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ApproachtothediagnosisofwideQRScomplextachycardias
Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreviewprocessiscomplete.
Literaturereviewcurrentthrough:Mar2016.|Thistopiclastupdated:Oct22,2015.
INTRODUCTIONTachycardiasarebroadlycategorizedbaseduponthewidthoftheQRScomplexontheelectrocardiogram(ECG).
AnarrowQRScomplex(<120msec)reflectsrapidactivationoftheventriclesviathenormalHisPurkinjesystem,whichinturnsuggeststhatthearrhythmia
originatesaboveorwithintheatrioventricular(AV)node(ie,asupraventriculartachycardia[SVT]).
AwidenedQRS(120msec)occurswhenventricularactivationisabnormallyslowforoneofthefollowingreasons(see'CausesofWCT'below):
Thearrhythmiaoriginatesoutsideofthenormalconductionsystem(ie,ventriculartachycardia[VT])
AbnormalitieswithintheHisPurkinjesystem(ie,SVTwithaberrancy)
PreexcitationwithaSVTconductingantegradeoveranaccessorypathway,resultingindirectactivationoftheventricularmyocardium
Awidecomplextachycardia(WCT)representsauniqueclinicalchallengefortworeasons:
DiagnosingthearrhythmiaisdifficultAlthoughmostWCTsareduetoventriculartachycardia(VT),thedifferentialdiagnosisincludesavarietyofSVTs.
Diagnosticalgorithmstodifferentiatethesetwoetiologiesarecomplexandimperfect.
UrgenttherapyisoftenrequiredPatientsmaybeunstableattheonsetofthearrhythmiaordeterioraterapidlyatanytime,particularlyiftheWCTisVT[14].
Theclinicalmanifestations,diagnosis,andinitialevaluationofpatientswithawideQRScomplextachycardiawillbediscussedhere.Themanagementofwide
QRScomplextachycardias,aswellasdiscussionofnarrowQRScomplextachycardias,ispresentedseparately.(See"ApproachtothemanagementofwideQRS
complextachycardias"and"Overviewoftheacutemanagementoftachyarrhythmias"and"Secondarypreventionofsuddencardiacdeathinheartfailureand
cardiomyopathy"and"Clinicalmanifestations,diagnosis,andevaluationofnarrowQRScomplextachycardias".)
INITIALAPPROACHThefirstprioritywhenevaluatingapatientwithawidecomplextachycardia(WCT)isanassessmentofpatientstability.Unstablepatients
shouldbetreatedimmediately,beforeanextensivediagnosticevaluation.(See'Assessmentofstability'belowand"ApproachtothemanagementofwideQRS
complextachycardias",sectionon'Unstablepatients'.)
Stablepatientswillmostoftenhavealreadyhadanelectrocardiogram(ECG)showingthepresenceofaWCT.Inastablepatient,theECGshouldbethoroughly
andsystematicallyreviewedinanefforttodeterminetheetiologyoftheWCT.(See'Evaluationoftheelectrocardiogram'below.)
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Inastablepatient,afocusedclinicalevaluationshouldincludethefollowing:
History
Physicalexamination
Laboratorytesting
Diagnosticmaneuversinselectedpatients
TheprimarygoalsoftheinitialevaluationofastablepatientwithWCTaretodeterminetheetiologyoftheWCT(throughevaluationoftheECG)andtoelucidate
anyunderlyingconditionsrelatedtotheevent(eg,heartfailure,myocardialischemia,drugreaction,orelectrolyteabnormalities).(See'Evaluationofthe
electrocardiogram'below.)
AssessmentofstabilityImmediateassessmentsofthepatient'ssymptoms,vitalsigns,andthelevelofconsciousnessareofprimaryimportance[5].Inthe
discussionsthatfollow,patientsarecategorizedasfollows:
UnstableAnunstablepatientwithWCTwillhaveevidenceofhemodynamiccompromise,suchashypotension,alteredmentalstatus,chestpain,orheart
failure,butgenerallyremainsawakewithadiscerniblepulse.Inthissetting,emergencysynchronizedcardioversionisthetreatmentofchoiceregardlessof
themechanismofthearrhythmia.(See"ApproachtothemanagementofwideQRScomplextachycardias",sectionon'Unstablepatients'.)
Patientswhobecomeunresponsiveorpulselessareconsideredtohaveacardiacarrestandaretreatedaccordingtostandardresuscitationalgorithms.(See
"Advancedcardiaclifesupport(ACLS)inadults"and"Basiclifesupport(BLS)inadults".)
StableAstablepatientwithWCTshowsnoevidenceofhemodynamiccompromisedespiteasustainedrapidheartrate.Suchpatientsshouldhave
continuousmonitoringandfrequentreevaluationsduetothepotentialforrapiddeteriorationaslongastheWCTpersists.
Thepresenceofhemodynamicstabilityshouldnotberegardedasdiagnosticofsupraventriculartachycardia(SVT)[4,6].Misdiagnosisofventricular
tachycardia(VT)asSVTbaseduponhemodynamicstabilityisacommonerrorthatcanleadtoinappropriateandpotentiallydangeroustherapy[3,4].(See
"ApproachtothemanagementofwideQRScomplextachycardias",sectionon'Pharmacologicinterventions'.)
HistoryWhenevaluatingthestablepatientwithaWCT,thefollowinghistoricalfeaturesmayhelpdeterminethelikelyetiologyand/orguidetherapy:
HistoryofheartdiseaseThepresenceofstructuralheartdisease,especiallycoronaryheartdiseaseand/orapreviousmyocardialinfarction,strongly
suggestsVTasanetiology[4,7].Itisalsoimportanttoestablishwhetheracardiacarrhythmiahasoccurredinthepastand,ifso,whetherthepatientisaware
oftheetiology.(See'Epidemiology'below.)
Presenceofanimplantablecardioverterdefibrillator(ICD)ThepresenceofanICDimpliesaknownincreasedriskofVTsandsuggestsstrongly(butdoes
notprove)thattheWCTisVT.(See"Generalprinciplesoftheimplantablecardioverterdefibrillator".)
PresenceofapacemakerThepatientshouldbeaskedaboutthepresenceofpacemaker,whichraisesthepossibilityofadeviceassociatedWCT.(See
'Supraventriculartachycardia'below.)
AtrialarrhythmiasInapatientknowntohavepersistentatrialfibrillation(AF),aregularWCTislikelyVTasaberrantconductionduringAFwouldcreatean
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irregularrhythm.AnexceptioniswhenAF"organizes"intoatrialflutterthiscanoccurspontaneouslybutoccursmuchmorecommonlyinthesettingof
antiarrhythmicdrugs(especiallyclassICagents,amiodarone,ordronedarone).
AgeInapatientovertheageof35years,aWCTislikelytobeVT(positivepredictivevalue85percentinoneseries)[8].SVTismorelikelyinyounger
patients(positivepredictivevalue70percent).However,VTmustbeconsideredinyoungerpatients,particularlythosewithafamilyhistoryofventricular
arrhythmiasorprematuresuddencardiacdeath.
DurationofthetachycardiaSVTismorelikelyifthetachycardiahasrecurredoveraperiodofmorethanthreeyears[5].Thefirstoccurrenceofthe
tachycardiaafteramyocardialinfarctionstronglyimpliesVT[7].
SymptomsSymptomsarenotusefulindeterminingthediagnosis,buttheyareimportantasanindicatoroftheseverityofhemodynamiccompromise.
Symptomsareprimarilyduetotheelevatedheartrate,associatedheartdisease,andthepresenceofleftventriculardysfunction[4,5,7].Somepatientswitha
WCThavefewornosymptoms(palpitations,lightheadedness,diaphoresis),whileothershaveseveremanifestationsincludingchestpainorangina,syncope,
shock,seizures,andcardiacarrest[5].
MedicationsManymedicationshaveproarrhythmiceffects,eitherdirectlybyprolongingtheQTintervalorindirectlyviaalterationsinelectrolytelevels,and
obtainingamedicationhistoryisamongthefirstprioritiesintheevaluationofapatientwithaWCT.ThemostcommondruginducedWCTisaformofpolymorphic
VTcalledtorsadesdepointes(TdP).ThisarrhythmiaisassociatedwithQTintervalprolongationwhenthepatientisinsinusrhythm.Manymedications(eg,
antiarrhythmicdrugs,antiinfectivedrugs,psychotropicdrugs,etc)areknowntoprolongtheQTinterval(table1)andareassociatedwithariskofpolymorphicVT.
AninternetresourcewithupdatedlistsofspecificdrugsthatcauseTdPisavailableatwww.crediblemeds.org/.(See"AcquiredlongQTsyndrome",sectionon
'DruginducedTdP'.)
TheclassIantiarrhythmicdrugs(table2)cancausebothaberrancyduringanSVTandalsoVT.Thesedrugs,especiallyclassICagents,slowconductionandhave
apropertyof"usedependency"(aprogressivedecreaseinimpulseconductionvelocityandwiderQRScomplexdurationatfasterheartrates).Asaresult,these
drugscancauseraterelatedaberrationandawideQRScomplexduringanySVT.However,theycanalsocauseVTwithaverywide,bizarreQRS,whichmaybe
incessant[9,10].(See'Supraventriculartachycardia'belowand"Myocardialactionpotentialandactionofantiarrhythmicdrugs".)
PhysicalexaminationAswiththehistory,theinitialphysicalexaminationshouldfocusuponevidenceofunderlyingcardiovasculardiseasewhichcanimpact
thelikelihoodthattheWCTisVT.
Findingssuggestiveofcardiovasculardiseaseinclude:
Signsofacuteorchronicheartfailure.(See"Treatmentofacutedecompensatedheartfailure:Generalconsiderations"and"Evaluationofthepatientwith
suspectedheartfailure".)
Ahealedsternalincisionasevidenceofpreviouscardiothoracicsurgery.
Thesequelaeofperipheralarterydiseaseorstroke.
ApacemakerorICD.Thesedevicesareusuallypalpableandareintheleftor,lesscommonly,rightpectoralareabelowtheclaviclesomeearlierICDsare
foundintheanteriorabdominalwall.
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AncillarytestingAnumberofadditionaltestsmayprovidefurtherinsighttothemechanismofthetachycardiaandthepresenceofassociatedconditions.
LaboratorytestingInitiallaboratorytestinginallpatientswithaWCTshouldincludeelectrolytesandcardiactroponin,withadditionaltestingforelevated
serumdruglevelsinpatientstakingcertainmedications.
Theplasmapotassiumandmagnesiumconcentrationsshouldbemeasuredaspartoftheinitialevaluation,sincehypokalemiaandhypomagnesemia
bothpredisposetothedevelopmentofVTs.HyperkalemiacancauseawideQRScomplexrhythmwiththelossofadetectablePwave,althoughthis
usuallyisasupraventricularrhythmwithaslowrate(socalled"sinoventricularrhythm").(See"Causesandevaluationofhyperkalemiainadults"and
"ECGtutorial:Miscellaneousdiagnoses",sectionon'Hyperkalemia'.)
CardiactroponintestingshouldbeperformedinpatientswithWCT,especiallyifthepatientishavingongoingchestpainorhemodynamicinstability.
Cardiactroponincanbeelevatedinthesettingofmyocardialischemia(astheresultofmyocardialoxygensupplyanddemandmismatch)ormyocardial
infarction(asapossiblecauseofthearrhythmia).Elevatedcardiactroponinisassociatedwithanincreasedriskofadverseoutcomesandmayguide
hospitaladmissiondecisions,cardiactesting,and/orantiischemictherapy.
Inpatientstakingdigoxin,quinidine,orprocainamide,plasmaconcentrationsofthesedrugsshouldbemeasuredtoassistinevaluatingpossibletoxicity.
ChestradiographAchestradiographcanprovideevidencesuggestiveofstructuralheartdisease,suchascardiomegaly.Evidenceofpreviouscardiothoracic
surgeryandthepresenceofapacemakerorICDcanalsobedetected.
Earlydiagnostic/therapeuticinterventionsInpatientswithaWCTwhoarehemodynamicallystable,certainvagalmaneuvers(ie,carotidsinusmassage)or
theadministrationofcertainintravenousmedications(eg,adenosine,betablockers,verapamil)maybebothhelpfulforestablishingthediagnosisandpotentially
therapeutic,althoughtheydocarryariskofhemodynamicdeteriorationandshouldonlybeperformedincloselymonitoredsettingsbyexperiencedclinicians.These
potentialinterventionsarediscussedindetailseparately.(See"ApproachtothemanagementofwideQRScomplextachycardias",sectionon'Vagalmaneuvers'.)
EPIDEMIOLOGYVentriculartachycardia(VT)isthemostcommoncauseofwidecomplextachycardia(WCT),particularlyinpatientswithahistoryofcardiac
disease.Inseriesofunselectedpatients,VTaccountedforupto80percentofcasesofWCT[2,4,5,11].VTfrequencycanexceed90percentinpatientswith
structuralheartdisease(eg,thosewithapriormyocardialinfarction)[7].
Supraventriculartachycardia(SVT)resultsinWCTmuchlessfrequentlythanVT.AmongpatientswithWCTduetoSVT,aberrantconductionisthemostcommon
reasonforawidenedQRS(21percentofcasesinoneseries)[11].However,anaberrantlyconductedSVTisstillmuchlesscommonthanVTasthecauseof
WCT.
Antidromicatrioventricularreentranttachycardia(AVRT)isarelativelyuncommoncauseofWCT(6percentofcasesinoneseries)[11].
CLINICALMANIFESTATIONSPatientswithwidecomplextachycardia(WCT)arerarelyasymptomatic,althoughthetypeandintensityofsymptomswillvary
dependingupontherateoftheWCT,thepresenceorabsenceofsignificantcomorbidconditions,andwhethertheWCTisventriculartachycardia(VT)or
supraventriculartachycardia(SVT).PatientswithWCTtypicallypresentwithoneormoreofthefollowingsymptoms:
Palpitations
Chestpain
Shortnessofbreath
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Syncopeorpresyncope
Suddencardiacarrest
FewphysicalexaminationfindingsinpatientswithaWCTareuniquetoWCT.Bydefinition,patientswillhaveapulseexceeding100beatsperminuterelatedto
thetachycardia.Patientsmaybehypotensive,whichmayresultinalterationsinconsciousness.Patientswithunderlyingheartdiseaseinwhomheartfailureresults
fromtheWCTmayhavecracklesonlungexamination.
Inaddition,thephysicalexaminationinpatientswithWCTcanrevealevidenceofatrioventricular(AV)dissociation,whichispresentinupto75percentofpatients
withVT,althoughitisnotalwayseasytodetect[5,7,12].DuringAVdissociation,thenormalcoordinationofatrialandventricularcontractionislost,whichmay
producecharacteristicphysicalfindings.ThepresenceofAVdissociationstronglysuggestsVT,althoughitsabsenceislesshelpful.
AlthoughAVdissociationistypicallydiagnosedontheelectrocardiogram(ECG),characteristicphysicalexaminationfindingsinclude(see'AVdissociation'below):
Markedfluctuationsinthebloodpressurebecauseofthevariabilityinthedegreeofleftatrialcontributiontoleftventricularfilling,strokevolume,andcardiac
output.
Variabilityintheoccurrenceandintensityofheartsounds(especiallyS1)("cacophonyofheartsounds"),whichisheardmorefrequentlywhentherateofthe
tachycardiaisslower.
Cannon"A"wavesCannonAwavesareintermittentandirregularjugularvenouspulsationsofgreateramplitudethannormalwaves.Theyreflect
simultaneousatrialandventricularactivation,resultingincontractionoftherightatriumagainstaclosedtricuspidvalve.ProminentAwavescanalsobeseen
duringsomeSVTs.Suchprominentwavesresultfromsimultaneousatrialandventricularcontractionoccurringwitheverybeat.(See"Examinationofthe
jugularvenouspulse".)
CAUSESOFWCTWidecomplextachycardias(WCTs)mostoftenresultfromventriculartachycardia(VT),withotherlesscommoncauseswhichinclude
supraventriculartachycardia(SVT)withaberrantconduction,SVTwithpreexcitation,SVTwithventricularpacing,andsometypesofartifactmimickingWCT(table
3).
VentriculartachycardiaVTusuallyoriginateswithintheventricularmyocardium,outsideofthenormalconductionsystem,resultingindirectmyocardial
activation.Comparedwithanormallyconductedsupraventricularbeat(whichactivatestheventricularmyocardiumviathenormalatrioventricular[AV]nodeHis
Purkinjesystem),ventricularactivationduringVTisslowerandproceedsinadifferentsequence.Thus,theQRScomplexiswideandabnormal(waveform1).As
theremaybeslightchangesoftheactivationsequenceduringtheVT,reflectingtheabnormalpathwayofimpulseconduction,theremaybesubtlechangesinQRS
complexmorphologyorintheSTTwaves.
VTmaybeeithermonomorphic(havingauniformandafairlystableQRSmorphologyduringanepisode),polymorphic(havingacontinuouslyvaryingQRScomplex
morphologyand/oraxisduringanepisode),orbidirectional(inwhicheveryotherbeathasadifferentaxisasittravelsalternatelydowndifferentconduction
pathways).ThefeaturesofeachformofVTarediscussedseparately.(See"Sustainedmonomorphicventriculartachycardia:Diagnosisandevaluation"and
"CatecholaminergicpolymorphicventriculartachycardiaandotherpolymorphicventriculartachycardiaswithanormalQTinterval"and"Clinicalfeaturesof
congenitallongQTsyndrome".)
ArtifactmimickingVTECGartifact,particularlywhenobservedonasingleleadrhythmstrip,maybemisdiagnosedasVT(waveform2)[13].Thepresenceof
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narrowcomplexbeatsthatcanbeseento"march"throughthesupposedWCTatafixedratestronglysupportsthediagnosisofartifact.
SupraventriculartachycardiaWhenanSVTconductstotheventriclesviathenormalAVnodeandHisPurkinjesystem,theactivationwavefrontspreads
quicklythroughtheventriclesandtheQRSisusuallynarrow.Inaddition,thepathwayofconductiontotheventriclesisfixedandthesameforeachimpulse,
accountingfortheuniformityoftheQRScomplexesandSTTwaves.However,SVTcanalsoproduceawidenedQRSbyanumberofmechanisms,including
aberrantconduction,preexcitation,andtheactivationofventricularpacing.
AberrantconductionTheconductionofasupraventricularimpulsecanbedelayedorblockedinthebundlebranchesorinthedistalPurkinjesystem,
resultinginawide,abnormalQRS.Thisphenomenonisreferredtoasaberrancy.(See"Basicapproachtodelayedintraventricularconduction".)
Aberrantconductionmayeitherbepresentatbaselineorundercertainconditions,suchasfasterheartrates.
Inpatientswithaleftbundlebranchblock(LBBB),rightbundlebranchblock(RBBB),oranonspecificintraventricularconductiondelay(IVCD)ontheir
baselineelectrocardiogram(ECG),anySVTwillhaveawidenedQRS.Thus,iftimeallows,reviewofabaselineECGcanbehelpfulindifferentiatingVTfrom
SVTwithaberrancy.ThepresenceofaconductionabnormalityonthebaselineECGdoesnotprovethatthetachycardiaisSVTwithaberrancy,butthemore
similartheQRSduringtheWCTistotheQRSduringsinusrhythm,themorelikelyitisthattheWCTisanSVTwithaberrancy.
InpatientswithaberrancyatbaselinewhomanifestaWCTinwhichtheQRScomplexisnarrowerthanthebaselineQRS,theWCTislikelyVToriginating
neartheventricularseptum,withearlyengagementofthespecializedconductingsystem.Thisscenarioisextremelyunusual.
InpatientswithanarrowQRScomplexatbaselinewhichwidensatfasterheartrates,conductionisnormalduringsinusrhythmbutaberrantduringthe
tachycardia.Themostcommonreasonforthisisraterelatedaberration(functionalbundlebranchblock),inwhichrapidlygeneratedimpulsesreachthe
conductingfibersbeforetheyhavefullyrecoveredfromthepreviousimpulse.SuchadelayinrecoverymayalsobetheresultofunderlyingdiseaseoftheHis
Purkinjesystem,hyperkalemia,ortheactionsofantiarrhythmicdrugs,particularlytheclassICagents(eg,flecainide,propafenone).(See"Myocardialaction
potentialandactionofantiarrhythmicdrugs".)
PreexcitationsyndromeInthepreexcitationsyndromes,AVconductioncanoccuroverthenormalconductionsystemandalsoviaanaccessoryAV
pathway(figure1AC).Thesetwopathwayscreatetheanatomicsubstrateforareentrantcircuit(macroreentrantcircuit),facilitatingthedevelopmentofacircus
movementorreentranttachycardiaknownasatrioventricularreentranttachycardia(AVRT).(See"ECGtutorial:Preexcitationsyndromes"and"Atrioventricular
reentranttachycardia(AVRT)associatedwithanaccessorypathway",sectionon'OrthodromicAVRT'and"Atrioventricularreentranttachycardia(AVRT)associated
withanaccessorypathway",sectionon'AntidromicAVRT'.)
AVRTcanpresentwithanarroworawideQRScomplex:
IfantegradeconductiontotheventriclesoccursovertheAVnodeandretrogradeconductionisovertheaccessorypathway,theQRScomplexwillbenarrow
(unlessthereisaberrantconductionatbaselinewithawideQRScomplex).ThisnarrowcomplexAVRTisknownasanorthodromicAVRT(figure2and
waveform3).OrthodromicAVRTcanalsooccurwithraterelatedaberrancy,creatingaWCT.
IfantegradeconductionoccursoveranaccessorypathwayandretrogradeconductionoccursovertheAVnodeorasecondaccessorypathway,theQRS
complexwillbewidewithanunusualmorphology.ThisisknownasanantidromicAVRT(figure3andwaveform4).AntidromicAVRTisdifficultto
differentiatefromVT,becauseventricularactivationstartsoutsidethenormalintraventricularconductionsysteminbothtypesoftachycardia(iethereisdirect
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myocardialactivation).(See'VTversusAVRT'below.)
Inaddition,patientswithanaccessorypathwaymaydevelopadifferentSVT(eg,atrialtachycardia,atrialfibrillation[AF],oratrialflutter).Insuchcases,theatrial
impulsesmayusetheaccessorypathwaytoconducttotheventricles,andtheQRScouldbeeithernarroworwide,dependinguponwhetherventricularactivation
occursoverthenormalconductionsystem,theaccessorypathway,orboth(waveform5andwaveform6andwaveform7).(See"Epidemiology,clinical
manifestations,anddiagnosisoftheWolffParkinsonWhitesyndrome",sectionon'ArrhythmiasassociatedwithWPW'.)
PacemakersWhentheventriclesareactivatedbyapacingdevice,theQRScomplexisgenerallywide:
Mosttransvenousventricularpacemakerspacetherightventricle,causingawideQRScomplexoftheLBBBtype.Typically,thesurfaceECGshowsabroad
RwaveinleadI,indicatingconductionfromrighttoleft.(See"Overviewofcardiacpacinginheartfailure".)
Pacemakersusedincardiacresynchronizationtherapy(CRT)usuallypacebothventricles.AlthoughCRTgeneratesaQRScomplexthatisnarrowerthanthe
patient'sbaseline(achronicallywidenedQRSisoneofthecomponentsoftheindicationforCRT),itisstillusuallylongerthan120msec.ThesurfaceECG
typicallyshowsaQwaveorQScomplexinleadI,indicatingactivationfromlefttoright.(See"Cardiacresynchronizationtherapyinheartfailure:Indications".)
RecognizingthataQRScomplexisduetoventricularpacingcanbechallenging,particularlyduringatachycardia.InadditiontocharacteristicQRSmorphology,a
pacing"spike"orstimulusartifactcanoftenbeidentified.Thestimulusartifactisanarrowelectricalsignaltoorapidtorepresentmyocardialdepolarization.
AmongpatientswithapacemakeroranICD,furtherpossibilitiesneedtobeconsideredinadditiontotheusualdifferentialdiagnosisofaWCT.Theseinclude:
InthepresenceofsinustachycardiaorsomeSVTs(eg,anatrialtachycardia,AF,oratrialfibrillation),thedevicemay"track"theatrialimpulseandpacethe
ventricleattherapidrate,resultinginaWCT.(See"Modesofcardiacpacing:Nomenclatureandselection",sectionon'Modeswitching'.)
AWCTcanresultifventricularpacedbeatsareconductedretrograde(backward)throughtheAVnodetotheatrium,resultinginanatrialsignal,whichthe
pacemakersensesandtrackswithanotherventricularstimulus.Thisventricularpacedbeatisalsoconductedretrograde,andthecyclerepeatsindefinitely,a
processtermedpacemakermediatedtachycardia(PMT)orendlesslooptachycardia.PMTusuallyoccursattheupperratelimit.Adifferentmechanismof
pacemakerassociatedtachycardia,nonreentrantrepetitiveVAsynchrony,alsocreatesawidecomplexrhythm,butusuallyatthelowerratelimitorsensor
mediatedrateratherthanattheupperratelimit.
Theseandotherarrhythmiasassociatedwithpacemakersarediscussedindetailseparately.(See"Unexpectedrhythmswithnormallyfunctioningdualchamber
pacingsystems",sectionon'Pacemakermediatedtachycardia'.)
EVALUATIONOFTHEELECTROCARDIOGRAMInmostpatients,aprobablediagnosis(ventriculartachycardia[VT]orsupraventriculartachycardia[SVT])
maybemadebycloselyreviewingtheelectrocardiogram(ECG),althoughdefinitivediagnosisisnotalwayspossibleandmaybetimeconsuming,especiallyfor
cliniciansunfamiliarwiththecriteriafordistinguishingVTfromSVT.ToperformanadequateECGanalysis,botha12leadECGandarhythmstripshouldbe
obtained.Ifavailable,apreviousECGwhenthepatientwasinnormalsinusrhythmmaybehelpful.However,ifthereareanyquestionsregardingthepatient's
stability,detailedECGevaluationshouldbedeferredinfavorofurgenttherapy,althoughiftimeallows,anECGshouldbeobtainedforlaterreviewpriortourgent
cardioversion.(See"ApproachtothemanagementofwideQRScomplextachycardias",sectionon'Unstablepatients'.)
BasicfeaturesAswiththeinterpretationofanyECG,thestandardinitialapproachincludesanassessmentofrate,regularity,axis,QRSduration,andQRS
morphology.
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RateTherateofthewidecomplextachycardia(WCT)isoflimiteduseindistinguishingVTfromSVT.Whentherateisapproximately150beatsperminute,
atrialflutterwith2:1atrioventricular(AV)blockandwithaberrantconductionshouldbeconsidered,althoughthisdiagnosisshouldnotbeacceptedwithout
othersupportingevidence.
RegularityVTisgenerallyregular,althoughslightvariationintheRRintervalsissometimesseen.SlightirregularitysuggestsVTasopposedtomostSVTs,
whicharecharacterizedbyuniformityoftheRRintervals.Whentheonsetofthearrhythmiaisavailableforanalysis,aperiodofirregularity("warmup
phenomenon"),suggestsVT.MoremarkedirregularityofRRintervalsoccursinpolymorphicVTandinatrialfibrillation(AF)withaberrantconduction.
MorphologyWhendescribingWCTs,theQRSmorphologyinleadV1isthekey.IfthecomplexisprimarilynegativeinleadV1,theWCTissaidtobeleft
bundlebranchblock(LBBB)like.IftheQRSisprimarilypositiveinleadV1,theWCTissaidtoberightbundlebranchblock(RBBB)like.(See'QRS
morphology'below.)
AxisTheQRSaxisinthefrontalplanecanbeusefulindistinguishingSVTfromVT.(See"Basicprinciplesofelectrocardiographicinterpretation",sectionon
'QRSaxis'.)
Arightsuperioraxis(axisfrom90to180degrees),sometimescalledanindeterminateor"northwest"axis,israreinSVTandstronglysuggestsVT[5].
Therearetwoexceptionstothisrule.Thefirstisanantidromicatrioventricularreentranttachycardia(AVRT)seenwithventricularpreexcitation.Inthis
situationthereisdirectactivationoftheventricularmyocardium,bypassingthenormalHisPurkinjesystem,andtheQRScomplexmayhavean
indeterminateaxis.ThesecondisabiventricularpacemakerinwhichtheaxisisoftenindeterminatewithaninitialQwaveinleadI.
Comparedwiththeaxisduringsinusrhythm(whenanoldECGisavailableforreview),anaxisshiftduringtheWCTofmorethan40degreessuggests
VT[14].
InapatientwithaRBBBlikeWCT,aQRSaxistotheleftof30degreessuggestsVT.(See'QRSmorphology'below.)
InapatientwithanLBBBlikeWCT,aQRSaxistotherightof+90degreessuggestsVT[15].(See'QRSmorphology'below.)
QRSdurationIngeneral,awiderQRSfavorsVT.InaRBBBlikeWCT,aQRSduration>140msecsuggestsVTwhileinaLBBBlikeWCT,aQRSduration
>160msecsuggestsVT[5,15].(See'QRSmorphology'below.)
Inananalysisofseveralstudies,aQRSduration>160msecwasastrongpredictorofVT(likelihoodratio>20:1)[16].However,aQRSduration>160msec
isnothelpfulinsomesettings,includingSVTwithanAVaccessorypathwaythepresenceofdrugscapableofslowingintraventricularconduction,suchas
classIantiarrhythmicdrugsandinassociationwithhyperkalemia[15,17,18].AverywideQRScomplexmayalsobeseenwithadilatedcardiomyopathyin
whichdiffusefibrosismayproduceamarkedslowingofimpulseconductionthroughtheventricularmyocardium.(See'VTversusAVRT'belowand
'Medications'above.)
AQRSduration<140msecdoesnotexcludeVT,sinceVToriginatingfromtheseptumorwithintheHisPurkinjesystem(asopposedtothemyocardium)
maybeassociatedwitharelativelynarrowQRScomplex.(See"Monomorphicventriculartachycardiaintheabsenceofapparentstructuralheartdisease",
sectionon'Idiopathicleftventriculartachycardia'.)
ConcordanceConcordanceispresentwhentheQRScomplexesinallsixprecordialleads(V1throughV6)aremonophasicwiththesamepolarity.Theycan
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eitherallbeentirelypositivewithtall,monophasicRwaves,orallbeentirelynegativewithdeepmonophasicQScomplexes.Ifanyofthesixleadshasabiphasic
QRS(qRorRScomplexes),concordanceisnotpresent.
NegativeconcordanceisstronglysuggestiveofVTbutisnotdefinitive.Rarely,SVTwithLBBBaberrancywilldemonstratenegativeconcordance,butthereis
almostalwayssomeevidenceofanRwaveinthelateralprecordialleads.
PositiveconcordanceismostoftenduetoVTbutcanalsooccurintherelativelyrarecaseofantidromicAVRTwithaleftposterioraccessorypathway[5,15].
(See"Anatomy,pathophysiologyandlocalizationofaccessorypathwaysinthepreexcitationsyndrome".)
WhilethepresenceofconcordancestronglysuggestsVT(>90percentspecificity),itsabsenceisnothelpfuldiagnostically(approximately20percentsensitivity)
[11].
AVdissociationAVdissociationischaracterizedbyatrialactivitythatisindependentofventricularactivity(waveform8).
InaWCTwithAVdissociation,anatrialrateslowerthantheventricularratestronglysuggestsVT.Anatrialratethatisfasterthantheventricularrateisseenwith
someSVTs,suchasatrialflutteroranatrialtachycardiawith2:1AVconduction.Inthesesettings,however,thereisaconsistentrelationshipbetweenthePwaves
andtheQRScomplexes,sothereisnottrueAVdissociation.
WhilethepresenceofAVdissociationlargelyestablishesVTasthediagnosis,itsabsenceisnotashelpfulfortworeasons:
AVdissociationmaybepresentbutnotobviousontheECG.
InsomecasesofVT,theventricularimpulsesconductbackwardsthroughtheAVnodeandcapturetheatrium(referredtoas1:1retrogradeconduction),soin
factthereisAVassociationratherthanAVdissociation[19].ThismaybeseenmorecommonlywhentherateofVTisslower.VTwithretrograde
Wenckebachconduction,orwith2:1VAconduction,technicallydoesnotexhibitAVdissociation,thoughtheventricularrateexceedstheatrialrate.Inall
casesinwhichthereisretrogradeVAconduction,thePwaveswillbeinvertedintheinferiorleads.
DissociatedPwavesPwavesaresaidtobedissociatediftheyarenotconsistentlycoupledtotheQRScomplexes,asevidencedbythefollowing:
PPandRRintervalsaredifferent
PRintervalsarevariable
ThereisnoassociationbetweenPandQRScomplexes
ThepresenceofaPwavewithone,butnotall,QRScomplexes
DuringaWCT,Pwavesareoftendifficulttoidentify.IfPwavesarenotevidentonthesurfaceECG,directrecordingsofatrialactivity(eg,viaanimplanted
pacemakerorimplantablecardioverterdefibrillator[ICD],orviaanesophagealelectrodeortemporarypacingcatheterorepicardialpacingwiresafterheartsurgery)
canrevealAVdissociation[20].
FusionandcapturebeatsFusionand/orcapturebeats,whenidentifiedonthesurfaceECGinapatientwithWCT,arediagnosticforVT.
Fusionbeatsoccurwhenoneimpulseoriginatingfromtheventricleandasecondsupraventricularimpulsesimultaneouslyactivatetheventricularmyocardium.
TheresultingQRScomplexhasamorphologyintermediatebetweenthatofasinusbeatandapurelyventricularcomplex(waveform9).Intermittentfusion
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beatsduringaWCTarediagnosticofAVdissociationandthereforeofVT.
Capturebeats,orDresslerbeats,areQRScomplexesduringaWCTthatareidenticaltothesinusQRScomplex(waveform9).Theterm"capturebeat"
impliesthatthenormalconductionsystemhasmomentarily"captured"controlofventricularactivationfromtheVTfocus.
Fusionbeatsandcapturebeatsaremorecommonlyseenwhenthetachycardiarateisslower.
QRSmorphologyFrequently,theabovecriteriadonotprovideadefinitivediagnosis.FurtherECGevaluationinvolvesassessmentofthemorphologyofthe
QRScomplex.
AnalysisofQRSmorphologyisbaseduponanunderstandingoftherelationshipsbetweenthesitesoftachycardiaorigin,ventricularactivationpatterns,andthe
resultingmorphologiesoftheQRScomplexinthe12standardECGleads.
DiagnosticcriteriaAnumberofcriteriahavebeendevelopedtofacilitatetheevaluationofQRSmorphology.Mostoftheseapproachesinvolveclassifying
theWCTsashavingoneoftwopatterns:
AnRBBBlikepatternQRSpolarityispositiveinleadV1
AnLBBBlikepatternQRSpolarityisnegativeinleadV1
Thisdistinctiondoesnot,byitself,makethediagnosis,butadditionalfeaturesfavorVTineitherRBBBlikeorLBBBlikeWCTs.However,thevalueofthese
morphologiccriteriaissubjecttoseverallimitations:
AssociationsbetweentheQRSmorphologyandWCTdiagnosisareoftenbaseduponstatisticalcorrelationswithsubstantialoverlap.
MorphologiccriteriafavoringVTcanbepresentinpatientswithanintraventricularconductiondelayorbundlebranchblockduringsinusrhythm,limitingtheir
applicabilityinthesecases[21].Onoccasionaraterelatedbundlebranchblockmayhaveatypicalfeatures,suggestingVT.
MorphologiccriteriatendtomisclassifyantidromicAVRTasVT.TheymayalsomisclassifySVTassociatedwithacardiomyopathy.(See'VTversusAVRT'
below.)
Inthediscussionsthatfollow,upperandlowercaselettersareusedtoindicatetherelativemagnitudeofthedescribedelectrocardiographicwaves.Asexamples,
theterm"qR"impliesasmallQwavefollowedbyalargeRwave.
V1positive(RBBB)patternInthepatientwithaWCTandpositiveQRSpolarityinleadV1,thefollowingassociationshavebeenmade[5,11,15,2224]:
FindingsinleadV1AmonophasicRorbiphasicqRcomplexinleadV1favorsVT.
AtriphasicRSR'orRsR'complex(thesocalled"rabbitear"sign)inleadV1usuallyfavorsSVT.Asanexception,iftheleftpeakoftheRsR'complexis
tallerthantherightpeak,VTismorelikely[16,25].
FindingsinleadV6AnrScomplex(RwavesmallerthanSwave)inleadV6favorsVT[16].Bycontrast,anRscomplex(RwavelargerthanSwave)
inleadV6favorsSVT.
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V1negative(LBBB)patternInthepatientwithaWCTandnegativeQRSpolarityinleadV1,thefollowingassociationshavebeenmade[5,11,15,2224]:
FindingsinleadV1orV2AbroadinitialRwaveof40msecdurationorlongerinleadV1orV2favorsVT.Incontrast,theabsenceofaninitialRwave
orasmallinitialRwaveoflessthan40msecinleadV1orV2favorsSVT.
TwootherfindingsthatfavorVTareaslurredornotcheddownstrokeoftheSwaveinleadV1orV2,andadurationfromtheonsetoftheQRScomplex
tothenadiroftheQSorSwaveof60msecinleadV1orV2.Inananalysisofseveralstudies,thepresenceofanyofthesethreecriteria(broadR
wave,slurredornotcheddownstrokeofSwave,anddelayednadirofSwave)wasastrongpredictorofVT[16].
Bycontrast,aswift,smoothdownstrokeoftheSwaveinleadV1orV2withadurationof<60msecfavorsSVT.
FindingsinleadV6ThepresenceofanyQorQSwaveinleadV6favorsVT[16].Bycontrast,theabsenceofaQwaveinleadV6favorsSVT.
VariationinQRSandSTTshapeSubtle,nonraterelatedfluctuationsorvariationsinQRSandSTTwaveconfigurationsuggestVTandmayreflect
variationsintheVTreentrantcircuitwithinthemyocardiumaswellasasubtledifferenceintheactivationsequenceofthemyocardiumreflectingactivationthat
bypassesthenormalconductionsystem.AVdissociationcancausevariabilityintheSTsegmentandTwavemorphology.Bycontrast,SVT,becauseitfollowsa
fixedconductionpathwaytoandthroughtheventricularmyocardium,ischaracterizedbyuniformityofQRSandSTTshapeunlesstheratechanges.
DIAGNOSISMostpatientswithwidecomplextachycardia(WCT)willhavesome,butnotall,oftheelectrocardiogram(ECG)featuresfavoringventricular
tachycardia(VT).ThereisnosinglecriterionorcombinationofcriteriathatprovidescompletediagnosticaccuracyinevaluatingaWCT.Itistypicallynecessary,
therefore,tointegratemultipleECGfindingsintoadiagnosticstrategy.Severalstrategieshavebeenproposed,ofwhichtheBrugadacriteriaarethemostwidely
known[16,26,27].(See'Brugadacriteria'below.)
However,becausethediagnosisofaWCTcannotalwaysbemadewithcompletecertaintyevenwhenusingmultipleECGcriteria,anunknownoruncertainrhythm
shouldbepresumedtobeVTintheabsenceofcontraryevidence[28].VTisfarmorecommonthansupraventriculartachycardia(SVT),byafactoroffourin
unselectedpopulationsandbyasmuchas10foldinpatientswithpriormyocardialinfarction.Additionally,presumingVTguardsagainstinappropriateandpotentially
dangeroustherapiesdirectedatanSVTwhichcanprecipitatehemodynamicdeteriorationinpatientswithVT,andtreatmentofSVTasifitwereVTissafeand
frequentlyeffectiveinrestoringsinusrhythm.(See"ApproachtothemanagementofwideQRScomplextachycardias",sectionon'Management'.)
AnalgorithmicapproachtothediagnosisofaWCTwillbereviewedhere,withemphasisonthedistinctionbetweenVTandSVT.TheapproachtoanarrowQRS
complextachycardiaisdiscussedseparately.(See"Clinicalmanifestations,diagnosis,andevaluationofnarrowQRScomplextachycardias".)
OurapproachOnceaWCThasbeenidentifiedontheECG,promptdiagnosisandmanagementisimportant.UnstablepatientsshouldbepresumedtohaveVT
andtreatedassuch.WhiletheBrugadacriteriaarethemostwidelyknownandappliedcriteriafordistinguishingVTfromSVT,timeand/ortechnicallimitationsmay
notallowforimmediatereviewoftheECGinsuchdetail,particularlyinasymptomaticorborderlineunstablepatient.OurapproachemphasizesimmediateECG
reviewforkeyhighyieldfeaturesinparallelwithabriefhistorythatcanguidethemanagementofmostpatientswithaWCT.
Istherhythmregularorirregular?VTandmostSVTsaregenerallyregular,thoughslightvariationoftheRRintervalcanbeseeninVT.AnirregularWCT
usuallyrepresentsatrialfibrillation(AF)withaberrantconduction,althoughpolymorphicVTshouldalsobeconsidered.(See'Basicfeatures'above.)
WhatistheQRSaxis?Arightsuperioraxis(axisfrom90to180degrees)stronglyfavorsVT,asdoesanyaxisshiftofgreaterthan40degreeswhen
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comparedwithbaselineorconcordanceoftheQRScomplexes.(See'Basicfeatures'aboveand'Concordance'above.)
Isthereatrioventricular(AV)dissociation?IfAVdissociationcanbequicklyidentified,anatrialrateslowerthantheventricularrate,alongwithanyfusionor
capturebeats,stronglysuggestsVT.(See'AVdissociation'above.)
Isthereahistoryofheartdiseaseorarrhythmias?Aquickhistoryfocusingonstructuralheartdisease,particularlycoronaryheartdiseaseand/orprior
myocardialinfarction,aswellasanyknownarrhythmiasorcardiacimplantableelectronicdevices(eg,pacemakerorimplantablecardioverterdefibrillator
[ICD]),canaidinidentifyingthemostlikelyetiologyofWCT.TheWCTisfarmorelikelytobeVTinpatientsover35yearsofagewithknowncoronaryheart
diseaseorpriormyocardialinfarction,andinthosewithanICD.(See'History'above.)
TheabsenceofthehistoricalorECGfeaturesofVTdoesnotconfirmadiagnosisofSVT.ThediagnosisofSVTshouldbeconsideredprimarilyinyoungpatients,
whoseheartsarestructurallynormal,inwhomnoneofthehistorical(eg,familyhistoryofsuddencardiacdeath),physical,orECGcriteriasupportingVTare
present,orinpatientswithahistoryofSVTwithasimilarpresentation.WhenthediagnosisofaWCTremainsuncertain,werecommendthatthepatientbetreated
asiftherhythmisVTuntildefinitivelyprovenotherwise.
BrugadacriteriaTheBrugadacriteriaareastepwiseapproachinwhichfourcriteriaforVTaresequentiallyassessed(algorithm1)[26].Ifanyofthecriteriais
satisfied,thediagnosisofVTismade,andifnonearefulfilled,anSVTisdiagnosed.Anexceptionisanantidromicatrioventricularreentranttachycardia(AVRT)in
WolffParkinsonWhitesyndrome.
Thestepsareasfollows:
LeadsV1V6areinspectedtodetectanRScomplex.IftherearenoRScomplexes,concordanceispresentandthediagnosisofVTcanbemade.(See
'Concordance'above.)
IfanRScomplexispresent,measuretheintervalbetweentheonsetoftheRwaveandthenadiroftheSwave(RSinterval).IfthelongestRSintervalinany
leadis>100msecandtheRwaveiswiderthantheSwave,thediagnosisofVTcanbemade.ThisreflectsthatwithVT,theentireQRScomplexiswide
andabnormal(eventheinitialRwaveportion),whileaberrationisduetoaterminaldelayresultinginawiderterminalportionoftheQRScomplex(ie,Swave).
Thiscriterion,however,maybelimitedinthepresenceofanunderlyingdiffusecardiomyopathy,asinthissituationeveninitialventricularactivationmaybe
slowandabnormal.
IfthelongestRSintervalis<100msec,thepresenceorabsenceofAVdissociationisassessed.IfAVdissociationisseen,thediagnosisofVTismade.
(See'AVdissociation'above.)
IfAVdissociationcannotclearlybedemonstrated,theQRSmorphologycriteriaforV1positiveandV1negativewideQRScomplextachycardiasare
considered.QRSmorphologycriteriaconsistentwithVTmustbepresentinleadsV1orV2andinleadV6todiagnoseVT.IfeithertheV1V2ortheV6criteria
arenotconsistentwithVT,anSVTisassumed.(See'QRSmorphology'above.)
AlternativeapproachesSeveralalternativeapproacheshavebeenproposedintheliterature,althoughnoneareascommonlyusedastheBrugadacriteria.
TheseapproachesaregenerallybestperformedinconsultationwithanelectrophysiologistwithexpertiseinthediagnosisofWCT.
Analternativealgorithm(Vereckeiapproach)usesastepwiseapproachsimilartotheBrugadacriteria,butincludesdifferentECGfeatures(algorithm2)[27].
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TwouniquefeaturesofthisalgorithmincludeaninitialRwaveinaVR(diagnosticofVT),andtheVi:Vtratio.ViandVtarethemagnitudeofvoltagechangein
theinitialandterminal40msecofaQRS,respectively.ViandVtshouldbemeasuredfromthesamebiphasicormultiphasicQRScomplex.AVi:Vtratio1is
diagnosticofVT.
Onestudyof51patientswithWCTinducedduringelectrophysiologystudyshowedequivalentsensitivityfordiagnosisbetweentheVereckeiandBrugada
approaches(89versus90percent),buttheVereckeiapproachyieldedsignificantlyfewerincorrectdiagnosesfollowingthefirststep(2versus27percent)and
wasslightlyfastertoperform(9.1versus9.9seconds)[29].
ABayesianapproachutilizeslikelihoodratios(LR)forsixECGcriteria[16].Patientsarepresumedtostartwitha"prioroddsratio"of4.0(4:1)infavorofVT.
Aseachcriterionisevaluatedsequentially,theassociatedLRismultipliedbytheprioroddsratiotocalculatethenewprobabilityofVT.Thefinaloddsratio
(posteriorprobability)isconsideredconsistentwithVTifthevalueis1.0,andSVTifthevalueis<1.0.
Intravenousadenosinemaybeadministeredasbothadiagnosticandpotentiallytherapeuticagent.(See"ApproachtothemanagementofwideQRScomplex
tachycardias",sectionon'Pharmacologicinterventions'.)
VTversusAVRTDifferentiationbetweenVTandantidromicAVRTisparticularlydifficult.Becausethereisdirectmyocardialactivationsinceventricular
activationbeginsoutsideofthenormalconductionsysteminbothVTandantidromicAVRT,manyofthestandardcriteriaarenotabletodiscriminateantidromic
AVRTfromVT.Theclinicalsignificanceofthisproblemisoftenlimited,however,becausepreexcitationisanuncommoncauseofWCT(6percentinoneseries),
particularlyifotherclinicalfactors(eg,age,underlyingheartdisease)suggestVT[11].
Forcasesinwhichpreexcitationisthoughttobelikely(suchasayoungpatientwithoutstructuralheartdisease,orapatientwithaknownaccessorypathway),a
separatealgorithmwasdevelopedwhichconsistsofthefollowingthreesteps(algorithm3)[26]:
ThepredominantpolarityoftheQRScomplexinleadsV4throughV6isdefinedeitheraspositiveornegative.Ifpredominantlynegative,thediagnosisofVT
canbemade.
IfthepolarityoftheQRScomplexispredominantlypositiveinV4throughV6,theECGshouldbeexaminedforthepresenceofaqRcomplexinoneormore
ofprecordialleadsV2throughV6.IfaqRcomplexcanbeidentified,VTcanbediagnosed.
IfaqRwaveinleadsV2throughV6isabsent,theAVrelationshipisthenevaluated(AVdissociation).Ifa1:1AVrelationshipisnotpresentandthereare
moreQRScomplexespresentthanPwaves,VTcanbediagnosed.
Whenanyofthesecriteriaaremet,VTislikely.However,iftheECGdoesnotdisplayanyofthethreemorphologiccharacteristicsdiagnosticofVTinthis
algorithm,thediagnosisofantidromicAVRTmustbeconsidered.Importantly,theQRScomplexmorphologyandSTTwavesareuniformwithAVRTasevery
impulsetotheventricleisconductedthroughthesameaccessorypathway.
AlgorithmperformanceAlgorithmsoftenperformwellininitialreports.However,suchstudiesincludeselectedpopulationsandexperiencedECGanalysts.
Initsinitialdescription,thereportedsensitivityandspecificityoftheBrugadacriteriawere98.7and96.5percent,respectively[26].However,intwo
subsequentreportsinwhichatotalofnineclinicians(twocardiologists,twoemergencydepartmentclinicians,andfiveinternists)usedthesecriteriain
interpretingatotalof168WCTsthathadbeendiagnosedwithelectrophysiologictesting,thesensitivityrangedfrom79to92percent,andspecificityfrom43
to70percent[30,31].
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InacomparisonoftheBrugadacriteriaandtheBayesianapproach,thetwoapproachesperformedsimilarly,withsensitivitiesof92and97andspecificitiesof
44and56percent,respectively[31].
Intheinitialdescriptionofthealternativealgorithmdescribedabove,itwassignificantlymoreaccuratethantheBrugadacriteria[27].Furtherstudyis
necessarytoconfirmboththeoverallaccuracyofthisapproachanditssuperioritytotheBrugadacriteria.
INFORMATIONFORPATIENTSUpToDateofferstwotypesofpatienteducationmaterials,"TheBasics"and"BeyondtheBasics."TheBasicspatient
educationpiecesarewritteninplainlanguage,atthe5thto6thgradereadinglevel,andtheyanswerthefourorfivekeyquestionsapatientmighthaveaboutagiven
condition.Thesearticlesarebestforpatientswhowantageneraloverviewandwhoprefershort,easytoreadmaterials.BeyondtheBasicspatienteducation
piecesarelonger,moresophisticated,andmoredetailed.Thesearticlesarewrittenatthe10thto12thgradereadinglevelandarebestforpatientswhowantin
depthinformationandarecomfortablewithsomemedicaljargon.
Herearethepatienteducationarticlesthatarerelevanttothistopic.Weencourageyoutoprintoremailthesetopicstoyourpatients.(Youcanalsolocatepatient
educationarticlesonavarietyofsubjectsbysearchingon"patientinfo"andthekeyword(s)ofinterest.)
Basicstopics(see"Patientinformation:Ventriculartachycardia(TheBasics)")
SUMMARYANDRECOMMENDATIONS
Ventriculartachycardia(VT)isthemostcommoncauseofwidecomplextachycardia(WCT),particularlyinpatientswithahistoryofcardiacdisease,while
supraventriculartachycardia(SVT)resultsinWCT(duetoaberrantconduction,preexcitation,orventricularpacing)muchlessfrequently.WCTisidentifiedas
VTinupto80percentofunselectedpatientsandmorethan90percentofpatientswithknownstructuralheartdisease.(See'Epidemiology'aboveand
'CausesofWCT'above.)
PatientswithWCTarerarelyasymptomatic,althoughthetypeandintensityofsymptomswillvarydependingupontherateoftheWCT,thepresenceor
absenceofsignificantcomorbidconditions,andwhethertheWCTisVTorSVT.PatientswithWCTtypicallypresentwithoneormoreofpalpitations,chest
pain,shortnessofbreath,syncope/presyncope,orsuddencardiacarrest.(See'Clinicalmanifestations'above.)
ThefirstprioritywhenevaluatingapatientwithaWCTisanimmediateassessmentofpatientstability,includingthepatient'ssymptoms,vitalsigns,andthe
levelofconsciousness.Anunstablepatientwillhaveevidenceofhemodynamiccompromise,suchashypotension,alteredmentalstatus,chestpain,orheart
failure.
Apatientwhoisunresponsiveorpulselessshouldbetreatedaccordingtostandardadvancedcardiaclifesupport(ACLS)algorithms(algorithm4).(See
'Assessmentofstability'aboveand"Advancedcardiaclifesupport(ACLS)inadults".)
Forapatientwhoisunstablebutconscious,werecommendimmediatesynchronizedcardioversion(Grade1B).(See'Assessmentofstability'above
and"ApproachtothemanagementofwideQRScomplextachycardias",sectionon'Unstablepatients'.)
Inastablepatient,orfollowingcardioversiontostabilizeanunstablepatient,ourinitialapproachincludesthefollowing:
Asuccincthistoryandphysicalexamination,focusingonthepresenceofstructuralheartdisease,especiallycoronaryheartdiseaseand/ora
previousmyocardialinfarction,aswellasthehistoryofanyarrhythmiasandthepresenceofapacemakerorimplantablecardioverterdefibrillator
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(ICD).(See'History'aboveand'Physicalexamination'above.)
Reviewofthepatientsmedicationsfordrugswhichmaybeproarrhythmic(byprolongingtheQTintervalorpromotingelectrolytedisturbances).
(See'Medications'above.)
Ancillarytestingincludingserumelectrolytelevels,cardiactroponin,andachestradiographinallpatients.(See'Ancillarytesting'above.)
InmostpatientswithWCT,aprobablediagnosis(VTorSVT)maybemadebycloselyreviewingtheelectrocardiogram(ECG),althoughdefinitivediagnosisis
notalwayspossibleandmaybetimeconsuming.ThestandardinitialapproachtoECGinterpretationincludesanassessmentofrate,regularity,axis,QRS
duration,andQRSmorphology.(See'Evaluationoftheelectrocardiogram'above.)
MostpatientswithWCTwillhavesome,butnotall,oftheECGfeaturesfavoringVT.Thereisnosinglecriterionorcombinationofcriteriathatprovides
completediagnosticaccuracyinevaluatingaWCT,evenwhenemployinganalgorithmicapproachtothediagnosisofaWCT,mostcommonlyusingthe
Brugadacriteria.(See'Diagnosis'above.)
ECGfeaturesconsistentwithVTincludeconcordance,AVdissociation,fusion/capturebeats,andspecificQRSmorphologies.
TheabsenceofthehistoricalorECGfeaturesofVTdoesnotconfirmadiagnosisofSVT.ThediagnosisofSVTshouldbeconsideredprimarilyinyoung
patients,whoseheartsarestructurallynormal,inwhomnoneofthehistorical(eg,familyhistoryofsuddencardiacdeath),physical,orECGcriteria
supportingVTarepresent,orinpatientswithahistoryofSVTwithasimilarpresentation.
WhenthediagnosisofaWCTisuncertain,werecommendthatthepatientbetreatedasiftherhythmisVT(Grade1B).
ACKNOWLEDGMENTTheeditorialstaffatUpToDatewouldliketoacknowledgePhilipPodrid,MD,whocontributedtoanearlierversionofthistopicreview.
UseofUpToDateissubjecttotheSubscriptionandLicenseAgreement.
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10.RangerS,TalajicM,LemeryR,etal.Amplificationofflecainideinducedventricularconductionslowingbyexercise.Apotentiallysignificantclinical
consequenceofusedependentsodiumchannelblockade.Circulation198979:1000.
11.MillerJM,HsiaHH,RothmanSA,etal.Ventriculartachycardiaversussupraventriculartachycardiawithaberration:electrocardiographicdistinctions.In:
CardiacElectrophysiologyFromCelltoBedside,ZipesDP,JalifeJose(Eds),W.B.Saunders,Philadelphia2000.p.696.
12.WellensHJ,BrFW,LieKI.ThevalueoftheelectrocardiograminthedifferentialdiagnosisofatachycardiawithawidenedQRScomplex.AmJMed1978
64:27.
13.KnightBP,PelosiF,MichaudGF,etal.Physicianinterpretationofelectrocardiographicartifactthatmimicsventriculartachycardia.AmJMed2001110:335.
14.GriffithMJ,deBelderMA,LinkerNJ,etal.Multivariateanalysistosimplifythedifferentialdiagnosisofbroadcomplextachycardia.BrHeartJ199166:166.
15.WellensHJ.Electrophysiology:Ventriculartachycardia:diagnosisofbroadQRScomplextachycardia.Heart200186:579.
16.LauEW,PathamanathanRK,NgGA,etal.TheBayesianapproachimprovestheelectrocardiographicdiagnosisofbroadcomplextachycardia.PacingClin
Electrophysiol200023:1519.
17.CrijnsHJ,vanGelderIC,LieKI.Supraventriculartachycardiamimickingventriculartachycardiaduringflecainidetreatment.AmJCardiol198862:1303.
18.MurdockCJ,KylesAE,YeungLaiWahJA,etal.Atrialflutterinpatientstreatedforatrialfibrillationwithpropafenone.AmJCardiol199066:755.
19.MilitianuA,SalacataA,MeissnerMD,etal.Ventriculoatrialconductioncapabilityandprevalenceof1:1retrogradeconductionduringinduciblesustained
monomorphicventriculartachycardiain305implantablecardioverterdefibrillatorrecipients.PacingClinElectrophysiol199720:2378.
20.HaleyJH,ReederGS.ImagesincardiovascularMedicine.Widecomplextachycardia.Circulation2000102:E52.
21.AlbercaT,AlmendralJ,SanzP,etal.EvaluationofthespecificityofmorphologicalelectrocardiographiccriteriaforthedifferentialdiagnosisofwideQRS
complextachycardiainpatientswithintraventricularconductiondefects.Circulation199796:3527.
22.KindwallKE,BrownJ,JosephsonME.Electrocardiographiccriteriaforventriculartachycardiainwidecomplexleftbundlebranchblockmorphology
tachycardias.AmJCardiol198861:1279.
23.RosenbaumMB.Classificationofventricularextrasystolesaccordingtoform.JElectrocardiol19692:289.
24.SwanickEJ,LaCameraFJr,MarriottHJ.Morphologicfeaturesofrightventricularectopicbeats.AmJCardiol197230:888.
25.GozenskyC,ThorneD.Rabbitears:anaidindistinguishingventricularectopyfromaberration.HeartLung19743:634.
26.BrugadaP,BrugadaJ,MontL,etal.AnewapproachtothedifferentialdiagnosisofaregulartachycardiawithawideQRScomplex.Circulation1991
83:1649.
27.VereckeiA,DurayG,SznsiG,etal.ApplicationofanewalgorithminthedifferentialdiagnosisofwideQRScomplextachycardia.EurHeartJ2007
28:589.
28.EuropeanHeartRhythmAssociation,HeartRhythmSociety,ZipesDP,etal.ACC/AHA/ESC2006guidelinesformanagementofpatientswithventricular
arrhythmiasandthepreventionofsuddencardiacdeath:areportoftheAmericanCollegeofCardiology/AmericanHeartAssociationTaskForceandthe
EuropeanSocietyofCardiologyCommitteeforPracticeGuidelines(WritingCommitteetoDevelopGuidelinesforManagementofPatientsWithVentricular
ArrhythmiasandthePreventionofSuddenCardiacDeath).JAmCollCardiol200648:e247.
29.KaiserE,DarrieuxFC,BarbosaSA,etal.DifferentialdiagnosisofwideQRStachycardias:comparisonoftwoelectrocardiographicalgorithms.Europace
201517:1422.
30.IsenhourJL,CraigS,GibbsM,etal.Widecomplextachycardia:continuedevaluationofdiagnosticcriteria.AcadEmergMed20007:769.
31.LauEW,NgGA.Comparisonoftheperformanceofthreediagnosticalgorithmsforregularbroadcomplextachycardiainpracticalapplication.PacingClin
Electrophysiol200225:822.
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GRAPHICS
SomereportedcausesandpotentiatorsofthelongQTsyndrome*
Congenital Acquired(continued)
JervellandLangeNielsensyndrome(including"channelopathies") Antihistamines
Idiopathic Antineoplasticdrugs
Hypomagnesemia Analgesic,anesthetic,andsedativedrugs
Hypocalcemia Chloralhydrate
Starvation Methadone,hydrocodone
Anorexianervosa Propofol
Liquidproteindiets Diuretics
Hypothyroidism Viaelectrolytechanges(especiallyhypokalemiaor
hypomagnesemia)
Bradyarrhythmias
Gastrointestinaldrugs
Sinusnodedysfunction
Antiemetics:ondansetron,granisetron,dolasetron,droperidol
Atrioventricular(AV)blocksecondorthirddegree
(maybesafeatthelowdosesusedbyanesthesiologists[0.625
Antiarrhythmicdrugs to1.25mg]),hydroxyzine,tropisetron
Quinidine,procainamide,disopyramide Promotility:cisapride(restrictedavailability),domperidone ,
Flecainide,propafenone metoclopramide
Sotalol Gonadotropinreleasinghormoneagonistsandantagonists
Dofetilide,ibutilide Buserelin,degarelix,goserelin,histrelin,leuprolide,triptorelin
Antianginaldrugs Neurologicdrugs
Apomorphine,donepezil,fingolimod,tetrabenazine
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Ranolazine,ivabradine Psychotropicdrugs
Antiinfectivedrugs Antipsychotics
Antimalarial Knownrisk:chlorpromazine,haloperidol,
Knownrisk:artemether,artemetherlumefantrine, methotrimeprazine(levomepromazine) ,pimozide,
chloroquine,halofantrine,lumefantrine,quinidine sulpiride ,thioridazine
Possibleorconditionalrisk:delamanid , Possibleorconditionalrisk:amisulpride ,aripiprazole,
hydroxychloroquine,mefloquine,primaquine,quinine asenapine,clozapine,cyamemazine ,iloperidone,
olanzapine,paliperidone,pipamperone ,quetiapine,
Antituberculous:bedaquiline
risperidone,sertindole ,ziprasidone
Azoleantifungals:fluconazole,itraconazole,ketoconazole
Tricyclicandtetracyclicantidepressants(TCAs)
(systemic),posaconazole,voriconazole
Selectiveserotoninreuptakeinhibitors(lowerriskthanTCAs):
Fluoroquinolones(systemic):ciprofloxacin,gatifloxacin ,
escitalopram,citalopram,fluoxetine
levofloxacin,moxifloxacin,ofloxacin,sparfloxacin
Others:atomoxetine,trazodone
HIVantiretrovirals(some):lopinavir,nelfinavir,saquinavir
Vasodilatordrugs
Macrolideantibiotics:azithromycin,erythromycin,clarithromycin,
telithromycin Bepridil ,cilostazol
Metronidazole Otherdrugsandherbs
Pentamidine(intravenous) Miscellaneous:anagrelide,alfuzosin,arformoterol,cocaine,
formoterol,mifepristone,papaverine(intravenous),pasireotide,
Telavancin
probucol ,terlipressin
Herbs:cinchona(containsquinine),licoriceextract(glycyrrhizin)
inoveruseleadingtoelectrolytechanges
Otherfactors
Myocardialischemiaorinfarction,especiallywithprominentT
waveinversions
Intracranialdisease
HIVinfection
Hypothermia
Toxicexposure:organophosphateinsecticides
ConnectivetissuediseaseswithantiRo/SSAantibodies
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*ThelongandgrowinglistofmedicationsandotherfactorscapableofprolongingtheQTrepresentsanevolvingareaofclinicalresearch.Insomecases
oflongQT,twoormorefactorsmaybeinvolved.ThisisnotacompletelistofalldrugsassociatedwithQTprolongation.Additionalclinicalinformationis
providedattheArizonaCenterforEducationandResearchonTherapeutics(CERT)website:http://crediblemeds.org/.
IncontrastwithotherclassIIIantiarrhythmicdrugs,amiodaroneisrarelyassociatedwithTdPrefertoaccompanyingtextwithinUpToDatetopic
reviewofacquiredlongQTsyndrome.
NotavailableintheUnitedStates.
Removedfrommarketinmostcountriesduetoadversecardiovasculareffects.
ThoughamoxapineandprotriptylinearenotincludedontheArizonaCERTlistofdrugsassociatedwithacquiredQTprolongation,overdoseofthese
tricyclicantidepressantshasbeenassociatedwithcardiovasculartoxicityandfatalities.
Datafrom:
1.NielsenJ,GraffC,KantersJ,etal.AssessingQTintervalprolongationanditsassociatedriskswithantipsychotics.CNSDrugs201125:473.
2.LiE,EsterlyJ,PohlS,etal.DruginducedQTintervalprolongation:Considerationsforclinicians.Pharmacotherapy201030:684.
3.CredibleMedsQTdrugslistwesbsitesponsoredbyScienceFoundationoftheUniversityofArizona.Availableathttp://crediblemeds.org/(Accessed
February20,2016).
4.LexicompOnline.Copyright19782016Lexicomp,Inc.AllRightsReserved.
Graphic57431Version52.0
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VaughanWilliamsclassificationofantiarrhythmicdrugs
ClassIAslowsconductionvelocity(lessthanclassIC)andprolongsactionpotentialduration
Disopyramide
Procainamide*
Quinidine
ClassIBhasnoeffectonconductionvelocityandmayshortenAPD
Lidocaine*
Mexiletine
Phenytoin
ClassICslowsconductionandmayprolongAPD(mild)
Flecainide
Propafenone
ClassIIblocksbetaadrenergicreceptors
Betablockers
ClassIIIprolongsAPDandhasnoeffectonconduction
Amiodarone
Dofetilide
Ibutilide*
Sotalol
Dronedarone
ClassIVcalciumchannelblockers
Nondihydropyridinecalciumchannelblockers(verapamilanddilitiazem)
APD:actionpotentialduration.
*AvailableonlyasanintravenouspreparationinUnitedStates.Oralprocainamideisavailableelsewhere.
lsotalolhasbetablockingandclassIIIactivitiesdsotalolisapureclassIIIagent.Commerciallyavailablesotalolisaracemic(equalpart)mixture.
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VaughanWilliamsEMClassifyingantiarrhythmicactions:byfactsorspeculationJClinPharmacol199232:964.
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CausesofawideQRScomplextachycardia
Ventriculartachycardia(VT)
Anytypeofsupraventriculartachycardia(SVT)withapreexistentbundlebranchblockoraraterelated(functional)bundlebranchblock
Sinustachycardia
Atrialtachycardia
Atrialflutter
Atrioventricularnodalreentranttachycardia
Atrioventricularreentranttachycardia(orthodromic)
AnySVTwhichoccursinapatientreceivinganantiarrhythmicdrug,primarilyclassIAorIC,orinapatientwithseverehyperkalemia
AnySVTwithantegradeconductionviaanaccessorypathway(WolffParkinsonWhitesyndrome)
Sinustachycardia
Atrialtachycardia
Atrialflutter
Atrioventricularreentranttachycardia(antidromic)
Electronicpacemakerincertainspecificsettings
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12leadelectrocardiogram(ECG)recordedinapatient
withrepetitivemonomorphicventriculartachycardia
(RMVT)arisingfromtheleftventricularoutflowtract
(LVOT)
Thiselectrocardiogram(ECG)illustratesrepetitivemonomorphicventricular
tachycardia(RMVT)witharightbundle,inferioraxismorphologysignifyingits
leftventricularsiteoforigin.ThisVTwaslocalizedtotheareaoftheaorto
mitralcontinuityintheleftventricularoutflowtract(LVOT).
Graphic81690Version3.0
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Tremorartifact
Thisdramaticexampleoftremorartifactdemonstratescomplexeswhich
simulatearunofventriculartachycardia.However,QRScomplexes
(arrows)canclearlybeseenmarchingthroughtherhythmstrip.
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AVconductionwithaconcealedaccessorypathway
Schematicrepresentationofatrioventricularconduction.Thenormal
pacemakerisinthesinoatrial(SA)nodeatthejunctionofthe
superiorvenacavaandtherightatrium.TheSAnodeactivatesthe
rightandleftatria(showningreen).Intheabsenceofanaccessory
pathway(AP)or,asinthiscase,iftheAPisconcealed,ventricular
activationresultsfromtheimpulsetraversingtheAVnode,the
specializedinfranodalconductingsystem(Hisbundleandbundleand
fascicularbranches,showninred),therebyactivatingtheventricular
myocardium(showninyellow).TheECGshowsanormalPRinterval
andanarrowQRScomplex.Theinsetontherightshowsthetimingof
SAnode(SAN),right(RA)andleftatrial(LA),Hisbundle(H),andthe
beginningofnormalventricularactivation(V N ).Allofventricular
activation(showninyellow)isduetonormalAVnodalandinfranodal
conduction.
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AVconductionthroughanovertaccessorypathway
Comparedtonormalconductionintheprecedingdiagram,the
accessorypathway(AP)isnowovert.Asaresult,ventricular
activationresultsfrombothearlyactivation(preexcitation)ofthefree
walloftheleftventricle(showninblue)andfromnormalactivation
(showninyellow).Thedegreeofunopposedpreexcitationdepends
uponthetimerequiredtoconductthroughtherightandleftatria,the
AP,andtheventricularmyocardiumascomparedtoconduction
throughthenormalpathways.TheinsetontherightshowstheECG
timingoftheseevents.TheneteffectisaQRScomplexthatisa
fusionofventricularpreexcitation(blue)andnormalexcitation
(yellow).EarlyactivationthroughttheAP(V P )occursataboutthe
sametimeasHisbundledepolarization(H).ThisleadstoashorterPR
interval,asmalldeltawave(arrow),andsomeprolongationofthe
QRSduration.
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ConductionthroughanaccessorypathwaywithAV
nodaldelay
ComparedtoconductionthroughanAPwithnormalAVnode
conduction,delayedconductionthroughtheAVnodeallowsmoreof
theventricularmyocardiumtobeactivatedbypreexcitation(shownin
blue).TheinsetontherightshowstheECGtimingoftheseevents.
TheatrialtoHisintervalisincreasedduetotheAVnodaldelay(RA
toH)Hisactivationissodelayedthatisfollowsactivationcausedby
theAP(V P ).ThePRintervalisshortduetothepreexcitation,the
deltawave(arrow)ismorepronouncedduetothegreaterand
unopposedearlyforces(blue),andtheQRSdurationisprolongeddue
tothelaterthannormalventricularactivationcausedbytheAVnodal
delay(yellow).
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Orthodromicatrioventricularreentranttachycardia
(AVRT)inthesettingofanaccessoryAVpathway
Therhythmstripshowsasinus(S)beatthathasashortPRinterval
andawideQRScomplexasaresultofadeltawave(d).PanelA
showsanatrialprematurebeat(APB,*)thatisblockedinthe
accessorypathway(AP)whichhasalongrefractoryperiodbutis
conductedantegradelythroughtheatrioventricularnode(N)andthe
HisPurkinjesystem,resultinginanormalPRintervalandanarrow
andnormalQRScomplex,asseenontherhythmstrip.Afternormal
myocardialactivation,theimpulseisconductedretrogradelyalongthe
AP,activatingtheatriuminaretrogradefashion(panelB)which
resultsinanegativePwave.Ifthisactivationsequencerepeatsitself
(panelC),anorthodromicatrioventricularreentrant(orreciprocating)
tachycardia(AVRT)isestablished.
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12leadelectrocardiogram(ECG)showingorthodromic
atrioventricularreentranttachycardia(AVRT)inapatient
withanaccessoryAVpathway
The12leadECGfromapatientwithWolffParkinsonWhiteshowsaregular
tachycardia.However,incontrasttotheQRSpatternduringsinusrhythm,theQRS
complexesarenarrow,withoutevidenceofadeltawaveorpreexcitationthisis
duetothefactthatantegradeventricularactivationoccursviathenormal
atrioventricularnodeHisPurkinjepathwaywhileretrogradeatrialactivationisvia
theaccessorypathway.Therefore,thisiscalledanorthodromicatrioventricular
reentranttachycardia(OAVRT).
CourtesyofMartinBurke,DO.
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ECGinWolffParkinsonWhite
The12leadECGshowsthetypicalfeaturesofWolffParkinsonWhitethePR
intervalisshort(*)andtheQRSdurationprolongedasaresultofadeltawave
(arrow),indicatingventricularpreexcitation.
CourtesyofMartinBurke,DO.
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Antidromicatrioventricularreentranttachycardia
(AVRT)inthesettingofanaccessoryAVpathway
Therhythmstripshowsasinus(S)beatthathasashortPRinterval
andawideQRScomplexasaresultofadeltawave(d).PanelA
showstheactivationsequencewithanatrialprematurebeat(APB,*).
Theimpulsereachestheatrioventricularnode(N)beforeithas
repolarizedandhenceisblockedinthisstructure.However,the
accessorypathway(AP),whichhasashortrefractoryperiod,isable
toconducttheimpulseantegradely,resultinginanAPBwitha
widenedQRSmorphologysimilartothesinusbeat.Asseeninpanel
B,followingmyocardialactivation,theimpulseisconducted
retrogradelyalongtheHisPurkinjesystemandAVnode,resultingin
retrogradeatrialactivation,seenontherhythmstripasaninvertedP
wave.Ifthisactivationsequencerepeatsitself(panelC),awideQRS
complexantidromicatrioventricularreentrant(orreciprocating)
tachycardia(AVRT)isestablished.
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12leadelectrocardiogram(ECG)showingantidromic
atrioventricularreentranttachycardia(AVRT)inapatient
withanaccessoryAVpathway
The12leadECGofapatientwithWolffParkinsonWhiteshowsaregular
tachycardia.TheQRScomplexesarewidenedandareidenticaltotheQRS
complexesseeninsinusrhythmtheantegradeconductiontotheventricleisvia
theaccessorypathwayandretrogradeconductionisviathenormalHis
atrioventicularnodepathway.Thisisthereforeanantidromicatrioventricular
reentanttachycardia(AAVRT).
CourtesyofMartinBurke,DO.
Graphic54484Version17.0
ECGinWolffParkinsonWhite
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The12leadECGshowsthetypicalfeaturesofWolffParkinsonWhitethePR
intervalisshort(*)andtheQRSdurationprolongedasaresultofadeltawave
(arrow),indicatingventricularpreexcitation.
CourtesyofMartinBurke,DO.
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12leadelectrocardiogram(ECG)showingatrial
fibrillationandpreexcitationintheWolff
ParkinsonWhite(WPW)syndrome
Thesurface12leadECGshowsatrialfibrillationwitharapid
ventricularresponse.TheQRScomplexesarewideneddueto
antegradeconductionoveraleftlateralaccessorypathway.However,
theQRScomplexesvaryinmorphologyanddurationbecauseof
variabilityinthedegreeofpreexcitationthereisoneQRScomplex
(*)thatisconductedwithoutpreexcitation.
Graphic60790Version4.0
NormalECG
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Normalelectrocardiogramshowingnormalsinusrhythmatarateof75beats/min,aPR
intervalof0.14sec,aQRSintervalof0.10sec,andaQRSaxisofapproximately75.
CourtesyofAryGoldberger,MD.
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12leadelectrocardiogramshowingatrialfibrillationwith
preexcitationinWolffParkinsonWhite(WPW)syndrome
The12leadECGinthispatientwithWolffParkinsonWhitesyndromeshowsatrial
fibrillationwitharapidventricularresponseofover300beatsperminuteandfully
aberrantQRScomplexes.Thisresultsfromrapidatrioventriculartransmissionof
impulsesviaarapidlyconductingaccessorypathway.
CourtesyofMortonFArnsdorf,MD.
Graphic75523Version6.0
NormalECG
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Normalelectrocardiogramshowingnormalsinusrhythmatarateof75beats/min,aPR
intervalof0.14sec,aQRSintervalof0.10sec,andaQRSaxisofapproximately75.
CourtesyofAryGoldberger,MD.
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Preexcitedtachycardiaduringatrialfibrillation
Theventricularrateinthisirregularlyirregulararrhythmiaisextremelyrapid,
approaching500beats/minute.TheQRScomplexesarewideoraberrantandhave
variablemorphologies,suggestingthattherearemultipleaccessoryatrioventricular
connections.Atelectrophysiologicstudy,leftposteriorandleftlateralpathways
wereidentifiedandsuccessfullyablated.
CourtesyofMortonArnsdorf,MD.
Graphic71133Version3.0
NormalECG
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Normalelectrocardiogramshowingnormalsinusrhythmatarateof75beats/min,aPR
intervalof0.14sec,aQRSintervalof0.10sec,andaQRSaxisofapproximately75.
CourtesyofAryGoldberger,MD.
Graphic76183Version3.0
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Atrioventriculardissociation
Independentactivationoftheatriaandventriclesresultsinnofixed
relationshipbetweenthePwaves(arrows)andtheQRScomplexesthePR
intervalsarevariableinarandomfashion.
Graphic52123Version2.0
Normalrhythmstrip
NormalrhythmstripinleadII.ThePRintervalis0.15secandthe
QRSdurationis0.08sec.BoththePandTwavesareupright.
CourtesyofMortonFArnsdorf,MD.
Graphic59022Version3.0
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Fusionbeats
Therhythmstripinapatientwithsustainedventriculartachycardiashowsa
fusionbeatandacapturebeat.Thefusionbeatoccurswhena
supraventricularimpulse(followingthefirstPwave)causesventricular
activation,whichfuseswiththecomplexoriginatingintheventricle,
producingahybridcomplex.ThecomplexfollowingthesecondPwavehas
theappearanceofanormalQRScomplexandisknownasacapturebeat.
Graphic72600Version4.0
Normalrhythmstrip
NormalrhythmstripinleadII.ThePRintervalis0.15secandthe
QRSdurationis0.08sec.BoththePandTwavesareupright.
CourtesyofMortonFArnsdorf,MD.
Graphic59022Version3.0
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BrugadaalgorithmforthediagnosisofwideQRS
tachycardia
Algorithmfordistinguishingventriculartachycardia(VT)from
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supraventriculartachycardia(SVT).
sens:sensitivityspec:specificity.
Graphic73159Version3.0
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Algorithmforthediagnosisofwidecomplex
tachycardia(WCT)
Algorithmforthediagnosisofwidecomplextachycardias.Instep4,
V i representsthemagnitudeofvoltagechangeintheinitial40
millisecondsoftheQRScomplex,whileV t representsthemagnitude
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ofvoltagechangeintheterminal40millisecondsoftheQRScomplex.
TheinitialV i andterminalV t voltagesshouldbemeasuredfromthe
samebiphasicormultiphasicQRScomplex.
AV:atrioventricularBBB:bundlebranchblockFB:fascicularblockSVT:
supraventriculartachycardiaVT:ventriculartachycardia.
Reproducedwithpermissionfrom:Vereckei,A,Duray,G,Szenasi,G,etal.
ApplicationofanewalgorithminthedifferentialdiagnosisofwideQRS
complextachycardia.EurHeartJ200728:589.Copyright2007Oxford
UniversityPress.
Graphic79624Version4.0
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AlgorithmforthediagnosisofwideQRStachycardia
inthesettingofventricularpreexcitation
Algorithmfordistinguishingventriculartachycardia(VT)from
supraventriculartachycardia(SVT)inthesettingofpreexcitation
syndrome.
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Sens:sensitivityspec:specificityECG:electrocardiography.
Graphic59336Version4.0
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Adultcardiacarrestalgorithm:2010ACLSguidelines
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CPR:cardiopulmonaryresuscitationET:endotrachealtubeEtCO2:endtidalcarbondioxideIO:
intraosseousIV:intravenousPEA:pulselesselectricalactivityVF:ventricularfibrillationVT:ventricular
tachycardia.
Reprintedwithpermission.AdultAdvancedCardiovascularLifeSupport:2010.AmericanHeartAssociation
GuidelinesforCardiopulmonaryResuscitationandEmergencyCardiovascularCare.2010American
HeartAssociation,Inc.
Graphic73862Version10.0
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ContributorDisclosures
LeonardIGanz,MD,FHRS,FACCSpeakersBureau:Amgen[Heartfailure(Ivabridine)]Pfizer,BMS[Anticoagulation(Apixaban)]St.JudeMedical,Biotronik
[Cardiacrhythm(Pacemaker/ICD)].Consultant/AdvisoryBoards:UnequalTechnologies[Commotiocordis(Protectiveequipment)].EquityOwnership/Stock
Options:UnequalTechnologies[Commotiocordis(Protectiveequipment/apparel)].PeterJZimetbaum,MDConsultant/AdvisoryBoards:Medtronic[Atrial
fibrillation(Linq)]AryLGoldberger,MDNothingtodisclose.JamesHoekstra,MDConsultant/AdvisoryBoards:AstraZeneca[ACS(Ticagrelor)]Janssen[ACS
(Rivaroxaban)]Novartis[CHF(Serelaxin)].BrianCDowney,MD,FACCNothingtodisclose.
Contributordisclosuresarereviewedforconflictsofinterestbytheeditorialgroup.Whenfound,theseareaddressedbyvettingthroughamultilevelreviewprocess,
andthroughrequirementsforreferencestobeprovidedtosupportthecontent.Appropriatelyreferencedcontentisrequiredofallauthorsandmustconformto
UpToDatestandardsofevidence.
Conflictofinterestpolicy
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