• Like
Wide complex Tachycardia by Dr. Vaibhav Yawalkar
Upcoming SlideShare
Loading in...5

Thanks for flagging this SlideShare!

Oops! An error has occurred.

Wide complex Tachycardia by Dr. Vaibhav Yawalkar


Presentation on wide QRS tachycardia

Presentation on wide QRS tachycardia

Published in Health & Medicine
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
No Downloads


Total Views
On SlideShare
From Embeds
Number of Embeds



Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

    No notes for slide


  • 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.
  • 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
  • 13. 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
  • 14. 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
  • 15. 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
  • 16. 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
  • 17. 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
  • 18. 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
  • 19. 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.
  • 20. 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.
  • 21. 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
  • 22. Chest x-ray Evidence suggestive of structural heart disease Evidence of previous cardiothoracic surgery Presence of a pacemaker or ICD.
  • 23. 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
  • 24. Regularity Marked irregularity of RR interval occurs in atrial fibrillation (AF) with aberrant conduction and polymorphic VT
  • 25. 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 .
  • 26. 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 .
  • 27. 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) .
  • 28. 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.)
  • 29. 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.
  • 30. 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
  • 31. Positive concordance Negative concordance
  • 32. 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 %)
  • 33. 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.
  • 34. 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.
  • 35. 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
  • 36. 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%)
  • 37. 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
  • 38. 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)
  • 39. Also look for…. VPCs Evidence of prior MI QT interval ECG clues to any other structural heart disease
  • 40. SVT vs VT ECG criteria: Brugada algorithm
  • 41. Step 1
  • 42. Step 2
  • 43. Step 3
  • 44. 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
  • 45. 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)
  • 46. V6 in LBBB type QRS qR Pattern QS Pattern
  • 47. 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
  • 48. V1 in RBBB type QRS qR wave Monophasic R wave
  • 49. Rsr’ pattern (Marriot’s Sign) Initial ventricular activation is independent of RBB. RBBB abberation affects only the latter QRS VT SVT
  • 50. V6 in RBBB type QRS •QS Complex • qRS pattern • qrS Pattern •rS Pattern
  • 51. “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
  • 52. Josephson’s sign Notching near the nadir of the S-wave Suggest VT
  • 53. Wellen’s Criteria • QRS width > 140 msec • Left axis deviation • AV dissociation • Configurational characteristics of the QRS morphology
  • 54. 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
  • 56. 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
  • 57. Sensitivity Specificity PPV NPV Brugada 89% 73% 92% 67% Vereckei 97% 75% 93% 87%
  • 58. VT vs AVRT ECG criteria
  • 59. 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.
  • 60. 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.
  • 61. 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.
  • 62. Torsades de pointes rhythm Give magnesium (load with 1-2 g over 5-60 min; then infuse
  • 63. 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
  • 64. 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.
  • 65. THANK YOU…….