This document provides an overview of the management of ventricular tachyarrhythmias. It begins with definitions of ventricular tachycardia and classifications based on ECG findings. It then discusses the initial presentation and diagnosis of unstable versus stable VT. Treatment approaches are outlined for acute management of various VT types as well as long-term management for secondary prevention. Specific considerations and guidelines for treatment of VT in the settings of ischemic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, and other inherited arrhythmias are also summarized.

1. MANAGEMENT OF VENTRICULAR
TACHYARRYTHMIAS
Dr. Chetana Sen
Chairperson: Dr.B.P. Chatterjee

2. Definition
• Ventricular tachyarrythmia defined as a
tachycardia (HR>100 bpm) in which the
driving circuit or focus originates solely in
ventricular tissue or Purkinje fibers.

3. Classification of Ventricular
Arrhythmia by ECG (ACC)
• Ventricular Tachycardia: VT is a cardiac arrythmia of 3 or
more consecutive complexes emanating from the ventricles
at a rate > 100bpm (cycle length less than 600ms)
1. Sustained VT: VT greater than 30s in duration and or
requiring termination for hemodynamic compromise in
less than 30s.
– Monomorphic- stable single QRS morphology
– Polymorphic-changing or polymorphic QRS, cycle length
between 600 and 180ms
2. Nonsustained VT: VT terminating spontaneously within
30seconds.
– Monomorphic
– Polymorphic

4. Classification of Ventricular Arrhythmia by
ECG (ACC)
• Bundle-branch re-entrant tachycardia
• Bidirectional VT
• Torsades de pointes
• Ventricular flutter
• Ventricular fibrillation

5. Initial Presentation
• Stable or Unstable
• History of CAD or previous MI
• History of syncope
• Depressed LV function
• Baseline ECG
Hemodynamically unstable:
• chest pain
• shortness of breath
• decreased level of
consciousness
• Cardiogenic Shock
• pulmonary congestion,
• congestive heart failure
• AMI• Wide complex or Narrow
complex
• Regular or Irregular
• Relation of P wave with
QRS
• Diagnosis?

6. • 60 yr old, with ischemic heart disease and h/o
MI 4 yrs ago presented with chest
pain,drowsiness, BP 80/50,PR 150/min.
Hemodynamically
Unstable
Wide QRS >
120ms

7. ACLS protocol for Hemodynamic
unstable Tachycardia with pulse

10. • VT or SVT with aberrancy???

11. ACC
Algorithm

12. A 45 yr woman with palpitations
• Wide QRS complex
• Irregularly irregular
• LBBB pattern, no
secondary R wave in
V1, no q in V6
Atrial fibrillation with LBBB

13. Brugada Criteria for SVT with aberrancy vs VT

14. Features favoring VT:
Taller left ‘rabbit ear’ in VT
N-W axis
Concordance

15. Reversible causes of VT
• Hypoxia
• Hyperthyroidism
• Catecholamines
• Hypokalemia
• Metabolic acidosis
• Hypomagenesemia
• Hypocalcemia
• Drugs
• Alcohol
• Starvation

16. Principles of Management
1. Acute Management
2. Long term management for secondary
prophylaxis of VT and prevention of Sudden
Cardiac Death
3. Management of specific VT
1. With structural heart disease/coronary artery
disease
2. Idiopathic VT
3. Inherited VT

17. Acute Management of Specific Arrhythmias
Sustained Monomorphic VT
• Wide-QRS tachycardia should be presumed to be VT if
diagnosis is unclear. (Class I)
• DC cardioversion in hemodynamic compromise.(Class I)
• Iv procainamide for initial treatment of patients with
stable sustained monomorphic VT.(IIa)
• Iv amiodarone if refractory. (IIa)
• Iv lidocaine-initial management in MI.(IIb)
• No response or frequently recurrent despite anti
arrythmics- transvenous catheter pacing. (IIa)
• Calcium channel blockers should not be used in
patients to terminate wide-QRS-complex tachycardia of
unknown origin, especially in patients with a history of
myocardial dysfunction(III)

18. Acute Management of Specific Arrhythmias
Polymorphic VT
• Hemodynamic compromise-DC cardioversion (I)
• IV beta blockers are useful for patients with recurrent
polymorphic VT, especially if ischemia is suspected or
cannot be excluded. (I)
• IV loading with amiodarone in recurrent polymorphic
VT in the absence of abnormal repolarization related to
congenital or acquired LQTS. (I)
• Urgent angiography with a view to revascularization
when myocardial ischemia cannot be excluded.(I)
• IV lidocaine in polymorphic VT specifically associated
with acute myocardial ischemia or infarction. (IIb)

19. Principles of management:
Long term management-Non sustained VT
• Goal of long-term therapy-prevent sudden cardiac
death and recurrence of symptomatic VT,
• Asymptomatic nonsustained ventricular
arrhythmias in low-risk populations -often need
not be treated.
• Symptomatic non-sustained tachycardia-
– beta blockers
– Class IC agents, sotalol, or amiodarone can be effective.
– class IC agents should be avoided in patients with
structural heart disease,especially CAD-Proarrythmic.

20. Principles of management:
Long term management-Sustained VT
• Sustained VT or cardiac arrest in patients with structural
heart disease
– Class III better than class I.
– empiric amiodarone-better survival than EP-guided
antiarrhythmic drugs, and
– ICDs provide better survival than amiodarone.
• In patients who have survived cardiac arrest or who have
sustained VT resulting in hemodynamic compromise and poor
LV function (EF<0.35):
– ICD is the treatment of choice.
– In patients who refuse an ICD, empiric amiodarone.

21. • Anti-Tachycardia
Pacing/Overdrive pacing
• Rate Discrimination
• Rhythm Discrimination
• Morphology Discrimination

22. Specific VT-VT in Ischemic
cardiomyopathy
• Healed MI is the most frequent clinical setting
for the development of sustained VT
• In the setting of a remote myocardial
infarction:
– the mechanism of VT is reentry
– Involves infarct scar and border zone
– VT in this setting typically monomorphic.
• Polymorphic VT or VF in the setting of ischemic
heart disease usually occurs during active
ischemia or infarction.

23. 55 yr male, h/o MI 5 yrs ago, with chest pain and
palpitations..
• Q waves (qR, QR or Qr) in
related leads
• Notched or wide QRS
complexes
• Low QRS voltage
• A-V dissociation
• Paroxysmal sustained episodes
Sustained monomorphic VT in old MI

24. • Lateral wall- RBBB
• Septal wall- LBBB
• QRS in Inferior leads:
• Inferior wall- superior axis Epicardial site of exit
• Anterior wall- superior or inferior axis
• QRS in precordial leads:
• Basal- Positive concordance
• Apical-Negative concordance

25. VT in Ischemic cardiomyopathy
Treatment:
ICD therapy is indicated in
1. patients resuscitated from VF when coronary revascularization is
not possible, and there is evidence of prior MI and significant LV
dysfunction (class I)
2. patients with LV dysfunction due to MI who present with
hemodynamically unstable VT (class I).
3. Primary prevention in patients with LV dysfunction due to prior
MI who are at least 40 days post-MI and have an LVEF ≤30%-40%
and NYHA class II or III (class I, level of evidence A).
4. Primary prevention in patients with LV dysfunction due to prior
MI who are at least 40 days post-MI, and have an LVEF ≤30%-35%
and NYHA class I (class Iia) patients with post-MI with normal LV
function and recurrent VT (class IIa).

26. • Drugs:
1. Amiodarone or sotalol, in combination with beta-blockers if
possible, as an adjunctive therapy to reduce symptoms in patients
with prior MI, LV dysfunction, and VT unresponsive to beta-
blockers alone/ frequent ICD shocks/ non candidates for ICD
2. Prophylactic antiarrhythmic drug therapy is not indicated to reduce
mortality, but only to reduce symptoms in patients fulfilling the
characteristics above mentioned. (III)
3. Class IC antiarrhythmic drugs in patients with a past history of MI
should not be used. (III)
• Ablation reserved for refractory VT or very well tolerated VT.
• Surgical endocardial resection of the scarred area in refractory VT
caused by previous infarction.
• For recurrent VT or VT storm refractory to medications or ablation,
cardiac sympathetic denervation has been effective in limited
studies.

27. VT in Dilated Cardiomyopathy
(non-ischemic)
• ventricular arrhythmias and sudden death
• Incidence of VT –50-60% DCM, resp for 8-50%
deaths
• Macro reentry -dominant mechanism
• Bundle branch reentry ventricular tachycardia
(BBRVT) is the most characteristic
• BBRVT Responsible for VT in up to 41% of
DCM

28. VT in Dilated Cardiomyopathy
(non-ischemic)
• EP testing-
– to diagnose bundle-branch reentrant tachycardia and to guide ablation.
– diagnostic evaluation in sustained palpitations, wide-QRS-complex
tachycardia, presyncope, or syncope (I)
• ICD –(receiving chronic optimal medical therapy, and who have
reasonable expectation of survival with a good functional status for
more than 1 year.)
1. significant LV dysfunction who have sustained VT or VF (I)
2. for primary prevention to reduce total mortality by a reduction in SCD
who have an LVEF less than or equal to 30% to 35%, are NYHA
functional class II or III. (I); or even in NYHA class I (IIb)
3. unexplained syncope, significant LV dysfunction
4. termination of sustained VT in patients with normal or near normal
ventricular function
• Amiodarone for sustained VT/VF (IIb)

29. Bundle Branch Reentrant VT
• Commonly in disease with severe LV dysfunction
like DCM & conduction abnormalities in the HPS
• BBR VT may also be seen in:
– Myotonic dystrophy
– Hypertrophic cardiomyopathy
– Ebstein anomaly
– Following valvular surgery
– Proarrhythmia due to Na channel blockers
• Presyncope, syncope or sudden death - VT with
fast rates > 200 bpm

30. ECG in sinus rhythm
- non-specific or
typical BBB patterns
with prolonged QRS
duration
• EPS:His electrograms
precede each V
• HV interval during
tachycardia > HV in
baseline
• Changes in V–V interval
follow the changes in H–H

31. Bundle Branch Reentrant VT
• High recurrence rate after drugs
• RFA - first line therapy; ablation of the RB
• A PPI should be implanted if the post-ablation
HV interval is 100 ms or longer
• ICD implant should be considered if
myocardial VT occur spontaneously or are
inducible or if EF < 35%

32. VT in Hypertrophic Cardiomyopathy
• SCD in adults with asymptomatic HCM- 1%,
NSVT – 8%
• On 24-hr Holter -90% have ventricular
arrhythmias
• Long term prophylactic pharmacologic therapy
now not recommended in high-risk population
• Risk Factors for SCD??
1. Family history of premature HCM-related death
2. Unexplained syncope, particularly in young patients, or if
demonstrated to be arrhythmia-based
3. Frequent, multiple, or prolonged episodes of NSVT
4. Hypotensive or attenuated BP response to exercise
5. Extreme LVH with maximum wall thickness ≥ 30 mm

33. VT in Hypertrophic Cardiomyopathy
• ICD (receiving chronic OMT with reasonable expectation
of survival with a good functional status for more than 1
year)
– sustained VT and/or VF.(I)
– primary prophylaxis against SCD.(IIa)
• Amiodarone therapy can be effective for treatment in
patients with HCM with a history of sustained VT and/or
VF, or for prophylaxis of SCD when an ICD is not
feasible.(IIa,IIB)
• EP testing may be considered for risk assessment for SCD
in patients with HCM.(IIb)

34. Arrythmogenic Right Ventricular
Dysplasia
• Ventricular arrhythmias are usually exercise-
related
• Sensitive to catecholamines
• Most Common- LBBB morphology VT
• RBBB VT - LV involvement or a left septal
breakthrough site

35. Arrythmogenic Right Ventricular
Cardiomyopathies
1. Prolonged QRS duration ≥ 110 ms
in V1-V3 (Sens-55%, Spec-100%)
2. T wave inversion in right
precordial leads (Seen in 60%)
3. Epsilon wave (Seen in 30%)
4. Low-voltage QRS amplitude
(Indicate severe cases)

36. Arrythmogenic Right Ventricular
Cardiomyopathies
• Documented VT/VF on chronic OMT, have
reasonable expectation of survival- ICD to
prevent SCD
• Severe disease LV inv, FH of SCD, undiagnosed
syncope, on chronic OMT-ICD
• Amiodarone or sotalol effective , when ICD
not feasible
• Ablation can be adjunctive
• EP testing might be useful for risk assessment

37. Bidirectional VT
• Bidirectional ventricular tachycardia (BVT) is a
rare ventricular dysrhythmia characterised by a
beat-to-beat alternation of the frontal QRS axis.
Causes
• most commonly associated with severe digoxin
toxicity.
• familial catecholaminergic polymorphic
ventricular tachycardia (CPVT).
• herbal aconite poisoning.

38. Bidirectional VT
• QRS axis shifts 180 degrees
from left to right with each
alternate beat.
• Another possible pattern is
alternating left and right
bundle-branch block

39. Idiopathic VT-RVOT/LVOT
• Only 10% of cases of VT occur in the absence
of structural heart disease, termed idiopathic
VT.
• The majority of idiopathic VTs (75-90%) arise
from the right ventricle — e.g right ventricular
outflow tract tachycardia(RVOT).

40. • Positive deflection in inferior
leads-Outflow tract ectopic
• First R wave in V3
• RVOT
• Positive deflection
in Inferior leads-
OT ectopic
• First R wave in
V1/V2
• LVOT

41. Fascicular VT
• Most common idiopathic VT of the left ventricle.
• It is a re-entrant tachycardia, typically seen in young patients
without structural heart disease.
• Diagnosis can be difficult and this rhythm is often
misdiagnosed as SVT with RBBB
• Verapamil is the first line treatment.
Causes
• Young healthy patients (15-40 years of age; 60-80% male).
• Most episodes occur at rest but may be triggered by exercise,
stress and beta agonists.
• A similar ECG pattern of fascicular VT may occur with
digoxin toxicity, but here the mechanism is enhanced
automaticity in the region of the fascicles.
• Digoxin-induced fascicular VT is responsive to Digoxin
Immune Fab.

42. • Monomorphic VT-fusion /capture beats,
AV dissociation.
• QRS duration 100 – 140 ms — this is
narrower than other forms of VT.
• Short RS interval of 60-80 ms — the RS
interval is usually > 100 ms in other
types of VT.
• RBBB Pattern.
• Posterior Fascicular-RBBB+LAD (90-
95%)
• Anterior Fascicular-RBBB+RAD
• Upper septal fascicular-atypical

43. 20yr female, went swimming, following which she had a syncope. Her ECG.
• Markedly prolonged QT
(QTc~700 ms)
• Wide and ample T waves in
V2-V4, deep T wave inversion
in the inferior leads
• T wave alternans
T wave alternans may be seen in a subgroup of patients with prolonged QT
and implies a very heterogeneous repolarization and a more imminent risk
of TdP. More typically seen in congenital long QT syndrome

44. Long QT syndrome
QT interval : total duration of ventricular
activity.
• Need for QTc Interval :The QT interval varies with RR interval. False
high values may be noted in Bradycardias.
• BAZETT’s Formula : QTc = QT ∕√ (RR) (RR in seconds)
• A useful rule of thumb is that, with a normal heart rate ( 60 - 100
bpm), the QT interval SHOULD NOT exceed half the RR interval.
• D/D for long QT:
• Electrolytes ( low K, low Mg, low Ca) (+other: hypothyroidism)
• Drugs (antiarrhythmics class I, III; macrolide or quinolone antibiotics;
antipsychotics…)
• Ischemia
• Congenital long QT syndrome (LQT 1,2,3)

45. Congenital Long QT syndrome
LQT1 Gene
• Most common type; 80% have first presentation < 20 yrs
• T wave is broad and occupies majority QT interval
• Most common triggers: exercise, emotional stress; Respond to beta-blockers
• Jervell Lange syndrome and Romano Ward syndrome are severe forms.
LQT2 Gene
• T wave tends to be bifid and notched
• Additional Trigger factors are sleep, auditory stimulation
• Respond to B-Blockers
LQT3 Gene
• Poorest prognosis amongst all
• T wave is asymmetrical or Late biphasic
• Trigger factor : Bradycardia ( sleep )
• B-Blockers Contraindicated; Exercise is not Restricted
Implantation of an ICD
along with use of beta
blockers is
recommended for LQTS
patients with previous
cardiac arrest or syncope or
VT.

46. Pt goes into this rhythm
Torsades de pointe (polymorphic VT with changing QRS polarity,
with a long baseline QTc)
VF (disorganized and chaotic rhythm, QRS almost vanishes
every now and then) Defibrillation
sinus

47. Torsades de Pointes
• 3 therapies:
1-Defibrillation
2-Magnesium 2 g IV (regardless of Mg level) + start
correcting K
3-Temporary pacing after the run of TdP has resolved.
Temporary pacing prevents TdP from recurring:
Usually, TdP occurs in a pt with prolonged QT who is also bradycardic.
Bradycardia further prolongs QT and furthers disperses repolarization
delays across the myocardium. Bradycardia is a major trigger of TdP,
particularly TdP in patients with acquired long QT. Pacing to a rate of 80-
100 bpm will prevent TdP recurrence.
Pacing does not apply to our pt here because he is tachycardic.
Congenital long QT, as opposed to acquired long QT, is often triggered by
catecholamine surge and may be associated with tachycardia
No Amiodarone. Amiodarone prolongs QT

48. 27 yr male, with syncope, family h/o SCD.
RBBB pattern ST elevation in
leads
V1 through V3.
Type 2 Brugada pattern with
a “saddleback” ST-segment
elevation greater than 1 mm
and a biphasic T wave in V1
(positive in V2-V3).
After
a procainamide challenge, the
prototypic changes on the ECG
are exaggerated, with an
increase in ST elevation, ECG
shows a type 1 pattern with a
downward-sloping
coved ST elevation and negative
T waves in V1-V3.

49. Brugada Syndrome
• RBBB and ST-segment elevation in the anterior precordial
leads, without any evidence of structural heart disease
• Type 1, type 2, or type 3 patterns on ECG
• Brugada syndrome should be suspected in :
– type 1 ECG pattern in >1 right precordial lead (V1 to V3) if there
is documented VF, polymorphic VT, family history of SCD,
Brugada-pattern ECG in other family members, or syncope.
– Type 2 and type 3 findings on the ECG are not diagnostic of
Brugada syndrome.
– If type 2 or type 3 ECG patterns (in more than one right
precordial lead) convert to a type 1 pattern after Procainamide
challenge + at least one clinical criterion (listed above) is also
present=consider the diagnosis of Brugada syndrome
• Mutations in genes for the sodium channel (SCN5A) and
calcium channel have been identified in many families

50. Brugada Syndrome
• ICD for prevention of SCD
• Isoproterenol for VT storm; also Quinidine.
• EP study for risk stratification in asymptomatic
Brugada Syndr.

51. Premature Ventricular Contraction

52. Accelerated Idioventricular Rhythm
• AIVR results when the rate of an ectopic
ventricular pacemaker exceeds that of the
sinus node.
• AIVR is classically seen in the reperfusion
phase of an acute STEMI, e.g. post
thrombolysis.
• Usually a well-tolerated, benign, self-limiting
arrhythmia.

53. AIVR
• Regular rhythm.
• Rate 50-110 bpm.
• >= 3 ventricular complexes.
• QRS complexes >120ms.
• Fusion and capture beats.
• Isorhythmic AV dissociation

54. Ventricular Flutter/Fibrillation
V. flutter
V. Fibrillation

55. Thank You