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Thiseditionﬁrstpublished2023

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Setin10/12ptWarnockProbyStraive,Chennai,India

9AblationofSupraventricularTachycardias 221

10AblationofPVCsandVentricularTachycardia 243

11AblationofAtrialFibrillation 268

12AblationofAtrialFlutter 289

13ConductionSystemPacing 310

14CardiacResynchronization:PacingTherapyforHeart Failure 318

15TheEvaluationofSyncope 330

16ElectrophysiologicTestinginPerspective:TheEvaluation andTreatmentofCardiacArrhythmias 344 Index 353

PrefacetotheSeventhEdition

Ourgoalinproducingthisseventheditionof Electrophysiologic Testing isthesameasithasbeenfromthebeginning–todemystify theﬁeldofcardiacelectrophysiologyforthenonelectrophysiologist. Thisbookismeantforstudents,residents,cardiologyfellows(or evencardiologists!),primarycarephysicians,physicianassistants, nurses,technicians,andanyoneelsewhoneedsabasicandrelatively quickunderstandingofelectrophysiologyandcardiacarrhythmias. Asalways,wehaveaimedtoexplain,asclearlyandsimplyaspossible, thekeyconceptsofthemechanisms,evaluation,andtreatment ofcardiacarrhythmias,aselucidatedintheelectrophysiology laboratory.

Inthisedition,wehavestriventoupdatewhatneededtobe updatedwithoutlosingsightofthatoriginal,motivatinggoal.Tokeep thingsassimpleaspossible,inthiseditionwehavedeemphasized (oreliminated)aspectsofelectrophysiologictestingthatwereonce importanttoelectrophysiologists,buttodayareofmainlyhistorical interest.Throughoutthebook,wehavefocusedonthebasicaspects ofcardiacelectrophysiologythatarecriticaltounderstandingand treatingcardiacarrhythmias.Wehavemostextensivelyupdatedthe chaptersonablationtherapy,themostrapidlyevolvingaspectof clinicalelectrophysiology.Additionally,wehaveaddedanewchapter onconductionsystempacing,whichwebelievewillbecomevery importanttocliniciansinthenearfuture.

viii PrefacetotheSeventhEdition

Wesincerelyhopeandtrustthatthisseventheditionof ElectrophysiologyTesting willremainashelpfultoanewgenerationofreaders as,wearetold,pasteditionshavebeentopreviousgenerations.

RichardN.Fogoros,MD

Danville,PA

JohnM.Mandrola,MD Louisville,KY

PartI

DisordersoftheHeartRhythm:BasicPrinciples

TheCardiacElectricalSystem

Theheartspontaneouslygenerateselectricalimpulses,andthese electricalimpulsesarevitaltoallcardiacfunctions.Onabasiclevel,by controllingtheﬂuxofcalciumionsacrossthecardiaccellmembrane, theseelectricalimpulsestriggercardiacmusclecontraction.Ona higherlevel,theheart’selectricalimpulsesorganizethesequenceof musclecontractionsduringeachheartbeat,importantforoptimizing thecardiacstrokevolume.Finally,thepatternandtimingofthese impulsesdeterminetheheartrhythm.Derangementsinthisrhythm oftenimpairtheheart’sabilitytopumpenoughbloodtomeetthe body’sdemands.

Theheart’selectricalsystemisfundamentaltocardiacfunction.The studyoftheelectricalsystemoftheheartiscalledcardiacelectrophysiology,andthemainconcernoftheﬁeldofelectrophysiologyisthe mechanismsandtherapyofcardiacarrhythmias.Theelectrophysiologystudy(EPstudy)isthemostdeﬁnitivemethodofevaluatingthe cardiacelectricalsystem.Itisthesubjectofthisbook.

AsanintroductiontotheﬁeldofelectrophysiologyandtotheEP study,thischapterreviewstheanatomyofthecardiacelectricalsystem anddescribeshowtheelectricalimpulseisgeneratedandpropagated.

Theanatomyoftheheart’selectricalsystem

Theheart’selectricalimpulseoriginatesinthesinoatrial(SA)node, locatedhighintherightatriumnearthesuperiorvenacava.The impulseleavestheSAnodeandspreadsradiallyacrossbothatria. Whentheimpulsereachestheatrioventricular(AV)groove,it encountersthe“skeletonoftheheart,”theﬁbrousstructuretowhich

thevalveringsareattached,andwhichseparatestheatriafrom theventricles.Thisﬁbrousstructureiselectricallyinertandacts asaninsulator–theelectricalimpulsecannotcrossthisstructure. Theelectricalimpulsewouldbepreventedfromcrossingoverto theventricularsideoftheAVgrooveifnotforthespecializedAV conductingtissues:theAVnodeandthebundleofHis(Figure1.1).

AstheelectricalimpulseenterstheAVnode,itsconductionis slowedbecauseoftheelectrophysiologicpropertiesoftheAVnodal tissue.ThisslowingisreﬂectedinthePRintervalonthesurface electrocardiogram(ECG).LeavingtheAVnode,theelectricalimpulse enterstheHisbundle,themostproximalpartoftherapidlyconductingHis–Purkinjesystem.TheHisbundlepenetratestheﬁbrous skeletonanddeliverstheimpulsetotheventricularsideoftheAV groove.

Onceontheventricularside,theelectricalimpulsefollowstheHis bundleasitbranchesintotherightandleftbundlebranches.BranchingofthePurkinjeﬁberscontinuesdistallytothefurthermostreaches

SA node

His bundle Purkinje fibers

Fibrous skeleton of the heart

oftheventricularmyocardium.Theelectricalimpulseisthusrapidly distributedthroughouttheventricles.

The“job”oftheheart’selectricalsystemistoorganizethesequence ofmyocardialcontractionwitheachheartbeat.First,astheelectricalimpulsespreadsovertheatriatowardtheAVgroove,theatria contract.ThedelayprovidedbytheAVnodeallowsforcompleteatrial emptyingbeforetheelectricalimpulsereachestheventricles.Once theimpulseleavestheAVnode,itisdistributedrapidlythroughout theventricularmusclebythePurkinjeﬁbers,providingforbriskand orderlyventricularcontraction.

Wenextconsiderthecharacteroftheelectricalimpulse,its generation,anditspropagation.

Thecardiacactionpotential

Thecardiacactionpotentialisoneofthemostmisunderstoodtopics incardiology.Thefactthatelectrophysiologistsclaimtounderstandit isalsoaleadingcauseofthemystiquethatsurroundsthemandtheir favoritetest,theEPstudy.Sincethepurposeofthisbookistodebunk themysteryofelectrophysiologystudies,wemustgainabasicunderstandingofthecardiacactionpotential.Fortunately,it’seasierthan legendwouldhaveit.

Althoughmostofuswouldliketothinkofcardiacarrhythmiasasan irritationor“itch”oftheheart(andofantiarrhythmicdrugsasabalm orasalvethatsoothestheitch),thisnotionofarrhythmiasiswrong andcanleadtothefaultymanagementofpatientswitharrhythmias. Infact,thebehavioroftheheart’selectricalimpulseandofthecardiac rhythmislargelydeterminedbytheshapeoftheactionpotential;the eﬀectofantiarrhythmicdrugsisdeterminedbyhowtheychangethat shape.

Theinsideofthecardiaccell,likealllivingcells,hasanegative electricalchargecomparedtotheoutsideofthecell.Theresulting voltagediﬀerenceacrossthecellmembraneiscalledthe transmembranepotential .Therestingtransmembranepotential(whichis 80 to 90mVincardiacmuscle)istheresultofanaccumulationof negativelychargedmolecules(calledions)withinthecell.Mostofthe body’scellsarehappywiththisarrangementandliveouttheirlives withoutconsideringanyotherpossibilities.

Figure1.2 Thecardiacactionpotential.

Cardiaccells,however,arediﬀerent–theyareexcitablecells.When excitablecellsarestimulatedappropriately,tinyporesorchannels inthecellmembraneopenandclosesequentiallyinastereotyped fashion.Theopeningofthesechannelsallowsionstotravelback andforthacrossthecellmembrane(againinastereotypedfashion), leadingtopatternedchangesinthetransmembranepotential.When thesestereotypicvoltagechangesaregraphedagainsttime,theresult isthecardiacactionpotential(Figure1.2).Theactionpotential reﬂectstheelectricalactivityofasinglecardiaccell.

Figure1.2showstheﬁvephasesoftheactionpotential,which encompassthreegeneralperiods:depolarization,repolarization,and therestingphase.

Depolarization

Thedepolarizationphase(phase0)iswherethe“action”oftheaction potentialis.Depolarizationoccurswhentherapidsodiumchannelsin thecellmembranearestimulatedtoopen.Whenthishappens,positivelychargedsodiumionsrushintothecell,causingarapid,positively directedchangeinthetransmembranepotential.Theresultantvoltage

spikeiscalled depolarization.Whenwespeakoftheheart’selectrical impulse,wearespeakingofthisdepolarization.

Depolarizationofonecelltendstocauseadjacentcardiaccellsto depolarize,becausethevoltagespikeofacell’sdepolarizationcauses thesodiumchannelsinthenearbycellstoopen.Thus,onceacardiac cellisstimulatedtodepolarize,thewaveofdepolarization(theelectricalimpulse)ispropagatedacrosstheheart,cellbycell.

Thespeedofdepolarizationofacell(reﬂectedbytheslopeofphase 0oftheactionpotential)determineshowsoonthenextcellwilldepolarize,andthusdeterminesthespeedatwhichtheelectricalimpulseis propagatedacrosstheheart.Ifwedosomethingtochangethespeedat whichsodiumionsenterthecell(andthuschangetheslopeofphase0), wethereforechangethespeedofconduction(theconductionvelocity) ofcardiactissue.

Repolarization

Onceacellisdepolarized,itcannotbedepolarizedagainuntiltheionic ﬂuxesthatoccurduringdepolarizationarereversed.Theprocessof gettingtheionsbacktowheretheystartediscalled repolarization. Therepolarizationofthecardiaccellroughlycorrespondstophases 1through3(i.e.,thewidth)oftheactionpotential.Becauseasecond depolarizationcannottakeplaceuntilrepolarizationoccurs,thetime fromtheendofphase0tolateinphase3iscalledthe refractoryperiod ofcardiactissue.

Repolarizationofthecardiaccellsiscomplexandincompletely understood.Themainideasbehindrepolarization,however,are simple.

• Repolarizationreturnsthecardiacactionpotentialtotheresting transmembranepotential.

• Ittakestimetodothis.

• Thetimethatittakestodothis,roughlycorrespondingtothewidth oftheactionpotential,istherefractoryperiodofcardiactissue.

Thereisanadditionalpointofinterestregardingrepolarization ofthecardiacactionpotential.Phase2oftheactionpotential,the so-calledplateauphase,canbeviewedasinterruptingandprolonging therepolarizationthatbeginsinphase1.Thisplateauphase,which isuniquetocardiaccells(e.g.,itisnotseeninnervecells),gives durationtothecardiacpotential.Itismostlymediatedbytheslow

usuallysecondarypacemakercells(oftenlocatedintheAVjunction) totakeoverthepacemakerfunctionoftheheart,butataslowerrate. Thus,theshapeoftheactionpotentialdeterminestheconduction velocity,refractoryperiod,andautomaticityofcardiactissue.Later, wewillseehowthesethreeelectrophysiologiccharacteristicsdirectly aﬀectthemechanismsofcardiacrhythms,bothnormalandabnormal.Toalargeextent,thepurposeoftheEPstudyistoassessthe conductionvelocities,refractoryperiods,andautomaticityofvarious portionsoftheheart’selectricalsystem.

Localizedvariationsintheheart’selectrical system

Inunderstandingcardiacarrhythmias,itisimportanttoconsider twoissuesinvolvinglocalizeddiﬀerencesintheheart’selectrical system:variationsintheactionpotentialandvariationsinautonomic innervation.

Localizeddiﬀerencesintheactionpotential

Diﬀerentcardiaccellshavediﬀerentlyshapedactionpotentials.The actionpotentialwehavebeenusingasamodel(seeFigure1.2)isa

Figure1.4 Localizeddifferencesinthecardiacactionpotential.Cardiacaction potentialsfromdifferentlocationswithinthehearthavedifferentshapes.These differencesaccountforthedifferencesseenintheelectrophysiologicproperties ofvarioustissueswithintheheart.

SA node

AV nodePurkinje fiberVentricular muscle

Atrial muscle

typicalPurkinjeﬁberactionpotential.Figure1.4showsrepresentative actionpotentialsfromseveralkeylocationsoftheheart–notethe diﬀerencesinshape.

TheactionpotentialsthatdiﬀermostradicallyfromthePurkinje ﬁbermodelarefoundintheSAandAVnodes.Notethattheaction potentialsfromthesetissueshaveslowinsteadofrapiddepolarization phases(phase0).ThisslowdepolarizationoccursbecauseSAand AVnodaltissueslacktherapidsodiumchannelsresponsibleforthe rapiddepolarizationphase(phase0)seeninothercardiactissues.In fact,theSAandAVnodesarethoughttobeentirelydependenton theslowcalciumchannelfordepolarization.Becausethespeedof depolarizationdeterminesconductionvelocity,theSAandAVnodes

Figure1.5 Relationshipbetweentheventricularactionpotential(top)andthe surfaceECG(bottom).Therapiddepolarizationphase(phase0)oftheaction potentialisreflectedintheQRScomplexonthesurfaceECG.Becausephase0is almostinstantaneous,theQRScomplexyieldsdirectionalinformationon ventriculardepolarization.Incontrast,therepolarizationportionoftheaction potentialhassignificantduration(phases2and3).Consequently,theportionof thesurfaceECGthatreflectsrepolarization(theSTsegmentandTwave)yields littledirectionalinformation.PRinterval,beginningofPtobeginningofQRS;ST segment,endofQRStobeginningofT;QTinterval,beginningofQRStoendofT.

conductelectricalimpulsesslowly.TheslowconductionintheAV nodeisreﬂectedinthePRintervalonthesurfaceECG(Figure1.5).

Localizeddiﬀerencesinautonomicinnervation

Ingeneral,anincreaseinsympathetictone,forexampleduring exercise,causesenhancedautomaticity(pacemakercellsﬁremore rapidly),increasedconductionvelocity(electricalimpulsesarepropagatedmorerapidly),anddecreasedactionpotentialdurationand thusdecreasedrefractoryperiods(cellsbecomereadyforrepeated depolarizationsmorequickly).Parasympathetictonehastheopposite eﬀect(i.e.,depressedautomaticity,decreasedconductionvelocity, andincreasedrefractoryperiods).

Sympatheticandparasympatheticﬁbersrichlyinnervateboththe SAandtheAVnode.Intheremainderoftheheart’selectricalsystem, whilesympatheticinnervationisabundant,parasympatheticinnervationisrelativelysparse.Thus,changesinparasympathetictonehavea relativelygreatereﬀectontheSAandAVnodaltissuesthanonother tissuesoftheheart.Thisfacthasimplicationsforthediagnosisand treatmentofsomeheartrhythmdisturbances.

Relationshipbetweenactionpotential andsurfaceECG

Thecardiacactionpotentialrepresentstheelectricalactivityofasinglecardiaccell.ButthesurfaceECGreﬂectstheelectricalactivityof theentireheart–essentially,thesumofalltheactionpotentialsofall cardiaccells.Consequently,theinformationonecangleanfromthe surfaceECGderivesfromthecharacteristicsoftheactionpotential (seeFigure1.5).

Formostcardiaccells,thedepolarizationphaseoftheaction potentialisessentiallyinstantaneous(occurringin1–3ms)and occurssequentially,fromcelltocell.Thus,theinstantaneouswave ofdepolarizationcanbefollowedacrosstheheartbystudyingthe ECG.ThePwaverepresentsthedepolarizationfrontasittraverses theatria,andtheQRScomplextracksthewaveofdepolarizationas itspreadsacrosstheventricles.Changesinthespreadoftheelectricalimpulse,suchasoccurinbundlebranchblockortransmural

myocardialinfarction,canbereadilydiagnosedbyinspectingthe ECG.Becausethedepolarizationphaseoftheactionpotentialis relativelyinstantaneous,thePwaveandtheQRScomplexcanyield speciﬁcdirectionalinformation(i.e.,informationonthesequenceof depolarizationofcardiacmuscle).

Incontrast,therepolarizationphaseoftheactionpotentialisnot instantaneous–indeed,repolarizationhassignificantduration.While depolarizationoccursfromcelltocellsequentially,repolarization occursinmanycardiaccellssimultaneously.Forthisreason,theST segmentandTwave(theportionsofthesurfaceECGthatreflect ventricularrepolarization)givelittledirectionalinformation,and abnormalitiesintheSTsegmentsandTwavesaremostoften(and quiteproperly)interpretedasbeingnonspecific.TheQTinterval representsthetimeofrepolarizationoftheventricularmyocardium andreflectstheaverageactionpotentialdurationofventricular muscle.

AbnormalHeartRhythms

Abnormalitiesintheelectricalsystemoftheheartresultintwogeneral typesofcardiacarrhythmia:heartrhythmsthataretooslow(bradyarrhythmias)andheartrhythmsthataretoofast(tachyarrhythmias).

Bradyarrhythmias

Therearetwobroadcategoriesofabnormallyslowheartrhythms–the failureofpacemakercellstogenerateappropriateelectricalimpulses (disordersofautomaticity)andthefailuretopropagateelectrical impulsesappropriately(heartblock).

Failureofimpulsegeneration

Failureofsinoatrial(SA)nodalautomaticity,resultinginaninsufﬁcientnumberofelectricalimpulsesemanatingfromtheSAnode (i.e.,sinusbradycardia[Figure2.1]),isthemostcommoncauseof bradyarrhythmias.Iftheslowedheartrateisinsuﬃcienttomeetthe body’sdemands,symptomsresult.Symptomaticsinusbradycardia iscalled sicksinussyndrome.Ifsinusslowingisprofound,subsidiary pacemakerslocatedneartheatrioventricular(AV)junctioncantake overthepacemakerfunctionoftheheart.Theelectrophysiologystudy (EPstudy),aswewillseeinChapter5,canbeusefulinassessingSA nodalautomaticity.

Figure2.3 Examplesofescapepacemakers.WhenblockislocalizedtotheAV node(toptracing),junctionalescapepacemakers(JE)areusuallystableenough topreventhemodynamiccollapse.Whenblockislocatedinthedistalconducting tissues(bottomtracing),escapepacemakersareusuallylocatedintheventricles (VE)andareslowerandmuchlessstable.

theventriclesisintermittent;thatis,someimpulsesareconducted andsomeareblocked.Third-degreeAVblockmeansthatblockis completeandnoatrialimpulsesareconductedtotheventricles.

Ifthird-degreeAVblockispresent,thensustaininglifedepends onthefunctionofsubsidiarypacemakersdistaltothesiteofblock. Thecompetenceofthesesubsidiarypacemakers,andthereforethe patient’sprognosis,dependslargelyonthesiteofblock(Figure2.3). WhenblockiswithintheAVnode,subsidiarypacemakersatthe AVjunctionusuallytakeoverthepacemakerfunctionoftheheart, resultinginarelativelystable,nonlife-threateningheartrhythm,with aratethatcanexceed50beats/min.Ontheotherhand,ifblockis distaltotheAVnode,thesubsidiarypacemakerstendtoproducea profoundlyslow(usuallylessthan40beats/min)andunstableheart rhythm.

Ifheartblockislessthancomplete(i.e.,ﬁrstorseconddegree),it isstillimportanttopinpointthesiteofblocktoeithertheAVnode ortheHis–Purkinjesystem.First-orsecond-degreeblockintheAV nodeisbenignandtendseithernottoprogressortoprogressslowly. Permanentpacingisrarelyrequired.First-andespeciallyseconddegreeblockdistaltotheAVnode,ontheotherhand,tendtoprogress toahigherdegreeofblockandprophylacticpacingcanbeindicated iftherearesymptoms.

DiﬀerentiatingthesiteofheartblockcanusuallybedonenoninvasivelybystudyingthesurfaceECGandtakingadvantageofthefactthat

theAVnodehasrichautonomicinnervationandtheHis–Purkinje systemdoesnot.Sometimes,however,theEPstudyisusefulin locatingthesiteofblock.Chapter5considersheartblockindetail.

Tachyarrhythmias

Cardiactachyarrhythmiascancausesigniﬁcantmortalityandmorbidity.ItistheabilityoftheEPstudytoaddresstheevaluationand treatmentoftachyarrhythmiasthathasbroughtthisprocedureinto widespreaduse.Wewilldiscussthreemechanismsfortachyarrhythmias:automaticity,reentry,andtriggeredactivity.

Automaticity

Automaticityaccountsfornormalpacemakerfunctionoftheheart. Butwhenabnormalaccelerationofphase4activityoccursinsome locationoftheheart,anautomatictachyarrhythmiaissaidtooccur (Figure2.4).Suchanabnormalautomaticfocuscanoccuranywhere intheheart.

Automaticityaccountsforlessthan10%ofallabnormaltachyarrhythmias.Automatictachyarrhythmiasareusuallyrecognizable bytheircharacteristicsandthesettingsinwhichtheyoccur.

Tounderstandautomatictachyarrhythmias,ithelpstoconsider thecharacteristicsofsinustachycardia,whichisa normal automatic tachycardia.Sinustachycardiausuallyoccursasaresultofappropriatelyincreasedsympathetictone(forinstance,inresponseto increasedmetabolicneedsduringexercise).Whensinustachycardia develops,theheartrategraduallyincreasesfromthebasic(resting)

Figure2.4 Abnormalautomaticitycausestherapidgenerationofaction potentialsandthusinappropriatetachycardia.