1. Practical Electrocardiography – Ventricular Tachycardia
Scott Ewing, D.O.
Cardiology Fellow
October 26, 2006

2. Terminology
Ventricular tachycardia (VT) – three or more ventricular extrasystoles in succession with rate > 120 bpm
Non-sustained VT (NSVT) – lasts < 30 sec
Sustained VT – lasts > 30 sec
Accelerated idioventricular rhythm – rate 100­120 bpm

3. NSVT

4. LBBB

5. RBBB

6. BBB Comparison Normal leads V1 and V6
Typical QRS-T patterns in RBBB and LBBB
Note the secondary T wave inversions in leads with an rSR' complex with RBBB and in leads with a wide R wave with LBBB

7. Varieties of Broad Complex Tachycardia
Ventricular - regular
Monomorphic ventricular tachycardia
Fascicular tachycardia
Right ventricular outflow tract tachycardia
Ventricular - irregular
Torsades de pointes tachycardia
Polymorphic ventricular tachycardia
Supraventricular
Bundle branch block with aberrant conduction
Atrial tachycardia with pre­excitation

8. Monomorphic vs. Polymorphic

9. Etiology VT usually a complication of severe heart disease
Early hours of MI, usually leading to ventricular fibrillation
Immediately after proximal obstruction of large artery
Chronically after large infarction, usually more stable form
May appear in “healthy” individuals
Originate from RV outflow tract
Posterior fascicle of the left bundle branch
Usually “cured” radiofrequency catheter ablation

10. Etiology
Many antiarrhythmic drugs proarrhythmic effects manifested as VT or torsades de pointes
Slow conduction and prolong the QRS complex and convert non-sustained VT into sustained VT
Prolong QTc interval and produce torsades de pointes
VT and proarrhythmic effect usually poor ventricular function and ischemic heart disease
Two aspects of the clinical history consistently predict a ventricular site of origin (90%)
Previous myocardial infarction
No previous tachyarrhythmia

11. Left Ventricle Tachycardia

12. Common Sources of Error
Believing VT cannot be well tolerated
Depending upon a single lead (Lead II)
Putting faith in irregularity
Depending upon independent atrial activity
Ignoring or neglecting QRS morphology

13. Believing That VT Cannot Be Well Tolerated
Commonly believed that VT is associated with a greater alteration of hemodynamics than are SVTs
Not true! Most are stable when first seen
Main factors that determine a patient's tolerance to a tachyarrhythmia of any origin
Ventricular rate
Size of the heart
Severity of underlying disease

14. Depending on a Single Lead
Lead II good for identifying P waves
Lead V1 (with its right-versus-left orientation) superior to lead II (with its base-to-apex orientation) for differentiating VT from an SVT
Lead V1 wide QRS complexes
V1-positive morphology, the differential diagnosis is between VT from the left ventricle and SVT with RBBB
V1-negative morphology, the differential diagnosis is between VT from the right ventricle and SVT with LBBB

15. Lead II vs. V1 Left-ventricular tachycardia or SVT with RBBB vs.
Right-ventricular tachycardia or SVT with LBBB

16. Putting Faith in Irregularity
VT is sometimes irregular, so is SVT
When an intermittent irregularity appears in the morphology of the QRS complex, either on time or slightly early, the most likely cause is a breakthrough of conduction of the atrial rhythm to the ventricles
Fusion beat
Capture beat
If fusion or capture beats are proven, diagnosis is almost certainly VT
Usually at rates < 160 bpm
Not common

17. Putting Faith in Irregularity
62 yo man who presented with acute SOB 2 months after an inferior–posterior MI
Arrows indicate capture beats and asterisks indicate fusion beats

20. Depending on Independent Atrial Activity
AV dissociation eliminates SVT originating from the atria or an accessory pathway, does not exclude SVT originating from AV node
Example of an AV-nodal tachycardia with LBBB aberrancy, confirmed by observing the similar QRS morphology occurring during sinus rhythm
However, this is the exception
With AV dissociation and wide-QRS-complex tachycardia, the diagnosis of VT is highly probable

21. AV Dissociation without VT
Recordings of limb leads I, II, and III during sinus rhythm (left) and AV-nodal tachycardia (right)
Arrows indicate the normally directed P waves visible in lead II without constant PR intervals

22. AV Dissociation with VT

23. Ignoring or Neglecting QRS Morphology
Duration of wide QRS complexes may provide important diagnostic information, particularly if a recording is available of the patient's QRS-complex morphology during sinus rhythm
QRS width > 0.14 sec good indicator of VT
May also be seen in LBBB or RBBB
Less wide QRS (0.12 – 0.14 sec) not necessarily indicative of SVT with aberrancy
In LVT, V1-positive QRS complex usually described by
Monophasic R wave or
Diphasic qR complex, or occasionally
Triphasic RSR’ complex
When V1 QRS complex has two positive peaks (an R and an R’, with or without an S wave between these two peaks), termed “rabbit ears”
Relative heights of these “ears” have been used to differentiate LVT from SVT with right bundle-branch (RBBB) aberrancy
R > R’ suggests the presence of LVT because RBBB aberration is characterized by R’ > R

24. Ignoring or Neglecting QRS Morphology
59 yo man after extensive anterior MI
Arrows taller first “rabbit ear” in lead V1
Asterisks indicate the QS pattern in lead V6

25. Ignoring or Neglecting QRS Morphology
Absence of any positive deflection (QS or rS complexes) in V6 diagnostic for VT originating from either ventricle
These patterns could not be produced by RBBB or LBBB
Such patterns in lead V6 appear with LVT and RVT
Conversely, triphasic qRs morphology in V6, is virtually diagnostic of SVT with aberrancy

26. Ignoring or Neglecting QRS Morphology
63 yo man with recurrent VT and heart failure awaiting cardiac transplantation while being maintained on propafenone therapy
Asterisks indicate the QS appearance in lead V6.

27. QRS Contours Favoring Ventricular Tachycardia

28. QRS Contours Favoring Ventricular Aberration

29. Ignoring or Neglecting QRS Morphology
Concordance precordial QRS complex directions another useful ECG clue
When all of the ventricular complexes from leads V1 to V6 are concordant negative or concordant positive
Diagnosis likely VT
Patterns highly atypical of either RBBB or LBBB
Concordant negativity virtually diagnostic of RVT
Concordant positivity virtually diagnostic of LVT

30. Ignoring or Neglecting QRS Morphology
Concordant negative (RVT)
Concordant positive (LVT)

31. Duration and Morphology of QRS Complex
Sequence of cardiac activation is altered, and the impulse no longer follows the normal intraventricular conduction pathway
Morphology of the QRS complex bizarre and duration prolonged (usually > 0.12 s)
Broader the QRS complex, more likely VT, esp. QRS > 01.6 s
QRS duration may exceed 0.2 s, particularly with electrolyte abnormalities, severe myocardial disease, or with antiarrhythmic drugs, such as flecainide
QRS complex in VT often has a RBBB or LBBB morphology
VT originating in the LV produces a RBBB pattern, whereas VT originating in the RV results in a LBBB pattern

32. Review

33. Rate and Rhythm VT rate normally 120­300 bpm
Rhythm is regular or almost regular ( < 0.04 s beat to beat variation), unless disturbed by the presence of capture or fusion beats
If a monomorphic broad complex tachycardia has an obviously irregular rhythm the most likely diagnosis is atrial fibrillation with either aberrant conduction or pre­excitation

34. Frontal Plane Axis
QRS axis normally - 30° to + 90°, with the axis most commonly ~60°
With VT mean frontal plane axis changes and often bizarre
Axis shift > 40° left or right suggestive of VT
Lead aVR is situated in the frontal plane at -210°
aVR negative with normal cardiac axis
aVR positive extremely abnormal axis to the left or right
aVR positive originates close to the apex, with depolarization moving upwards towards base of the heart

35. Axis Shift Favoring VT

36. Direct Evidence of Independent Atrial Activity
With VT, sinus node continues to initiate atrial contraction
P waves are dissociated from the QRS complexes and are positive in leads I and II
Atrial rate usually slower than the ventricular rate
AV dissociation usually diagnostic for VT, lack of direct evidence of independent P wave activity does not exclude the diagnosis

37. Indirect Evidence of Independent Atrial Activity
Capture beat
Occasionally an atrial impulse may cause ventricular depolarization via the normal conduction system
The resulting QRS complex occurs earlier than expected and is narrow
Such a beat shows that even at rapid rates the conduction system is able to conduct normally, thus making a diagnosis of supraventricular tachycardia with aberrancy unlikely
Capture beats are uncommon, and though they confirm a diagnosis of ventricular tachycardia, their absence does not exclude the diagnosis

38. Indirect Evidence of Independent Atrial Activity
Fusion beats
Fusion beat occurs when a sinus beat conducts to the ventricles via the AV node and fuses with a beat arising in the ventricles
As the ventricles are depolarized partly by the impulse conducted through the His­Purkinje system and partly by the impulse arising in the ventricle, the resulting QRS complex has an appearance intermediate between a normal beat and a tachycardia beat
Fusion beats are uncommon, and though they support a diagnosis of ventricular tachycardia, their absence does not exclude the diagnosis

39. Indirect Evidence of Independent Atrial Activity
QRS concordance throughout the chest leads
QRS complexes in precordial leads are either predominantly positive or predominantly negative
Presence of concordance suggests that the tachycardia has a ventricular origin
Positive concordance probably indicates that the origin of the tachycardia lies on the posterior ventricular wall; the wave of depolarization moves towards all the chest leads and produces positive complexes
Similarly, negative concordance is thought to correlate with a tachycardia originating in the anterior ventricular wall

42. Right Ventricular Outflow Tract Tachycardia
Tachycardia originates from RVOT and impulse spreads inferiorly
Typically right axis deviation with a LBBB pattern
Tachycardia may be brief and self terminating or sustained
May be provoked by catecholamine release, sudden changes in heart rate, and exercise
Usually responds to β-blockers or CCB
Occasionally stops with adenosine treatment and so may be misdiagnosed as a supraventricular tachycardia

44. Torsades de pointes Tachycardia
Torsades de pointes (“twisting of points”) is a type of polymorphic ventricular tachycardia in which the cardiac axis rotates over a sequence of 5­20 beats, changing from one direction to another and back again
QRS amplitude varies similarly, such that the complexes appear to twist around the baseline
Usually associated with conditions that prolong QT interval
Usually not sustained
Recur unless the underlying cause is corrected
May be prolonged
May degenerate into ventricular fibrillation
Transient prolongation of the QT interval is often seen in the acute phase of myocardial infarction and may lead to torsades de pointes
Management different from the management of other VTs

45. Torsades de pointes

46. Torsades de pointes 62 yo woman on diuretics with syncope
Syncope recurred during this ECG recording
Serum potassium concentration was 2.3 mEq/L

48. Polymorphic Ventricular Tachycardia
Polymorphic ventricular tachycardia has the electrocardiographic characteristics of torsades de pointes but in sinus rhythm the QT interval is normal
Much less common than torsades de pointes
If sustained often leads to hemodynamic collapse
Occur in acute myocardial infarction and may deteriorate into ventricular fibrillation
Must be differentiated from atrial fibrillation with pre­excitation, as both have the appearance of an irregular broad complex tachycardia with variable QRS morphology

52. Ventricular Fibrillation
67 yo man at the onset of a cardiac arrest
Arrow indicates the early-occurring VPB that initiates the ventricular flutter that rapidly deteriorates into ventricular fibrillation

54. VT with Rate 170 bpm
RBBB morphology is atypical (monomorphic R, rather than rSR', in V1), and the R:S ratio is less than 1 in V6, both suggestive of ventricular tachycardia
Most common underlying diagnosis in adult North American patients with sustained monomorphic VT is coronary heart disease status post myocardial infarction
This patient had a non-ischemic cardiomyopathy
Morphology of the VT is suggestive of origin from the left side of the heart, near the base (RBBB with inferior/rightward axis)

56. Accelerated Idioventricular Rhythm
67 yo man with previous acute MI with normal QRS duration. What is the most likely diagnosis for the rhythm?
Most consistent with AIVR, originating from the left ventricle and therefore accounting for the atypical RBBB morphology
ST elevations in the precordial leads are likely due to the injury current from underlying acute myocardial infarction
AIVR may be marker of reperfusion following acute MI
83 bpm too slow for VT and too fast for complete heart block

58. VT with Underlying ST and AV Dissociation
77 yo with coronary artery disease
Wide complex tachycardia at 165 bpm and RBBB morphology
Underlying sinus tachycardia at 136 bpm and AV dissociation confirming the diagnosis of VT (Note the clear sinus P wave just after 5th QRS)
QRS morphology and axis are consistent with origin of the VT from the posterior septum
Patient had had a prior large inferior-posterior MI

60. Torsade de pointes
74 yo woman with syncope with life-threatening finding
Complex ECG showing
Underlying atrial fibrillation
Long Q-T(U)
Ventricular pacing with intermittent sensing failure
Run of torsade de pointes-type of polymorphic ventricular tachycardia

62. Ventricular Fibrillation / Ventricular Flutter
51 year male seen in the emergency department
Classic ECG obtained during a VF cardiac arrest
Findings typical of ventricular fibrillation with more organized ventricular electrical activity in the second half of the strip consistent with ventricular flutter
Characteristic systematic variation in QRS axis of torsade is not seen here (although torsade may degenerate terminally into ventricular fibrillation)

64. NSVT 28 yo female with palpitations and lightheadness
Sinus rhythm (normal QTc) with non-sustained monomorphic VT (starting 2nd beat, rate 170 bpm)
Ventricular beats have a LBBB pattern and inferior / borderline rightward QRS axis raising consideration of monomorphic VT arising from the RVOT
Isolated PVCs and two ventricular couplets with the same morphology
Retrograde P waves
Patient had an idiopathic cardiomyopathy with global mild ventricular hypokinesis

66. VT with LBBB Morphology
89 year-old male admitted for chest pain and tachycardia
First 4 beats show termination of a run of wide-complex tachycardia at rate about 150 bpm
5th and the 6th beats supraventricular conduction with underlying atrial fibrillation
Conducted supraventricular beats suggest underlying inferior myocardial infarction with prominent Q waves in leads II and aVF and a borderline intraventricular conduction delay (QRS = 110 msec)
Starting with the 7th beat and continuing to the end, the wide-complex tachycardia resumes
Wide-complex tachycardia (QRS = 160 msec) has LBBB morphology, with an inferior QRS axis
Two features strongly favoring VT over SVT with LBBB aberrancy
Broad R wave (40 msec or more in duration) in leads V1-V2
Delayed intrinsicoid deflection great than 70 msec in V1-V2 measured from the initial onset of the QRS to the nadir of the S wave
Patient ruled in for a small acute myocardial infarction with an elevated troponin

68. VT with RBBB Morphology
78 year-old man with a history of “heart attack” comes into the emergency department with complaints of palpitations and shortness of breath
Very wide-complex (between msec) tachycardia at a rate about 180 bpm with a right bundle branch (RBBB) morphology
The diagnosis of monomorphic ventricular tachycardia with a RBBB morphology is strongly supported
Wide QRS (greater than 140 ms) in the absence of drugs or hyperkalemia (the QRS here is extremely wide)
Wide monophasic R wave in lead V1 (or RS or QR complex in that lead)
QR complexes in the inferior leads with extreme axis deviation
rS or QS waves in V6
Patient had a complicated cardiac history of coronary artery disease, status post bypass graft surgery and prior inferior infarction