arritmias

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http://accessmedicine.mhmedical.com.consultaremota.upb.edu.co/content.aspx?bookid=385&sectionid=40357251 1/39

CURRENTDiagnosis&TreatmentEmergencyMedicine,7e>

Chapter35.CardiacArrhythmiasJosephHeidenreich,MD

CardiacArrhythmias:IntroductionPatientswithcardiacarrhythmiasoftenpresenttotheemergencydepartment.Thepatient'sclinicalpresentationdeterminestheurgencywithwhichtheassessmentandmanagementshouldproceed.Patientswithserioussignsandsymptoms(ie,shock,hypotension,congestiveheartfailure(CHF),severeshortnessofbreath,alteredlevelofconsciousness,ischemicchestpain,oracutemyocardialinfarction)requireimmediatetreatment.Withstablepatients,moretimeisaffordedforreviewofthe12leadelectrocardiogram(ECG)andrhythmstriptodiagnosethecardiacarrhythmia.ReviewofavailablepriorECGsmayalsoassistinarrhythmiadiagnosis.

ElevenHelpfulHintsforEmergencyDepartmentArrhythmias1. Obtainasmuchinformationasavailable.Alwayslookatall12leadsandbesureofname,date,age,correct

leadplacement,andstandardization.

2. Knowwhateachleadlookslikenormally(Figure351)eg,leadI(andusuallyleadIIandaVF)shouldlooklikethetextbookPQRSTexceptnoQwave.InleadI,theP,QRS,andTshouldallbeupright,theintervalsshouldbenormalandthePRandSTbaselinesshouldbeisoelectric.

3. Aregulartachycardiawitharatecloseto150shouldpromptasearchforatrialflutter.

4. Precisediagnosisofwidecomplextachycardias(WCTs)canbedifficult.Ifventricularrateisirregularconsideratrialfibrillation(AF)oratrialflutterwithvariableconductionandunderlyingbundlebranchblock(BBB).

5. Donotrelyoncomputerreadings.Theymayormaynotbecorrect.

6. Singleleadrhythmstripsmaynothaveenoughinformation.Iftimepermits,alwaysobtaina12leadECG.

7. YoucannothavetoomanyECGs.SerialECGsareimportant.Sinustachycardiaratestendtochangeovertime.

8. ArrhythmiasarecommoninacuteSTelevationmyocardialinfarctions.

9. TachyarrhythmiasaredividedintonarroworwideQRSwidthandthenintoregularorirregular.

10. Arrhythmiaclassificationsandterminologiescanbeconfusingandtheychangeasnewinformationbecomesavailable.

11. Iftheheartrhythmisslowandthepatientishypotensivewithsignsofpoorperfusion,assumetransthoracicortransvenouspacingwillbeneeded.

FIGURE351.

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NormalECG.

ANoteonCardioversionandDefibrillation

NoconsensusexistsoncorrectpadpositioningandcurrentACLSguidelinesendorseboththeconventionalorsternalapicalpositioning(onepadonthesuperioranteriorrightchestjustbelowtheleveloftheclavicleandonepadontheinferolateralleftchest)andtheanteroposterior(theanteriorpadasintheconventionalmethodandtheposteriorpadontherightorleftupperback).However,someauthorsfeelthatanteroposteriorplacementwiththeanteriorpadovertherightatriumandtheposteriorpadatthetipoftheleftscapulaoptimizescardioversionofatrialtachyarrhythmiaswhileplacementoftheanteriorpadovertheventriclesandposteriorpadagainatthetipoftheleftscapulaworkswellforventriculararrhythmias.

Allcurrentlymanufactureddefibrillatorsusebiphasicwaveformssounlessyouareusinganoldermachine,theenergysettingwillrangefrom0Joules(J)to200J.Allenergydosesmentionedinthischapterwillbeforbiphasicdefibrillators.Inadditiontodiseasespecificenergyrecommendations,therearedevicespecificrecommendationsforthedifferentbiphasicdefibrillatormodelsforfirstshockenergydoseinsomesituations.Notably,inventricularfibrillation(VF)orpulselessventriculartachycardia(VT)theinitialshockis120fordevicesusingarectilinearwaveformand150200Jfordevicesusingatruncatedexponentialwaveformrangingfrom120to200J.ACLS

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guidelinesrecommendthatIFTHEOPERATORISUNSUREofdevicespecificrecommendationsthenthedefibrillator'shighestenergylevelshouldbeusedinthissettingthiswillbe200Jforallbiphasicunitsand360Jifyouhappentostillhaveamonophasicunit.Thebottomlineisthatifyouareuncertainontheenergydoseinanyemergentsituationwhereelectricityisrequiredforanadultyourbestbetisturntheenergyupashighasitwillgoasevenmaximaldosesofenergyarefelttoberelativelysafe.

TachyarrhythmiasImmediatesynchronizedcardioversionshouldbeperformedonallunstablepatientswithtachydsrythmias.Thespecificarrhythmiadiagnosis(supraventricularorventricular)doesnotneedtobemadeimmediatelybecauseinitialmanagementisthesame.Patientswithpolymorphicventriculartachycardia(PMVT)of30secondsormoreandallunstablepatientsshouldbetreatedwithimmediatedefibrillation.

Instablepatients,theinitialmedicalmanagementwillbeguidedbytheunderlyingrhythmandadetailedhistoryandphysicalexamination.Inrecentyears,themoretraditionalapproachtocategorizepatientsaseitherstableorunstablehasbeenmodified.Hemodynamicallystablepatientscanbefurthersubdividedintothosewithpreservedorimpairedcardiacfunction.Findingsofimpairedcardiacfunctioninapatientwhoisotherwisestablemayalterthepharmacologictreatment.

SupraventricularArrhythmias

SinusTachycardia

ClinicalFindings

(SeeAppendix,Figure353.)Sinustachycardiaoccurswhenthesinusrateisfasterthan100beats/min.Usuallytherateis101160beats/min.Young,healthyadultscanacceleratetheirheartrateupto180200beats/min,particularlyduringexercise.Youngchildrenhavebeennotedtohavesinusratesupto220beats/min.Sinustachycardiashouldnotbeviewedasaprimaryarrhythmiabutmoreasaresponsetoanunderlyingillnessorcondition.Itisoftennormalininfancyandearlychildhoodbutcanoccurasaresultofanumberofconditionsincludingpain,fever,stress,hyperadrenergicstates,anemia,hypovolemia,hypoxia,myocardialischemia,pulmonaryedema,shock,andhyperthyroidism.Certainmedicationsandillicitdrugscanalsocausetachycardia.ThePwaveinsinustachycardiashouldhaveapositiveaxisinthefrontalplane,ie,thePwaveshouldbepositiveinleadIandaVF.

TreatmentandDisposition

Thetreatmentofsinustachycardiaisdirectedattheunderlyingcause.Thismayincludecorrectionofdehydrationwithintravenousfluids,analgesicorantipyreticadministration,orsupplementaloxygentocorrecthypoxia.Treatmentaimedatcorrectingtheheartrateratherthantheunderlyingconditionmaybeharmfulifthetachycardiaiscompensatoryandissupportingthecardiacoutput.Gradualslowingoftheheartratewithtreatmentoftheunderlyingconditionorduringcarotidsinusmassagemayhelptodifferentiatesinustachycardiafromothersupraventriculararrhythmias.Adenosineadministrationwitha12leadrhythmstripishelpfulindifferentiatingfromothercausesoftachyarrhythmias.Furthermanagement,includingtheneedforhospitalization,dependsontheunderlyingcondition.

ParoxysmalSupraventricularTachycardia

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ClinicalFindings

(SeeAppendix,Figures356,357,358,359,3510,and3511.)Paroxysmalsupraventriculartachycardia(PSVT)isageneraltermthatreferstoanumberoftachyarrhythmiasthatarisefromabovethebifurcationoftheHisbundle.Approximately90%ofthesearrhythmiasoccurasaresultofareentrantmechanismtheremaining10%occurasaresultofincreasedautomaticity.

Atrioventricularnodalreentranttachycardia(AVNRT)isthemostcommonformofPSVT,accountingfor5060%ofcases.Theheartrateisusually180200beats/minandischaracterizedbysuddenonsetandsuddentermination.BecausethereentrantmechanismoccurswithintheAVnodeitself,virtuallysimultaneousexcitationoftheatriaandventriclesoccurs.Asaresult,thePwavesoccurconcurrentwiththeQRScomplexesandaredifficulttovisualizeontheECG.Often,patientswithAVNRTdonothaveunderlyingheartdisease.Commonprecipitatingfactorsincludealcohol,caffeine,andsympathomimeticamines.PatientswithAVNRTusuallypresentintheirthirdorfourthdecadeoflife,andthemajority(approximately70%)arefemale.

Atrioventricularreciprocatingtachycardia(AVRT)accountsfor30%ofPSVT.Inmostcases,theimpulsetravelsdowntheAVnodeandfollowsaretrogradepathuptheaccessorybypasstract.Becauseactivationoftheventriclesoccursthroughnormalconductionpathways,theaccessorypathwayisconcealed,andtheQRSmorphologyisnormal.ConsiderAVRTiftheheartrateisfasterthan200beats/minorifPwavesareseenfollowingtheQRScomplex.

SinusnodereentryandintraatrialreentryareuncommoncausesofPSVT,accountingforapproximately5%ofcases.Inthesearrhythmias,theheartrateisusually130140beats/min.Moreoften,patientswiththesearrhythmiashaveunderlyingheartdisease.

Automaticatrialtachycardiaisanotheruncommonarrhythmia,accountingforlessthan5%ofcasesofPSVT.Theheartrateisusually160250beats/minbutmaybeasslowas140beats/min.Inthiscase,theunderlyingmechanismisincreasedautomaticityratherthanreentry.Automaticatrialtachycardiaiscommonlyassociatedwithunderlyingheartdisease.Thisarrhythmiaisdifficulttotreatandmayberefractorytostandardmeasuresincludingcardioversion.

PSVTcanbeclassifiedasAVnodaldependentorindependent.Thisstrategymayproveusefulinformulatingtreatmentoptions.AVNRTandAVRTareAVnodaldependent,meaningthattheAVnodeisinvolvedinthereentrantcircuit.Fortheserhythms,pharmacologicmanagementisdesignedtodecreaseconductionthroughtheAVnode.

Treatment

UNSTABLEPATIENTS

PatientswithPSVTwhoarehemodynamicallyunstablerequireimmediatesynchronizedDCcardioversion.Currentrecommendationsaretostartwithlowenergylevels(50100J)andthentoincreasetheinitialdoseby50Jasneededuntilsinusrhythmisrestored.Ifclinicalcircumstancespermit,administerintravenoussedatives.Avoidthecommonerrorofdelayingemergencycardioversiontoperformotherpatientcareactivities.Ifimmediatecardioversionisunavailable,physicalmaneuversthatcausevagalstimulationcanbeattempted.

Adenosine,blocker,orcalciumchannelblockermaybeadministered.

STABLEPATIENTS

TachycardiaassociatedwithPSVTisusuallywelltoleratedunlessthepatienthasunderlyingheartdiseaseorleftventriculardysfunction.

PhysicalManeuvers

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Instablepatients,physicalmaneuverscausingvagalstimulationcanbeattemptedpriortomedicationadministration.ManeuversthatstimulatethevagusnervesuchastheValsalvamaneuver(expirationagainstaclosedglottis),Muellermaneuver(deepinspirationagainstaclosedglottis),coldwaterfacialimmersion,andcarotidsinusmassageareattimeseffectiveinterminatingPSVTthatresultsfromAVnodalandsinoatrial(SA)nodaldependentmechanisms.Performcarotidsinusmassageonlyafterauscultationforcarotidbruits.

PharmacologicTreatment

Ifvagalstimulationiscontraindicatedorineffective,adenosineisconsideredfirstlinemedicaltherapyforconversionofPSVT.Ingeneral,pharmacologicagentswithAVnodalblockingpropertiessuchasadenosine,blockers,calciumchannelblockers,anddigoxinareusedfortheacutemanagementandpreventionofAVnodaldependentPSVT.Otherantiarrhythmicagents,suchasprocainamideandamiodarone,whichexerteffectsatvariouslevelsofthecardiacconductionsystemareusedforthemanagementandpreventionofAVnodalindependentPSVT.AntiarrhythmicmedicationsmaybeconsideredforconversionofPSVTwhenAVnodalblockingagentsareunsuccessful.

Adenosine

AdenosineisanendogenousnucleosidethatslowsconductionthroughtheAVnodeandissuccessfulinterminatingmorethan90%ofPSVTsresultingfromAVnodalreentrymechanisms(AVNRTandAVRT).Adenosinemayalsobeeffectiveinterminatingsinusnodereentrytachycardiabutisusuallyineffectiveinterminatingautomaticatrialtachycardia.OftenadenosinewillcauseatransientAVblock,brieflyexposingtheunderlyingatrialactivity.AdministrationofamedicationwithmoreprolongedeffectontheAVnode(blockersorcalciumchannelblockers)mayprovideamoresustainedreductioninventricularrate.

Administeradenosinerapidly,andfolloweachdoseimmediatelywitha20ccsalineflush.Althoughcurrentrecommendationsaretoadministeraninitialintravenousdoseof6mgover13secondsrepeatedat2and4minuteswith12mgdosesifthisdoesnotterminatethePSVT,manyclinicianschoosetoforgotheinitial6mgdoseandwillincreasethedoseto18mgifthe12mgdosedoesnotproduceAVblockade.The18mgdosehasbeenshowntobebothsafeandeffective.Commonsideeffectsincludeunexplainablefeelingofimpendingdoom,facialflushing,hyperventilation,dyspnea,andchestpain.Thesesideeffectsareoftentransientowingtotheshorthalflifeofadenosine(lessthan5seconds).Prewarningtothepatientofthesesymptomsishelpful.Theeffectsofadenosineareantagonizedbycaffeineandtheophyllineandpotentiatedbydipyridamoleandcarbamazepine.Hearttransplantpatientsmaybeoverlysensitivetotheeffectsofadenosineifnecessary,usesmallerdoses.Becauseadenosinecanprovokebronchospasm,usecautionifitisbeingadministeredtopatientswithahistoryofreactiveairwaydisease.

AdenosinecanalsobeadministeredtoastablepatientwithawideQRScomplextachycardiasuspectedtobesupraventricularinorigin.Adenosineispreferredovercalciumchannelblockersinpatientswithhypotensionorimpairedcardiacfunctionandinpatientsconcomitantlyreceivingadrenergicblockingagents.

BlockingAgents

blockerssuchasmetoprololoresmololslowSAnodeimpulseformationandslowconductionthroughtheAVnode.ThesemedicationsshouldbeusedwithcautioninpatientswithahistoryofseverereactiveairwaydiseaseandCHF.

Metoprololisanalternativetocalciumchannelblockers,andisadministeredintravenouslyatadoseof5mgevery5minutesforthreedoses.Esmololisanultrashortacting1selectiveblockerthathastheadvantageofabriefhalflife(10minutes)andarapidonsetofaction.Administeraloadingdoseof0.5mg/kgover1minute.Thisisfollowedbyamaintenanceinfusionof50g/kg/min.Iftheresponseisinadequate,anotherdoseof0.5mg/kgcanbeadministeredafter4minutesandthemaintenanceinfusionincreasedto100g/kg/min.Whenheart

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ratecontrolisachieved,reducethemaintenanceinfusionto25g/kg/min.

CalciumChannelBlockers

CalciumchannelblockerssuchasdiltiazemorverapamilareeffectiveinconvertingPSVTtosinusrhythm.Theefficacyofdiltiazemandverapamilintermsofconversionrates,rapidityofresponse,andsafetyprofileappearsimilar.ThesemedicationsdecreaseSAandAVnodeconductionandcauseprolongationoftheAVnoderefractoryperiod.Calciumchannelblockersalsodecreasemyocardialcontractilityandperipheralvascularresistance.UsecalciumchannelblockerswithcautioninpatientswithleftventriculardysfunctionorCHF.AvoidthesemedicationsinpatientswithWCTofunknownorigin,ventriculartachycardia(VT),ortachycardiawithventricularpreexcitation.Hypotensionisthemostconcerningsideeffectofintravenousadministrationandoccursin1015%ofpatients.

Verapamil

Theinitialdoseofverapamilis510mgadministeredintravenouslyover12minutes.Additionaldosesof510mgcanbeadministeredevery15minutesasneededuntilthedesiredeffectisachievedoratotalof30mghasbeenadministered.

Diltiazem

Theinitialdoseofdiltiazemis0.25mg/kgadministeredintravenouslyover2minutes(20mgfortheaverageadult).Ifnecessary,adoseof0.35mg/kgcanbeadministeredin15minutes.Afterconversion,amaintenanceinfusioncanbestartedat510mg/handcanbeincreasedtoamaximumof15mg/hifneeded.

Thechoicebetweenblockersandcalciumchannelblockersdependsonmultiplefactors,butbothshouldnotbegivenintravenouslytothesamepatient.Bothhaverapidonset(minutes)andbothshouldbeusedwithcautioninsevereCOPDandsevereCHF.Medicationthatthepatientiscurrentlytakingandphysicianpreferenceareconsiderations.Inpatientswithhyperthyroidismandcongenitalheartdisease,blockersarethebestchoice.

Digoxin

Digoxinadministrationwillincreasevagaltonewhilereducingsympatheticactivity.Asaresult,conductionthroughtheAVnodeisslowed.Digoxinmaybeadministeredasanintravenousbolusdoseof0.5mg.Additionaldosesof0.25mgmaybegivenasneededevery46hours,withatotaldosenottoexceed1.25mgin24hours.Theimmediatebenefitofdigoxinislessenedbyitsslowonsetofaction.Whenusedincombination,digoxinmayallowforlowerdosesofsubsequentlyadministeredantiarrhythmicagents.AvoiddigoxininpatientswithAFwithventricularpreexcitation.

Amiodarone

AmiodaroneisaclassIIIantiarrhythmicagentwithsodiumandpotassiumchannelblockingpropertiesandblockingandcalciumchannelblockingproperties.Byvirtueofitsblockingandcalciumchannelblockingproperties,amiodaroneslowsconductionthroughtheAVnode.InpatientswithimpairedcardiacfunctionorCHF,treatmentoptionsnarrow.Amiodaronehasasolidsafetyprofileandmaybeaneffectivealternativeagentinthissituation.Amiodaronecanbeadministeredasaslowintravenousinfusionof150mgover10minutes.Thisisfollowedbyamaintenanceinfusionof1mg/minfor6hoursandthen0.5mg/min.Additionalbolusdosesof150mgcanberepeatedasneededforresistantorrecurrentPSVTuptoatotaldailydoseof2g.

Procainamide

ProcainamideisaclassIAantiarrhythmicagentwithsodiumchannelblockingproperties.ProcainamidewillslowconductionthroughboththeAVnodeand,ifpresent,anaccessorybypasstract.ProcainamidecanbeconsideredforpatientswithPSVTrefractorytoAVnodalblockingagents.Therecommendedloadingdoseofprocainamideis

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17mg/kgadministeredasaslowintravenousinfusionatarateof2030mg/min(1gforanaverageadult).Stoptheinitialinfusionifthearrhythmiaissuppressed,hypotensiondevelops,ortheQRScomplexwidensbymorethan50%ofitsoriginalduration.Afterarrhythmiasuppression,startamaintenanceinfusionat14mg/min.

Disposition

HospitalizationshouldbeconsideredforpatientsinPSVTwithaccompanyingserioussignsandsymptoms,patientsrequiringemergencycardioversion,patientsinPSVTwithventricularpreexcitation,andpatientswitharrhythmiasrefractorytostandardtreatment.OutpatientfollowupcareshouldbeprovidedfortheotherwisehealthypatientwithatransientepisodeofPSVTconvertedtosinusrhythmintheemergencydepartment.

AtrialFibrillation

ClinicalFindings

(SeeAppendix,Figures3512and3513.)InAF,theatrialrateisdisorganizedandis300600beats/min.AFischaracterizedbyanirregularlyirregularventricularratewiththeabsenceofdiscerniblePwaves.

AFisthemostcommonsustainedcardiacarrhythmiainadults.ItisestimatedthatAFaffectsmorethan2millionpersonsintheUnitedStatesitsprevalenceincreaseswithage,approaching10%inthoseolderthan80years.AFcanoccurintheabsenceofunderlyingheartdiseaseormaybeassociatedwithanumberofconditions,includingchronichypertension,valvulardisease,cardiomyopathy,myocardialischemia,myocarditis,pericarditis,orcongenitalheartdisease.AFmayalsooccurinthepresenceofothersystemicdisorders,includinghyperthyroidism,pulmonaryembolism,hypoxia,andexcessconsumptionofalcoholorcaffeine.

PatientswithnonvalvularAFhaveapproximatelya5%annualincidenceofstrokeasaresultofathromboembolicevent.Thisriskincreasesfourfoldinpatientswithmitralstenosisandincreasesdramaticallyinolderpatients,approaching30%inpatientsaged8089years.

Treatment

AcutemanagementofAFincludesventricularratecontrolandpreventionofthromboemboliccomplications.Additionalmanagementconsiderationsincluderestorationandmaintenanceofsinusrhythm.

UNSTABLEPATIENTS

PatientsinAFwitharapidventricularresponsewhoarehemodynamicallyunstablerequireimmediatesynchronizedDCcardioversion.Recommendationsaretostartbetween100and200Jbiphasicandthentoincreasethedoseinstepwisefashionasneededuntilsinusrhythmisrestored.

STABLEPATIENTS

Instablepatientswitharapidventricularresponse,theinitialgoalisratecontrol.Thiscanusuallybeachievedwithblockers,calciumchannelblockers,ordigoxin.blockersmayprovemosthelpfulinpatientswithhyperthyroidismbutarerelativelycontraindicatedinpatientswithacutedecompensatedCHF.Diltiazemandverapamilcanoftenslowtheventricularrateandhavetheaddedbenefitofantianginaleffectsandbloodpressurecontrolinhypertensivepatients.Inmorethan90%ofpatients,areductioninheartrateofatleast20%isnoted.DiltiazemappearstobesafeforuseinpatientswithmildCHF.DigoxincanalsohelpcontroltheventricularrateinpatientswithAFandmaybeusefulinpatientswithleftventriculardysfunction.Itssloweronsetofactionascomparedtootheragentsmakesitlessusefulforacuteratecontrol.InpatientswithmildtomoderateCHF,theadministrationofamiodaronemayproveuseful.Intravenousamiodaronecanalsobeconsideredanalternativeagentforratecontrolwhentheaboveagentsfail.Thespecificmedicationchoicewilloftenbedictatedbythe

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urgencyofthesituation,themedicationprofile,physicianpreference,andthepatient'sunderlyingcondition.

Anticoagulants

ProphylacticanticoagulationwithwarfarinhasbeenshowntosignificantlyreducetheincidenceofstrokeinpatientswithAF.IfnewonsetAFisofundetermineddurationorgreaterthan48hoursduration,initiationofanticoagulationisnecessary.Currentrecommendationsincludeanticoagulationfor3weeks,followedbyelectivecardioversionandthencontinuedoutpatientanticoagulationforfourmoreweeks.Analternativestrategyisinitialanticoagulationwithunfractionatedorlowmolecularweightheparinfollowedbytransesophagealechocardiographytoevaluatetheleftatrialappendageforthepresenceofclot.Ifnoclotisidentified,thepatientmaysafelyundergocardioversion,followedbyanticoagulationfor4weeks.Ifaleftatrialappendageclotisidentifiedbytransesophagealechocardiography,recommendationsincludeanticoagulationfor3weeks,followedbycardioversionandthencontinuedanticoagulationforfouradditionalweeks.InpatientswithAFoflessthan48hoursduration,anticoagulationisnotrecommended.

Antiarrhythmics

Variousantiarrhythmicagents,includingamiodarone,procainamide,andsotalol(classIII),areusedtochemicallyconvertAF.PharmacologicorelectricalcardioversionmaybeconsideredinselectedstableemergencydepartmentpatientswithAFoflessthan48hoursduration.Remodeling,bothanatomicallyandelectrically,occurssoonaftertheonsetofAF.Postponingcardioversioncouldleadtoanincreasedresistancetoattemptsatconversion.

Disposition

PatientswithchronicratecontrolledAFdonotrequirehospitaladmission.InpatientswithnewonsetAF,hospitalizationisoftenrequiredforventricularratecontrol,initiationofanticoagulation,andsometimesforinitiationofantiarrhythmictherapy.Ifapatientpresentswiththromboemboliccomplications,hospitaladmissionwillalsobenecessary.

AtrialFlutter

ClinicalFindings

(SeeAppendix,Figure3514)Inatrialflutter,theatrialrateisusually250350beats/min.Itisthemostcommonunderdiagnosedtachyarrhythmia.SawtoothflutterwavesmaysometimesbeseenonECG,butshouldnotbereliedupon.Typically,atrialflutterwillpresentwith2:1AVconduction.Forthisreason,itisimportanttoconsideratrialflutterinthedifferentialdiagnosisofaregulartachycardiaatapproximately150beats/min,evenintheabsenceofflutterwaves.AtrialflutterismostcommonlyidentifiedasnegativewavesinII,III,andaVFwithpositiveflutterwavesinleadV1.

Ifatrialflutterissuspected,severaloptionsareavailabletobetteridentifyatrialactivity.Vagalmaneuversoradministrationofadenosinewitha12leadrhythmstripmayunmaskflutterwaves.

Treatment

Acutemanagementofatrialflutterincludesventricularratecontrolandpreventionofthromboemboliccomplications.Additionalmanagementconsiderationsincluderestorationandmaintenanceofsinusrhythm.

UNSTABLEPATIENTS

PatientsinatrialflutterwitharapidventricularresponsewhoarehemodynamicallyunstablerequireimmediatesynchronizedDCcardioversion.Currentrecommendationsaretostartwithbetween50and100Jbiphasicand

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thenincreasetheenergydoseinstepwisefashionasneededuntilsinusrhythmisrestored.

STABLEPATIENTS

Instablepatientswitharapidventricularresponse,theinitialgoalisratecontrol.Adequateheartratecontrolcanbeachievedwiththeadministrationofeitherblockersorcalciumchannelblockers.Digoxinisoftenlesseffectiveacutelybecauseofitsslowonsetofaction.AmiodaroneanddiltiazemarealternativesforratecontrolinthestablepatientwithimpairedcardiacfunctionorCHF.

ThestrokeriskforpatientsinatrialflutterislessthanthatofAF.ThesameanticoagulationguidelinesexistforatrialflutterasinAF.

Disposition

Patientswithchronicratecontrolledatrialflutterdonotrequirehospitaladmission.Inpatientswithnewonsetatrialflutter,hospitalizationisoftenrequiredforventricularratecontrol,initiationofanticoagulation,andsometimesforinitiationofantiarrhythmictherapy.

MultifocalAtrialTachycardia

ClinicalFindings

(SeeAppendix,Figure3515)Inmultifocalatrialtachycardia(MAT)theheartrateistypically100130beats/min.ThecharacteristicECGfindingisatleastthreedifferentPwavemorphologies.TherhythmoftenappearsirregularandcanattimesbeconfusedwithAF.VaryingPRintervalsmayalsobenoted.Whentherateisslowerthan100beats/min,thetermwanderingatrialpacemakerisapplied.Unlessunderlyingaberrantconductionispresent,theQRScomplexesarenarrow.Severeunderlyingchronicobstructivepulmonarydiseaseaccountsforapproximately6085%ofcases.TheophyllineanddigoxinlevelsshouldbecheckedsincetoxicityofthesedrugscancauseMAT.

Treatment

TheinitialtreatmentofMATisdirectedatcorrectingtheunderlyingcause.AswithAF,theinitialgoaloftherapyistoachieveheartratecontrol.BecauseMATdoesnotrespondtoelectricalcardioversion,pharmacologicinterventionmayberequired.

MagnesiummaybeeffectiveinconvertingMATandcanbeadministeredasa2gintravenousbolusover1minute.Thisisfollowedbya2g/hinfusionfor5hours.Magnesiumcanstillbeeffectiveifserummagnesiumlevelsareinthenormalrange.Potassiumrepletionmaybehelpfulinpatientswhoarehypokalemic.

Amiodarone,digoxin,ordiltiazemmaybeconsideredasalternativeagentsforratecontrol,especiallywhenthepatientexhibitsfindingsofCHF.

Disposition

PatientsmayrequirehospitalizationforMATiftheheartrateisdifficulttocontrolorforfurthermanagementoftheunderlyingcondition.

PreexcitationArrhythmias

ClinicalFindings

(SeeAppendix,Figures3511and3513)PatientswithWolffParkinsonWhite(WPW)syndromehavean

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accessorypathway.AnatomicallocationvariesandthepathwayscanbeAV(Kent),atrioHis(James),intranodal,andnodoventricular(Mahain).OntheECG,ashortPRinterval(lessthan120ms)andthepresenceofawave(initialupwardslurringoftheQRScomplex)signifyventricularpreexcitation.

AvarietyofarrhythmiasmayoccurinpatientswithWPWsyndromeapproximately70%isorthodromicAVRT.Inthiscase,thecardiacimpulsetravelsdowntheAVnode(antegradeconduction)andstimulatestheventriclesthroughthenormalconductionpathways.TheaccessoryAVbypasstractservesastheretrogradelimbofthecircuit.IntheabsenceofaberrantventricularconductionorafixedBBB,themorphologyoftheQRScomplexisnarrowwithoutevidenceofventricularpreexcitation(absentwave).ThebypasspathwayisconsideredconcealediftheshortPRandwavearenotpresentonthebaselineECG.

Rarely,antidromicAVRToccurswherebytheaccessoryAVpathwayactsastheantegradelimbofthecircuitandtheAVnodeastheretrogradelimb.AntidromicAVRTwillproduceawideQRScomplextachycardiaandmaymasqueradeasVT.Thetachycardiamaybeextremelyrapid(withventricularrate220300),leadingtoventricularfibrillation(VF)asaresultofanRonTphenomenon.

AFisthesecondmostcommonarrhythmiaassociatedwithWPWsyndrome.AFwithventricularpreexcitationhasahighpotentialtoprecipitatehemodynamiccompromise.AFwitharapidventricularrateischaracterizedbyanirregulartachycardiaandawideQRScomplexresultingfromventricularpreexcitation.

Treatment

PatientswithorthodromicAVRTwhoarehemodynamicallyunstablerequireimmediatesynchronizedDCcardioversion.Currentrecommendationsaretostartbetween50Jand100Jbiphasicandthentoincreasetheinitialdoseinstepwisefashionasneededuntilsinusrhythmisrestored.InpatientswithknownWPWsyndromepresentingwithanarrowcomplexregulartachycardia,orthodromicAVRTcanbeassumed.Instablepatients,themedicaltreatmentwillbethesameasinAVNRT.Pharmacologictreatmentwithadenosine,adrenergicblockingagents,orcalciumchannelblockerscanbeadministeredasdeemednecessaryandappropriatefortheindividualcase.Ingeneral,thetreatmentoforthodromicAVRTwithAVnodalblockingagentsissafe.Theriskofenhancingantegradeconductiondownthebypasstractisverylow.

TreatmentofAFwithventricularpreexcitation(antidromicAVRT)isdifferentfromthatoforthodromicAVRT.Ifthepatientishemodynamicallyunstable,immediatesynchronizedDCcardioversionstartingat100200Jiswarranted.TheuseofAVnodalblockingagents,specificallyblockers,calciumchannelblockers,anddigoxin,iscontraindicated.IfconductionthroughtheAVnodeisslowed,conductiondowntheaccessorypathwaymaybeenhanced,possiblydegeneratingtoVF.BecauseprocainamidewillslowconductionthroughboththeAVnodeandtheaccessorypathway,itisthemedicationofchoicewhenAFwitharapidventricularresponseisassociatedwithventricularpreexcitation.ProcainamideisalsothemedicationofchoiceinantidromicAVRT.AmiodaronecanbeusedasanalternativeagentintreatingAFwithventricularpreexcitationandfindingsofCHF.

Disposition

HospitalizationisnotrequiredforpatientswhoareasymptomaticwithevidenceofventricularpreexcitationontheECG(sinusrhythm,shortPR,andawave).Considerhospitalizingpatientswhohaveserioussignsandsymptomsorthoserequiringcardioversion.Inaddition,hospitalizationisrecommendedforpatientswithAFandventricularpreexcitationorantidromicAVRT.PatientswhopresentwithstableorthodromicAVRTmaybedischargedwithcloseoutpatientfollowupafterpharmacologicconversionintheemergencydepartment.

2005AmericanHeartAssociationGuidelinesforCardiopulmonaryResuscitationandEmergencyCardiovascularCare.Circulation2005112:IV35IV46[PubMed:16314375].DelacrtazE:Clinicalpractice.Supraventriculartachycardia.NEnglJMed2006354:10391051[PubMed:16525141].

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InnesJA:Reviewarticle:Adenosineuseintheemergencydepartment.EmergMedAustralas200820:209215[PubMed:18549383].RaghavanAVetal:Managementofatrialfibrillationintheemergencydepartment.EmergMedClinNorthAm200523:11271139[PubMed:16199341].StahmerSA,CowanR:Tachydysrhythmias.EmergMedClinNorthAm200624:1140[PubMed:16308111].SulkeN,SayersF,LipGY:Rhythmcontrolandcardioversion.Heart200793(1):2934[PubMed:16963490].WatsonT,ShanstilaE,LipGY:Modernmanagementofatrialfibrillation.ClinMed20077:2834[PubMed:17348571].

VentricularArrhythmias

VentricularTachycardia

ClinicalFindings

(SeeAppendix,Figures3516and3517)VentriculartachycardiaisthemostcommoncauseofwideQRScomplextachycardia.ThetermVTisusedwhensixormoreconsecutiveventricularbeatsoccur.Theventricularrateisusually150220beats/min,althoughratesslowerthan120beats/minmayoccur.NonsustainedVTischaracterizedbyanepisodelastinglessthan30seconds.SustainedVTischaracterizedbyanepisodelastinglongerthan30seconds,associatedwithhemodynamiccompromise,orrequiringtherapeuticinterventionfortermination.WCTreferstoaregulartachycardiawithaQRScomplexgreaterthan0.12seconds(120ms)induration.WCTmostoftenoccursasaresultofeitherVTorSVTwithaberrantconduction(underlyingorratedependentBBB).

Inmorethan75%ofpatientspresentingintheemergencydepartmentwithregularWCT,theunderlyingarrhythmiaisVT.Thepresenceofstructuralheartdisease,coronaryarterydisease,priormyocardialinfarction,orCHFstronglysuggestsVT.CertainECGfindingsfavorVToverSVTwithaberrantconduction.ThesefindingsincludeaQRScomplexwiderthan160ms,thepresenceoffusionbeats,andevidenceofAVdissociation.AVdissociationoccursinabout20%ofpatientswithVTandconfirmsthediagnosis(thisisusuallyseenwithventricularrateslessthan150).AcommonclinicalerrorthatmustbeavoidedistoassumethatWCTisSVTwithaberrantconduction.AllcasesofWCTofunknownoriginshouldbemanagedasVT.

Electricalstormisasomewhatrarebutwelldescribedentitythatconsistsofrecurrentventriculartahchycardia,usuallywithanimplanteddefrillatorthatdischargesrepeatedly.Patientswiththisconditionhaveahighmortalityandwilllikelyneedsedationaswellassympatheticblockadetocontroltherecurrentdysrhythmias.AntiarrhythmicsuseisusuallyrequiredandIVamiodaroneisthedrugofchoice.

TenTipsfortheDiagnosisofRegularWCT

1. AWCTismostlikelyVT.

2. Considertoxicityalwaysthinkofhyperkalemia,tricyclicantidepressants,anddigoxin.Treatmentisdifferentandcardioversionisnothelpful.

3. Ifunstable,treatimmediatelywithcardioversion.

4. Asktwoquestions:PriorMI?TachycardianewsinceMI?AnsweringyesincreaseslikelihoodofVTto>90%.

5. TwelveleadECGisalwaysbest,ifpossible,before,during,andaftertreatment.Savealltracings.

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6. OldECGsareinvaluablewhenlookingforsimilarBBBpatterns.

7. TherearemanyalgorithmsfordeterminingVT(vsSVTwithBBB,aberrancy)andnoneare100%accurate.Therulesaredifficulttorememberandinterpret.VTislikelyifthefollowingareidentified:

a. RSabsentinallprecordialleads(seeninlessthan25%ofVT).IfcannotfindRS(onlyQS,QR,monophasicR,orrSRcomplexes)thisfavorsVT.

b. OnsetofRtonadirofS>.10msinanyprecordiallead.

d. AVdisassociation.

f. Fusionbeats,capturebeats.

h. Concordanceallpositiveorallnegativeprecordialleaddeflections.

j. FrontalplaneQRSaxisusuallyabnormal.

l. IfRBBBlike,thenlookformonophasicRorRSR'inV1andforR/S30ms),onsetofRtonadirofS>100msinV1orV2,andQRorQSinV6.

8. IfstillunsuretreatforVT.

9. Besttreatmentiscardioversion.

10. Stabilizerhythmbeforeadmission.

Treatment

UnstablePatients

PatientswithVTorWCTofunknownoriginwhoarehemodynamicallyunstablewithserioussignsandsymptomsrequireimmediatesynchronizedDCcardioversion.Recommendationsaretostartwith50100Jandthenincreasetheinitialdoseby50Jasneededuntilsinusrhythmisrestored.

StablePatients

Traditionally,patientswithstableVTareadministeredanantiarrhythmicagentforchemicalcardioversion.Anumberofmedicationsareavailable.Thechoiceforaparticularpatientisoftenbasedonphysicianpreferenceandexperience,findingsofpreservedorimpairedcardiacfunction,andtheunderlyingcauseoftheVT.

LIDOCAINE

LidocaineisaclassIbantiarrhythmicwithsodiumchannelblockingproperties.Becauseitcanbeadministeredrapidlywithfewsideeffects,someauthorsconsiderittheagentofchoiceforventriculararrhythmiasassociatedwithacutemyocardialischemiaorinfarction.Therecommendedintravenousloadingdoseis1.01.5mg/kg.Ifrequired,asecondbolusdoseof0.751.5mg/kgcanbeadministeredin510minutes.Ifventricularectopypersists,anadditionalbolusdoseof0.50.75mg/kgcanbeadministeredevery510minutestoamaximumdoseof3mg/kg.Afterrhythmsuppression,startamaintenanceinfusionat24mg/min.Lidocainehasthelowestincidenceoftoxicityofallcurrentlyusedantiarrhythmicmedications.

OTHERDRUGS

ProcainamideisanalternativeagenttolidocaineforthetreatmentofstablemonomorphicVT.AmiodaronemaybepreferabletootherantiarrhythmicagentsforVTinpatientswithCHF.Althoughrecommended,amiodarone'sefficacymaynotbefastenoughforuseonanemergencybasis.

Disposition

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HospitalizationisrecommendedforallpatientswhopresentwithVT.

PolymorphicVentricularTachycardia(IncludingTorsadesDePointes)

ClinicalFindings

(SeeAppendix,Figure3518)PolymorphicventriculartachycardiaisaformofVTwithvaryingQRScomplexmorphology.Therhythmisoftenirregularandhemodynamicallyunstable,anditcandegeneratetoVF.

TorsadesdepointesisaformofPMVTassociatedwithaprolongedQTintervalonthebaselineECG.Therhythmisoftendescribedashavingatwistingonpointappearanceandcanbeeitherparoxysmalorsustained.Theheartrateisusually200250beats/min.HereditarylongQTsyndromesassociatedwithtorsadesdepointesincludeLangeNielsensyndromeandRomanoWardsyndrome.Torsadesdepointesmayalsooccurasaresultofnumerousmedicationinteractions.AcompletelistofmedicationsthathavebeenreportedtoprolongtheQTintervalisavailableatwww.qtdrugs.org.

PMVTcanalsooccurintheabsenceofaprolongedQTinterval.Inthiscase,cardiacischemiaorunderlyingstructuralheartdiseaseisoftenthecause.


PatientswithPMVTwhoarehemodynamicallyunstablewithserioussignsandsymptomsrequireimmediatecardioversionordefibrillation.Recommendationsaretostartwith200J.Topreventrecurrence,discontinueallagentsthatcanprolongtheQTinterval.

MagnesiumisthemedicationofchoiceforthemanagementoftorsadesdepointesassociatedwithcongenitalandacquiredformsoflongQTsyndrome.Itmaybeeffectiveevenwhenserumlevelsarenormal.A2gintravenousdosecanbeadministeredasaslowpushover5minutes.Followthebolusdosebyamaintenanceinfusionof12g/h.Considersupplementalpotassiumasanadjunctivetherapytomaintainserumpotassiumlevelsinthehighnormalrange.Temporarytransvenouspacingatratesaround100beats/minmaybeusefultopreventrecurrences,especiallyinpatientswithbradycardiaorpauses.HospitalizationisrecommendedforallpatientswhopresentwithPMVT.

VentricularFibrillation

ClinicalFindings

(SeeAppendix,Figure3519)VentricularfibrillationischaracterizedbyanirregularventricularrhythmwithnodiscernibledistinctionbetweentheQRScomplex,STsegment,andTwaves.VFisacommoncauseofsuddencardiacdeathandremainsasignificantcontributortomortalityinthefirst24hoursafteranacutemyocardialinfarction.Intheabsenceofearlybystandercardiopulmonaryresuscitationandinitiationofadvancedcardiaclifesupport,includingdefibrillation,survivalratesarepoor.


WitnessedVForpulselessVT,istreatedwithimmediatetreatmentisasynchronousdefibrillationfollowedbyCPRfor2minutesbeforerhythmcheck.IfVTorpulselessVTpersists,repeatdefibrillationfollowedbyeitherepinephrineorvasopressinandcontinuedCPRfor2minutes.IfVTorpulselessVTstillpersistsagainrepeatdefibrillationfollowedbyeitheramiodaroneorlidocaineandCPRfor2minutes.AllpatientswhohavebeensuccessfullyresuscitatedfromVForpulselessVTshouldbestartedonadripofthelastantiarrhythmic

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administeredandadmittedtotheintensivecareunitforcloseobservation.Ifanacutecoronarysyndromeissuspectedasthecauseofthearrest,thepatientmayrequirecardiaccatheterizationforevaluationandtreatment.Chapter9offersamoreindepthdiscussionofthemanagementofcardiacarrest.

ACC/AHA/ESC2006Guidelinesformanagementofpatientswithventriculararrhythmiasandthepreventionofsuddencardiacdeathexecutivesummary.Circulation2006114:10881132[PubMed:16949478].GoldbergerZD,RhoRW,PageRL:Approachtothediagnosisandinitialmanagementofthestableadultpatientwithawidecomplextachycardia.AmJCardiol2008101:14561466[PubMed:18471458].HollowellH,MattuA,PerronAD,HolstegeC,BradyWJ:Widecomplextachycardia:beyondthetraditionaldifferentialdiagnosisofventriculartachycardiavssupraventriculartachycardiawithaberrantconduction.AmJEmergMed200523:876889[PubMed:16291445].HuangDT,TraubD:Recurrentventriculararrhythmiastormsintheageofimplantablecardioverterdefibrillatortherapy:acomprehensivereview.ProgCardiovascDis200851:229236[PubMed:19026857].MarrillKA,deSouzaIS,NishijimaDK,StairTO,SetnikGS,RuskinJN:Amiodaroneispoorlyeffectivefortheacuteterminationofventriculartachycardia.AnnEmergMed200647:217224[PubMed:16492484].StahmerSA,CowanR:Tachydysrhythmias.EmergMedClinNorthAm200624:1140.[PubMed:16308111]VohraJ:TheLongQTSyndrome.HeartLungCirc200716:S5S12[PubMed:17627884].

Bradyarrhythmias,ConductionDisturbances,andEscapeRhythmsAsintachycardiamanagement,ifabradycardicpatientishemodynamicallyunstable,immediateinterventionisrequiredregardlessoftheoriginoftheunderlyingarrhythmia(eg,SAblock,AVblock,andventricularescaperhythm).Transcutaneouscardiacpacingfollowedassoonaspossiblewithtransvenouspacingistheinitialinterventionofchoiceforpatientswithserioussignsandsymptomsthatoccurasaresultofabradyarrhythmia.Instablepatients,orinpatientswithmildsymptoms(eg,dizziness,lightheadedness),pharmacologictreatmentisofteninitiatedwithorwithoutstandbypacing.Medicalmanagementcanbeinitiatedinpatientswithsymptomaticbradycardiaasabridgetocardiacpacing,ormaybeinitiatedifemergencycardiacpacingisunavailable.

Primaryconductionsystemdisturbancesaccountfor15%ofbradyarrhythmiasencounteredintheemergencydepartmentsetting.Theremaining85%occurasaresultofvarioussecondarycausessuchasacutecoronaryischemia(40%),medicationsortoxicologicalcauses(20%),metaboliccauses(5%),neurologicalcauses(5%),permanentpacemakerfailure(2%),andothermiscellaneouscauses(13%).SymptomaticbradycardiaresultingfromAVconductiondisturbancesorsicksinussyndromeismorecommonintheelderlythemajorityofpatientspresentatage65yearsorolder.

SinusBradycardia

ClinicalFindings

(SeeAppendix,Figure354)Sinusbradycardiaoccurswhenthesinusrateisslowerthan60beats/min.Usuallytherateis4559beats/min,butonrareoccasionitmaybeasslowas35beats/min.Sinusbradycardiaiscommonlyassociatedwithsinusarrhythmiaandisoftenanormalfindinginyoung,healthy,athleticindividuals.Sinusbradycardiaisoftenbenignanddoesnotnecessarilyindicatesinusnodedysfunction.Althoughcommonlyphysiologic,sinusbradycardiamaybepathologicwhenpatientsexperiencesymptomsofcerebralhypoperfusionorwhentheheartratedoesnotincreaseappropriatelywithactivityorexercise.Certainunderlyingconditionshavebeenassociatedwithaslowingoftheheartrate,includinghypothermia,hypothyroidism,andincreasedintracranialpressure.Inaddition,anumberofdifferentmedications,includingblockers,calciumchannelblockers,clonidine,digoxin,andlithium,cancausebradycardia.

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Usuallynotreatmentisrequiredforasymptomaticsinusbradycardia.Whenserioussignsandsymptomsarepresent,medicalmanagement,pacemakerplacement,andhospitaladmissionareindicated.

SinusArrest

Sinusarrestisdefinedasafailureofsinusnodeimpulseformation.OntheECG,randomperiodsofabsentcardiacactivitymaybenoted.Unlessescapebeatsoccur,lengthypausesarenoted.Whenpausesoccur,patientsmaycomplainofdizzinessorlightheadednessormayhavesyncope.Ifuntreated,pauseslongerthan2.5secondsmayprogresstoasystole.

SinoatrialBlock

SAblockdiffersfromsinusarrestinthatSAblockisaformofexitblockratherthanfailureofimpulseformation.Likesinusarrest,SAblockmayoccurasaresultofanumberofconditions,includingacutemyocardialinfarction,myocarditis,fibrosisoftheSAnode,excessivevagaltone,anddigoxintoxicity.AnalogoustoAVblock,SAblockcanbeclassifiedintofirst,second,andthirddegreeheartblock.

FirstdegreeSinoatrialBlock

FirstdegreeSAblockdoesnotproduceanyECGchanges.Thediagnosiscanbemadeonlythroughelectrophysiologictesting.

SecondDegreeSinoatrialBlock(MobitzTypeI)

(SeeAppendix,Figure3524)SeconddegreeMobitztypeISAblock,alsoknownasSAWenckebach,ischaracterizedbyPPintervalsthatgraduallyshortenwhilethePRintervalremainsconstant.ThiscycleterminateswithablockedPwave.ThelengthofthepauseisshorterthantwicetheprecedingPPcycle.

SecondDegreeSinoatrialBlock(MobitzTypeII)

SeconddegreeMobitztypeIISAblockischaracterizedbyfixedpauses.OntheECG,thePPintervalremainsconstantandisthenfollowedbyablockedPwave.ThePPinterval,includingtheblockedPwave,willbetwicethelengthofthenormalPPinterval.

ThirdDegreeSinoatrialBlock

ThirddegreeSAblockmaybedifficulttodistinguishfromsinusarrest.PatientswitheitherconductiondisturbancepresentwithvariablepausesontheECGuntilanescaperhythmoccursorsinusrhythmisrestored.

SickSinusSyndrome

ClinicalFindings

Sicksinussyndromeisamanifestationofsinusnodedysfunction.Patientswiththesyndromemaypresentwithawiderangeofbradyarrhythmias.Numerousarrhythmiasareassociatedwithsicksinussyndrome,includingmarkedsinusbradycardia,sinuspause,sinusarrest,andSAblock.Onoccasion,patientsmayalsopresentwithventricularoratrialtachyarrhythmias.


Treatmentmaybeindicatedwhenpausesofmorethan23secondsoccurorifthepatientissymptomatic.Administrationofatropineorinitiationoftemporarycardiacpacingmayberequired.Symptomaticpatientswillrequirehospitaladmission,oftenforpermanentpacemakerplacement.

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AtrioventricularBlock

AVblockreferstoagroupofconductiondisturbanceswithintheAVjunctionaltissue.Ingeneral,AVblockischaracterizedbyprolongedconductiontimeorafailuretoconductimpulsesthroughtheAVnode.Theconductiondisturbancecanbepartial(firstorseconddegreeAVblock)orcomplete(thirddegreeAVblock).Ingeneral,thehemodynamiceffectswilldependontheventricularrateandthepresenceofunderlyingheartdisease.AVconductionblocksaretraditionallyclassifiedasfirst,second,orthirddegreeheartblock.

FirstDegreeAtrioventricularBlock

(SeeAppendix,Figure3525)FirstdegreeAVblockisthemostcommonconductiondisturbanceandischaracterizedbyaPRintervalthatisprolongedforgreaterthan0.2seconds.Ingeneral,thePRintervalisconstant,andeachatrialimpulseisconductedtotheventricles.FirstdegreeAVblockcanbeanormalvariantinyoungorathleticindividualsduetoexcessivevagaltone.FirstdegreeAVblockisalsocommoninelderlypatientswithoutunderlyingheartdisease.Itmayoccurinpatientswithmyocarditis,milddigoxintoxicity,andinferiorwallmyocardialinfarctionsecondarytoAVnodalischemia.

SecondDegreeAtrioventricularBlock(MobitzTypeI)

(SeeAppendix,Figure3526)SeconddegreeMobitztypeIAVblockisalsoknownasWenckebachAVblock.ThistypeofblockischaracterizedbyaprogressivelengtheningofthePRintervalfollowedbyanonconductedPwaveleadingtoadroppedQRScomplex.Classically,thePPintervalremainsconstantexceptwhensinusarrhythmiaispresent.TheRRintervalwillhaveacharacteristiccyclethroughouttheconductiondisturbance.TheRRintervalthatincludestheblockedPwaveisthelongestinduration.ThisisthenfollowedbyRRintervalsthatsubsequentlybecomeshorteruntilthenextPwaveisblocked.

Onarhythmstrip,groupedbeatingisoftenevidentandcanfurtherhelpdistinguishseconddegreefromthirddegreeAVblock.TheblockedPwavesmayoccurfrequentlyorperiodically,andmayormaynotoccurwithregularity.BecauseMobitztypeIAVblockisattheleveloftheAVnode,theQRScomplexisnormalinconfigurationunlessaberrantventricularconductionoranunderlyingBBBexists.Ingeneral,MobitztypeIAVblockdoesnotusuallyproducehemodynamicallysignificantsymptoms.Itcanbeseeninpatientswithacutemyocardialinfarction(usuallyinferiorwall)anddoesnotcommonlyprogresstocompleteheartblock(CHB).IfCHBdoesoccur,theescaperhythmpacemakerisusuallylocatedintheAVjunctionaltissueandisoftenfastenoughtomaintainanadequatecardiacoutput.

SecondDegreeAtrioventricularBlock(MobitzTypeII)

(SeeAppendix,Figure3528)SeconddegreeMobitztypeIIAVblockischaracterizedbyaconstantPRinterval,eithernormalorprolonged,thatisfollowedbyanonconductedPwave.InMobitztypeIIAVblock,theQRScomplexisusuallywide.ThisoccursbecauseMobitztypeIIAVblockrepresentsaninfranodalblock.Attimes,everyotherPwaveisblocked.Thisisdescribedas2:1AVconduction.Whenthisoccurs,onecannotdistinguishbetweenMobitztypeIortypeIIAVblock(seeAppendix,Figure3527).MobitztypeIIAVblockiscommoninpatientswithacutemyocardialinfarction(usuallyanteriorwall)andcansuddenlyprogresstoCHBresultinginsyncope.

ThirdDegreeAtrioventricularBlock(CompleteHeartBlock)

ClinicalFindings

(SeeAppendix,Figures3529,3530,and3531)ThirddegreeAVblock,orCHB,ischaracterizedbyindependentatrialandventricularactivity.AsaresultofcompleteAVblock,noatrialimpulsesareconductedthroughtheAVnode.Theventricularrateisdeterminedbytheintrinsicescaperhythm,AVjunctionalescape

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(usually4560beats/min),oranidioventricularescaperhythm(usually3040beats/min).Theatrialratemaybesinusinoriginormaybefromanectopicatrialfocus.InCHBtheatrialrateistypicallyfasterthantheventricularrate.AsnotedwithseconddegreeAVblock,thehemodynamicconsequencesdependontheventricularrateandthepresenceofunderlyingheartdisease.SyncopeorCHFcommonlyaccompanyacuteacquiredCHB.CompleteAVblockismostcommonlycausedbycoronaryarterydiseaseorbydegenerationofthecardiacconductionsystem.

Treatment

UNSTABLEPATIENTS

Emergencycardiacpacingisindicatedforpatientswithhemodynamicallyunstablebradycardia,especiallyforpatientswhohavefailedmedicaltherapy,patientswithmalignantescaperhythms,andpatientsinbradyasystolicarrest.Transcutaneouscardiacpacingistheinitialinterventionbecauseofitseaseofapplication,comparedtotemporarytransvenouspacing.Inunstablepatients,medicalmanagementcanbeinitiated,althoughattimesitsutilityisonlytemporary.

STABLEPATIENTS

Atropine

AtropineisananticholinergicmedicationwithparasympatholyticpropertiesleadingtoenhancedSAnodeautomaticityandAVnodeconduction.Theinitialintravenousdoseofatropineis0.51.0mg,whichcanberepeatedevery5minutestoatotaldoseof0.04mg/kg(3mgfortheaverageadult).Themaximaldoseproducescompletevagalblockade.Atropineisrecommendedfor,butnotlimitedto,patientswithsymptomaticbradycardiaorrelativebradycardia,bradycardiawithmalignantescaperhythms,andasystole.

Rarely,aparadoxicreductioninheartratehasbeenobservedinpatientswithadvancedAVblockafteradministrationofatropine.Therefore,useatropinewithcautioninpatientswithinfranodalAVblock(MobitztypeII,andCHBwithwideQRScomplexes).Otherrarelyencounteredsideeffectsofatropineadministrationincludeworseningofcardiacischemiainpatientswithanacutemyocardialinfarction,orthedevelopmentofaventriculartachyarrhythmia.Theseadverseeffectsareuncommon,butknowledgeofsuchresponsesmayassistwithproperpatientselection.Atropineisnoteffectiveinthemanagementofthehearttransplantpatientwithsymptomaticbradycardiabecauseofsurgicaldenervationofthevagusnerve.

Isoproterenol

Isoproterenolisanonspecificadrenergicagonistthatcausesanincreaseinheartrateandcardiaccontractility.Thecombinedeffectsleadtoincreasesincardiacoutputandsystolicbloodpressureanddecreasesinsystemicandpulmonaryvascularresistanceanddiastolicbloodpressure.Asaresult,nosignificantchangeinmeanarterialpressureoccurs.Myocardialoxygendemandisincreasedasaresultoftheincreasedheartrateandcontractility.Inaddition,isoproterenolcausessmoothmusclerelaxationandbronchodilation.Isoproterenolmaybeusedtotreatsymptomaticbradycardiainhearttransplantpatients.Theinitialintravenousdoseofisoproterenolis1g/min,titratedslowlyuntilthedesiredhemodynamiceffectsareachieved.Themaximuminfusionrateis4g/min.

Dopamine

Dopamineisanendogenouscatecholaminewithdoserelatedeffects.Atdosesof3.07.5g/kg/min,ithasagonistpropertiesresultinginincreasedheartrateandcardiacoutput.Theagonisteffectsarelesspronouncedthanthoseofisoproterenol.Dopamineisthepreferredcatecholamineforsymptomaticbradycardiarefractorytoatropine.

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Aminophylline

Aminophylline,amethylxanthinederivative,isacompetitiveantagonistofadenosine.Conductiondisturbancesduringanacutemyocardialinfarctionmaybepartiallymediatedbytheendogenousreleaseofadenosine.Aminophyllinecanbeadministeredintravenouslyatadoseof56mg/kginfusedover5minutes.Amaintenanceinfusionmayberequiredandcanbeinitiatedat0.5mg/kg/h.

Glucagon

Glucagonstimulatescyclicadenosinemonophosphateproduction.Itmaybebeneficialinthetreatmentofbradycardiaassociatedwithblockerorcalciumchannelblockertoxicity.Aninitialintravenousdoseof0.050.15mg/kgisrecommended,althoughoptimaldoseshavenotbeendetermined.

Disposition

Hospitalizeallpatientswhohavesymptomaticbradycardia.DiscontinuemedicationswithAVnodalblockingproperties.AlthoughsomepatientswithadvancedAVconductionblockswillbeasymptomatic,itisrecommendedthatallpatientswithnewlydiagnosedseconddegreeMobitztypeIIAVblockandCHBbehospitalized.

OftenpatientswithWenckebachAVblockwillbeasymptomatic.Treatmentisusuallynotnecessaryunlesssymptomsoccur.Ingeneral,notreatmentisnecessaryforpatientswithfirstdegreeAVblock.Attimes,hospitalizationwillbenecessarytotreattheunderlyingconditionsuchasmyocardialischemiaordigoxintoxicity.

IdioventricularRhythm

ClinicalFindings

Idioventricularrhythmreferstotheoccurrenceofsixormoreconsecutiveventricularescapebeats.Therateofanidioventricularescaperhythmisusually3040beats/min.ThedurationoftheQRScomplexoftenexceeds0.16seconds.ThemorphologyoftheQRScomplexissimilartothatinprematureventricularcontractions(PVCs)butvariesdependingonthelocationoftheectopicventricularfocus.EscaperhythmsoftendevelopinresponsetoseverebradycardiaoranadvancedAVblock.Iftherateis50100beats/min,therhythmiscalledacceleratedidioventricularrhythm(AIVR).AIVRcanalsobeseenafteradministrationofthrombolytictherapyforacutemyocardialinfarctionandmayserveasamarkerofreperfusion.


Treatmentmaybeindicatediftheventricularescaperhythmisunabletomaintainadequatecerebralperfusionorifthepatientisunstable.IfventricularescapebeatsoccurinresponsetoadvancedAVblock,itcouldbedangeroustoabolishtheescaperhythm.Inthiscase,theescaperhythmmaybehelpingtomaintainadequateperfusion.ManagementisdirectedattreatingtheunderlyingAVblock.IfAIVRoccurssecondarytoreperfusion,notreatmentisgenerallyneeded.BecauseanidioventricularescaperhythmoftenoccursasaresultofadvancedAVblock,themajorityofpatientswillrequirehospitalization.

AtrioventricularJunctionalRhythm

ClinicalFindings

AVjunctionalescaperhythmreferstotheoccurrenceofsixormoreconsecutivejunctionalescapebeats.Theventricularrateisusually4560beats/min.AVjunctionalrhythm,likeAVjunctionalprematurebeats,mayoriginatefromanylocationintheAVjunctionaltissue.BecausetheoriginoftherhythmistheAVjunctionaltissue,

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theQRScomplexisnarrowunlessthepatienthasapreexistingBBB.Ifthejunctionalescaperhythmisfasterthan60beats/min,thetermAVjunctionaltachycardiaisapplied.Ifthisrhythmispresent,digoxintoxicityshouldberuledout.


PatientswithsinusbradycardiaandoccasionalorintermittentAVjunctionalescapebeatsdonotgenerallyrequireintervention.Treatmentincludinghospitalizationwilldependontheunderlyingcauseofthecardiacarrhythmia.

HaydenGE,BradyWJ,PollackM,HarriganRA:Electrocardiographicmanifestations:Diagnosisofatrialventricularblockintheemergencydepartment.JEmergMed200426:95106[PubMed:14751485].HoodRE,ShorofskySR:Managementofarrhythmiasintheemergencydepartment.CardiolClin200624:125133[PubMed:16326262].SherbinoJ,VerbeekPR,MacDonaldRD,SawadskyBV,McDonaldAC,MorrisonLJ:Prehospitaltranscutaneouscardiacpacingforsymptomaticbradycardiaorbradyasystoliccardiacarrest:asystematicreview.Resuscitation200670:193200[PubMed:16814446].UfbergJW,ClarkJS:Bradydysrhythmiasandatrioventricularconductionblocks.EmergMedClinNorthAm200624:19[PubMed:16308110].

PermanentCardiacPacemakersandImplantableCardioverter

DefibrillatorsItisestimatedthatmorethan100,000implantablecardioverterdefibrillators(ICDs)andmorethan200,000permanentcardiacpacemakersareimplantedintheUnitedStatesannually.Thesedeviceshavedramaticallyreduceddeathfromsuddencardiacdeathandotherarrhythmias.However,theyoccasionallyfailandemergencymedicinephysiciansshouldbefamiliarwithbothnormalpacemakerandAICDcommonmalfunctions.Itisestimatedthatpermanentpacemakershavea6%yearlyincidenceofmalfunctionandalthoughmanyofthesemalfunctionswillbeidentifiedduringroutineevaluation,somemalfunctionswilloccurunexpectedly,resultinginanemergencydepartmentvisit.

TypesofPacemakers

Pacemakersareeithersinglechamber(rightatriumorrightventricle)dualchamber(rightatriumandrightventricle)orbiventricular(rightatrium,rightventricleandleftventricle)devices.Insinglechamberpacemakers,asingleleadpacesandsensesinthesamechamber,mostoftentherightventricle.Indualchamberpacemakers,onepacingandsensingleadisintherightatriumandtheotherisintherightventricle.Thebiventricularpacemakerissimilartothedualchamberunitsexceptthatthereisalsoaleftventricuallead.BiventricularpacingisusedwithincreasingfrequencytooptimizetreatmentofCHFwithconductiondelayordysynchrony.

Since1990,almostallpacemakerleadsarebipolar.Bipolarleadshavetwoelectrodesonthesamepacinglead,adistalcathode,andaproximalanodelocatedapproximately1cmapartnearthedistaltipofthepacemakerlead.Bipolarleadsproduceasmallelectricalfieldbetweenthetwoelectrodes.Thisproducesasmall,sometimesbarelynoticeable,pacingspikeontheECG.Olderpacemakerleadswereunipolarindesign.Thecathodewaslocatedatthedistalendoftheleadandthepulsegeneratorservedastheanode.UnipolarleadsproducealargerelectricalfieldandgiverisetolargerpacemakerspikesontheECG.Unipolarleadsaremorelikelytosensenoncardiacelectricaleventssuchaspectoralismuscleactivity.Thiscanresultininappropriateinhibitionofpacemakeractivity(myopotentialinhibition).Theintroductionofbipolarleadshasvirtuallyeliminatedthistypeofoversensingmalfunction.

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TypesofICDs

SincereceivingUSFoodandDrugAdministrationapprovalin1985,ICDshaveundergonesignificanttechnologicadvances.Initially,deviceswereimplantedintheabdominalwallandepicardialpatchesweresewninplaceviaamediansternotomy.Newerthirdgenerationdevicesaresmaller,andmostareimplantedinthesubpectoralfasciausingatransvenousleadsystem,similartopermanentpacemakersystems.Ascomparedtoearliermodels,thirdgenerationdeviceshavemoreadvancedtachycardiadetectionandterminationfeatureswithlongerbatterylife(78years).Theadvancedtachycardiaterminationfeaturesincludeantitachycardiapacing(ATP),lowenergycardioversion,andhighenergydefibrillation.NewerICDsarealsocapableofrateresponsivedualchamberbackuppacing.

ComplicationsofImplantableCardiacPacemakersandICDs

VenousAccess

Althoughuncommon,themajorityofvenousaccesscomplicationsoccurearlyafterimplantation.Venousaccesscomplicationsincludebleeding,pneumothorax,hemothorax,andrarelyairembolism.Venousthrombosisisanotherrarecomplicationofpacemakerplacement.Patientsmaypresentwithunilateralupperextremitypainandswelling.

PacemakerandICDPocketSite

Usuallyplacedintheleftsubclaviculararea,earlydevicepocketsitecomplicationsincludebleedingwithhematomaformation,wounddehiscence,orinfection.EarlypocketsiteinfectionsareusuallycausedbyStaphylococcusaureus.Latecomplications(greaterthan30daysafterimplantation)canincludepacemakersiteerosion,keloidformation,pacemakermigration,andinfection.LateinfectionsareusuallycausedbyStaphylococcusepidermidis.Approximately6%ofpatientswithpermanentpacemakersdeveloppocketsiteinfections.

LeadComplications

AnumberofcomplicationscanoccurwithendocardialpacemakerandICDleads.Leaddislodgementisuncommonforpacemakersratesarelessthan2%forventricularleadsandlessthan5%foratrialleads.ICDleaddislodgementapproaches10%.Ifleaddislodgementissuspected,obtainposteroanteriorandlateralchestradiographsandcomparethemwithpriorchestXray.Leadfractureorinsulationbreakmayalsooccur.Leadfracturesgenerallyoccuratthreesites:(1)closetothepulsegenerator,(2)atthevenousentrysite,and(3)withtheheart.LeadfracturesmaybediagnosedbychestXrayorbypacemakerinterrogation.

Cardiacperforationisanotheruncommonbutpotentiallyseriousleadcomplication.Suspectperforationinthepatientwithanewpacedrightbundlebranchblock(RBBB)patternonECG,intercostalmuscleordiaphragmaticcontractions(hiccups),pericardialeffusion,ortamponade.Cardiacperforationmayalsobeidentifiedbyaplainchestradiographdemonstratingthetipofthepacemakerleadoutsidethecardiacsilhouette.Echocardiographymaybeinvaluableindiagnosingapericardialeffusion.Mostcases(80%)ofperforationoccurwithinthefirst4daysofpacemakerinsertion.AnotheruncommonleadcomplicationisTwiddler'ssyndrome.Thisoccurswhenapatientwigglesorrotatesthepacemakergenerator,eventuallydislodgingthepacemakerleads.

DeviceMalfunction

GeneralConsiderations

Themostcommonpacemakermalfunctionsaresensingabnormalities.Sensingmalfunctionsarefurthersubdividedintoundersensingoroversensing.Undersensingoccurswhenthepacemakerfailstosenseintrinsic

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electricalcardiacactivity(PwaveorQRScomplex).OntheECG,apacingspikeisprecededbyanintrinsicPwaveorQRScomplex.Oversensingorcrosstalkmisinterpretationbyoneleadofthesignalgeneratedbytheotherleadcancausethepacemakertoinappropriatelyinhibitapacingstimulus.OntheECG,thisisevidentbyapausethatislongerthantheprogrammedpacemakerrate.

Otherpacemakermalfunctionsincludefailuretopaceandfailuretocapture.Failuretopaceischaracterizedbyanabsenceofanappropriatepacingstimulus.Failuretocaptureoccurswhenapacingstimulusfailstodepolarizethemyocardium.Physiologicfailuretocapturemayoccurifthepacingstimulusoccursduringtheventricularrefractoryperiod(within300msafteranativedepolarization).Thisisnotamalfunction,butreprogrammingmaystillbenecessary.

Leadcomplicationsarecommoncausesofpacemakermalfunction.Anincreaseinthepacingthresholdmayalsocausesensingmalfunctionsandfailuretocapture.Thiscanoccurasaresultoffibrosisattheleadtip,hyperkalemia,hypoxemia,myocardialischemia,andantiarrhythmicdrugtoxicity.Batterydepletionorcomponentfailuremayresultinfailuretopaceorundersensing.Electromagneticinterferencefromelectrocauteryormagneticresonanceimaging(MRI)canleadtooversensing.PatientswithimplantablecardiacpacemakersshouldnotundergoMRI.Variableeffectshavebeendocumented,includingpacemakermotion,functionmodification,heatingofthepacemakergenerator,andinductionofvoltageorcurrentinthepacingleads.

Pacemakermediatedtachycardia(PMT)isanuncommoncomplicationthatcanoccurwithdualchamberpacemakers.PMTcanbetriggeredbyaPVCwithventriculartoatrial(VA)conduction.Retrogradeatrialactivitytriggersaventricularpacedbeat.AstheventricularpacedbeatundergoesVAconduction,anotherventricularpacedbeatistriggeredandthecyclecontinues.PMTwillbeevidentbysustainedpacingattheupperlimitoftheprogrammedpacingrate(100140beats/min).TheECGwillcharacteristicallyrevealawidecomplexpacedtachycardia.PMTisoftennotlifethreateningbecausetheheartratedoesnotusuallyresultinhemodynamicinstability.RunawaypacemakerisanotherrarecauseofawideQRScomplexpacedtachycardia.Inthiscase,themalfunctioningpulsegeneratordischargesatarateaboveitspresetupperlimit.

ClinicalFindings

PatientsmaypresentwithanumberofsymptomssuggestiveofpacemakerorICDmalfunction.Theseincludedizziness,lightheadedness,nearsyncope,syncope,palpitations,shortnessofbreath,orchestpain.Thesymptomsmostconcerningarethoseassociatedwithcerebralhypoperfusion.Patientsmaypresentafterbluntchesttraumaorexternaldefibrillationleadingtopacemakermalfunction.Bradycardiamaybeanindicatorormalfunctionbecausethelowerlimitoffixedratepacingistypically5060beats/min.Thismayoccurasaresultofoversensingorfailuretopace.Theupperlimitofrateresponsivepacemakersisgenerally100140beats/min.Apacedrhythmatthisratemayormaynotbepacemakermalfunction.

Althoughuncommon,frequentorrecurrentshocksmayrepresentanICDmalfunction.Anincreasedfrequencyofshocksmaybecausedbyanumberofconditionsincludinganincreasedfrequencyofventriculararrhythmias,deviceinefficacy,oranICDsensingmalfunction.ThemostcommoncauseofanincreasedfrequencyofICDshocksisanincreasedfrequencyofVTorVF.Ventriculararrhythmiascanoccurasaresultofworseningleftventriculardysfunction,myocardialischemia,orchangesinantiarrhythmictherapy.AnICDsensingmalfunctionmayleadtodoublecountingoftheTwavesorinappropriaterecognitionofSVTasVT.LeadcomplicationsmayalsocauseinappropriateICDshocks.

OccasionallyapatientmaypresentwithasustainedventriculararrhythmiawithoutICDintervention.Althoughrare,thismayoccurasaresultofafailuretodetectthearrhythmiaorexhaustionoftherapies.InpatientswithICDs,antibradycardiapacingmalfunctionswillbesimilartothoseexperiencedbypatientswithimplantablecardiacpacemakers.

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EvaluationofthepatientsuspectedofhavingICDorpacemakermalfunctionincludesa12leadICGandrhythmstrip.Ifavailable,acomparisonECGmaybehelpful.Achestradiographshouldalsobeobtained.Labtesting,specificallyofpotassium,magnesium,creatinine,thyroidscreening,andantiarrhythmiclevels,maybenecessary.

Asystematicapproachtotheevaluationofthe12leadECGandrhythmstripmayhelptoidentifypacemakermalfunction.TheECGshouldbeevaluatedtodeterminethepresenceorabsenceofappropriatepacingspikes.Anormallyfunctioningpacemakershouldbeinhibitedfromfiringwhenthepatient'sintrinsicrateisfasterthantheprogrammedrate.Pacemakerfunctioncannotbeevaluatedwhentheintrinsicrateisfasterthantheprogrammedrate.Whenproperlyinhibited,nopacingspikesareseenontheECG.

Magnetapplicationmayprovideinformationregardingbatterydepletionormalfunction.WhenappliedcorrectlyoverapacemakerorICDgenerator,themagnettriggersareedswitch,whichinactivatesthesensingfunction.Pacemakersshouldreverttoanasynchronouspacingmodeatarate(magnetrate)presetbythemanufacturer.Amagnetratethatisslowerthanthemanufacturer'spresetratesuggestsbatterydepletion.Ifnopacemakerspikesoccuraftermagnetapplication,leadfractureoranothermalfunctionmaybethecause.WhenappliedoveranICD,allantitachycardiafunctions(ATPandshocktherapies)aredisabled.Antibradycardiapacingfunctionsareunaffected.AlthoughmostpacemakersandICDsrespondimmediatelywhenamagnetisappliedcorrectly,thereisnoindustrystandardandresponsesaresomewhatmanufacturerdependent.MRIiscontraindicatedinpatientswithbothimplantablepacemakersandICDs.Thestrongmagneticfieldmaydamagethegeneratorandinterferewithnormaldevicefunctioning.

MajorICDfunctionsincludesensing,detection,provisionoftherapytoterminateVTorVF,andpacingforbradycardia.Whenatachycardiaisdetectedtwotherapiesarepossible.First,ATP,whichcommonlyconsistsofburstpacingatarate610beatsfasterthantheventricularrate,isusuallyattempted.ATPmaybefeltbutisnotpainful.Second,ifATPdoesnotterminatethetachyarrhythmia,thenhighenergyshocks(140J)willbedeliveredbetweentherightventriclecoilelectrodeandtheICDcasingand/oranotherelectrode.Theseshocksarepainfulifthepatientisconscious.


Treatvenousaccesscomplicationsaccordingly.Admitforparenteralantibioticsanypatientssuspectedofhavingpocketsiteinfections.

Forpatientspresentingwithpacemakermalfunctionleadingtosymptomaticbradycardia,institutepharmacologictreatmentoremergencypacingmeasures.Iftranscutaneouscardiacpacingisinitiated,placetheanteriorpacingpadasfarawayfromthepacemakergeneratoraspossible.Inthesettingofsymptomaticbradycardia,amagnetcanalsobeappliedtoreverttoasynchronouspacing.IfapatientrequiressynchronizedDCcardioversionordefibrillation,placethepaddlesorpadsasfarfromthepulsegeneratoraspossible.

Intheemergencydepartment,treatmentofPMTmaybeundertakenbyanumberofdifferentmaneuvers.First,amagnetmaybeappliedtoterminatethetachycardia.Ifamagnetisunavailableorunsuccessful,chestwallstimulationusingatranscutaneouspacemakercanbeattempted.Therequiredstimulusisusually1020mA.Thisislessthanthestimulusgenerallyrequiredfortranscutaneouspacing.Ifunsuccessful,isometricexercisescanbetried.Finally,chestthumpshavehadsuccessinterminatingPMTnomorethantwoarerecommended.Eachofthementionedtechniquesisdesignedtoaffectthesensingfunctionofthepacemaker,inhibitventricularpacing,andterminatePMT.Iftheseareunsuccessful,cardiologyconsultationforpacemakerinterrogationandreprogrammingwillbenecessary.

Runawaypacemakerisararelyencounteredproblem.Pharmacologicinterventionormagnetapplicationcanbeattemptedbutwillmostlikelybeunsuccessful.Definitivetreatmentmayrequiredisconnectingthepacemakerleadsorremovalofthepulsegenerator.

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Obtaincardiologyconsultationforpatientssuspectedofhavingpacemakermalfunction.Unlessthepacemakercanbeinterrogatedintheemergencydepartment,themajorityofpatientswithsuspectedpacemakermalfunctionwillrequirehospitalization.ForICDmalfunctionresultinginfrequentinappropriateshocks,temporarydevicedeactivationmaybenecessary.Similartocardiacpacemakers,magnetapplicationshouldtriggeramagneticallyactivatedreedswitch.Thisdisablesallantitachycardiafunctions(ATPandshocktherapies).Antibradycardiapacingfunctionsareunaffected.AlthoughmostICDsareimmediatelydeactivatedwhenamagnetisappliedcorrectly,responsesaresomewhatmanufacturerdependent.Deactivationisnotcommonlyperformed,however,becausethemostcommonreasonforfrequentshocksisanincreaseinthefrequencyofVTorVF.

IfrecurrentventriculararrhythmiasresultinfrequentICDshocks,antiarrhythmicadministrationandsedationmaybenecessary.Iftheventriculararrhythmiaisincessant,externalcardioversionordefibrillationmaybeneeded.PlacethedefibrillatorpadsorpaddlesasfarfromICDgeneratoraspossible.OlderICDswithepicardialelectrodeshavebeenreportedtoincreasethedefibrillationthresholdbypreventingexternallyappliedcurrentfrompassingintothemyocardium.Thismaydecreasethelikelihoodofsuccessfuldefibrillation.

CesarioDA,TurnerJW,DecGW:Biventricularpacinganddefibrillatoruseinchronicheartfailure.CardiolClin200725:595603[PubMed:18063163].ChanTC,CardallTY:Electronicpacemakers.EmergMedClinNorthAm200624:179194[PubMed:16308119].GehiAK,MehtaD,GomesJA:Evaluationandmanagementofpatientsafterimplantablecardioverterdefibrillatorshock.JAMA2006296:28392847[PubMed:17179461].HoodRE,ShorofskySR:Managementofarrhythmiasintheemergencydepartment.CardiolClin200624:125133[PubMed:16326262].StevensonWG,ChaitmanBR,EllenbogenKA,EpsteinAE,GrossWL,HayesDL,StrickbergerSA,SweeneyMO:SubcommitteeonElectrocardiographyandArrhythmiasoftheAmericanHeartAssociationCouncilonClinicalCardiologyHeartRhythmSociety:Clinicalassessmentandmanagementofpatientswithimplantedcardioverterdefibrillatorspresentingtononelectrophysiologists.Circulation2004110:38663869[PubMed:15611390].

Appendix:CommonlyEncounteredCardiacArrhythmias

NormalSinusRhythm

(Figure352)Theheartrateis60100beats/min.ThereisaconstantandnormalPRinterval,andthePwavewillbeuprightinleadIIandinvertedinleadaVR.

FIGURE352.

Normalsinusrhythmatarateof90beats/min.

SinusTachycardia

(Figure353)Theheartrateisfasterthan100beats/min.Usuallytherateis101160beats/min.ThePwavemorphologyisthesameasinnormalsinusrhythm.

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FIGURE353.

Sinustachycardiaatarateof130beats/min.

SinusBradycardia

(Figure354)Theheartrateisslowerthan60beats/min.Usuallytherateis4559beats/min.Sinusbradycardiaiscommonlyassociatedwithsinusarrhythmia.ThePwavemorphologyisthesameasinnormalsinusrhythm.

FIGURE354.

Sinusbradycardiaatarateof45beats/min.

SinusArrhythmia

(Figure355)Theheartrateisusually45100beats/min.ThePwavemorphologyisthesameasinnormalsinusrhythm.ThePPorRRcyclesvaryby0.16secondsormore.Mostcommonly,sinusarrhythmiaoccursinrelationtotherespiratorycycle.Thesinusratewillgraduallyincreasewithinspirationandslowwithexpiration.

FIGURE355.

Sinusarrhythmia.Theheartratevariesbetween60and80beats/min.

AutomaticAtrialTachycardia

(Figure356)Theheartrateisusually160250beats/minbutmaybeasslowas140beats/min.ThePwavemorphologyisusuallydifferentfromthatofnormalsinusrhythm.ThePPandRRcyclesareregularinmostcases.Whentheatrialrateisslowerthan200beats/min,1:1AVconductioniscommonlynoted.Whentheatrialrateisfasterthan200beats/min,theventricularrateisoftenhalftheatrialratebecauseoftherefractorinessoftheAVnode.

FIGURE356.

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Automaticatrialtachycardiaatarateof140beats/min.

AtrioventricularNodalReentrantTachycardia

(Figures357,358,359,and3510)Theheartrateisusually180200beats/min.ThePwavesoccurconcurrentwiththeQRScomplexandareoftendifficulttovisualizeontheECG.

FIGURE357.

Atrioventricularnodalreentranttachycardiaatarateof175beats/min.NotetheabsenceofclearlydiscerniblePwaves.

FIGURE358.

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A:AVnodalreentranttachycardiawithaleftbundlebranchblockatarateof155beats/min.B:ThebaselineECGinthesamepatientshowingsinusrhythmwithaLBBBatarateof95beats/min.Notethatthe11thbeatisaprematureventricularcontraction.

FIGURE359.

A:AVnodalreentranttachycardiaatarateof150beats/min.B:Secondslateraftertheadministrationofadenosine,thesamepatientconvertstosinusrhythm.

FIGURE3510.

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Paroxysmalsupraventriculartachycardiaatarateof150beats/mininapatientwhoishemodynamicallyunstable.Aftertheseventhbeat,thepatientiscardiovertedwith50Jtosinusrhythm.

AtrioventricularReciprocatingTachycardia

(Figure3511)Theheartrateisusuallyfasterthan200beats/min.Becauseactivationoftheventricleoccursthroughnormalconductionpathways,theaccessorypathwayisconcealedandtheQRSmorphologyisnormal.

FIGURE3511.

A:AVreciprocatingtachycardiaatarateof250beats/min.B:Thesamepatientafterpharmacologicconversionshowingsinusrhythmwithventricularpreexcitation.

AtrialFibrillation

(Figures3512and3513)Theatrialrateisdisorganizedandis400650beats/min.Theventricularrateisirregularlyirregular.NoPwavesarediscernibleonECG.

FIGURE3512.

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A:Atrialfibrillationwithacontrolledventricularresponse.B:Atrialfibrillationataventricularrateof130beats/min.

FIGURE3513.

A:Atrialfibrillationwithventricularpreexcitation.B:Thesamepatientafterpharmacologicconversionshowingsinusrhythmwithventricularpreexcitation.

AtrialFlutter

(Figure3514)Theatrialrateisusually250350beats/min.CharacteristicsawtoothflutterwavesmaybeseenontheECG,particularlyinleadII.VariableAVconductionmaybenoted.Typically,2:1AVconductionoccurs,resultinginaventricularrateofapproximately150beats/min.

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FIGURE3514.

A:Atrialflutterwith4:1AVconduction.B:Atrialflutterwith2:1AVconduction.Theventricularrateis145beats/min.

MultifocalAtrialTachycardia

(Figure3515)Theheartrateistypically100130beats/min.ThecharacteristicECGfindingisatleastthreedifferentPwavemorphologies.VaryingPRintervalsmayalsobenoted.

FIGURE3515.

Multifocalatrialtachycardiaatarateof145beats/min.NotethedifferentPwavemorphologies.

VentricularTachycardia

(Figures3516and3517)Theventricularrateisusually180250beats/min,althoughratesslowerthan160beats/minmayoccur.TheQRScomplexiswide(greaterthan0.12sinduration)andoftenbizarreinappearance.FusionbeatsorAVdissociationmaybenoted.IfAVdissociationispresent,thediagnosisofVTisconfirmed.

FIGURE3516.

Therhythmstripshowsarunofventriculartachycardiatherateis150beats/min.After16beatstheventriculartachycardiaspontaneouslyconvertstosinustachycardia.

FIGURE3517.

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Ventriculartachycardiaatarateof145beats/min.

PolymorphicVentricularTachycardia(TorsadesDePointes)

(Figure3518)Theheartrateisusually200250beats/min.Torsadesdepointesisdescribedashavingatwistingonpointappearance.

FIGURE3518.

Polymorphicventriculartachycardia.

VentricularFibrillation

(Figure3519)VFischaracterizedbyanirregularlyirregularventricularrhythmwithnodiscernibledistinctionbetweentheQRScomplex,theSTsegment,andTwaves.

FIGURE3519.

Ventricularfibrillation.Aftersixbeats,sinusrhythmdegeneratesintoventricularfibrillation.

PrematureAtrialContractions

(Figure3520)Aprematureatrialcontraction(PAC)mayoriginatefromanywhereintheatriaexceptthesinusnode.ThePwavemorphologyisusuallydifferentfromthatofnormalsinusrhythm.Itiscommontoseea

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postectopicpauseafteraPAC.TheQRScomplexisnarrowunlessaberrantlyconducted.

FIGURE3520.

Sinusrhythmwithprematureatrialcontractionsinabigeminalpattern.TheconfigurationofthePwavesoftheprematureatrialcontractionsaredifferentfromthatofnormalsinusrhythm.

PrematureVentricularContractions

(Figure3521)APVCmayoriginatefromanywhereintheventricles.TheQRScomplexis0.12secondorlongerindurationandresembleseitheraLBBBorRBBB.UniformPVCsoriginatefromthesamefociandhavethesameappearance.MultiformPVCshavedifferentmorphologybecausetheyoriginatefromdifferentventricularfoci.

FIGURE3521.

A:Sinusrhythmwithfrequentprematureventricularcomplexesinapatternofbigeminy.B:Sinusrhythmwithfrequentprematureventricularcomplexesinapatternoftrigeminy.

IdioventricularRhythm

(Figure3522)Theventricularrateisusually3040beats/min.ThemorphologyoftheQRScomplexeswillbesimilartoPVCsbutwillvarydependingonthelocationoftheventricularfoci.Iftheventricularrateis50100beats/min,therhythmiscalledAIVR.

FIGURE3522.

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A:Atrialfibrillationwithanidioventricularescaperhythm.B:Acceleratedidioventricularrhythmatarateof50beats/min.

AtrioventricularJunctionalRhythm

(Figure3523)Theventricularrateisusually4560beats/min.TheQRScomplexisnarrowunlessaberrantlyconducted.Ifthejunctionalrhythmisfasterthan60beats/min,thetermAVjunctionaltachycardiaisapplied.

FIGURE3523.

AVjunctionalrhythmatarateof40beats/min.

SinoatrialBlock

(Figure3524)SAblockischaracterizedbyblockedPwaves,evidentbyalongPPinterval.ThePPintervalsbeforetheblockedPwavemaygraduallyshorten(SAWenckebach),orthePPintervalsmaybeconstant(seconddegreeMobitztypeIISAblock).

FIGURE3524.

SinusrhythmwithseconddegreeMobitztypeISAblock.NotethatthePPintervalsgraduallyshorten,whereasthePRintervalsremainconstant.ThecycleterminateswithablockedPwave.ThelengthofthepauseisshorterthantwicetheprecedingPPcycle.

FirstDegreeAtrioventricularBlock

(Figure3525)ThePRintervalisconstantbutcharacteristicallyprolongedgreaterthan0.2second.

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FIGURE3525.

SinusrhythmwithfirstdegreeAVblock.ThePRintervalis0.44s.

SecondDegreeAtrioventricularBlock(MobitzTypeI)

(Figure3526)ThereisprogressivelengtheningofthePRintervalfollowedbyanonconductedPwaveleadingtoadroppedQRScomplex.Classically,thePPintervalremainsconstant.TheRRintervalthatincludestheblockedPwaveisthelongestinduration.

FIGURE3526.

SinusbradycardiawithseconddegreeMobitztypeIAVblock.NotetheprogressivelengtheningofthePRintervaluntilaQRScomplexisdropped.

SecondDegreeAtrioventricularBlock

(Figure3527)WheneveryotherPwaveisblocked,onecannotdistinguishbetweenMobitztypeIorMobitztypeIIAVblock.Thisisdescribedas2:1AVconduction.

FIGURE3527.

SinusrhythmwithseconddegreeAVblock.

SecondDegreeAtrioventricularBlock(MobitzTypeII)

(Figure3528)ThePRintervalisregularandcanbeeithernormalorprolonged.Periodically,aPwaveisnotconducted,leadingtoadroppedQRScomplex.

FIGURE3528.

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SinusrhythmwithseconddegreeMobitztypeIIAVblock.NotethevariableAVconduction.

ThirdDegreeAtrioventricularBlock(CompleteHeartBlock)

(Figures3529,3530,and3531)ThePPinterval(atrialrate)isusuallyshorter(faster)thantheRRinterval(ventricularrate).BecausenoatrialimpulsesareconductedthroughtheAVnode,norelationshipexistsbetweentheatrialandventricularactivity.

FIGURE3529.

ThirddegreeAVblock.Theatrialrateis92beats/minandtheventricularrateis50beats/min.

FIGURE3530.


FIGURE3531.

ThirddegreeAVblockwithanacceleratedidioventricularescaperhythmwithaventricularrateof60beats/min.

SingleChamberVentricularPacing

(Figures3532and3533)Whentheintrinsicheartrateisfasterthantheprogrammedpacemakerrate,thepacemakerisinhibitedfromfiring.Whentheintrinsicrateisslower,thepacemakeristriggered,takingoverasthedominantpacemakeroftheheart.

FIGURE3532.

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Asynchronousventricularpacing.Inthiscase,theintrinsicheartrateisslowerthantheprogrammedpacemakerrate.Whenthisoccurs,thepacemakeristriggered,takingoverasthedominantpacemakeroftheheart.

FIGURE3533.

VVIpacing.Althoughthepacemakerspikesaredifficulttoappreciate,beats38areventricularpacedbeats.Whentheintrinsicheartrateisfasterthantheprogrammedrate,thepacemakerisinhibitedfromfiring.

DualChamberAtrioventricularPacing

(Figures3534and3535)Thepacemakeriscapableofpacingandsensingtheatriaandventricles.Dependingontheintrinsicrate,thepacemakercaneitherbetriggeredorinhibited.

FIGURE3534.

AVsequentialpacinginadualchamberpacemaker.Inthiscase,thepacemakerwillpaceboththeatriaandventricleswhennointrinsiccardiacactivityissensed.

FIGURE3535.

DualchamberpacemakerfunctioningintheVATmode.Thepacemakerpacestheventriclesandsensestheatria.Ifintrinsicatrialdepolarizationsaresensed,aventricularpacingspikeistriggered.ThisisevidentontheECGbythepresenceofatrialtracking.

FailuretoCapture

(Figure3536)Failuretocaptureoccurswhenanappropriatepacemakerdischargefailstodepolarizethemyocardium.Physiologicfailuretocapturecanoccurifthepacingstimulusoccursduringtheventricularrefractoryperiod.

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FIGURE3536.

A:Singlechamberventricularpacemakershowingfailuretocapture.TheunderlyingrhythmisseconddegreeMobitztypeIAVblock.Aventricularpacingspikeoccursafterthefifthatrialcomplex(Pwave).Thispacingspikefailstodepolarizetheventricularmyocardium.B:Dualchamberpacemakershowingfailuretocapture.Beat3showsanatrialpacingspikethatfailstodepolarizetheatrialmyocardium.Thepacemakerthenproceedstopacetheventricle.Beats1,2,and49showanatrialpacingspikewithcapturefollowedbynormalAVconduction.(PartAreproduced,withpermission,fromGarsonA:StepwiseapproachtotheunknownpacemakerECG.AmHeartJ1990119:924.)

FailuretoSense(Undersensing)

(Figure3537A)Undersensingoccurswhenthepacemakerfailstodetectintrinsicelectricalcardiacactivity.OntheECG,aPwaveorQRScomplexisinappropriatelyfollowedbyapacingspike.

FIGURE3537.

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A:Undersensing.Thefifthbeatisaprematureventricularcontraction(PVC).Thenextbeatisaventricularpacedbeat.NotethatthepacedbeatoccurssoonafterthePVC,indicatingafailuretosensetheprecedingcomplex.B:ThefirstandsecondbeatsarepacedandthethirdandfourthbeatsshownormalAVconduction.Thereisalongerthanexpectedpausebetweenthefourthandfifthbeats.Thisoccurssecondarytoventricularoversensing.(Reproduced,withpermission,fromGarsonA:StepwiseapproachtotheunknownpacemakerECG.AmHeartJ1990119:924.)

Oversensing

(Figure3537B)Oversensingistheinappropriateinhibitionofapacingstimulus.OntheECG,itisevidentbyapausethatislongerthantheprogrammedpacemakerrate.

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YourIPaddressis200.3.144.114

NormalECG.

Normalsinusrhythmatarateof90beats/min.

Sinustachycardiaatarateof130beats/min.

Sinusbradycardiaatarateof45beats/min.

Sinusarrhythmia.Theheartratevariesbetween60and80beats/min.

Automaticatrialtachycardiaatarateof140beats/min.

Atrioventricularnodalreentranttachycardiaatarateof175beats/min.NotetheabsenceofclearlydiscerniblePwaves.

A:AVnodalreentranttachycardiawithaleftbundlebranchblockatarateof155beats/min.B:ThebaselineECGinthesamepatientshowingsinusrhythmwithaLBBBatarateof95beats/min.Notethatthe11thbeatisaprematureventricularcontraction.

A:AVnodalreentranttachycardiaatarateof150beats/min.B:Secondslateraftertheadministrationofadenosine,thesamepatientconvertstosinusrhythm.

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Paroxysmalsupraventriculartachycardiaatarateof150beats/mininapatientwhoishemodynamicallyunstable.Aftertheseventhbeat,thepatientiscardiovertedwith50Jtosinusrhythm.

A:AVreciprocatingtachycardiaatarateof250beats/min.B:Thesamepatientafterpharmacologicconversionshowingsinusrhythmwithventricularpreexcitation.

A:Atrialfibrillationwithacontrolledventricularresponse.B:Atrialfibrillationataventricularrateof130beats/min.

A:Atrialfibrillationwithventricularpreexcitation.B:Thesamepatientafterpharmacologicconversionshowingsinusrhythmwithventricularpreexcitation.

A:Atrialflutterwith4:1AVconduction.B:Atrialflutterwith2:1AVconduction.Theventricularrateis145beats/min.

Multifocalatrialtachycardiaatarateof145beats/min.NotethedifferentPwavemorphologies.

Therhythmstripshowsarunofventriculartachycardiatherateis150beats/min.After16beatstheventriculartachycardiaspontaneouslyconvertstosinustachycardia.

Ventriculartachycardiaatarateof145beats/min.

Polymorphicventriculartachycardia.

Ventricularfibrillation.Aftersixbeats,sinusrhythmdegeneratesintoventricularfibrillation.

Sinusrhythmwithprematureatrialcontractionsinabigeminalpattern.TheconfigurationofthePwavesoftheprematureatrialcontractionsaredifferentfromthatofnormalsinusrhythm.

A:Sinusrhythmwithfrequentprematureventricularcomplexesinapatternofbigeminy.B:Sinusrhythmwithfrequentprematureventricularcomplexesinapatternoftrigeminy.

A:Atrialfibrillationwithanidioventricularescaperhythm.B:Acceleratedidioventricularrhythmatarateof50beats/min.

AVjunctionalrhythmatarateof40beats/min.

SinusrhythmwithseconddegreeMobitztypeISAblock.NotethatthePPintervalsgraduallyshorten,whereasthePRintervalsremainconstant.ThecycleterminateswithablockedPwave.ThelengthofthepauseisshorterthantwicetheprecedingPPcycle.

SinusrhythmwithfirstdegreeAVblock.ThePRintervalis0.44s.

SinusbradycardiawithseconddegreeMobitztypeIAVblock.NotetheprogressivelengtheningofthePRintervaluntilaQRScomplexisdropped.

SinusrhythmwithseconddegreeAVblock.

SinusrhythmwithseconddegreeMobitztypeIIAVblock.NotethevariableAVconduction.



ThirddegreeAVblockwithanacceleratedidioventricularescaperhythmwithaventricularrateof60beats/min.

Asynchronousventricularpacing.Inthiscase,theintrinsicheartrateisslowerthantheprogrammedpacemakerrate.Whenthisoccurs,thepacemakeristriggered,takingoverasthedominantpacemakeroftheheart.

VVIpacing.Althoughthepacemakerspikesaredifficulttoappreciate,beats38areventricularpacedbeats.

8/6/2015


Whentheintrinsicheartrateisfasterthantheprogrammedrate,thepacemakerisinhibitedfromfiring.

AVsequentialpacinginadualchamberpacemaker.Inthiscase,thepacemakerwillpaceboththeatriaandventricleswhennointrinsiccardiacactivityissensed.

DualchamberpacemakerfunctioningintheVATmode.Thepacemakerpacestheventriclesandsensestheatria.Ifintrinsicatrialdepolarizationsaresensed,aventricularpacingspikeistriggered.ThisisevidentontheECGbythepresenceofatrialtracking.

A:Singlechamberventricularpacemakershowingfailuretocapture.TheunderlyingrhythmisseconddegreeMobitztypeIAVblock.Aventricularpacingspikeoccursafterthefifthatrialcomplex(Pwave).Thispacingspikefailstodepolarizetheventricularmyocardium.B:Dualchamberpacemakershowingfailuretocapture.Beat3showsanatrialpacingspikethatfailstodepolarizetheatrialmyocardium.Thepacemakerthenproceedstopacetheventricle.Beats1,2,and49showanatrialpacingspikewithcapturefollowedbynormalAVconduction.(PartAreproduced,withpermission,fromGarsonA:StepwiseapproachtotheunknownpacemakerECG.AmHeartJ1990119:924.)

A:Undersensing.Thefifthbeatisaprematureventricularcontraction(PVC).Thenextbeatisaventricularpacedbeat.NotethatthepacedbeatoccurssoonafterthePVC,indicatingafailuretosensetheprecedingcomplex.B:ThefirstandsecondbeatsarepacedandthethirdandfourthbeatsshownormalAVconduction.Thereisalongerthanexpectedpausebetweenthefourthandfifthbeats.Thisoccurssecondarytoventricularoversensing.(Reproduced,withpermission,fromGarsonA:StepwiseapproachtotheunknownpacemakerECG.AmHeartJ1990119:924.)

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