basic approach to tachy arrhythmias

1. APPROACH TO WIDE COMPLEX
TACHYCARDIA(WCT)
DR.K.ABHISHEK

3. widened QRS complex
• ≥120 milliseconds
• occurs when ventricular activation is abnormally slow.
1. arrhythmia originates outside of the normal conduction
system and below the AV node [VT]
2. Abnormalities within the His-Purkinje system (SVT with
aberrancy)
3. Pre-excitation with an SVT conducting antegrade over an
accessory pathway, resulting in direct activation of the ventricular
myocardium

4. EPIDEMIOLOGY
• VT is the MCC of WCT (80% cases of WCT), particularly in
patients with h/o cardiac disease.
• Among pt with structural heart diseases VT incidence 90%
• SVT results in WCT much less frequently than VT.
• aberrant conduction is the most common reason for a widened
QRS
• AV reentrant tachycardia (AVRT) is a relatively uncommon
cause of WCT

5. Causes of wide QRS TACHYCARDIA
VT MACROREENTRANT VT
FOCAL VT
SVT WITH ABERRANCY FUNCTIONAL BBB
PREEXISTENT BBB
PREEXCITED SVT ANTIDROMIC AVRT
AT OR AVNRT WITH BYSTANDER BYPASS
TRACT
ANTIARRYTHMIC DRUGS CLASS 1A,CLASS 1C
AMIODARONE
ELECTROLYTE ABNORMALITIES HYPERKALEMIA

6. History
• H/O heart disease - especially coronary heart disease and/or a
previous myocardial infarction (MI), strongly suggests VT.
• Presence of an ICD – implies a known increased risk of VTs and
suggests strongly the WCT is VT.
• Presence of a pacemaker – raises the possibility of a device-
associated WCT
• Age – >35 years presenting to ER, a WCT is likely to be VT .
SVT is more likely in younger patients
VT must be considered in younger patients, particularly those
with a family history of ventricular arrhythmias or premature sudden
cardiac death.

7. • Atrial arrhythmias
• In a patient with persistent AF - a regular WCT is likely VT, as aberrant
conduction during AF would create an irregular rhythm.
• An exception is when AF "organizes" into atrial flutter; this can occur
spontaneously but occurs much more commonly in the setting of
antiarrhythmic drugs (especially class IC agents, amiodarone,
or dronedarone).

8. Medications
• antiarrhythmic drugs
• anti-infective drugs
• psychotropic drugs
• are known to prolong the QT interval and are associated with a risk of
polymorphic VT.

9. CLINICAL MANIFESTATIONS
Patients with WCT typically present with one or more of the following:
• Palpitations
• Chest pain
• Shortness of breath
• Syncope or presyncope
• Sudden cardiac arrest

10. On Examination
• Tachycardia
• Hypotension
• Hypoxia & lung crepts- pt’s pulmonary congestion and heart
failure result from the WCT may have hypoxia and crackles
• Evidence of AV dissociation- presence of AV dissociation strongly
suggests VT

11. AV dissociation –by examination
• Marked fluctuations in the blood pressure
• Variability in the occurrence and intensity of heart sounds (especially
S1)
• Cannon "A" waves – Cannon A waves are intermittent and irregular
jugular venous pulsations of greater amplitude.
reflect simultaneous atrial and ventricular activation.
• Prominent A waves can also be seen during some SVTs, but they are
usually regular.

12. old ECG if available ? Look for
• Baseline QRS
• VPCs
• Evidence of prior MI
• QT interval
• ECG clues to any other structural heart disease

13. Ventricular tachycardia
• originates within the ventricular myocardium outside of the
normal conduction system, resulting in direct myocardial
activation.
• ventricular activation during VT is slower and proceeds in a
different sequence. Thus QRS complex is wide and abnormal.
• Monomorphic – uniform and a fairly stable QRS morphology
• Polymorphic – continuously varying QRS complex morphology/ axis
• Bidirectional – Every other beat has a different axis as it travels
alternately down different conduction pathways

14. 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 .

15. AXIS
• 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 .

16. • 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 %)

17. 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.

18. • 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

19. Negative concordance

20. Positive concordance

21. 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) .

22. • A QRS duration <140 msec does not exclude VT
SEPTAL VT
FASCICULAR VT

23. 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.

24. 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.

25. 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

26. Fusion beats
• 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%)

27. Capture beats
Capture beats, or Dressler beats, are 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

30. RBBB morphology wide QRS tachycardia
• VT
Structurally normal heart
• LVOT VT
• Fasicular VT
Abnormal heart
• LV myocardial VT
• Bundle Branch Reentrant VT
SVT
SVT with pre existing RBBB
SVT with functional RBBB

31. Repetitive monomorphic ventricular tachycardia (RMVT)
arising from the left ventricular outflow tract (LVOT)
right bundle, inferior axis morphology signifying its left ventricular site of origin

32. VT WITH RBBB
predominantly positive terminal deflection in V1;r S/ QS V6; R in v1 exceeds R’

33. LBBB morphology wide QRS tachycardia
• VT
Structurally normal heart
• RVOT VT
Abnormal heart
• Right ventricular myocardial VT
• ARVD
SVT
• Mahaim fibre mediated tachycardia
• SVT with LBBB

34. VT WITH LBBB

35. Supraventricular tachycardia
• SVT conducts to the ventricles via the normal AV node and His-
Purkinje system, the activation wave front spreads quickly through
the ventricles, and the QRS is usually narrow.
• supraventricular impulse can be delayed or blocked in the bundle
branches or in the distal Purkinje system, resulting in a wide,
abnormal QRS. ABERRANCY

36. SVT with ABBERANCY
• No fusion/capture beats/ no AV dissociation
• Consistent onset of tachycardia with premature “p”wave
• Very short RP interval(0.1 sec)
• QRS configuration same as that occurring from unknown supraventricular
conduction at similar rate
• P wave QRS rate & rhythm linked to suggest that ventricular activation
depends on atrial discharge (AV wenckebach block)
• Slowing/termination of tachycardia by vagal manoeuvres.

37. Pre-excitation syndrome
• AV conduction can occur over the normal conduction system and also
via an accessory AV pathway
• two pathways create the anatomic substrate for a reentrant circuit
(macro-reentrant circuit), facilitating the development of a circus
movement or reentrant tachycardia known as AV reentrant
tachycardia (AVRT)
• AVRT can manifest pre-excitation, WPW syndrome or concealed
accessory pathways, can present with a narrow or a wide QRS
complex:

38. ECG in Wolff-Parkinson-White

39. AVRT in the setting of an accessory AV pathway

40. Antidromic AVRT in a patient with an accessory
AV pathway

41. orthodromic atrioventricular reentrant tachycardia
(AVRT) in a patient with an accessory AV pathway

42. pre-excited atrial fibrillation
atrial fibrillation in a patient with antegrade conduction through both the AV node and
an accessory pathway.

43. Pacemakers
• When the ventricles are activated by a pacing device, the QRS complex is
generally wide
• Most transvenous ventricular pacemakers pace the right ventricle, causing
a wide QRS complex of the LBBB type. Typically, the surface ECG shows a
broad R wave in lead I, indicating conduction from right to left.
• chronically widened QRS is one of the components of the indication for CRT

44. Artifact mimicking ventricular tachycardia
• when observed on a single-lead rhythm strip, may be misdiagnosed
as VT .
• presence of narrow-complex beats that can be seen to "march"
through the supposed WCT at a fixed rate strongly supports the
diagnosis of artifact.

45. VT vs SVT
IN A PATIENT WITH WIDE QRS TACHYCARDIA ???????????????????

46. Brugada algorithm -diagnosis of VT & SVT

47. Step 1

48. Step 2

49. Step 3

50. 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

51. V6 in LBBB type QRS
• True LBBB
Monophasic R with slow upstroke
• VT
qR or QS pattern

52. 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

53. “R/S ratio in V6 rule”
• R/S ratio in RBB type wide QRS tachycardia less than one, favors VT
Sensitivity-0.73
Specificity-0.79
Positive predictive value 0.9

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

55. Rabbit’s ear

56. Ultra-simple 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 (positive likelihood ratio 34.8)
.
Pava LF, Perafán P, Badiel M, Arango JJ, Mont L, Morillo CA, and Brugada J. R-wave peak time at DII: a new criterion
for differentiating between wide complex QRS tachycardias. Heart Rhythm 2010 Jul; 7(7) 922-6

57. Vereckei A, Duray G, Szénási G, Altemose GT, and Miller JM.Application of a new algorithm in the differential diagnosis of wide
QRS complex tachycardia. Eur Heart J 2007 Mar; 28(5) 589-600.

58. • Vi –initial 40 ms in v1 (initial ventricular activation velocity)
• Vt - terminal 40ms in v1(late ventricular activation velocity)
• WCT caused by SVT-initial activation of the septum is rapid followed by
conduction delay which manifest in later part of qrs-------vi/vt more than 1
• In Vt vi/vt is less than 1
• Vi/vt less than 1 in EXCEPTION SVT with old anteroseptal MI
• Vi/vt more than 1 in FASCICULAR VT

59. Vi/Vt

60. aVR algorithm-(if answer is yes, then VT)
Criteria looks ONLY at lead aVR :
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?
Vereckei et al, Heart Rhythm 2008

61. Sensitivity Specificity PPV NPV
• Brugada 89% 73% 92% 67%
• Vereckei 97% 75% 93% 87%
Vereckei A, Duray G, Szénási G, Altemose GT, and Miller JM.Application of a new algorithm in the differential diagnosis of wide
QRS complex tachycardia. Eur Heart J 2007 Mar; 28(5) 589-600.

62. Sensitivity & Specificity For VT
• 88% and 53% by aVR algorithm

64. Assessment of hemodynamic stability
• Unstable – WCT has evidence of hemodynamic compromise but
generally remains awake with a discernible pulse. In this setting,
emergency synchronized cardioversion (after intravenous sedation,
whenever possible) is the treatment of choice regardless of the
mechanism of the arrhythmia.
• Patients who become unresponsive or pulseless are considered to
have a cardiac arrest and are treated according to standard
resuscitation algorithms ACLS/BLS/PALS.

65. • Stable – A stable patient with WCT shows no evidence of
hemodynamic compromise despite a sustained rapid heart rate. Such
patients should have continuous monitoring and frequent
reevaluations due to the potential for rapid deterioration as long as
the WCT persists.
• The presence of hemodynamic stability should not be regarded as
diagnostic of SVT Misdiagnosis of VT as SVT based upon
hemodynamic stability is a common error that can lead to
inappropriate and potentially dangerous therapy