Ventricular tachycardia

1. Ventricular Tachycardia
Part-II

2. The site of origin of arrythmia
SVT
• SA NODE
• ATRIA
• AV NODE
• HIS BUNDEL
VENTRICULAR ARRYTHMIA
• PURKINJE FIBRE
• VENTRICUALR MYOCARDIUM

3. In SVT, the QRS is narrow

4. VENTRICULAR ARRYTHMIA
• Ventricular myocardium
• His-Purkinje system
• QRS IS WIDE >120 milli seconds

5. VENTRICULAR ARRYTHMIA
• MECHANISM
• Abnormal impulse formation: Automaticity and triggered activity in the ventricular
myocardium or Purkinje system
• Reentry in the ventricular myocardium or Purkinje system
• Depolarization wavefront that propagates through the ventricles independent of
activation from the atrium and AV node
• Abnormal QRS complex exceeding 120 msec
• T wave is typically broad and in the opposite direction of the major QRS
deflection
• It is typically not preceded by a P-wave
• Premature atrial or junctional beats that conduct with bundle branch block
can mimic PVCs

6. CLASSIFICATION VENTRICULAR ARRYTHMIA
• Premature ventricular complexes(PVCs)
• Vventricular Bigeminy
• Couplet
• Triplet
• Nonsustained ventricular tachycardias
• Sustained ventricular tachycardias (VT)
• MONOMOPHIC
• POLYMORHIC
• TORSDE DE POINTES
• IDIOVENTRICUALR RHYTHM
• Ventricular fibrillation (VF)
• VENTRICLAUR FLUTTER
• ELECTRICAL STORM

7. CAUSES OF SOME MONOMOPHIC VT
Monomorphic VT Cardiac Structure Sinus ECG FH/Genetics VT Features Usual Initial
Management
Coronary disease Old infarction Abnormal CAD+ Multiple morphologies ICD
NICM Fibrosis, often in the basal LV Usually abnormal 40%—LMNA, TTN, PLM,
desmosomal
Multiple morphologies ICD
Post-viral Fibrosis after healing Lateral subepicardial LV origin
most common
ICD
ARVC RV fibrosis starts epicardial, LV
involvement in some
Abnormal, PVCs >60% desmosomal
mutations
LBBB, multiple morphologies ICD
Sarcoidosis LV, RV fibrosis. + FDG PET if
active inflammation
AV conduction impairment
common, PVCs
RBBB or LBBB, endocardial
and epicardial
ICD
Repaired TOF, VSD Ventricular fibrosis, patch
material
RBBB common LBBB Dependent on
biventricular function
Idiopathic outflow VT Normal Normal, PVCs Single monomorphic VT, PVCs
often present
Beta-blocker
Idiopathic LV fascicular
reentrant VT
Normal Normal Single RBBB monomorphic VT Beta-blocker, verapamil

8. CAUSES OF POLYMORPHIC VT
Polymorphic VT/VF
Coronary disease Acute ischemia Abnormal CAD+ Variable initiation Reperfusion,
CAD management
LV failure/hypertrophy from any
cause
LVH, fibrosis, dilation Abnormal ICD
Acquired LQTS Normal or any disease QTc usually >0.48 sec, but can
be short
Occasional Pause dependent PMVT/torsade
de pointes
Mg, removal of inciting
factors
Idiopathic VF Normal Normal or early
repolarization
Occasional PMVT ICD, quinidine, ablation
Congenital LQTS Normal QT prolongation, but variable Mutations in ion channel
genes
PMVT/torsade de pointes Beta-blocker
Catecholaminergic polymorphic VT Normal Normal, PVCs on exertion Mutation in RyR2,
Calsequestrin
Exertion, stress induced
polymorphic PVCs, VT
Beta-blocker, flecainide
Brugada syndrome Normal Normal or ST elevation V1—2 20%–30% SCN5A, others Nocturnal cardiac arrest ICD
Early repolarization Normal, small
epicardial scars?
J-point elevation Occasional PMVT/VF ICD quinidine
Short QT syndrome Normal QTc <0.34 – 0.36s Yes AF, PMVT ICD, quinidine

9. Premature Ventricular Complexes
• A- Late PVC results in a
compensatory pause
• B- Earlier PVC result in
retrograde atrial excitation (P′)
• C- PVC with a non-
compensatory pause
• D- Interpolated multifocal PVCs
• E - Hemodynamic effect of PVCs

11. Ventricular bigeminy
• One SINUS and one PVC go
together

12. Couplets
• Two consecutive PVCs are referred to as a PVC couplet
• Three consecutive beats is a triplet
• VT is also characterized by its QRS morphology
• Monomorphic VT has the same QRS morphology from beat to beat consistent with a
single origin for each beat
• Polymorphic VT has a continually changing QRS morphology
• The initial beats of a run of monomorphic VT may have a variable QRS morphology

13. NSVT :MORE THAN THREE CONSECUTIVE PVC
BUT LESS THAN FOR 30 SECONDS

14. Accelerated
Idioventricular
Rhythm
• ACUTE MI : Blood flow is
restored to ischemic
myocardium by TLT or PTCA
• HR is less than 120/bpm
• Called mini VT

15. Sustained VT
• VT MORE THAN 30 SECONDS
• Ventricular tachycardia can be due to reentry, triggered activity, or
automaticity
• The management and prognosis depend on the specific type of VT
and underlying heart disease.

16. VPC –bigeminy-
couplet-PMVT-
VFIB
• A, Normal ECG with normal repolarization,
QT
• B, Ventricular bigeminy with short
coupled premature ventricular complexes
interrupting the T-wave of the preceding
sinus beat initiate polymorphic VT
degenerating to ventricular fibrillation
• C and D, During acute myocardial
ischemia ventricular couplets with close
coupling to the preceding sinus beat. D,
Closely coupled PVCs are present and
initiate polymorphic VT.

17. Monomorphic Ventricular Tachycardia
• Wide QRS tachycardia
• Same QRS configuration from beat to beat indicating a stable ventricular
depolarization sequence for each beat
• The QRS duration typically exceeds 120 msec
• Occasionally shorter for VTs originating in the septum or that utilize a
portion of the Purkinje system
• It is usually regular
• 20 msec variation in cycle length is not uncommon
• Occasionally marked cycle length variation is encountered in the presence
of antiarrhythmic medications, or at the onset and prior to spontaneous
termination
• Rates can range from slower than 100/min to faster than 270/min.

18. Sustained monomorphic VT

19. Left fascicular VT:RBBB pattern and narrow

20. Sustained monomorphic VT with P/H of IWMI
• A:LBBB pattern
• B:RBBB pattern

21. Polymorphic Ventricular Tachycardia
• Continually changing QRS morphology : changing ventricular activation sequence
• Torsade de pointes is a specific type of polymorphic VT that has a waxing and waning QRS
amplitude and is often associated with QT prolongation prior to initiation
• The tachycardia is unstable and either terminates spontaneously or degenerates to VF
• The distinction of where polymorphic VT ends and VF begins is often not clear
• Polymorphic VT presents with light-headedness, syncope, or cardiac arrest
• Polymorphic VT can be associated with
• myocardial ischemia
• left ventricular hypertrophy, or scar
• Genetic sudden death syndromes (long QT, short QT, early repolarization [ER], Brugada, catecholaminergic
polymorphic VT) as well as digoxin toxicity
• The mechanism may be reentry with continually changing reentry paths and has been associated with
marked dispersion of ventricular repolarization
• In CPVT and digoxin toxicity it is likely due to multiple competing foci of triggered activity
• Unlike sustained monomorphic VT it is less likely to be associated with areas of ventricular scar

22. Long QT to Torsade de pointes
• A, During hypokalemia there is
marked QT prolongation with
broad-based T waves
• B, PVCs with initiation of the
polymorphic VT torsade de
pointes
• C, After restoration of
potassium, QT interval has
shortened markedly

23. Torsade de pointes
• D-F Long QT syndrome type 2
• D, QT prolongation with
notched T-waves. E, PVCs and
couplets
• F, A pause initiates torsade de
pointes

24. Ventricular fibrillation
• VF is always fatal
• Irregular undulations of varying contour and amplitude without distinct QRS complexes
• Hemodynamic collapse
• Ischemia or metabolic
• Must be corrected within 3 to 5 minutes
• Basic life support and advanced cardiac life support
• Asynchronous DC cardioversion using 200 J to 400 J is mandatory therapy for VF, ventricular flutter, and
pulseless VT
• Cardiopulmonary resuscitation is performed until cardioversion can be performed and resumed immediately
after each shock
• If the first shock is ineffective subsequent shocks should be delivered at maximum defibrillator output
• A bolus of intravenous amiodarone of 300 mg can be administered if initial shocks are unsuccessful
• Cardiopulmonary resuscitation is continued
• Recurrent fibrillation is common after an initially successful shock
• Treat the underlying cause

25. Ventricular flutter
• A sinusoidal tachycardia
• QRS and ST-T not distinguish
• Faster than 280 beats/minute
• QRS wide
• Monomorphic VT
• Acute myocardial infarction
• Severe metabolic derangements
• Hemodynamic collapse and
degenerates to VF
• Immediate electrical cardioversion
or defibrillation is required

26. ELECTRICAL STROM
1. VT that occurs 3 or more times within 24 hours has been defined as an
“electrical storm”
2. Difficult to control VT and increased mortality
3. Ongoing electrical storm with VT that recurs frequently after cardioversion or
is incessant despite termination attempts is a life-threatening emergency
4. Precipitating factors, most commonly elevated sympathetic tone, should be
addressed
5. Very wide sinusoidal tachycardia should prompt immediate consideration
6. Treatment for hyperkalemia
7. Intravenous amiodarone
8. Measures to reduce sympathetic tone should be initiated
9. The nonselective beta-blocker propranolol was more effective than metoprolol
10. Sedation escalating to general anesthesia is often effective
11. Reducing cardiac sympathetic stimulation include percutaneous stellate
ganglion block
12. High thoracic epidural anesthesia
13. ICD
14. Emergent catheter ablation

27. INVESTIGATION
• INESSANT VT :cardiac lymphoma
by LV apical lymphoma by F-18
DG PET

28. WIDE QRS :VT or SVT

29. Treatment of VT

30. TREATMENT OF VENTRICULAR ARRYTHMIA

31. ICD for defibrillation for VT
• A: Initiation of sustained
polymorphic VT by a premature
ventricular complex is followed
by burst pacing from an
implanted defibrillation, which
fails to terminate the VT,
although the QRS becomes more
organized
• B: VT continues, and the ICD
delivers a shock that converts
the rhythm to sinus

32. CATHETER ABLATION