EP DIAGNOSTIC APPROACH OF

WIDE COMPLEX TACHYCARDIA

Dr Awadhesh Kumar Sharma

DM 2nd YR

INTRODUCTION Wide Complex Tachycardia(WCT) often presents a

diagnostic dilemma for the physician particularly in determining its site of origin, which can be either ventricular or supraventricular.

Correct diagnosis is important both for acute management and also subsequent management.

In one series, only 32% of clinicians correctly diagnosed ventricular tachycardia (VT) in patients who presented with WCT.

The surface ECG is the standard and most clinically used tool for identifying the underlying cause of wide complex tachycardia.

Ann Int Med. 1988;109; 905-912.

OBJECTIVES OF SEMINAR Definition of WCT Differential Diagnosis of wide complex

tachycardia ECG diagnosis of wide complex

tachycardia EP Approach of wide complex

tachycardia

DEFINITION Wide complex tachycardia (WCT) refers

to a cardiac rhythm of more than 100 beats per minute with a QRS duration of 120 ms or more on the surface electrocardiogram (ECG).

DIFFERENTIAL DIAGNOSIS OF WCT Regular wide complex tachycardia

includes three major categories 1-Ventricular tachycardia (VT)

2-Supraventricular tachycardia (SVT) with aberrancy

3-Preexcited tachycardia.Irregular WCT 1- Afib + pre-excitation, Afib + BBB,

Aflutter + BBB, MAT + BBB, polymorphic Vtach (torsades)

THE ECG DIAGNOSIS- POINTS TO BE SEEN

AV dissociation. Width of the QRS complex. QRS axis in the frontal plane. Configurational characteristics of the

QRS complex( morphological criteria). Value of the ECG during sinus rhythm. Vagal maneuvers

SANode

Ventricular Focus

ATRIA AND VENTRICLESACT INDEPENDENTLY

AV Dissociation

SVT VS VT- AV DISSOCIATION Presence off this largely establishes the

diagnosis of VT but its absence is not helpful

May sometimes not be evident on ECG Some cases of VT, the ventricular

impulses conduct retrograde through the AV node and capture the atrium, preventing dissociation

THE BRUGADA ALGORITHM

THE DIAGNOSIS OF WCT STARTS FROM OUTSIDE THE EP LABORATORY

Many diagnostic clues have been proposed to differentiate between SVT with abberation & VT starting with-------

History Physical examination ECG analysis EPS

EP DIAGNOSIS OF WCT

ROLE OF ELECTROPHYSIOLOGICAL STUDY IN DIAGNOSIS OF PATIENTS WITH WIDE QRS COMPLEX TACHYCARDIAS

Class I Patients with wide QRS complex

tachycardia in whom correct diagnosis is unclear after analysis of available ECG tracings and for whom knowledge of the correct diagnosis is necessary for patient care

Class II None

ACC/AHA Guidelines for Clinical Intracardiac Electrophysiological and Catheter Ablation Procedures 1995

Class III Patients with VT or supraventricular

tachycardia with aberrant conduction or preexcitation syndromes diagnosed with certainty by ECG criteria and for whom invasive electrophysiological data would not influence therapy.

However, data obtained at baseline electrohysiological study in these patients might be appropriate as a guide for subsequent therapy.

NOMENCLATURE & MEASUREMENT OF BASELINE COND. INTERVALS

Cycle length = 60.000/ HR length of time bet. Heart beats

V

A

V

SCLP

BASELINE COND. INTERVALS SCL= interval bet. 2 successive A

waves AH interval ( 50—120 msec) AVN HV interval (35 – 55 msec) His-

purk His deflection (cond. Via His

bundle)

DIAGNOSTIC MANEUVERS IN EP LAB1-VA /AV Dissociation2-Measurement of HV during tachycardia3-Measurement of His-atrial (HA) during

tachycardia and during RV pacing 4-Introduction of premature atrial extra stimuli

during tachycardia5-Atrial overdrive pacing6-Response to Adenosine

Josephson M,clinical cardiac electrophysiology,2002,322-424

ELECTROPHYSIOLOGIC EVALUATION OF WCT

Relationship between atrial and ventricular activity-

Placing a catheter within the atrium provides unequivocal evidence for the timing of atrial activity.

If atrial activity is independent of or intermittently associated with ventricular activity, atrioventricular dissociation is present and ventricular tachycardia overwhelmingly becomes the most likely diagnosis.

There are two very rare conditions in which true AV dissociation can be observed in the setting of wide complex tachycardia other than VT.

The first is a tachycardia arising from the AV node region associated with both retrograde block and bundle branch block aberrancy.

The second is a reentrant circuit using a nodo ventricular accessory pathway.

The best way to rule these unusual arrhythmias out is to identify the presence of dissociation between ventricular signals and His bundle signals.

The situation is much more difficult in the setting of a 1 : 1 ventricular and atrial relationship.

There are several strategies that can be tried, but the most commonly used approach is to use adenosine to produce retrograde block within the AV node and evaluate whether the wide complex tachycardia terminates.

Continuation of wide complex tachycardia in the presence of transient ventriculo atrial block establishes the likely diagnosis of ventricular tachycardia

ATRIAL ACTIVATION SEQUENCE Delievering an atrial premature stimulus

during tachycardia-can preexcite the ventricle in VT OR AVRT although a change in QRS morphology expected in VT

Right atrial pacing– minimal or no preexcitation in case of left sided accessory pathway

Coronary sinus pacing—preexcitation increased in case of left accessory pathway

His –synchronous atrial extrastimulus cannot preexcite the ventricle if the mechanism of tachycardia is AVNRT with aberrancy but could preexcite the ventricle during SVT with a bystander AP changing the QRS morphology.

The sequence of His and Right bundle branch(RBB)activation during tachycardia

RBB activation preceds H activation- favours VT or antidromic AVRT

AV dissociation- rules out antidromic AVRT

H-A INTERVAL Comparing H-A during tachycardia to H-

A during RV pacing- AVRT,VT-same H-A during both

phase AVNRT with aberration – HA tachy <

HA RV pacing

ATRIAL OVERDRIVE PACING Atrial overdrive pacing- development of

constant QRS fusion seen in- 1-VT in the presence of

bystander AP 2- AVRT with multiple AP 3- BBRTNot in----- 1-Antidromic AVRT without

another AP 2- Aberrant SVT

JT BBRT VT(MYOCARDIAL)

HB act Antegrade Retrograde Retrograde

BB act Preceeding V Before & after

Obscured (after V)

H-H/V-V H-H preceeds V-V

H-H preceeds V-V

V-V preceeds H-H

Fahmy T,Hammouda M, Mokhtar M,2001

Fahmy T,Hammouda M, Mokhtar M,2001

THANKS

The method for induction and termination of ventricular tachycardia provides clues for the mechanism of tachycardia.

Most patients with structural heart disease due to myocardial infarction develop ventricular tachycardia caused by reentrant circuits that use protected channels of viable tissue within scar. Premature beats will block in one portion of the channel, propagate slowly in another channel, and set up a reentrant circuit.

The ability to induce a ventricular arrhythmia with premature ventricular beats strongly suggests reentry as a mechanism.

In contrast, automatic ventricular tachycardias often require infusion with a beta-agonist (isoproterenol is usually used in the electrophysiology laboratory) and are related to high ventricular rate either by atrial pacing or by ventricular pacing.

ANATOMY AND ELECTROPHYSIOLOGY IN AP

The electrophysiologic properties of accessory pathways can vary significantly

Most commonly accessory pathways are composed of tissue histologically and electrophysiologically like atrial or ventricular tissue, with a rapid phase 0 upstroke and a plateau phase.

Accessory pathways can usually conduct in both directions, from atrium to ventricle and from ventricle to atrium.

However, some accessory pathways can only conduct in one direction,usually from ventricle to atrium.

These accessory pathways are often called “concealed,” because their presence is not observed during sinus rhythm (no atrioventricular activation) but they can participate in supraventricular tachycardia because of robust ventricle-to-atrium depolarization.

Some accessory pathways conduct very slowly, more like AV node tissue.

Three types of arrhythmias can develop in the presence of an accessory pathway .

The most common type of tachycardia is orthodromic atrioventricular reentrant tachycardia (orthodromic AVRT), in which a reentrant circuit develops that activates the AV node in the normal fashion (ortho is Greek for regular), and, after activating ventricular tissue, the wave of depolarization travels retrogradely over the accessory pathway to depolarize the atria.

This arrhythmia is often described as reciprocating or “circus movement”

The ECG during orthodromic reciprocating tachycardia will display a regular narrow complex tachycardia, because the ventricles are activated normally via the AV node.

In some cases the presence of a retrograde P wave can be seen in the ST segment

Patients can also develop antidromic atrioventricular reentrant tachycardia (antidromic reciprocating tachycardia), in which the direction of the reentrant circuit is reversed and the ventricles are activated via the accessory pathway and the atria are activated by the AV node.

Antidromic reciprocating tachycardia is characterized by a regular wide complex tachycardia (since the ventricles are depolarized by the accessory pathway).

Sustained antidromic tachycardia is very rare.

Finally, patients can develop atrial fibrillation with rapid ventricular activation.

If atrial fibrillation develops in the presence of an accessory pathway, the ventricles can be depolarized very rapidly.

In fact the triad of an irregular, very fast, wide complex rhythm should always arouse suspicion for the presence of an accessory pathway and atrial fibrillation.

It is generally agreed by most investigators that sudden death occurs in patients with accessory pathways because of rapid ventricular activation from atrial fibrillation initiating ventricular fibrillation.

ELECTROPHYSIOLOGIC TESTING Baseline evaluation Electrophysiology studies can help

delineate the properties of accessory pathways and evaluate risk for sudden cardiac death and mechanisms of arrhythmia initiation.

At baseline, the HV interval will be very short and in some cases negative.

The PR interval is significantly shortened and that the beginning of the QRS actually precedes His bundle depolarization (H) for a negative HV interval.

ATRIAL PACING With progressively more rapid atrial

pacing, the delta wave will become more prominent as more of the ventricle is activated via the accessory pathway

With more rapid atrial pacing the observed response will depend on the relative refractory properties of the AV node and the accessory pathway.

If the refractory period in the accessory pathway is reached first, the QRS will suddenly normalize due to conduction down the AV node alone.

As the atrial pacing rate is increased, and the refractory period of the AV node is reached, eventually an atrial paced beat without a QRS complex will be seen.

Patients with accessory pathways who develop sudden cardiac death often have a shorter accessory pathway refractory period, since a shorter refractory period means that more rapid ventricular depolarization can occur.

Most experts suggest that risk of sudden cardiac death is increased in those patients with accessory pathway refractory periods of less than 270 ms.

VENTRICULAR PACING With ventricular pacing in a patient with

an accessory pathway, retrograde depolarization of the atria can occur via two routes: the AV node and the accessory pathway.

VENTRICULAR TACHYCARDIA Ventricular tachycardia in the setting of

no structural heart disease is almost always due to abnormal automaticity or triggered activity.

In contrast, in patients with structural heart disease reentry is the most common mechanism for ventricular tachycardia, due to the presence of “patchy scars” that increase the likelihood of “protected channels” forming the substrate for reentry.

Electrophysiology testing can provide clues to the mechanism for tachycardia.

Induction of ventricular tachycardia with premature ventricular extra stimuli suggests an underlying reentrant mechanism, although triggered activity can also be initiated this way.

Initiation of ventricular tachycardia due to automaticity is often rate-related and is usually performed by ventricular pacing or atrial pacing at a constant rate.

In addition, isoproterenol is often required to initiate the tachycardia.

PROGRAMMED STIMULATION FOR INITIATIONOF VENTRICULAR TACHYCARDIA

A stepwise stimulation protocol for initiation of sustained VT.

After ventricular pacing for 8 to 15 beats, a single extra stimulus is used to scan electrical diastole until it encounters refractoriness or reaches a very short coupling interval (<200 ms).

Second, third, and, in some cases, fourth stimuli are then added.

Two or more different basic pacing rates (drive cycles) typically are used (e.g., 100 and 150 beats/min) before premature stimulus delivery.

If pacing at the right ventricular apex fails to induce VT, pacing at a second right ventricular site (e.g., the right ventricular outflow tract) generally is used.

In general, pacing with up to three extrastimuli at two cycle lengths and two sites induces VT in approximately 90% of patients who have had this arrhythmia spontaneously after MI.

The addition of rapid burst pacing, left ventricular stimulation, and programmed stimulation during isoproterenol infusion further increases sensitivity.

As the number of extrastimuli increases, the risk of initiating nonspecific, polymorphic VT or VF increases.

Limiting the closest coupling interval to greater than 200 ms reduces the risk of initiating ventricular fibrillation

VT initiated by isoproterenol infusion or with rapid burst pacing during isoproterenol administration, but not in response to coupled extrastimuli, is believed to be more likely caused by abnormal automaticity rather than by re-entry.

CONFIRMING THE DIAGNOSIS In contrast to ECGs, in which atrial

activity may be difficult to detect, direct recordings from the atrium always allow clear delineation of whether AV dissociation is present.

When AV dissociation is present, the diagnosis is VT, with the rare exception of junctional ectopic tachycardia with ventriculoatrial (VA) block or rare forms of SVT without atrial tissue participation.

When AV dissociation is present and depolarization of the bundle of His does not precede each QRS complex, the diagnosis of VT is unequivocal.

POLYMORPHIC VENTRICULAR TACHYCARDIA Polymorphic VT indicates a continually

changing ventricular activation sequence.

Spontaneous polymorphic VT is most commonly caused by myocardial ischemia or TdP associated with Q-T interval prolongation.

Polymorphic VT also occurs in idiopathic VF, Brugada syndrome, and hypertrophic cardiomyopathy as well as other cardiomyopathies.

Sustained polymorphic VT (lasting >30 seconds or requiring termination) is initiated less commonly in normal hearts and usually requires aggressive stimulation (three or more extrastimuli and relatively short stimulus coupling intervals of <200 ms).

Initiation of polymorphic VT is of possible relevance in patients with suspected Brugada syndrome.

Polymorphic VT, often induced with two or fewer extrastimuli, is induced in approximately 80% of patients with Brugada syndrome who have been resuscitated from cardiac arrest

In patients with hypertrophic cardiomyopathy, sustained VT (usually polymorphic) is inducible in 66% of those who had a prior cardiac arrest compared with 23% of patients without a history of cardiac arrest or syncope

BUNDLE BRANCH RE-ENTRY VENTRICULAR TACHYCARDIA

A bundle of His deflection is consistently present before each QRS during an uncommon type of VT caused by re-entry through the bundle branches

The re-entry wave front circulates up the left bundle branch, down the right bundle branch, and then through the intra ventricular septum to re-enter the left bundle.

Ventricular depolarization proceeds from the right bundle, giving rise to a tachycardia with an LBBB configuration.

Rarely, the circuit revolves in the opposite direction (down the left bundle and back up the right bundle) or is confined to the fascicles of the left bundle branch system, giving rise to a tachycardia with an RBBB configuration.

The diagnosis is confirmed by showing that the atria can be dissociated but that the bundle of His depolarization is closely linked to the circuit.

Electrophysiologic study in ventricular tachycardia. (Re entry type from previous MI)

(a) A single extrastimulus (S2) after an 8 beat drive at 550ms cycle length (S1 S1) initiates sustained monomorphic ventricular tachycardia (VT) . Note the presence of atrioventricular dissociation and the absence of a His potential before the QRS. (b) A burst of rapid ventricular pacing (RVP) is used to restore normal sinus rhythm (NSR).

Electrophysiologic findings in bundle branch re entry. The tracings shown are surface ECG leads 1, aVF and V1, and intracardiac recordings from the high right atrium (HRA), the bundle of His (HBE) and the right ventricular apex (RVA). The surface leads show the typical pattern of left bundle branch block. The intracardiac recordings show atrioventricular dissociation and a His potential preceding each ventricular depolarization .