WIDE COMPLEX TACHYCARDIA

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 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.

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%)

Other causes..

HyperkalemiaAcidosisAntiarrhythmics-IA,ICVentricular pacing

Functional Bundle Branch BlockFunctional 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 PHENOMENON

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 .

AVRT

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

RBBB morphology wide QRS tachycardia• VTa. Structurally normal heart

LV Outflow Tract VTFascicular VT

b. Abnormal heartLV myocardial VTBundle Branch Reentrant VT

SVTSVT with pre existing RBBBSVT with functional RBBB

LBBB morphology wide QRS tachycardiaVTa. Structurally normal heart

RV Outflow Tract VT

b. Abnormal heartRight ventricular myocardial VTArhythmogenic Right Ventricular Dysplasia (ARVD)

SVTMahaim fibre mediated tachycardia

SVT with LBBB

Unique clinical challengeDiagnosing 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 → Torsades 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% VTCardiomyopathy,Family h/o Sudden Cardiac Death

Pacemakers or ICD Increased risk of ventricular tachyarrhythmia

SVT vs VT SVTDuration :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

ManeuversThe 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.

VTAV dissociation -

-variable systolic BP

-cannon A waves

-variable intensity of S1Unaffected by vagal maneuvers such as carotid sinus

pressure or valsalvaMay slow or block retrograde conduction.

Exposes AV dissociation

Rarely, VT terminates in response to carotid sinus pressure.

Laboratory testsThe 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

Chest x-rayEvidence 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

RegularityMarked irregularity of RR interval occurs in

atrial fibrillation (AF) with aberrant conduction and polymorphic VT

AxisA 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 durationIn 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) .

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.)

ConcordanceConcordance 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

Positive concordance Negative concordance

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 %)

AV dissociationAV 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 VTAV 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 BeatFusion 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%)

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

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

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-V2 in LBBB type QRSVTR >30 msec,QRS onset to S nadir>70 msec Notching and slurring of QRS complex –

myocardial disease(sensitivity-0.78,specificity 0.85)

V6 in LBBB type QRS qR Pattern

QS Pattern

Step 4: RBBB - type wide QRS complexSVT 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 qR wave

Monophasic R wave

Rsr’ pattern (Marriot’s Sign) Initial ventricular activation is independent of RBB.RBBB abberation affects only the latter QRS

VT SVT

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-0.79

Josephson’s sign Notching near the nadir of the S-waveSuggest VT

Wellen’s Criteria   •   QRS width > 140 msec

  •   Left axis deviation

  •   AV dissociation

  •  Configurational characteristics of the QRS morphology

Ultrasimple Brugada criterionJoseph 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

VERECKEI ALGORITHM

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?

Sensitivity & Specificity For VT 88% and 53% by aVR algorithm

Sensitivity Specificity PPV NPV

Brugada 89% 73% 92% 67%

Vereckei 97% 75% 93% 87%

VT vs AVRTECG criteria

ManagementUntil proven otherwise, any WCT should be

managed as if it were VT, in keeping with the consideration of "First, do no harm"

Unstable PatientIf 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.

PatientPatient is in

ventricular tachycardia or uncertain rhythm.

TreatmentAmiodarone 150 mg

IV over 10 min; repeat as needed to

maximum dose of 2.2 g in 24 hours.

Prepare for elective synchronized cardioversion.

PatientSupraventricular

tachycardia with aberrancy

TreatmentAdenosine 6 mg

rapid IV push If no conversion,

give adenosine 12 mg rapid IV push; may repeat 12 mg dose once.

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 symptomatic impact, and protect the patient against sudden cardiac death

Features s/o VTAbsence of typical RBBB or LBBB morphologyExtreme 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 leadsBrugada’s sign –  The distance from the onset of the

QRS complex to the nadir of the S-wave is > 100msJosephson’s sign – Notching near the nadir of the S-

waveMarriot’s sign :RSr’ complexes with a taller left rabbit

ear: most specific finding in favour of VT.

THANK YOU…….