WIDE COMPLEX TACHYCARDIA Dr.PradeepSreekumar
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: supraventriculartachycardias with antegrade conduction over an accessory pathway into the ventricular myocardium.
SVT (20%) VT (80%) Stewart RB. Ann Intern Med 1986
Causes of wide QRS complex tachycardia • Supraventricular tachycardia - with prexsisting BBB - with BBB due to heart rate (aberrant conduction) - antidromic tachycardia in WPW syndrome • Ventricular 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 Linking: a dynamic electrophysiologic phenomenon in macroreentrycircuits,Michael h. lehmann et al, Circulation. 1985;71:254-265 Mechanism for perpetuation of functional anterograde bundle branch block due to repetitive transseptal retrograde concealed penetration by impulses propagating along the contralateral bundle.
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 .
Mahaimfibre mediated tachycardia • Antegrade conduction : Mahaim pathway • Retrograde conduction:AV node • LBBB morphology • Left axis deviation • Pre-excitation during sinus rhythm is uncommon
RBBB morphology wide QRS tachycardia • VT Structurally normal heart • LVOT VT • Fasicular VT Abnormal heart • LV myocardial VT • Bundle Branch Reentrant VT
SVT SVT with pre existing RBBB SVT with functional RBBB
LBBB morphology wide QRS tachycardia • VT Structurally normal heart • RVOT VT Abnormal heart • Right ventricular myocardial VT • ARVD
SVT Mahaimfibre 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
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 msecsuggests VT In a LBBB-like WCT, a QRS duration >160 msecsuggests 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 %)
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 wavefrontscharacterised 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