Presentation on wide QRS tachycardia

1. Dr. Vaibhav Yawalkar

2. Definitions
Wide QRS complex tachycardia is a rhythm with a
rate of ≥100 b/m and QRS duration of ≥ 120 ms
VT – Three or more consequtive ventricular beats
with rate of 100/minute or more
SVT- Tachycardia requiring participation of structures
above bundle of His.

3. LBBB morphology-QRS
complex duration ≥ 120 ms
with a predominantly
negative terminal
deflection in lead V1
RBBB morphology -QRS
complex duration ≥ 120 ms
with a predominantly
positive terminal
deflection in V1

4. Why QRS is wide?
A widened QRS (≥120 msec) occurs when ventricular
activation is abnormally slow
Arrhythmia originates outside of the normal conduction
system (ventricular tachycardia)
Abnormalities within the His-Purkinje system
(supraventricular tachycardia with aberrancy).
Pre-excited tachycardias: supraventricular tachycardias
with antegrade conduction over an accessory pathway into
the ventricular myocardium.

5. Causes of wide QRS complex tachycardia
Supraventricular tachycardia(20%)
- with prexsisting BBB
- with BBB due to heart rate (aberrant conduction)
- antidromic tachycardia in WPW syndrome
Ventricular tachycardia(80%)

6. Other causes..
Hyperkalemia
Acidosis
Antiarrhythmics-IA,IC
Ventricular pacing

7. Functional Bundle Branch Block
Functional aberration results from sudden change in
cycle length when parts of the His-Purkinje system
are partially or wholly inexcitable
Functional RBBB more common.

8. Linking phenomenon
Mechanism for perpetuation of functional
anterograde bundle branch block due to repetitive
transseptal retrograde concealed penetration by
impulses propagating along the contralateral
bundle.

9. LINKING PHENOMENON

10. AVRT
Orthodromic AVRT –
Antegrade conduction :AV node
Retrograde conduction : Accessory pathway.
Wide QRS is produced only if aberrant conduction
(rate related or preexisting BBB)
Antidromic AVRT –
Antegrade conduction : over the accessory pathway
Retrograde conduction : over the AV node .

11. AVRT

12. Mahaim fibre mediated tachycardia
 Anterograde conduction : Mahaim pathway(atrio-
facsicular pathway)
 Retrograde conduction :AV node
 LBBB morphology
 Left axis deviation
Pre-excitation during sinus rhythm is uncommon

14. RBBB morphology wide QRS
tachycardia
• VT
a. Structurally normal heart
LV Outflow Tract VT
Fascicular VT
b. Abnormal heart
LV myocardial VT
Bundle Branch Reentrant VT
SVT
SVT with pre existing RBBB
SVT with functional RBBB

15. LBBB morphology wide QRS
tachycardia
VT
a. Structurally normal heart
RV Outflow Tract VT
b. Abnormal heart
Right ventricular myocardial VT
Arhythmogenic Right Ventricular Dysplasia (ARVD)
SVT
Mahaim fibre mediated tachycardia
SVT with LBBB

16. Unique clinical challenge
Diagnosing the arrhythmia is difficult —
Diagnostic algorithms are complex and imperfect.
Urgent therapy is often required —
Patients may be unstable at the onset of the arrhythmia or
deteriorate rapidly at any time.
Risks associated with giving therapy for an SVT to a
patient who actually has VT

17. SVT vs VT
Clinical history
Medication Drug-induced tachycardia → Torsades de pointes
Diuretics
Digoxin-induced arrhythmia → [digoxin] ≥2ng/l or
normal if hypokalemia
Age - ≥ 35 ys → VT (positive predictive value of 85%)
Underlying heart disease Previous MI → 90% VT
Cardiomyopathy,
Family h/o Sudden Cardiac Death
Pacemakers or ICD Increased risk of ventricular tachyarrhythmia

18. SVT vs VT
SVT
Duration :If tachycardia has recurred over a period of
more than three years
 Termination of WCT in response to maneuvers like
Valsalva , carotid sinus pressure, or adenosine

19. Maneuvers
The response of the arrhythmia to maneuvers may
provide insight to the mechanism of the WCT
Carotid sinus pressure — Enhances vagal tone ,
depresses sinus and AV nodal activity

20. Carotid sinus pressure
Sinus tachycardia will gradually slow with carotid
sinus pressure and then accelerate upon release.
Atrial tachycardia or atrial flutter-the ventricular
response will transiently slow.
The arrhythmia is unaffected.
Paroxysmal SVT frequently terminates with carotid
sinus pressure.

21. VT
AV dissociation -
-variable systolic BP
-cannon A waves
-variable intensity of S1
Unaffected by vagal maneuvers such as carotid sinus
pressure or valsalva
May slow or block retrograde conduction.
Exposes AV dissociation
Rarely, VT terminates in response to carotid sinus
pressure.

23. Laboratory tests
The plasma potassium and magnesium concentrations
(hypokalemia and hypomagnesemia predispose to the
development of ventricular tachyarhythmias. )
Digoxin, quinidine, or procainamide levels-to rule out
drug toxicity

24. Chest x-ray
Evidence suggestive of structural heart disease
Evidence of previous cardiothoracic surgery
Presence of a pacemaker or ICD.

25. Rate
Limited use in distinguishing VT from SVT.
When the rate is approximately 150 beats per minute,
atrial flutter with aberrant conduction should be
considered.
Ventricular rate > 200-suspect preexcitation
tachycardia

26. Regularity
Marked irregularity of RR interval occurs in
atrial fibrillation (AF) with aberrant conduction and
polymorphic VT

27. Axis
A right superior axis (axis from -90 to ±180º)- “northwest"
axis, strongly suggests VT .
(sensitivity 20%,specificity 96%)
Exception -antidromic AVRT in Wolff-Parkinson-White
(WPW) syndrome .

28. Compared to the axis during sinus rhythm, an axis
shift during the WCT of more than 40º suggests VT .
In a patient with a RBBB-like WCT, a QRS axis to the
left of -30º suggests VT.
In a patient with an LBBB-like WCT, a QRS axis to
the right of +90º suggests VT .

29. QRS duration
In general, wider QRS favors VT.
In a RBBB-like WCT, a QRS duration >140 msec suggests VT
In a LBBB-like WCT, a QRS duration >160 msec suggests
VT
In an analysis of several studies, a QRS duration >160 msec
was a strong predictor of VT (likelihood ratio >20:1) .

30. Narrow QRS VT
A QRS duration <140 msec does not exclude VT
( VT originating from the septum or within the
His-Purkinje system may be associated with a
relatively narrow QRS complex.)

31. Concordance
Concordance is present when the QRS complexes in
all six precordial leads (V1 through V6) are
monophasic with the same polarity.
Either -entirely positive with tall, monophasic R
waves, or entirely negative with deep monophasic
QS complexes.
If any of the six leads has a biphasic QRS (qR or RS
complexes), concordance is not present.

32. Negative concordance is strongly suggestive of VT
exception:SVT with LBBB aberrancy may demonstrate
negative concordance
Positive concordance -also indicates VT
exception: antidromic AVRT with a left posterior accessory
pathway

33. Positive concordance Negative concordance

34. Presence of concordance strongly suggests VT (90
percent specificity)
Absence is not helpful diagnostically (approximately
20 percent sensitivity)
Higher specificity for Positive concordance compared
to negative concordance(specificity 95% vs 90 %)

35. AV dissociation
AV dissociation is characterized by atrial activity that is
independent of ventricular activity
Atrial rate slower than the ventricular rate diagnostic of VT.
Atrial rate that is faster than the ventricular rate - SVTs.

36. Absence of AV dissociation in VT
AV dissociation may be present but not obvious on
the ECG.
The ventricular impulses conduct backwards
through the AV node and capture the atrium (
retrograde conduction), preventing AV
dissociation.

37. Dissociated P waves
PP and RR intervals are different
PR intervals are variable
There is no association between P and QRS
complexes
The presence of a P wave with some , but not all, QRS
complexes

38. Fusion Beat
Fusion beat-produced by fusion of two ventricular activation
wave fronts characterized by QRST morphology intermediate
between normal and fully abnormal beat.
Fusion beats during a WCT are diagnostic of AV dissociation
and therefore of VT.
Low sensitivity(5-20%)

39. Capture beats
Here QRS complexes during a WCT that are identical
to the sinus QRS complex .
Implies that the normal conduction system has
momentarily "captured" control of ventricular
activation from the VT focus.
Fusion beats and capture beats are more commonly
seen when the tachycardia rate is slower

40. If old ecg available…
Ideal QRS configuration between baseline and
WQRST-suggest SVT(exception :bundle branch
reentrant VT)
Contralateral BBB patterns in baseline vs WQRST
ECGs-suggest VT
WQRST complexes narrower than baseline ECG-
suggest VT(the baseline ecg must have a bundle
branch block pattern)

41. Also look for….
VPCs
Evidence of prior MI
QT interval
ECG clues to any other structural heart disease

42. SVT vs VT
ECG criteria: Brugada algorithm

43. Step 1

44. Step 2

45. Step 3

46. Step 4: LBBB - type wide QRS complex
SVT VT
small R wave notching of S wave
R wave >30ms
fast downslope
of S wave
no Q wave
Q wave
> 70ms
V1
V6

47. V1-V2 in LBBB type QRS
VT
R >30 msec,
QRS onset to S nadir>70 msec
Notching and slurring of QRS complex –myocardial
disease
(sensitivity-0.78,specificity 0.85)

48. V6 in LBBB type QRS
qR Pattern
QS Pattern

49. Step 4: RBBB - type wide QRS complex
SVT VT
V1
V6
or
or
R/S > 1 R/S ratio < 1 QS complex
rSR’ configuration monophasic R wave qR (or Rs) complex

50. V1 in RBBB type QRS
qR wave
Monophasic R wave

51. Rsr’ pattern (Marriot’s Sign)
Initial ventricular activation is independent of
RBB.
RBBB abberation affects only the latter QRS
VT SVT

52. V6 in RBBB type QRS
•QS Complex
• qRS pattern
• qrS Pattern
•rS Pattern

53. “R/S ratio in V6 rule”
R/S ratio in RBB type wide QRS tachycrdia less than one,
favours VT
Sensitivity-0.73
Specificity-0.79

54. Josephson’s sign
Notching near the nadir of the S-wave
Suggest VT

55. Wellen’s Criteria
• QRS width > 140 msec
• Left axis deviation
• AV dissociation
• Configurational characteristics of the QRS
morphology

56. Ultrasimple Brugada criterion
Joseph Brugada - 2010
R wave peak time in Lead II
Duration of onset of the QRS to the first change in
polarity (either nadir Q or peak R) in lead II.
If the RWPT is ≥ 50ms the likelihood of a VT very
high

58. VERECKEI ALGORITHM

59. aVR algorithm
Criteria looks ONLY at lead aVR (if answer is
yes, then VT):
1. Is there an initial R wave?
2. Is there a r or q wave > 40 msec
3. Is there a notch on the descending limb of a
negative QRS complex?
4. Measure the voltage change in the first (vi) and
last 40 msec (vt). Is vi / vt < 1?
Sensitivity & Specificity For VT
88% and 53% by aVR algorithm

61. Sensitivity Specificity PPV NPV
Brugada 89% 73% 92% 67%
Vereckei 97% 75% 93% 87%

62. VT vs AVRT
ECG criteria

63. Management
Until proven otherwise, any WCT should be managed
as if it were VT, in keeping with the consideration of
"First, do no harm"
Unstable Patient
If Patients with low blood pressure, pulmonary edema,
severe angina, or other evidence of poor perfusion
cardioverted back into normal rhythm,
using synchronized electrical direct current.

64. Patient
Patient is in ventricular
tachycardia or uncertain
rhythm.
Treatment
Amiodarone 150 mg IV
over 10 min;
repeat as needed to
maximum dose of 2.2 g
in 24 hours.
Prepare for elective
synchronized
cardioversion.

65. Patient
Supraventricular
tachycardia with
aberrancy
Treatment
Adenosine 6 mg rapid IV
push
If no conversion, give
adenosine 12 mg rapid IV
push; may repeat 12 mg
dose once.

66. Torsades de pointes
rhythm
Give magnesium (load
with 1-2 g over 5-60 min;
then infuse

67. After the acute management :
Long-term plans should be made to prevent the
recurrence of the episodes, minimize their
symptomatic impact, and protect the patient against
sudden cardiac death

68. Features s/o VT
Absence of typical RBBB or LBBB morphology
Extreme axis deviation (“northwest axis”)
Very broad complexes (>160ms)
AV dissociation (P and QRS complexes at different rates)
Capture beats
Fusion beats
Positive or negative concordance throughout the chest
leads
Brugada’s sign – The distance from the onset of the QRS
complex to the nadir of the S-wave is > 100ms
Josephson’s sign – Notching near the nadir of the S-wave
Marriot’s sign :RSr’ complexes with a taller left rabbit
ear: most specific finding in favour of VT.

69. THANK YOU…….