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?