Dr. Vaibhav Yawalkar
Definitions
Wide QRS complex tachycardia is a rhythm with a
rate of ≥100 b/m and QRS duration of ≥ 120 ms
VT – Three or ...
LBBB morphology-QRS
complex duration ≥ 120 ms
with a predominantly
negative terminal
deflection in lead V1
RBBB morphology...
Why QRS is wide?
A widened QRS (≥120 msec) occurs when ventricular
activation is abnormally slow
Arrhythmia originates out...
Causes of wide QRS complex tachycardia
Supraventricular tachycardia(20%)
- with prexsisting BBB
- with BBB due to heart ra...
Other causes..
Hyperkalemia
Acidosis
Antiarrhythmics-IA,IC
Ventricular pacing
Functional Bundle Branch Block
Functional aberration results from sudden change in
cycle length when parts of the His-Purk...
Linking phenomenon
Mechanism for perpetuation of functional
anterograde bundle branch block due to repetitive
transseptal ...
LINKING PHENOMENON
AVRT
Orthodromic AVRT –
Antegrade conduction :AV node
Retrograde conduction : Accessory pathway.
Wide QRS is produced only...
AVRT
Mahaim fibre mediated tachycardia
 Anterograde conduction : Mahaim pathway(atrio-
facsicular pathway)
 Retrograde conduc...
RBBB morphology wide QRS
tachycardia
• VT
a. Structurally normal heart
LV Outflow Tract VT
Fascicular VT
b. Abnormal heart...
LBBB morphology wide QRS
tachycardia
VT
a. Structurally normal heart
RV Outflow Tract VT
b. Abnormal heart
Right ventricul...
Unique clinical challenge
Diagnosing the arrhythmia is difficult —
Diagnostic algorithms are complex and imperfect.
Urgent...
SVT vs VT
Clinical history
Medication Drug-induced tachycardia → Torsades de pointes
Diuretics
Digoxin-induced arrhythmia ...
SVT vs VT
SVT
Duration :If tachycardia has recurred over a period of
more than three years
 Termination of WCT in respons...
Maneuvers
The response of the arrhythmia to maneuvers may
provide insight to the mechanism of the WCT
Carotid sinus pressu...
Carotid sinus pressure
Sinus tachycardia will gradually slow with carotid
sinus pressure and then accelerate upon release....
VT
AV dissociation -
-variable systolic BP
-cannon A waves
-variable intensity of S1
Unaffected by vagal maneuvers such as...
Laboratory tests
The plasma potassium and magnesium concentrations
(hypokalemia and hypomagnesemia predispose to the
devel...
Chest x-ray
Evidence suggestive of structural heart disease
Evidence of previous cardiothoracic surgery
Presence of a pace...
Rate
Limited use in distinguishing VT from SVT.
When the rate is approximately 150 beats per minute,
atrial flutter with a...
Regularity
Marked irregularity of RR interval occurs in
atrial fibrillation (AF) with aberrant conduction and
polymorphic ...
Axis
A right superior axis (axis from -90 to ±180º)- “northwest"
axis, strongly suggests VT .
(sensitivity 20%,specificity...
Compared to the axis during sinus rhythm, an axis
shift during the WCT of more than 40º suggests VT .
In a patient with a ...
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,...
Narrow QRS VT
A QRS duration <140 msec does not exclude VT
( VT originating from the septum or within the
His-Purkinje sys...
Concordance
Concordance is present when the QRS complexes in
all six precordial leads (V1 through V6) are
monophasic with ...
Negative concordance is strongly suggestive of VT
exception:SVT with LBBB aberrancy may demonstrate
negative concordance
P...
Positive concordance Negative concordance
Presence of concordance strongly suggests VT (90
percent specificity)
Absence is not helpful diagnostically (approximately...
AV dissociation
AV dissociation is characterized by atrial activity that is
independent of ventricular activity
Atrial rat...
Absence of AV dissociation in VT
AV dissociation may be present but not obvious on
the ECG.
The ventricular impulses condu...
Dissociated P waves
PP and RR intervals are different
PR intervals are variable
There is no association between P and QRS
...
Fusion Beat
Fusion beat-produced by fusion of two ventricular activation
wave fronts characterized by QRST morphology inte...
Capture beats
Here QRS complexes during a WCT that are identical
to the sinus QRS complex .
Implies that the normal conduc...
If old ecg available…
Ideal QRS configuration between baseline and
WQRST-suggest SVT(exception :bundle branch
reentrant VT...
Also look for….
VPCs
Evidence of prior MI
QT interval
ECG clues to any other structural heart disease
SVT vs VT
ECG criteria: Brugada algorithm
Step 1
Step 2
Step 3
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 wav...
V1-V2 in LBBB type QRS
VT
R >30 msec,
QRS onset to S nadir>70 msec
Notching and slurring of QRS complex –myocardial
diseas...
V6 in LBBB type QRS
qR Pattern
QS Pattern
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 w...
V1 in RBBB type QRS
qR wave
Monophasic R wave
Rsr’ pattern (Marriot’s Sign)
Initial ventricular activation is independent of
RBB.
RBBB abberation affects only the latte...
V6 in RBBB type QRS
•QS Complex
• qRS pattern
• qrS Pattern
•rS Pattern
“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....
Josephson’s sign
Notching near the nadir of the S-wave
Suggest VT
Wellen’s Criteria
• QRS width > 140 msec
• Left axis deviation
• AV dissociation
• Configurational characteristics of the ...
Ultrasimple Brugada criterion
Joseph Brugada - 2010
R wave peak time in Lead II
Duration of onset of the QRS to the fir...
VERECKEI ALGORITHM
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 ...
Sensitivity Specificity PPV NPV
Brugada 89% 73% 92% 67%
Vereckei 97% 75% 93% 87%
VT vs AVRT
ECG criteria
Management
Until proven otherwise, any WCT should be managed
as if it were VT, in keeping with the consideration of
"First...
Patient
Patient is in ventricular
tachycardia or uncertain
rhythm.
Treatment
Amiodarone 150 mg IV
over 10 min;
repeat as n...
Patient
Supraventricular
tachycardia with
aberrancy
Treatment
Adenosine 6 mg rapid IV
push
If no conversion, give
adenosin...
Torsades de pointes
rhythm
Give magnesium (load
with 1-2 g over 5-60 min;
then infuse
After the acute management :
Long-term plans should be made to prevent the
recurrence of the episodes, minimize their
symp...
Features s/o VT
Absence of typical RBBB or LBBB morphology
Extreme axis deviation (“northwest axis”)
Very broad complexes ...
THANK YOU…….
Wide complex Tachycardia by Dr. Vaibhav Yawalkar
Wide complex Tachycardia by Dr. Vaibhav Yawalkar
Wide complex Tachycardia by Dr. Vaibhav Yawalkar
Wide complex Tachycardia by Dr. Vaibhav Yawalkar
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Wide complex Tachycardia by Dr. Vaibhav Yawalkar

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Presentation on wide QRS tachycardia

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Wide complex Tachycardia by Dr. Vaibhav Yawalkar

  1. 1. Dr. Vaibhav Yawalkar
  2. 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. 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. 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. 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. 6. Other causes.. Hyperkalemia Acidosis Antiarrhythmics-IA,IC Ventricular pacing
  7. 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. 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. 9. LINKING PHENOMENON
  10. 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. 11. AVRT
  12. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 22. Chest x-ray Evidence suggestive of structural heart disease Evidence of previous cardiothoracic surgery Presence of a pacemaker or ICD.
  23. 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. 24. Regularity Marked irregularity of RR interval occurs in atrial fibrillation (AF) with aberrant conduction and polymorphic VT
  25. 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. 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. 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. 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. 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. 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. 31. Positive concordance Negative concordance
  32. 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. 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. 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. 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. 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. 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. 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. 39. Also look for…. VPCs Evidence of prior MI QT interval ECG clues to any other structural heart disease
  40. 40. SVT vs VT ECG criteria: Brugada algorithm
  41. 41. Step 1
  42. 42. Step 2
  43. 43. Step 3
  44. 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. 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. 46. V6 in LBBB type QRS qR Pattern QS Pattern
  47. 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. 48. V1 in RBBB type QRS qR wave Monophasic R wave
  49. 49. Rsr’ pattern (Marriot’s Sign) Initial ventricular activation is independent of RBB. RBBB abberation affects only the latter QRS VT SVT
  50. 50. V6 in RBBB type QRS •QS Complex • qRS pattern • qrS Pattern •rS Pattern
  51. 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. 52. Josephson’s sign Notching near the nadir of the S-wave Suggest VT
  53. 53. Wellen’s Criteria • QRS width > 140 msec • Left axis deviation • AV dissociation • Configurational characteristics of the QRS morphology
  54. 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
  55. 55. VERECKEI ALGORITHM
  56. 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. 57. Sensitivity Specificity PPV NPV Brugada 89% 73% 92% 67% Vereckei 97% 75% 93% 87%
  58. 58. VT vs AVRT ECG criteria
  59. 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. 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. 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. 62. Torsades de pointes rhythm Give magnesium (load with 1-2 g over 5-60 min; then infuse
  63. 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. 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. 65. THANK YOU…….

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