Ventricular arrhythmias

Ventricular arrhythmias

1. VENTRICULAR
ARRHYTHMIAS
Moderator : Lt Col Brahamjit Singh
Presenter : Lt Phuntsho Choden

2. Arrhythmias that originate in the ventricular myocardium or His
Purkinje system include:
•Premature ventricular beats
•Ventricular tachycardia
•Ventricular fibrillation

3. •Emerge from focus of myocardium and purkinje fibres
•Conduction away from the ventricular focus through the ventricular
myocardium is slower than activation of the ventricles over the
Purkinje system.
•QRS wide, typically >0.12 s

4. Premature Ventricular Contraction
•Premature ventricular ectopic beats arising in the diastolic period of
preceding sinus beat
•Unifocal
•Multifocal
•Ventricular Couplets
•Caused by electrical irritability
•Ischemia
•Electrolyte imbalances
•Drug intoxication

6. Multiform premature ventricular complexes
(PVCs)
The normally conducted QRS complexes exhibit a left bundle branch block contour
(arrowhead) and are followed by PVCs with three different morphologies.

7. Ventricular couplets

8. • Three or more PVC's in a row (run of V-tach)
• They come close to or on top of a preceding T-wave (R on T)
• They are frequent (> 30% of complexes)
• They are increasing in frequency
• PVC's come from different foci ("multifocal" or "multiformed")
May preclude the occurrence of :
• Ventricular Tachycardia
• Ventricular Fibrillation
PVCs : CLINICAL SIGNIFICANCE
sinus beats Unconverted V-tach r V-fib V-tach
“R on T phenomenon”
time

9. Fusion beat -
note p-wave in
front of PVC
and the PVC is
narrower than
the other
PVC’s – this
indicates the
beat is a
product of both
the sinus node
and an ectopic
ventricular
focus
Capture beat -
note that the
complex is narrow
enough to suggest
normal ventricular
conduction. This
indicates that an
atrial impulse has
made it through and
conduction through
the ventricles is
relatively normal.
Fusion and capture beats during ventricular tachycardia.

10. VENTRICULAR
TACHYCARDIA

11. Ventricular Tachycardia (VT)
•Three or more consecutive ventricular ectopic beats at a rate > 100
beats/min
•Originates in the ventricles
•Nonsustained < 30secs
•Sustained > 30secs
•Most patients have significant heart disease
•Coronary artery disease
•A previous myocardial infarction
•Cardiomyopathy

12. V1
Ventricular Tachycardia
(VT)
• Rates range from 100-250 beats/min
• Non-sustained or sustained
• P waves often dissociated (as seen here)

13. SA
Node
Ventricular
Focus
ATRIA AND
VENTRICLES
ACT
INDEPENDENTLY
AV Dissociation

14. Mechanisms of VT
•Reentrant
•Reentry circuit (fast and slow pathway) is confined to the ventricles and/or
bundle branches
•Automatic
•Automatic focus occurs within the ventricles
•Triggered activity
•Early after depolarizations (phase 3)
•Delayed after depolarizations (phase 4)

15. Reentrant
•Reentrant ventricular arrhythmias
•Premature ventricular complexes
•Idiopathic left ventricular tachycardia
•Bundle branch reentry
•Ventricular tachycardia and fibrillation when associated with chronic heart
disease:
•Previous myocardial infarction
•Cardiomyopathy

16. Automatic
•Automatic ventricular arrhythmias
•Premature ventricular complexes
•Ischemic ventricular tachycardia
•Ventricular tachycardia and fibrillation when associated with acute medical
conditions:
•Acute myocardial infarction or ischemia
•Electrolyte and acid-base disturbances, hypoxemia
•Increased sympathetic tone
•Drugs

17. Automaticity
Abnormal Acceleration of Phase 4
Fogoros: Electrophysiologic Testing. 3
rd
ed. Blackwell Scientific 1999; 16.

18. Triggered
•Triggered activity ventricular arrhythmias
•Pause-dependent triggered activity
•Early afterdepolarization (phase 3)
•Hypokalemia, TdP
•Polymorphic ventricular tachycardia
•Catechol-dependent triggered activity
•Late afterdepolarizations (phase 4)
•Local catecholamines, hypercalcemia
•Digitalis intoxication
•Idiopathic right ventricular tachycardia

19. IDIOVENTRICULAR TACHYCARDIA
•Enhanced inherent idioventricular rhythm
•Manifests when the rate equals sinus rate
•Characterised by:
•Bizarre QRS complexes or Fusion beats
•Rapid idioventricular rate (70-80beats/min)
•AV dissociation and capture beats
•Absence of pacemaker protection – abolished by faster sinus rhythm

20. Ectopic
ventricular activation
Normal
ventricular activation
Fusion
beat
Accelerated Idioventricular Rhythm
(> Ventricular Escape Rate, but < 100
bpm)
Sinus
acceleration

22. •Hemodynamically well tolerated
•Beta blockers and CCBs for prevention
•Catheter ablation
•No risk of sudden cardiac deaths

23. ECG Clues Supporting the Diagnosis of
Ventricular Tachycardia
•AV dissociation (capture beats, fusion beats)
•Concordance of QRS complex in all precordial leads
•Frontal plane: LAD with QRS > 140 ms
•Precordial leads: RS pattern ; Onset of R to Nadir of S >100ms
•RBBB pattern with
- V6 : QS or dominant S
- V1 : R > R’
- V1 : Monophasic R or biphasic qR or R/S with initial deflection different from sinus
initiated QRS
•LBBB pattern with
- Right axis : Negative deflection in V1 > V6
- V6 : qR or QS
- V1 : R > 40 ms

24. Monomorphic VT

25. Polymorphic VT

27. TORSADES DE POINTES
•‘Twisting of the points’
•Etiology:
•Congenital long QT
•Drugs – Quinidine, Phenothiazines
•Hypokalemia/ hypomagnesemia
•Bradyarrhythmias -3
rd
degree blocks

28. ECG Recognition
•QRS morphology continuously changes
•Complexes alternates from positive to negative

29. Mechanism
•Events leading to TdP are:
•Hypokalemia
•Prolongation of the action potential duration
•Early afterdepolarizations
•Critically slow conduction that contributes to reentry

30. Brugada Syndrome
•RBBB + persistent ST elevation in Right precordial leads
•Sudden cardiac death
•3 patterns
•Type 1 - J point elevation with ST segment elevation ≥0.2mV followed by
Negative T wave
•Type 2 – saddle back configuration of ST elevation >0.2mV – downsloping ST
elevation – positive or biphasic T wave not touching baseline
•Type 3 – ST elevation <0.1mV with either of the morphologies

33. The Brugada Criteria

34. Morphology Criteria for VT
qRqRAbsent Q

35. ACUTE MANAGEMENT OF
SUSTAINED VT
Hemodynamic decompensation
NO YES
Termination by medical treatment
AMIODARONE
PROCAINAMIDE
SOTALOL
LIDOCAINE
No Response DC Cardioversion
AMIODARONE
15 mg/min over 10 min f/b
1 mg/min for 6 hours f/b
0.5 mg/min for 18 hours.

36. LONG TERM THERAPY
PREVENTION OF RECURRENCE/SUDDEN DEATH
•Asymptomatic
Nonsustained
Preserved LV function
•Symptomatic
Nonsustained
Preserved LV function
•Symptomatic
Nonsustained
LV dysfunction (EF < 0.35)
Need not be treated
Beta blockers
Class IC agents
Sotalol
Amiodarone
ICD

37. LONG TERM THERAPY
SECONDARY PREVENTION
Survivors of cardiac arrest/ Sustained VT with
hemodynamic compromise
PLUS
Poor LV function
ICD IS THE TREATMENT OF CHOICE
Empirical Amiodarone/ Beta blocker is the next best
therapy

38. Implantable Cardioverter Defibrillator

39. Intracardiac Cardioverter Defibrillator

40. THANK YOU!