specific

AV Dissociation Fusion Beats Capture beats

96% Specific

R-S interval > 100mS Specificity 96%

A-V Dissociation

Demonstrated on ECG by evidence of two distinct rhythms

Sinus rhythm or sinus tachy A Rate slower than V Rate On an EGM, more V’s than A’s

Fusion and capture beats virtually diagnostic

Example A-V Dissociation

Example A-V Dissociation

Fusion Beats

Ventricular Concordance

Look at precordial Leads

Concordance defined when all precordial leads are either up or down

Positive concordance R Waves

Negative concordance QS complexes

Example Concordance

QRS Width

Helpful if no pre-existing BBB

If during tachycardia: RBBB morpholgy

QRS > 140 mS suggests VT

LBBB morpholgy QRS > 160 mS suggests VT

R-S Interval

Axis

If axis different during tachycardia when compared to sinus rhythm

If “Northwest Axis” s/o VT

In someone with normal QRS in NSR, if develops LBBB morphology tachycardia with RAD

Always VT b/c activation in LBBB aberration always right to left

Precordial Leads

V1 and V2

RBBB Morphology RsR’, rsR’both suggest SVT with aberrancy R, Rr’, qR or RS favors VT R Wave > 40mS in duration favors VT

LBBB Morphology QRS duration key

Greater than 160mS If time to nadir of QRS > 70 mS, suggests VT

WCT with R in V1 (RB Morphology)

WCT with LBBB Morphology

Others…

If BBB or IVCD noted during NSR, look at QRS duration

If narrower when HR faster, suggestive of VT Exception left sided free wall AP

Epicardial VT

With infarcts, not always transmural….can go through endocardium to M layer, or extend from M layer to epicardium

Thus can have re-entry in “layers” of myocardium

Epicardial VT…cont’

Epicardial VT…

Look at Total QRS duration

Then look at time to peak height of QRS or intrinsicoid deflection

“Initial upstroke”

If intial upstroke > 55% of total QRS duration, highly suggestive of epicardial foci

Epicardial VT

Signal Averaged ECG (SAECG)

Filtered ECG that is able to detect low amplitude potentials filtered out of standard ECGs.

Myocardial scar creates zones of slow conduction that appear as low amplitude late potentials on SAECG. Areas of slow conduction are necessary components for reentry.

Late potentials from within scar sometimes are not detected in SAECG

Bundle branch block delays depolarization ipsilateral to the site of block. The delayed conduction may conceal late potentials on SAECG.

The base of the left ventricle is the last area to depolarize when bundle branch block is not present. Inferior scar is easier to detect on SAECG than anterior scar because the inferior scar border zone is activated later than the anterior wall. Therefore, the late potentials are not concealed by depolarization in other areas of the ventricle.

Criteria for abnormal SAECG

Root mean squared voltage of the terminal 40 msec is less than 20 microvolts.

This shows low voltage potentials late in ventricular depolarization and reflect depolarization in slowly conducting scar border zones

Total QRS duration greater than 114 msec

Duration of the low amplitude signal that is less than 40 microvolts and is greater than 38 msec

Predictive valueof SAECG

The negative predictive value of SAECG is 97%. The positive predictive value is only 20%.

It is useful in that a negative test result has been associated with improved cardiovscular outcomes in post MI patients.

Example SAECG

Prognostic Value of late potentials after acute myocardial infarction.

Several studies in post myocardial infarction patients have shown an increased likelihood of spontaneous VT or sudden cardiac death in patients who have an abnormal SAECG.

Abnormal SAECGs are found in 26 to 40% of postmyocardial infarction patients when the recording is made prior to hospital discharge.

SAECGFourteen to 29% of patients recovering from myocardial infarction with abnormal SAECGs will experience sustained VT during the first year.

This compared to 0.8 to 4.5% of those with a normal recording.

A majority of patients who have an abnormal SAECG do not develop a serious arrhythmia.

SAECG

The negative SAECG coupled with normal left ventricular function suggests less need for concern about arrhythmias and less need for ambulatory monitoring and drug therapy of of ventricular ectopy.

Patients with abnormal SAECGs are more prone to inducible, sustained monomorphic VT, ventricular fibrillation, or sudden death.

ECG Localization of VT

Wavefront towards positive electrode upright Towards lead is upright

Wavefront away is opposite Away from lead- deflection downward

Myocardial Activation in VT

Initial activation eminates from exit site of scar

ECG Localization

Initial forces of the QRS complexes

Slurred or broad initial forces Suggest tachycardia arising from scarred myocardium

Or potentially epicardial focus Use the following formula: Time to peak of QRS complex/Total duration of QRS If ratio greater than 0.55, suggests epicardial locale

If rapid normal upstroke, suggests arising from normal myocardial substrate

QRS Morpholgy

VT’s arising from RV should have a LBBB morphology

VT’s arising from LV should have a RBBB morphology

VT’s arising from septum can still have a LBBB morphology if VT exits from the septum to the RV

LBBB VT in patients with CAD are most often from the LV, with this mechanism explaining it

VT exits septum, activates RV first, LV last.

QRS Width

QRS generally wider in VT’s arising from free wall (particularly epicardial)

Free wall VT’s activate ventricles sequentially

VT’s from septum usually activate ventricles simultaneously

Caveat: Septal VT’s with large scar and markedly slowed conduction

QRS Axis

Axis is related to the superior/inferior and right/left direction the VT travels away from the site of origin or exit to activate the rest of the heart

QRS Axis….Cont’ VT’s arising from superior aspect of heart have an inferior axis

VT’s arising from inferior wall will have a superior axis

VT’s arising from inferobasal septal LV and inferior RV will have a left superior axis

VT’s arising from inferoapical LV will have a QS in limb leads Right superior axis

Anterior (apical) Versus Basal

VT’s arising at base of heart will have vectors pointing anteriorly

R Waves dominate precordial leads

VT’s arising near apex will have posteriorly directed forces

Negative complexes precordial leads

Precordial Leads…Cont’

Positive Concordance R Waves V1 – V6

Wavefront travelling back to front

Associated with VT’s from base of the heart Aortic-Mitral continuity Basal aspect LV septum

Negative Concordance QS complexes V1-V6

Wavefront - front to back

VT usually from apical septum Typically anterior infarction

RV Apical Pacing…..

EPS in Ischemic VT

Beyond the scope of our talk today Programmed Ventricular Stim Entrainment Pace Map Activation Sequence If VT inducible…..very helpful

Treatment of VT

Hemodynamic Stability Medical Interventional (catheter based) Surgical

Give it a shot!

Next few slides are a collection of WCT’s:

Decide first: VT or SVT with aberrancy

Then if VT: Identify site of origin

Patient 1

Patient 2…..

Patient 3

Patient 4

Patient 5

Patient 6

Patient 7

Salient Points

In general, the wider the QRS in VT, the slower the intraventricular conduction

Marked “splintering” of QRS suggests scar

VT in CAD is almost exclusively re-entrant

The narrower the QRS, the more likely the VT arises from septum and/or be associated with a normal heart

Further away from normal conduction system….more bizarre

The End!

Thank you for your attention. Questions?