2. Overview
• Case scenario
• ECG based diagnosis
• Introduction
• Wide complex tachycardia and diagnostic algorithm
• VT vs SVT
• VT
– Classification
– Etiology
– Localization
• ECG examples
3. Case
• 40 Y old male, Taxi driver
• Non smoker, occasional tobacco
• K/C/O Bronchial asthma, No other co-morbidities
• C/O
– Retro-sternal burning sensation
– Palpitation
• Past history: Episodic palpitations from last 10 yrs
• Holter study: Sinus bradycardia with occasional VPCs (May’2011)
• Family history: NAD
On examination
• PR 256/ min
• BP 90/60 mm Hg
• SE:
– CVS: S1/S2 + , no murmur, no added sounds
– R/S: bilateral equal vesicular BS
6. • CBC: 15/12050/141000
• RFT: 17.63/1.24
• Na/K: 146/5.7
• Trop T : 0.032
• Echo: Normal chamber dimensions, Normal LV systolic function,
LVEF 55%, RA, RV normal, RVOT-PLAX- 16, PSAX- 21
• Cardiac MRI: Normal biventricular size and function, focal non
specific enhancement at inferior RV insertion point, no e/o
ischemic/fibrotic changes
Diagnosis
Hemodynamically unstable sustained monomorphic VT ? Idiopathic
7. Introduction
• Most common cause of WCT(80%)
• Relatively organized tachyarrhythmia with discrete QRS
• Major cause of
– Morbidity and mortality in pt with structural heart disease
– Sudden cardiac death (60% cases) on holter monitoring
• Diagnosis on presentation…….. still a challenge
• Reentry is most common mechanism
• Recurrence is common in less than year
• ICD implantation is absolute indication in presence of LVEF< 30%
All WCT is VT until proven otherwise
András Vereckei et al, current Cardiology Reviews, 2014, 1
10. Brugada algorithm for
D/D of WCTs
Brugada P et al,A new approach to the differential diagnosis of a regular tachycardia with a wide QRS
complex. Circulation 1991; 83: 1649-59.
11. Adam M. May. Journal of the American Heart Association. Wide Complex Tachycardia Differentiation: A
Reappraisal of the State‐of‐the‐Art, 2020 Volume: 9, Issue: 11
12. Classification of VT
• On basis of
– Clinical presentation
– ECG (Duration and morphological) presentation
– Disease entity
ACC/AHA/ESC 2006 guidelines
23. VT in patients with CAD
• Typically based on a reentrant mechanism
Principles for noninvasive localization of the VT circuit’s exit
1.Post-MI VTs almost always arise in the left ventricle or IVS.
•Knowledge of the location of the prior infarct facilitates the localization
process
•VTs associated with inferior MI arise from the inferobasal septum or free
wall
•VTs associated with anterior MI arise from the antero-apical or infero-
apical septum or free wall.
2. VTs arising from the IVS have narrower QRS durations compared to free
wall VTs.
3.LBBB VTs almost always localize to the septum, (or within 1 cm of the
septum) while RBBB VTs can arise anywhere in the left ventricle, posing a
greater challenge for localization.
4.The presence of positive or negative concordance in the precordial leads
strongly suggests a basal or apical exit site, respectively.
5.A superior axis in general points to an IVT exit location (thus many inferior
MI VTs have a superior axis) or apical locations (in anterior MI), while an
inferior axis generally implies an antero-basal location.
Masry et al Thoracic key 2018
24. Schematic representation of anatomical areas in right anterior
oblique (RAO) and left anterior oblique (LAO) views. LAO: left
anterior oblique; RAO: right anterior oblique.
Algorithm for identification of exit sites of VT.
Condori-Leandro HI, et al. Journal of Geriatric Cardiology (2019) 16: 362 377
25.
26. VT in absence of Structural heart disease
• ~ 10% of all patients present with VT
• An absence of structural heart disease is usually suggested if an ECG
(except in Brugada syndrome and LQTS]), echo, and coronary
arteriogram collectively are normal.
• Types of VT in absence of structural heart disease:
– RV outflow tract (RVOT) VT
– LV outflow tract (LVOT) VT
– Idiopathic LV tachycardia (ILVT)
– Idiopathic propranolol-sensitive (automatic) VT (IPVT)
– Catecholaminergic polymorphic VT (CPVT),
– Brugada syndrome, and LQTS.
• Idiopathic VT -RVOT VT, LVOT VT, ILVT, and IPVT
Komandoor Srivathsan et al, Indian Pacing and Electrophysiology Journal (ISSN 0972-6292), 5(2): 106-121 (2005)
27. Diagnostic scheme for monomorphic ventricular tachycardia in structurally normal
hearts (collectively normal electrocardiogram, echo, and coronary angiogram)
Komandoor Srivathsan et al, Indian Pacing and Electrophysiology Journal (ISSN 0972-6292), 5(2): 106-121 (2005)
28. Proposed diagnostic scheme for polymorphic VT or ventricular fibrillation in
structurally normal hearts (collectively normal electrocardiogram [except in
Brugada syndrome and LQTS], echocardiogram, and coronary angiogram).
Komandoor Srivathsan et al, Indian Pacing and Electrophysiology Journal (ISSN 0972-6292), 5(2): 106-121 (2005)
31. LVOT VT ECG
ECG illustrating LVOT VT. The S wave in LI and R-wave transition in V1
suggest LVOT VT. In addition, an R:S amplitude ratio of 30% and an R:QRS
duration ratio of 50% are seen. Presence of an S wave in leads V5 and V6
suggests an infravalvular origin of the tachycardia.
32. Leandro et al, Journal of Geriatric Cardiology (2019) 16: 362 377
34. Epicardial VT
•A pseudo delta wave ≥ 34 ms
(measured from the earliest
ventricular activation to the earliest
fast deflection in any precordial lead)
•Intrinsicoid deflection V2 ≥ 85 ms
(defined as the interval measured from
the earliest ventricular activation to
the peak of QRS in V2)
•Shortest RS complex ≥ 121 ms
(defined as the interval measured from
the earliest ventricular activation to
the nadir of the first S wave in any
precordial lead)
Leandro et al, Journal of Geriatric Cardiology (2019) 16: 362 377
35. Brugada type ECG
RBBB with ST elevation in V1 to V3
ECG of a patient with Brugada syndrome. The right bundle branch block pattern with coved ST
segment elevation (J-point elevation) is more than 2 mm, particularly in lead V2.