V tach

1. WELCOME
TO TODAY’S WEEKLY
PRESENTATION.
 TOPICS: Ventricular Tachycardia(VT or V-tach)
Dr.Muzahidul Islam.
MBBS
RMO(Cardiology)
AFC Health Fortis Heart Institute, Khulna

2. What is Ventricular
Tachycardia?
Ventricular Tachycardia is diagnosed by ECG.
If it fulfill the following criteria we can call it
Ventricular Tachycardia –
1. Three or more consecutive ventricular beat
2. Tachycardia: >120 bpm
3. Wide QRS complex: >140 msec

3. 1. Sustained(>30sec) Or Non
Sustained(<30sec)
2. Pulse Or Pulse less VT
3. Stable Or Unstable VT
4. Monomorphic, Polymorphic VT

5. Polymorphic VT
Here QRS morphology changing

6. AVIR:Accelerated idioventricular
rhythm
 Wide complex Ventricular rhythm usually
at a rate of 40-120 beat/min
 Usually Haemodynamically stable
 Cause: reperfusion arrhythmia in 1st
12hours after acute MI
 Typically preceding by a sinus slowing.
 Self limiting, so usually doesn’t require
any treatment.

7.  Cardiac: MI, Cardiomyopathy, Myocarditis, Brugada syndrome,
Arrhythmogenic right ventricular dysplasia (ARVD)
 Biochemical abnormalities: Hypo/Hyperkalaemia, Hypomagnesaemia,
Hypocalcaemia
 Drugs:Ionotrops, Digitalis, Cocaine, Methamphetamine, Theophylline
 Acidosis
 Alcohol
 Starvation
 Systemic disease affecting Myocardium: Sarcoidosis, Amyloidosis,
SLE, RA

8. How a VT may
presents to you?
 Lightheadedness
 Dizziness
 Sweating
 Racing of heart
 Chest pain
 Chest discomfort
 Shortness of breath
 Syncope
 Cardiac arrest, in extreme cases

9. Investigation:
 ECG
 S.Electrolytes
 S.Magnesium
 ABG

10. DIFFERENTIAL DIAGNOSIS:
OF WIDE COMPLEX TACHYCARDIA
1. Ventricular Fibrillation
2. SVT with aberrant conduction
3. WPW syndrome
4. ECG lead motion abnormality
5. Pacemaker Rhythm
6. Accelerated Idioventricular rhythm
7. Premature Ventricular contraction

11. POINTS FAVORING TO V-TACH:
1) AV dissociation.
2) Capture beat.
3) Fusion beat.
4) Prior MI.
5) QRS>160msec.
6) Extreme left axis deviation.

12. AV dissociation: it is a hallmark of VT. AV
dissociation occurs because the sinus node is depolarizing the
atria at a rate that is slower than the pathologic, faster
ventricular rate. At times, P waves can be seen in between or
embedded in the QRS complexes, but the P waves and QRS
complexes have their own independent rates.

13. Capture beat: it is a hallmark of
VT

14. Fusion beat: it is a hallmark of
VT

16. Ultra Simple Brugada Criteria-2010

17. 1. Acute management.
2. Long term management

18. Acute Management:
it depends whether patient is stable or Unstable compromised.
Symptoms of Unstable VT includes-
 Pulse less
 HR:≥150/min
 BP-systolic:≤90 mmHg
 Chest pain.
 Heart failure.
Rx. Immediate DC cardioversion (200j→300j→360j) then I/V
amiodarone 300mg over 20-60min, or I/V lidocaine 50mg over
2min then may repeat every 5min interval upto 200mg followed by
I/V infusion 2mg/hr…
In case of Pulseless VT, after each DC cardioversion Immediate
CPR should be given(30:2) at a rate of 100-120/min for 5 cycle
before rechecking Pulse, Also Adrenaline 1mg IV given every 3-
5min interval.

19. Management of Stable VT
Monomorphic VT:
1. If LV function good, then intravenous Amiodarone,
Procainamide or Sotalol
2. If LV function is impaired, Amiodarone (or lidocaine) is
preferred to Procainamide for pharmacologic conversion
because of the latter drug’s potential for exacerbating heart
failure
3. If above measure fails then DC cardioversion.

20. Polymorphic VT
Polymorphic VT in stable patient typically terminates on its
own. However it tends to recur. After returning to sinus
rhythm ECG should be analyzed.
1. If QT is normal then treat as Monomorphic VT.
2. If QT is prolonged then Intravenous Magnesium salphate is given in
bolus dose of 8mg. Intravenous Lidocaine may be used to shorten QT
interval but Amiodarone or Procainamide is contraindicated because it
will prolong QT.

21. Long term management:
 VT with structurally normal heart, these patient almost always managed by
medication or ablation.
 Amiodarone in combination with beta blockers, can be useful for patients
with left ventricular dysfunction due to previous myocardial infarction (MI)
 Patient with Heart Failure are treated with Beta-blocker(carvedilol,
bisoprolol, metoprolol), Aldosterone antagonist, ACEI/ARB

22. Risk of recurrence after successful
resuscitation is 30-40%.
1. Management of intercurrent disease
2. ICD
3. Long term therapy on Amiodarone and Beta
blocker

23. ANTI-ARRHYTHMIC SURGERY
 Surgical resection of arrhythmogenic foci
 Cardiac sympathectomy
 Aneurysm resection

24. Select 2017 AHA/ACC/HRS recommendations
• Patients with heart failure and reduced LVEF (≤40%): Administer a beta blocker,
mineralocorticoid receptor antagonist, and either an angiotensin-converting
enzyme inhibitor (ACEI) or an angiotensin-receptor blocker (ARB), or an
angiotensin receptor-neprilysin inhibitor (ARNI) to reduce the risk of sudden
cardiac death and all-cause mortality.
• Patients with ischemic heart disease and sustained monomorphic VT: More than
coronary revascularization alone is needed to prevent recurrent VT.
• Patients with nonischemic cardiomyopathy, symptomatic heart failure (New
York Heart Association [NYHA] class II-III symptoms), and an LVEF of 35% or
below while on guideline-directed therapy: Place an ICD if the expected survival is
longer than 1 year.
• Patients with previous MI and recurrent symptomatic sustained VT, or present
with VT/VF storm, and are refractory to/intolerant of amiodarone: Perform
catheter ablation.
• Patients requiring arrhythmia suppression for symptoms or declining ventricular
function probably owing to frequent premature ventricular complexes for whom
antiarrhythmics are not effective, tolerated, or preferred: Catheter ablation
provides benefit.

25. Catecholaminergic polymorphic ventricular
tachycardia
 Catecholaminergic polymorphic VT (CPVT) is
characterized by polymorphic VT that can be
triggered by stress, exercise, or even strong
emotional states. It can be induced by
catecholamine administration. Patients may
present with syncope or with sudden cardiac
death if the dysrhythmia degrades into VF.
Physical examination or electrocardiography
(ECG) during rest will likely be normal.
 CPVT may be caused by mutations in the CASQ2
or RYR2 genes. [26] An additional locus has been
mapped to chromosome 7p22-p14. This disorder
shares clinical characteristics with the
bidirectional VT sometimes seen in digitalis
toxicity

26. Thank you