Wide Complex Tachycardia(WCT) often presents adiagnostic dilemma for the physician particularly indetermining its site of origin, which can be eitherventricular or supraventricular. Correct diagnosis is important both for acute managementand also subsequent management. In one series, only 32% of clinicians correctly diagnosedventricular tachycardia (VT) in patients who presentedwith WCT. The surface ECG is the standard and most clinically usedtool for identifying the underlying cause of wide complextachycardia.Ann Int Med. 1988;109; 905-912.
Definition of WCT Differential Diagnosis of wide complextachycardia ECG diagnosis of wide complex tachycardia EP Approach of wide complex tachycardia
Wide complex tachycardia (WCT) refers to acardiac rhythm of more than 100 beats perminute with a QRS duration of 120 ms ormore on the surface electrocardiogram(ECG).
Regular wide complex tachycardiaincludes three major categories1-Ventricular tachycardia (VT)2-Supraventricular tachycardia (SVT) withaberrancy3-Preexcited tachycardia.Irregular WCT1- Afib + pre-excitation, Afib + BBB,Aflutter + BBB, MAT + BBB, polymorphicVtach (torsades)
AV dissociation. Width of the QRS complex. QRS axis in the frontal plane. Configurational characteristics of the QRScomplex( morphological criteria). Value of the ECG during sinus rhythm. Vagal maneuvers
SANodeVentricularFocusATRIA AND VENTRICLESACT INDEPENDENTLYAVDissociation
Presence off this largely establishes thediagnosis of VT but its absence is not helpful May sometimes not be evident on ECG Some cases of VT, the ventricular impulsesconduct retrograde through the AV node andcapture the atrium, preventing dissociation
Many diagnostic clues have been proposed todifferentiate between SVT with abberation &VT starting with-------HistoryPhysical examinationECG analysisEPS
Class IPatients with wide QRS complex tachycardiain whom correct diagnosis is unclear afteranalysis of available ECG tracings and forwhom knowledge of the correct diagnosis isnecessary for patient care Class IINoneACC/AHA Guidelines for Clinical IntracardiacElectrophysiological and Catheter AblationProcedures 1995
Class IIIPatients with VT or supraventricular tachycardiawith aberrant conduction or preexcitationsyndromes diagnosed with certainty by ECGcriteria and for whom invasiveelectrophysiological data would not influencetherapy.However, data obtained at baselineelectrohysiological study in these patients mightbe appropriate as a guide for subsequenttherapy.
Cycle length = 60.000/ HR length of time bet. Heart beatsVAVSCLP
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)
1-VA /AV Dissociation2-Measurement of HV during tachycardia3-Measurement of His-atrial (HA) duringtachycardia and during RV pacing4-Introduction of premature atrial extra stimuliduring tachycardia5-Atrial overdrive pacing6-Response to AdenosineJosephson M,clinical cardiac electrophysiology,2002,322-424
Relationship between atrial and ventricularactivity- Placing a catheter within the atrium providesunequivocal evidence for the timing of atrialactivity. If atrial activity is independent of orintermittently associated with ventricularactivity, atrioventricular dissociation is presentand ventricular tachycardia overwhelminglybecomes the most likely diagnosis.
There are two very rare conditions in which true AVdissociation can be observed in the setting of widecomplex tachycardia other than VT. The first is a tachycardia arising from the AV node regionassociated with both retrograde block and bundle branchblock aberrancy. The second is a reentrant circuit using a nodo ventricularaccessory pathway. The best way to rule these unusual arrhythmias out is toidentify the presence of dissociation between ventricularsignals 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 themost commonly used approach is to use adenosine toproduce retrograde block within the AV node and evaluatewhether the wide complex tachycardia terminates. Continuation of wide complex tachycardia in the presenceof transient ventriculo atrial block establishes the likelydiagnosis of ventricular tachycardia
Delievering an atrial premature stimulusduring tachycardia-can preexcite theventricle in VT OR AVRT although a change inQRS morphology expected in VT Right atrial pacing– minimal or nopreexcitation in case of left sided accessorypathway Coronary sinus pacing—preexcitationincreased in case of left accessory pathway
His –synchronous atrial extrastimulus cannotpreexcite the ventricle if the mechanism oftachycardia is AVNRT with aberrancy butcould preexcite the ventricle during SVT witha bystander AP changing the QRS morphology.
The sequence of His and Right bundlebranch(RBB)activation during tachycardia RBB activation preceds H activation- favoursVT or antidromic AVRT AV dissociation- rules out antidromic AVRT
Comparing H-A during tachycardia to H-Aduring RV pacing-AVRT,VT-same H-A during both phaseAVNRT with aberration – HA tachy < HARV pacing
Atrial overdrive pacing- development ofconstant QRS fusion seen in-1-VT in the presence ofbystander AP2- AVRT with multiple AP3- BBRTNot in-----1-Antidromic AVRT withoutanother AP2- Aberrant SVT
JT BBRT VT(MYOCARDIAL)HB act Antegrade Retrograde RetrogradeBB act Preceeding V Before &afterObscured (after V)H-H/V-V H-H preceedsV-VH-Hpreceeds V-VV-V preceeds H-H
The method for induction and termination ofventricular tachycardia provides clues for themechanism of tachycardia. Most patients with structural heart disease dueto myocardial infarction develop ventriculartachycardia caused by reentrant circuits that useprotected channels of viable tissue within scar.Premature beats will block in one portion of thechannel, propagate slowly in another channel,and set up a reentrant circuit.
The ability to induce a ventricular arrhythmiawith premature ventricular beats stronglysuggests reentry as a mechanism. In contrast, automatic ventricular tachycardiasoften require infusion with a beta-agonist(isoproterenol is usually used in theelectrophysiology laboratory) and are related tohigh ventricular rate either by atrial pacing or byventricular pacing.
The electrophysiologic properties of accessorypathways can vary significantly Most commonly accessory pathways arecomposed of tissue histologically andelectrophysiologically like atrial or ventriculartissue, with a rapid phase 0 upstroke and aplateau phase. Accessory pathways can usually conduct in bothdirections, from atrium to ventricle and fromventricle to atrium. However, some accessory pathways can onlyconduct in one direction,usually from ventricleto atrium.
These accessory pathways are often called―concealed,‖ because their presence is notobserved during sinus rhythm (noatrioventricular activation) but they canparticipate in supraventricular tachycardiabecause of robust ventricle-to-atriumdepolarization. Some accessory pathways conduct veryslowly, more like AV node tissue.
Three types of arrhythmias can develop inthe presence of an accessory pathway . The most common type of tachycardia isorthodromic atrioventricular reentranttachycardia (orthodromic AVRT), in which areentrant circuit develops that activates theAV node in the normal fashion (ortho isGreek for regular), and, after activatingventricular tissue, the wave of depolarizationtravels retrogradely over the accessorypathway to depolarize the atria.
This arrhythmia is often described asreciprocating or ―circus movement‖ The ECG during orthodromic reciprocatingtachycardia will display a regular narrowcomplex tachycardia, because the ventriclesare activated normally via the AV node. In some cases the presence of a retrograde Pwave can be seen in the ST segment
Patients can also develop antidromicatrioventricular reentrant tachycardia(antidromic reciprocating tachycardia), in whichthe direction of the reentrant circuit is reversedand the ventricles are activated via theaccessory pathway and the atria are activated bythe AV node. Antidromic reciprocating tachycardia ischaracterized by a regular wide complextachycardia (since the ventricles are depolarizedby the accessory pathway). Sustained antidromic tachycardia is very rare.
Finally, patients can develop atrialfibrillation with rapid ventricular activation. If atrial fibrillation develops in the presenceof an accessory pathway, the ventricles canbe depolarized very rapidly. In fact the triad of an irregular, very fast,wide complex rhythm should always arousesuspicion for the presence of an accessorypathway and atrial fibrillation.
It is generally agreed by most investigatorsthat sudden death occurs in patients withaccessory pathways because of rapidventricular activation from atrial fibrillationinitiating ventricular fibrillation.
Baseline evaluation Electrophysiology studies can help delineatethe properties of accessory pathways andevaluate risk for sudden cardiac death andmechanisms of arrhythmia initiation. At baseline, the HV interval will be veryshort and in some cases negative. The PR interval is significantly shortened andthat the beginning of the QRS actuallyprecedes His bundle depolarization (H) for anegative HV interval.
With progressively more rapid atrialpacing, the delta wave will become moreprominent as more of the ventricle isactivated via the accessory pathway With more rapid atrial pacing the observedresponse will depend on the relativerefractory properties of the AV node and theaccessory pathway. If the refractory period in the accessorypathway is reached first, the QRS willsuddenly normalize due to conduction downthe AV node alone.
As the atrial pacing rate is increased, and therefractory period of the AV node isreached, eventually an atrial paced beat withouta QRS complex will be seen. Patients with accessory pathways who developsudden cardiac death often have a shorteraccessory pathway refractory period, since ashorter refractory period means that more rapidventricular depolarization can occur. Most experts suggest that risk of sudden cardiacdeath is increased in those patients withaccessory pathway refractory periods of lessthan 270 ms.
With ventricular pacing in a patient with anaccessory pathway, retrograde depolarizationof the atria can occur via two routes: the AVnode and the accessory pathway.
Ventricular tachycardia in the setting of nostructural heart disease is almost always dueto abnormal automaticity or triggeredactivity. In contrast, in patients with structural heartdisease reentry is the most commonmechanism for ventricular tachycardia, dueto the presence of ―patchy scars‖ thatincrease the likelihood of ―protectedchannels‖ forming the substrate for reentry.
Electrophysiology testing can provide clues tothe mechanism for tachycardia. Induction of ventricular tachycardia withpremature ventricular extra stimuli suggests anunderlying reentrant mechanism, althoughtriggered activity can also be initiated this way. Initiation of ventricular tachycardia due toautomaticity is often rate-related and is usuallyperformed by ventricular pacing or atrial pacingat a constant rate. In addition, isoproterenol is often required toinitiate the tachycardia.
A stepwise stimulation protocol for initiation ofsustained VT. After ventricular pacing for 8 to 15 beats, asingle extra stimulus is used to scan electricaldiastole until it encounters refractoriness orreaches a very short coupling interval (<200 ms). Second, third, and, in some cases, fourth stimuliare then added. Two or more different basic pacing rates (drivecycles) typically are used (e.g., 100 and 150beats/min) before premature stimulus delivery.
If pacing at the right ventricular apex fails toinduce VT, pacing at a second right ventricularsite (e.g., the right ventricular outflow tract)generally is used. In general, pacing with up to three extrastimuliat two cycle lengths and two sites induces VT inapproximately 90% of patients who have had thisarrhythmia spontaneously after MI. The addition of rapid burst pacing, leftventricular stimulation, and programmedstimulation during isoproterenol infusion furtherincreases sensitivity.
As the number of extrastimuli increases, therisk of initiating nonspecific, polymorphic VTor VF increases. Limiting the closest coupling interval togreater than 200 ms reduces the risk ofinitiating ventricular fibrillation VT initiated by isoproterenol infusion or withrapid burst pacing during isoproterenoladministration, but not in response tocoupled extrastimuli, is believed to be morelikely caused by abnormal automaticityrather than by re-entry.
In contrast to ECGs, in which atrial activitymay be difficult to detect, direct recordingsfrom the atrium always allow cleardelineation of whether AV dissociation ispresent. When AV dissociation is present, thediagnosis is VT, with the rare exception ofjunctional ectopic tachycardia withventriculoatrial (VA) block or rare forms ofSVT without atrial tissue participation.
When AV dissociation is present anddepolarization of the bundle of His does notprecede each QRS complex, the diagnosis ofVT is unequivocal.
Polymorphic VT indicates a continuallychanging ventricular activation sequence. Spontaneous polymorphic VT is mostcommonly caused by myocardial ischemia orTdP associated with Q-T intervalprolongation. Polymorphic VT also occurs in idiopathicVF, Brugada syndrome, and hypertrophiccardiomyopathy as well as othercardiomyopathies.
Sustained polymorphic VT (lasting >30 seconds orrequiring termination) is initiated less commonlyin normal hearts and usually requires aggressivestimulation (three or more extrastimuli andrelatively short stimulus coupling intervals of<200 ms). Initiation of polymorphic VT is of possiblerelevance in patients with suspected Brugadasyndrome. Polymorphic VT, often induced with two or fewerextrastimuli, is induced in approximately 80% ofpatients with Brugada syndrome who have beenresuscitated from cardiac arrest
In patients with hypertrophiccardiomyopathy, sustained VT (usuallypolymorphic) is inducible in 66% of those whohad a prior cardiac arrest compared with 23%of patients without a history of cardiac arrestor syncope
A bundle of His deflection is consistently presentbefore each QRS during an uncommon type of VTcaused by re-entry through the bundle branches The re-entry wave front circulates up the leftbundle branch, down the right bundlebranch, and then through the intra ventricularseptum to re-enter the left bundle. Ventricular depolarization proceeds from theright bundle, giving rise to a tachycardia with anLBBB configuration.
Rarely, the circuit revolves in the oppositedirection (down the left bundle and back upthe right bundle) or is confined to thefascicles of the left bundle branchsystem, giving rise to a tachycardia with anRBBB configuration. The diagnosis is confirmed by showing thatthe atria can be dissociated but that thebundle of His depolarization is closely linkedto the circuit.
Electrophysiologic study inventricular tachycardia. (Reentry type from previous MI) (a) A single extrastimulus (S2)after an 8 beat drive at550ms cycle length (S1 S1)initiates sustainedmonomorphic ventriculartachycardia (VT) . Note thepresence of atrioventriculardissociation and the absenceof a His potential before theQRS. (b) A burst of rapidventricular pacing (RVP) isused to restore normal sinusrhythm (NSR).
Electrophysiologic findings inbundle branch re entry. Thetracings shown are surfaceECG leads 1, aVF and V1, andintracardiac recordings fromthe high right atrium (HRA),the bundle of His (HBE) andthe right ventricular apex(RVA). The surface leadsshow the typical pattern ofleft bundle branch block. Theintracardiac recordings showatrioventricular dissociationand a His potential precedingeach ventriculardepolarization .