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…….