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

 Cansee 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

 Studydone 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

 Ifaxis different during tachycardia when

compared to sinus rhythm

 If “Northwest Axis” s/o VT

 Insomeone 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
 Withinfarcts, 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”

 Ifintial 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 value
of SAECG
 Thenegative 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.
SAECG
Fourteen 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’sarising at base of heart will have vectors

pointing anteriorly
 R Waves dominate precordial leads

 VT’sarising 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?