wide complex tachycardia

WIDE COMPLEX TACHYCARDIA

Dr.Pradeep Sreekumar

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.

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

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.

Stewart RB. Ann Intern Med 1986

VT (80%)

SVT (20%)

Supraventricular tachycardia

- with prexsisting BBB

- with BBB due to heart rate (aberrant conduction)

- antidromic tachycardia in WPW syndrome Ventricular tachycardia

Causes of wide QRS complex tachycardia

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-Purkinje system are partially or wholly inexcitable

Functional RBBB more common.

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.

Linking: a dynamic electrophysiologic phenomenonin macroreentry circuits,Michael h. lehmann et al, Circulation. 1985;71:254-265

LINKING PHENOMENON

AVRT

Orthodromic AVRT –

Antegrade conduction :AVnode

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 and retrograde conduction over the AV node .

AVRT

Mahaim fibre mediated tachycardia

Antegrade conduction : Mahaim pathway

Retrograde conduction:AV node

LBBB morphology

Left axis deviation

Pre-excitation during sinus rhythm is uncommon

Bundle Branch Reentrant VT

RBBB morphology wide QRS tachycardia

VTStructurally normal heart

LVOT VT Fasicular VT

Abnormal heart LV myocardial VT Bundle Branch Reentrant VT

SVT

SVT with pre existing RBBBSVT with functional RBBB

LBBB morphology wide QRS tachycardia

VTStructurally normal heart

RVOT VT

Abnormal heart Right ventricular myocardial VT ARVD

SVTMahaim fibre mediated tachycardia

SVT with LBBB

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

SVT vs VT Clinical history

Medication Drug-induced tachycardia → Torsade de pointesDiureticsDigoxin-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

Pacemakers or ICD Increased risk of ventricular tachyarrhythmia

Duration of the tachycardia — SVT is more likely if the tachycardia has recurred over a period of more than three years

SVT vs VT

AV dissociation

-cannon A waves

-variable intensity of S1

Termination of WCT in response to maneuvers like

Valsalva, carotid sinus pressure, or adenosine favor

SVT

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

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.

VT

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.

Laboratory tests

The plasma potassium and magnesium concentrations (hypokalemia and hypomagnesemia predispose to the development of ventricular tachyarrhythmias. )

Digoxin, quinidine, or procainamide levels-to rule out drug toxicity

Chest x-ray

Evidence suggestive of structural heart disease

Evidence of previous cardiothoracic surgery

Presence of a pacemaker or ICD.

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

Regularity

Marked irregularity of RR interval occurs in

atrial fibrillation (AF) with aberrant conduction and polymorphic VT

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 .

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 .

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) .

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.)

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.

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

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 %)

Negative concordance

Positive concordance

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.

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.

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

Fusion beats

Fusion beat-produced by fusion of two ventricular activation wavefronts characterised 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%)

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

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)

Also look for….

VPCs

Evidence of prior MI

QT interval

ECG clues to any other structural heart disease

SVT vs VTECG criteria: Brugada algorithm

Brugada P. Ciculation 1991

Step 1

Step 2

Step 3

Step 4: LBBB - type wide QRS complex

SVT VT

small R wave notching of S waveR wave >30ms

fast downslopeof S wave

no Q wave

Q wave

> 70ms

V1

V6

V1 in LBBB type QRS

True LBBB R-R duration <- 30 msecInterval from QRS onset to S nadir ≤70 msec

(85% of SVT –A)VTR >30 msec,QRS onset to S nadir>70 msec (sensitivity-0.78,specificity 0.85,positive predictive value 0.97)Notching and slurring of QRS complex –myocardial disease

V6 in LBBB type QRS

True LBBBMonophasic R with slow

upstroke

VTqR or 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 wave qR (or Rs) complex

V1 in RBBB type QRS

Initial ventricular activation is independent of RBB.RBBB abberation affects only the latter QRS

True RBBBrR’,rsR’,rSr’,rSR’

VTqR,Rsr’,monophasic R wave

(Sensitivity 0.97,specificity 0.88)

VT SVT

V6 in RBBB type QRS

RBBB abberation-small s wave.qRs or Rs pattern

RBBB type VT-VT from left ventricle-LV and RV

voltage contributes to SqRS,qrS,rS,QS patterns seen

“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

Positive predictive value 0.9

Josephson’s sign 

Notching near the nadir of the S-wave

Suggest VT

Wellens Criteria

  •   QRS width > 140 msec

  •   Left axis deviation

  •   AV dissociation

  •  Configurational characteristics of the QRS morphology

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 (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.

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.

aVR algorithmCriteria 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?

Vereckei et al, Heart Rhythm 2008

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.

Sensitivity & Specificity For VT

88% and 53% by aVR algorithm

VT vs AVRTECG criteria

Brugada P. Ciculation 1991

THANK YOU…….