Basics of Electrophysiologic Study, (part4)

Dr. Salah Atta, MD

Cosultant Electrophysiologist, SBCC

Professor of Cardiology

Assiut University, Egypt

Role of EPS in the Diagnosis and Management of Arrhythmias

Mechanisms of Arrhythmia

Abnormal automaticity automatic impulse generation from unusual site

or overtakes sinus node

Triggered activity secondary depolarization during or after

repolarization Dig toxicity, Torsades de Pointes

Reentry 90 % of arrhythmias

Reentry

Most common mechanism

Requires two separate paths of conduction

Requires an area of slow conduction

Requires unidirectional block

EP diagnosis of narrow QRS EP diagnosis of narrow QRS tachycardiatachycardia

Differential Dx of Regular SVT

Short RP tachycardia AV nodal reentrant

tachycardia (AVNRT) ORT( Orthodromic

reciprocating tachycardia)= AVRT

atrial tachycardia when associated with slow AV nodal conduction

Short RP interval

Differential Dx of Regular SVT Long RP tachycardia

Atrial tachycardia Sinus node reentry Sinus tachycardia Atypical AV nodal

reentrant tachycardia Permanent form of

junctional reciprocating tachycardia (PJRT) = AVRT over a slow retrograde conducting AP.

Long RP interval

Forms of abnormal Sinus Tachycardia

Sinus node reentrant abrupt onset and offset P wave complex same as

sinus Amenable to calcium

channel blockers, much less responsive to beta blockers

Amenable to catheter ablation

Syndrome of inappropriate sinus tachycardia typical sinus tachycardia

with lowest rate on Holter of 130 bpm

Treated with high dose beta blockers

Poor results with catheter ablation

Regular SVT in adults

90% reentrant, 10 % non reentrant 60% AV nodal reentrant tachycardia (AVNRT) 30% orthodromic reciprocating tachycardia

(ORT) 10% Atrial tachycardia

Supraventricular TachycardiasDiagnosis

ECG is cornerstone Observe zones of transition for clues as to

mechanism: onset termination slowing, AV nodal block bundle branch block

Stepwise assessment of the induced tachycardia:Stepwise assessment of the induced tachycardia:

Once the tachycardia is induced, the following Once the tachycardia is induced, the following observations help establish the mechanism:observations help establish the mechanism:

• Mode of initiation and termination.Mode of initiation and termination.• A-V relationship: 1:1 or variable, V-A relation and A-V relationship: 1:1 or variable, V-A relation and

intervalinterval• Atrial activation sequence, AV relationship, Atrial activation sequence, AV relationship,

ventricular activation sequence during the ventricular activation sequence during the tachycardia.tachycardia.

• Cycle length , Effect of pacing maneuvers and Cycle length , Effect of pacing maneuvers and drugs on the tachycardiadrugs on the tachycardia

• Other specific tests related to each type.Other specific tests related to each type.

AV Nodal Reentrant Tachycardia

2 pathways within or limited to perinodal tissue anterograde conduction

down fast pathway blocks with conduction down slow pathway, with retrograde conduction up fast pathway.

May have very short RP interval with retrograde P wave visible as an R’ in lead V1 or psuedo-S wave in inferior leads in 1/3 of cases . No p wave seen in 2/3

Slow pathway

Fast pathway

AVNRT Mechanism

AV Nodal Reentrant Tachycardia

Responds to vagal maneuvers in 1/3 cases

Very responsive to AV nodal blocking agents such as beta blockers, CA channel blockers, adenosine.

Recurrences are the norm on medical therapy

Catheter ablation 95% successful with 1% major complication rate

EPS Diagnostic criteria of AVNRT:

1-The initiation of AVNRT is dependent on a critical delay in the AH interval (AH jump).

2- The occurence of atrial activation simultaneously with or before the ventricular activation

AVNRTAVNRT

EPS diagnosis of AVNRT

3- Retrograde VA during AVNRT is earliest on HBE with a VA interval ≤70 msec.

4- Inability of His synchronous ventricular extrastimuli to pre-excite the atria during AVNRT.

5- BBB block has no effect on the tachycardia cycle length.

WPW syndrome

ECG criteria: Accelerated AV conduction PR <120 msec Prolonged QRS > 120 msec Abnormal slurred upstroke of QRS ( delta wave) Abnormal depolarization and repolarization may

lead to pseudoinfarction pattern

WPW

WPW epidemiology Present in 0.3% of the

population Risk of sudden death 1 per

1000 patient-years Sudden death due to atrial

fibrillation with rapid ventricular conduction

Atrial fibrillation often induced from rapid ORT

ORT(orthodromic reciprocating tachycardia

WPW pathophysiology Short AV conduction

early excitation of ventricle at site of accessory pathway

Bizarre upstroke of QRS abnormal initial site of

depolarization

Wide QRS early initiation of

ventricular depolarization

The result is fusion of both normal and accessory conduction

No conductio

n

delay

AV node Accessory

pathway

EP criteria of Manifest pre-excitation:

Shows the following electrophysiologic criteria: In sinus rhythm, the AH interval is normal while the

HV interval is shorter than 35 msec. The anterograde curve is non decremental showing a

fixed AV interval, with closer atrial extrastimuli with increasing pre-excitation, till the ERP of the AP is reached and the AP conduction is blocked. At this coupling interval the QRS complex normalizes as the impulse is blocked in the AP and is conducted exclusively over the AV node.

the eccentericc ventricular activation sequence

EPS of WPW

Antegrade ERP of the AP

Safe AP

Concealed pre-excitation (unidirectional retrograde conduction over the AP):

Has the same electrophysiologic properties of manifest APs in the retrograde direction. Anterogradely, conduction is decremental as the impulses proceed over the AV node.

Orthodromic Reciprocating Tachycardia

Anterograde over AV node and retrograde conduction of an accessory pathway.

RP interval short but longer than AVNRT due to required conduction through ventricle prior to conduction up accessory pathway

Frequently presents in patients with WPW patients as narrow complex tachycardia

Up accessory

pathway

Conduction down AVnode

ORT Amenable to AV nodal

blocking agents in absence of WPW syndrome (anterograde conduction of pathway)

Amenable to catheter ablation with 95% success and 1% rate major complication

Conduction down AVnode

Up accessory

pathway

AVRT is induced and terminated by VPD, APDs or pacing.

The retrograde atrial activation sequence during AVRT is eccentric and fixed independent of the SVT cycle length.

During ventricular pacing with extrastimulation, the retrograde curve is also non decremental. The retrograde atrial activation sequence simulates that during orthodromic AVRT.

ParaHisian pacing: constant V-A interval.

EPS of AVRT

Both the atrium and the ventricle are necessary for initiation and continuation of AVRT. AV or VA block would interrupt the AVRT.

His synchronous VPDs, during AVRT, either terminates the tachycardia or conducts up the AP pre-exciting (advancing) the atria.

In case of free wall AP: Epsilateral BBB produces prolongation of the SVT Cycle length and the VA by 35 msec or more.

EPS of AVRT

His synchronized ventricular ES

EP criteria of AVRT

The shortest VA interval during AVRT is generally greater than 60 milliseconds and QRS to HRA interval of at least 95 milliseconds.

In the presence of septal AP the VA interval during RV pacing tends to be similar to the VA interval during AVRT.

In AVNRT, VA during RV pacing tends to be longer than during tachycardia. In AVNRT there is simult-aneous antegrade and retrograde conduction from the AVN, resulting in a short VA interval.

Orthodromic AVRTOrthodromic AVRT

Atrial Fibrillation and WPW

AV nodal blocking agents may paradoxically increase conduction over accessory pathway by removing concealed retrograde penetration into accessory pathway.

Concealed penetration into the pathway causes intermittent block of pathway

conduction

Management of Atrial Fibrillation with WPW

Avoid AV nodal blockers IV procainamide to slow accessory pathway

conduction Amiodarone if decreased LVEF DC cardioversion if symptomatic with

hypotension

Management of Patients with WPW

All patients with symptomatic AF & WPW should be evaluated with EPS

Accessory pathways capable of conducting faster than 240 BPM should be ablated (ERP<250ms)

Patients with inducible arrhythmias involving pathway should be ablated

WPW patients in high risk professions should be evaluated.

Differentiation by pacing during the SVT

What is entrainment?

It is widely taught that a His-refractory ventricular premature beat (VPB) can advance atrial timing during AVRT. The VPB depolarizes the ventricles earlier than the tachycardia wavefront would have, and this in turn advances atrial activation so that the AVRT circuit is reset. If this rather basic electrophysiologic concept is well understood, then entrainment, which is nothing more than thecontinual resetting of such a circuit by a series of consecutive VPB's (ie. a pacing train slightly faster than the tachycardia), should be easily understood also.

Tachycardia reappearnce after pacing cessation with same sequence, morphology and cycle length is a mandatory condition for the definition of entrainment.

Concealed entrainment (QRS complex is that of a paced beat) is different

from entrainment with concealed fusion (QRS complex is that of the native tachycardia). This

subtle distinction in nomenclature is commonly overlooked .

During orthodromic AVRT, the overdrive ventricular pacing site most likely

to result in entrainment with fusion is at the base, near the insertion of the AP. Thus,

entrainment with concealed fusion indicates that the pacing site is close to the ventricular insertion of the AP and can be used to map the AP.

On reappearance of the tachycardia after stopping pacing, certain criteria can be checked for diagnosis of the re-entry circuit and nature of the SVT.....

Differentiation by pacing during the SVT

A cPPI-TCL (post pacing interval – tachycardia cycle length) > 110 ms is consistent with AVNRT,

while a cPPI-TCL < 110 ms is consistent with AVRT employing a non-left sided AP.

A cPPI-TCL > 110 ms can occur with AVRT employing a left sided AP simply because the RVA pacing site is far from such a circuit. During a long RP interval SVT, a cPPI-TCL > 110 ms should also prompt conside-ration of orthodromic AVRT employing a slowly conducting AP with decremental conduction properties.*

Differentiation by pacing during the SVT

*In these challenging situations, fusion during entrainment by ventricular pacing and delay of atrial timing by a His refractory VPB should be considered proof of the involvement of an AP regardless of the PPI-TCL value.

SA-VA(Stimulus to Atrium – Ventricle to A) differences < 85 ms are consistent with AVRT, while SA-VA differences > 85 ms are consistent with AVNRT.

the cPPI-TCL and SA-VA differences may be unreliable during SVTs with marked spontaneous beat-to-beat variation in TCL (>40 ms).

Differentiation by pacing during the SVT

Differentiation by pacing during the SVT

Differentiation by pacing during the SVT

A proposed algorithm to arrive at a diagnosis for regular sustained SVT based on the results of overdriveventricular pacing. Non-diagnostic responses may contain partial diagnostic information and include (i) terminationwith conduction to the atria, (ii) termination of SVT with septal VA ≥ 70 ms by a VPB prior to His bundlerefractoriness that does not conduct to the atrium (excludes AT), and (iii) dissociation of the ventricles from thetachycardia (excludes AVRT). A=atrium; V=ventricle; AT=atrial tachycardia; AVNRT=atrioventricular nodereentry tachycardia; AVRT=atrioventricular reciprocating tachycardia; S=stimulus; PPI=post pacing interval;TCL=tachycardia cycle length; HRVPB=His refractory ventricular premature beat.

Atrial Flutter

An atrial flutter (Macrore-entry in the right atrium with atrial rate: 300/min) with two to one conduction to the ventricles with LBBB aberration was evident.

Atrial Tachycardia

Most are due to abnormal automaticity and have right atrial focus

May be reentry particularly in patients with previous atriotomy scar, such as CABG or congenital repair patients

Atrial Tachycardia

Atrial rate between 150 and 250 bpm Does not require AV nodal or infranodal

conduction as the origin is atrial. P wave morphology different than sinus P-R interval > 120 msec differentiating from

junctional tachycardia Origin inferred from P wave morphology.

Atrial tachycardia

P wave upright lead V1 and negative in aVL consistent with left atrial focus.

P wave negative in V1 and upright in aVL consistent with right atrial focus.

Adenosine may help with diagnosis if AV block occurs and continued arrhythmia likely atrial tachycardia

70-80% will also terminate with adenosine.

Atrial Tachycardia Therapy

Frequently treated with antiarrhythmics Class 1 agents procainamide, quinidine, flecainide

may be used in patients without structural heart disease.

Class III agents sotalol, amiodarone, dofetilide may be used with caution according to specific side effects

AV Nodal blocking agents for rate control. Catheter ablation effective in 70-80%

EP Diagnosis of Wide-Complex Tachycardia

(WCT)

Basic EPS

Definition:Tachycardia with a QRS duration > 120 msec, which is related to an asynchronous, or sequential activation of the ventricular

myocardium.

Wide Complex Tachycardia (WCT(

It comprises a broad range of cardiac rhythm abnormalities:

•Supraventricular tachycardia (SVT), with

permanent or functional BBB.•Pre-excited tachycardia including:

•Antidromic tachycardia

• SVT with a by stander accessory pathway•Ventricular tachycardia.

WCT

Causes of WCT

WCT

Causes of WCT in structually normal heart patients (Eckardt et al., Heart 2006;92;704-711(

WCT

Causes of WCT in structually normal heart patients (Eckardt et al., Heart 2006;92;704-711(

WCT

Many diagnostic clues have been proposed to

differentiate between SVT with aberration, and VT,

starting with

•History,

•Physical examination,

•ECG analysis and

•EPS: being the most definitive way for diagnosis.

The diagnosis of WCT starts from outside the EP laboratory:

Intracardiac Electrocardiography (EPS) of WCT

Basic EPS

--Identifies whether broad-complex Identifies whether broad-complex tachycardias are ventricular or tachycardias are ventricular or supraventricular in origin: supraventricular in origin:

which is the leading the atrium or the which is the leading the atrium or the ventricle ?!ventricle ?!

During the Culprit During the Culprit arrhythmiaarrhythmia?!

Basic EPS

Fahmy T, Hammouda M, Mokhtar M, 2001

Basic EPS

Fahmy T, Hammouda M, Mokhtar M, 2001

Thank you