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Practical Electrocardiography – Ventricular Tachycardia

Practical Electrocardiography – Ventricular Tachycardia. Scott Ewing, D.O. Cardiology Fellow October 26, 2006. Terminology. Ventricular tachycardia (VT) – three or more ventricular extrasystoles in succession with rate > 120 bpm Non-sustained VT (NSVT) – lasts < 30 sec

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Practical Electrocardiography – Ventricular Tachycardia

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  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

  18. 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

  19. 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

  20. AV Dissociation with VT

  21. 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

  22. 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

  23. 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

  24. 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.

  25. QRS Contours Favoring Ventricular Tachycardia

  26. QRS Contours Favoring Ventricular Aberration

  27. 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

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

  29. 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

  30. Review

  31. 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

  32. 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

  33. Axis Shift Favoring VT

  34. 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

  35. 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

  36. 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

  37. 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

  38. 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

  39. 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

  40. Torsades de pointes

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

  42. 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

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