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CURRENTDiagnosis&TreatmentEmergencyMedicine,7e>
Chapter35.CardiacArrhythmias
JosephHeidenreich,MD
CardiacArrhythmias:Introduction
Patientswithcardiacarrhythmiasoftenpresenttotheemergencydepartment.Thepatient'sclinicalpresentation
determinestheurgencywithwhichtheassessmentandmanagementshouldproceed.Patientswithserioussigns
andsymptoms(ie,shock,hypotension,congestiveheartfailure(CHF),severeshortnessofbreath,alteredlevel
ofconsciousness,ischemicchestpain,oracutemyocardialinfarction)requireimmediatetreatment.Withstable
patients,moretimeisaffordedforreviewofthe12leadelectrocardiogram(ECG)andrhythmstriptodiagnose
thecardiacarrhythmia.ReviewofavailablepriorECGsmayalsoassistinarrhythmiadiagnosis.
ElevenHelpfulHintsforEmergencyDepartmentArrhythmias
1. Obtainasmuchinformationasavailable.Alwayslookatall12leadsandbesureofname,date,age,correct
leadplacement,andstandardization.
2. Knowwhateachleadlookslikenormally(Figure351)eg,leadI(andusuallyleadIIandaVF)shouldlook
likethetextbookPQRSTexceptnoQwave.InleadI,theP,QRS,andTshouldallbeupright,theintervals
shouldbenormalandthePRandSTbaselinesshouldbeisoelectric.
3. Aregulartachycardiawitharatecloseto150shouldpromptasearchforatrialflutter.
4. Precisediagnosisofwidecomplextachycardias(WCTs)canbedifficult.Ifventricularrateisirregularconsider
atrialfibrillation(AF)oratrialflutterwithvariableconductionandunderlyingbundlebranchblock(BBB).
5. Donotrelyoncomputerreadings.Theymayormaynotbecorrect.
6. Singleleadrhythmstripsmaynothaveenoughinformation.Iftimepermits,alwaysobtaina12leadECG.
7. YoucannothavetoomanyECGs.SerialECGsareimportant.Sinustachycardiaratestendtochangeover
time.
8. ArrhythmiasarecommoninacuteSTelevationmyocardialinfarctions.
9. TachyarrhythmiasaredividedintonarroworwideQRSwidthandthenintoregularorirregular.
10. Arrhythmiaclassificationsandterminologiescanbeconfusingandtheychangeasnewinformationbecomes
available.
11. Iftheheartrhythmisslowandthepatientishypotensivewithsignsofpoorperfusion,assumetransthoracicor
transvenouspacingwillbeneeded.
FIGURE351.
http://accessmedicine.mhmedical.com.consultaremota.upb.edu.co/content.aspx?bookid=385&sectionid=40357251
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NormalECG.
ANoteonCardioversionandDefibrillation
NoconsensusexistsoncorrectpadpositioningandcurrentACLSguidelinesendorseboththeconventionalor
sternalapicalpositioning(onepadonthesuperioranteriorrightchestjustbelowtheleveloftheclavicleandone
padontheinferolateralleftchest)andtheanteroposterior(theanteriorpadasintheconventionalmethodand
theposteriorpadontherightorleftupperback).However,someauthorsfeelthatanteroposteriorplacementwith
theanteriorpadovertherightatriumandtheposteriorpadatthetipoftheleftscapulaoptimizescardioversionof
atrialtachyarrhythmiaswhileplacementoftheanteriorpadovertheventriclesandposteriorpadagainatthetip
oftheleftscapulaworkswellforventriculararrhythmias.
Allcurrentlymanufactureddefibrillatorsusebiphasicwaveformssounlessyouareusinganoldermachine,the
energysettingwillrangefrom0Joules(J)to200J.Allenergydosesmentionedinthischapterwillbeforbiphasic
defibrillators.Inadditiontodiseasespecificenergyrecommendations,therearedevicespecificrecommendations
forthedifferentbiphasicdefibrillatormodelsforfirstshockenergydoseinsomesituations.Notably,inventricular
fibrillation(VF)orpulselessventriculartachycardia(VT)theinitialshockis120fordevicesusingarectilinear
waveformand150200Jfordevicesusingatruncatedexponentialwaveformrangingfrom120to200J.ACLS
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guidelinesrecommendthatIFTHEOPERATORISUNSUREofdevicespecificrecommendationsthenthe
defibrillator'shighestenergylevelshouldbeusedinthissettingthiswillbe200Jforallbiphasicunitsand360Jif
youhappentostillhaveamonophasicunit.Thebottomlineisthatifyouareuncertainontheenergydoseinany
emergentsituationwhereelectricityisrequiredforanadultyourbestbetisturntheenergyupashighasitwillgo
asevenmaximaldosesofenergyarefelttoberelativelysafe.
Tachyarrhythmias
Immediatesynchronizedcardioversionshouldbeperformedonallunstablepatientswithtachydsrythmias.The
specificarrhythmiadiagnosis(supraventricularorventricular)doesnotneedtobemadeimmediatelybecause
initialmanagementisthesame.Patientswithpolymorphicventriculartachycardia(PMVT)of30secondsormore
andallunstablepatientsshouldbetreatedwithimmediatedefibrillation.
Instablepatients,theinitialmedicalmanagementwillbeguidedbytheunderlyingrhythmandadetailedhistory
andphysicalexamination.Inrecentyears,themoretraditionalapproachtocategorizepatientsaseitherstableor
unstablehasbeenmodified.Hemodynamicallystablepatientscanbefurthersubdividedintothosewithpreserved
orimpairedcardiacfunction.Findingsofimpairedcardiacfunctioninapatientwhoisotherwisestablemayalter
thepharmacologictreatment.
SupraventricularArrhythmias
SinusTachycardia
ClinicalFindings
(SeeAppendix,Figure353.)Sinustachycardiaoccurswhenthesinusrateisfasterthan100beats/min.Usually
therateis101160beats/min.Young,healthyadultscanacceleratetheirheartrateupto180200beats/min,
particularlyduringexercise.Youngchildrenhavebeennotedtohavesinusratesupto220beats/min.Sinus
tachycardiashouldnotbeviewedasaprimaryarrhythmiabutmoreasaresponsetoanunderlyingillnessor
condition.Itisoftennormalininfancyandearlychildhoodbutcanoccurasaresultofanumberofconditions
includingpain,fever,stress,hyperadrenergicstates,anemia,hypovolemia,hypoxia,myocardialischemia,
pulmonaryedema,shock,andhyperthyroidism.Certainmedicationsandillicitdrugscanalsocausetachycardia.
ThePwaveinsinustachycardiashouldhaveapositiveaxisinthefrontalplane,ie,thePwaveshouldbepositive
inleadIandaVF.
TreatmentandDisposition
Thetreatmentofsinustachycardiaisdirectedattheunderlyingcause.Thismayincludecorrectionofdehydration
withintravenousfluids,analgesicorantipyreticadministration,orsupplementaloxygentocorrecthypoxia.
Treatmentaimedatcorrectingtheheartrateratherthantheunderlyingconditionmaybeharmfulifthe
tachycardiaiscompensatoryandissupportingthecardiacoutput.Gradualslowingoftheheartratewith
treatmentoftheunderlyingconditionorduringcarotidsinusmassagemayhelptodifferentiatesinustachycardia
fromothersupraventriculararrhythmias.Adenosineadministrationwitha12leadrhythmstripishelpfulin
differentiatingfromothercausesoftachyarrhythmias.Furthermanagement,includingtheneedforhospitalization,
dependsontheunderlyingcondition.
ParoxysmalSupraventricularTachycardia
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ClinicalFindings
(SeeAppendix,Figures356,357,358,359,3510,and3511.)Paroxysmalsupraventriculartachycardia
(PSVT)isageneraltermthatreferstoanumberoftachyarrhythmiasthatarisefromabovethebifurcationofthe
Hisbundle.Approximately90%ofthesearrhythmiasoccurasaresultofareentrantmechanismtheremaining
10%occurasaresultofincreasedautomaticity.
Atrioventricularnodalreentranttachycardia(AVNRT)isthemostcommonformofPSVT,accountingfor5060%
ofcases.Theheartrateisusually180200beats/minandischaracterizedbysuddenonsetandsudden
termination.BecausethereentrantmechanismoccurswithintheAVnodeitself,virtuallysimultaneousexcitation
oftheatriaandventriclesoccurs.Asaresult,thePwavesoccurconcurrentwiththeQRScomplexesandare
difficulttovisualizeontheECG.Often,patientswithAVNRTdonothaveunderlyingheartdisease.Common
precipitatingfactorsincludealcohol,caffeine,andsympathomimeticamines.PatientswithAVNRTusuallypresent
intheirthirdorfourthdecadeoflife,andthemajority(approximately70%)arefemale.
Atrioventricularreciprocatingtachycardia(AVRT)accountsfor30%ofPSVT.Inmostcases,theimpulsetravels
downtheAVnodeandfollowsaretrogradepathuptheaccessorybypasstract.Becauseactivationofthe
ventriclesoccursthroughnormalconductionpathways,theaccessorypathwayisconcealed,andtheQRS
morphologyisnormal.ConsiderAVRTiftheheartrateisfasterthan200beats/minorifPwavesareseen
followingtheQRScomplex.
SinusnodereentryandintraatrialreentryareuncommoncausesofPSVT,accountingforapproximately5%of
cases.Inthesearrhythmias,theheartrateisusually130140beats/min.Moreoften,patientswiththese
arrhythmiashaveunderlyingheartdisease.
Automaticatrialtachycardiaisanotheruncommonarrhythmia,accountingforlessthan5%ofcasesofPSVT.The
heartrateisusually160250beats/minbutmaybeasslowas140beats/min.Inthiscase,theunderlying
mechanismisincreasedautomaticityratherthanreentry.Automaticatrialtachycardiaiscommonlyassociated
withunderlyingheartdisease.Thisarrhythmiaisdifficulttotreatandmayberefractorytostandardmeasures
includingcardioversion.
PSVTcanbeclassifiedasAVnodaldependentorindependent.Thisstrategymayproveusefulinformulating
treatmentoptions.AVNRTandAVRTareAVnodaldependent,meaningthattheAVnodeisinvolvedinthe
reentrantcircuit.Fortheserhythms,pharmacologicmanagementisdesignedtodecreaseconductionthroughthe
AVnode.
Treatment
UNSTABLEPATIENTS
PatientswithPSVTwhoarehemodynamicallyunstablerequireimmediatesynchronizedDCcardioversion.
Currentrecommendationsaretostartwithlowenergylevels(50100J)andthentoincreasetheinitialdoseby
50Jasneededuntilsinusrhythmisrestored.Ifclinicalcircumstancespermit,administerintravenoussedatives.
Avoidthecommonerrorofdelayingemergencycardioversiontoperformotherpatientcareactivities.Ifimmediate
cardioversionisunavailable,physicalmaneuversthatcausevagalstimulationcanbeattempted.
Adenosine,blocker,orcalciumchannelblockermaybeadministered.
STABLEPATIENTS
TachycardiaassociatedwithPSVTisusuallywelltoleratedunlessthepatienthasunderlyingheartdiseaseorleft
ventriculardysfunction.
PhysicalManeuvers
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Instablepatients,physicalmaneuverscausingvagalstimulationcanbeattemptedpriortomedication
administration.ManeuversthatstimulatethevagusnervesuchastheValsalvamaneuver(expirationagainsta
closedglottis),Muellermaneuver(deepinspirationagainstaclosedglottis),coldwaterfacialimmersion,and
carotidsinusmassageareattimeseffectiveinterminatingPSVTthatresultsfromAVnodalandsinoatrial(SA)
nodaldependentmechanisms.Performcarotidsinusmassageonlyafterauscultationforcarotidbruits.
PharmacologicTreatment
Ifvagalstimulationiscontraindicatedorineffective,adenosineisconsideredfirstlinemedicaltherapyfor
conversionofPSVT.Ingeneral,pharmacologicagentswithAVnodalblockingpropertiessuchasadenosine,
blockers,calciumchannelblockers,anddigoxinareusedfortheacutemanagementandpreventionofAVnodal
dependentPSVT.Otherantiarrhythmicagents,suchasprocainamideandamiodarone,whichexerteffectsat
variouslevelsofthecardiacconductionsystemareusedforthemanagementandpreventionofAVnodal
independentPSVT.AntiarrhythmicmedicationsmaybeconsideredforconversionofPSVTwhenAVnodal
blockingagentsareunsuccessful.
Adenosine
AdenosineisanendogenousnucleosidethatslowsconductionthroughtheAVnodeandissuccessfulin
terminatingmorethan90%ofPSVTsresultingfromAVnodalreentrymechanisms(AVNRTandAVRT).
Adenosinemayalsobeeffectiveinterminatingsinusnodereentrytachycardiabutisusuallyineffectivein
terminatingautomaticatrialtachycardia.OftenadenosinewillcauseatransientAVblock,brieflyexposingthe
underlyingatrialactivity.AdministrationofamedicationwithmoreprolongedeffectontheAVnode(blockersor
calciumchannelblockers)mayprovideamoresustainedreductioninventricularrate.
Administeradenosinerapidly,andfolloweachdoseimmediatelywitha20ccsalineflush.Althoughcurrent
recommendationsaretoadministeraninitialintravenousdoseof6mgover13secondsrepeatedat2and4
minuteswith12mgdosesifthisdoesnotterminatethePSVT,manyclinicianschoosetoforgotheinitial6mg
doseandwillincreasethedoseto18mgifthe12mgdosedoesnotproduceAVblockade.The18mgdosehas
beenshowntobebothsafeandeffective.Commonsideeffectsincludeunexplainablefeelingofimpendingdoom,
facialflushing,hyperventilation,dyspnea,andchestpain.Thesesideeffectsareoftentransientowingtotheshort
halflifeofadenosine(lessthan5seconds).Prewarningtothepatientofthesesymptomsishelpful.Theeffectsof
adenosineareantagonizedbycaffeineandtheophyllineandpotentiatedbydipyridamoleandcarbamazepine.
Hearttransplantpatientsmaybeoverlysensitivetotheeffectsofadenosineifnecessary,usesmallerdoses.
Becauseadenosinecanprovokebronchospasm,usecautionifitisbeingadministeredtopatientswithahistoryof
reactiveairwaydisease.
AdenosinecanalsobeadministeredtoastablepatientwithawideQRScomplextachycardiasuspectedtobe
supraventricularinorigin.Adenosineispreferredovercalciumchannelblockersinpatientswithhypotensionor
impairedcardiacfunctionandinpatientsconcomitantlyreceivingadrenergicblockingagents.
BlockingAgents
blockerssuchasmetoprololoresmololslowSAnodeimpulseformationandslowconductionthroughtheAV
node.Thesemedicationsshouldbeusedwithcautioninpatientswithahistoryofseverereactiveairwaydisease
andCHF.
Metoprololisanalternativetocalciumchannelblockers,andisadministeredintravenouslyatadoseof5mg
every5minutesforthreedoses.Esmololisanultrashortacting1selectiveblockerthathastheadvantageof
abriefhalflife(10minutes)andarapidonsetofaction.Administeraloadingdoseof0.5mg/kgover1minute.
Thisisfollowedbyamaintenanceinfusionof50g/kg/min.Iftheresponseisinadequate,anotherdoseof0.5
mg/kgcanbeadministeredafter4minutesandthemaintenanceinfusionincreasedto100g/kg/min.Whenheart
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ratecontrolisachieved,reducethemaintenanceinfusionto25g/kg/min.
CalciumChannelBlockers
CalciumchannelblockerssuchasdiltiazemorverapamilareeffectiveinconvertingPSVTtosinusrhythm.The
efficacyofdiltiazemandverapamilintermsofconversionrates,rapidityofresponse,andsafetyprofileappear
similar.ThesemedicationsdecreaseSAandAVnodeconductionandcauseprolongationoftheAVnode
refractoryperiod.Calciumchannelblockersalsodecreasemyocardialcontractilityandperipheralvascular
resistance.UsecalciumchannelblockerswithcautioninpatientswithleftventriculardysfunctionorCHF.Avoid
thesemedicationsinpatientswithWCTofunknownorigin,ventriculartachycardia(VT),ortachycardiawith
ventricularpreexcitation.Hypotensionisthemostconcerningsideeffectofintravenousadministrationandoccurs
in1015%ofpatients.
Verapamil
Theinitialdoseofverapamilis510mgadministeredintravenouslyover12minutes.Additionaldosesof510
mgcanbeadministeredevery15minutesasneededuntilthedesiredeffectisachievedoratotalof30mghas
beenadministered.
Diltiazem
Theinitialdoseofdiltiazemis0.25mg/kgadministeredintravenouslyover2minutes(20mgfortheaverage
adult).Ifnecessary,adoseof0.35mg/kgcanbeadministeredin15minutes.Afterconversion,amaintenance
infusioncanbestartedat510mg/handcanbeincreasedtoamaximumof15mg/hifneeded.
Thechoicebetweenblockersandcalciumchannelblockersdependsonmultiplefactors,butbothshouldnotbe
givenintravenouslytothesamepatient.Bothhaverapidonset(minutes)andbothshouldbeusedwithcautionin
severeCOPDandsevereCHF.Medicationthatthepatientiscurrentlytakingandphysicianpreferenceare
considerations.Inpatientswithhyperthyroidismandcongenitalheartdisease,blockersarethebestchoice.
Digoxin
Digoxinadministrationwillincreasevagaltonewhilereducingsympatheticactivity.Asaresult,conductionthrough
theAVnodeisslowed.Digoxinmaybeadministeredasanintravenousbolusdoseof0.5mg.Additionaldosesof
0.25mgmaybegivenasneededevery46hours,withatotaldosenottoexceed1.25mgin24hours.The
immediatebenefitofdigoxinislessenedbyitsslowonsetofaction.Whenusedincombination,digoxinmayallow
forlowerdosesofsubsequentlyadministeredantiarrhythmicagents.AvoiddigoxininpatientswithAFwith
ventricularpreexcitation.
Amiodarone
AmiodaroneisaclassIIIantiarrhythmicagentwithsodiumandpotassiumchannelblockingpropertiesand
blockingandcalciumchannelblockingproperties.Byvirtueofitsblockingandcalciumchannelblocking
properties,amiodaroneslowsconductionthroughtheAVnode.InpatientswithimpairedcardiacfunctionorCHF,
treatmentoptionsnarrow.Amiodaronehasasolidsafetyprofileandmaybeaneffectivealternativeagentinthis
situation.Amiodaronecanbeadministeredasaslowintravenousinfusionof150mgover10minutes.Thisis
followedbyamaintenanceinfusionof1mg/minfor6hoursandthen0.5mg/min.Additionalbolusdosesof150
mgcanberepeatedasneededforresistantorrecurrentPSVTuptoatotaldailydoseof2g.
Procainamide
ProcainamideisaclassIAantiarrhythmicagentwithsodiumchannelblockingproperties.Procainamidewillslow
conductionthroughboththeAVnodeand,ifpresent,anaccessorybypasstract.Procainamidecanbeconsidered
forpatientswithPSVTrefractorytoAVnodalblockingagents.Therecommendedloadingdoseofprocainamideis
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17mg/kgadministeredasaslowintravenousinfusionatarateof2030mg/min(1gforanaverageadult).Stop
theinitialinfusionifthearrhythmiaissuppressed,hypotensiondevelops,ortheQRScomplexwidensbymore
than50%ofitsoriginalduration.Afterarrhythmiasuppression,startamaintenanceinfusionat14mg/min.
Disposition
HospitalizationshouldbeconsideredforpatientsinPSVTwithaccompanyingserioussignsandsymptoms,
patientsrequiringemergencycardioversion,patientsinPSVTwithventricularpreexcitation,andpatientswith
arrhythmiasrefractorytostandardtreatment.Outpatientfollowupcareshouldbeprovidedfortheotherwise
healthypatientwithatransientepisodeofPSVTconvertedtosinusrhythmintheemergencydepartment.
AtrialFibrillation
ClinicalFindings
(SeeAppendix,Figures3512and3513.)InAF,theatrialrateisdisorganizedandis300600beats/min.AFis
characterizedbyanirregularlyirregularventricularratewiththeabsenceofdiscerniblePwaves.
AFisthemostcommonsustainedcardiacarrhythmiainadults.ItisestimatedthatAFaffectsmorethan2million
personsintheUnitedStatesitsprevalenceincreaseswithage,approaching10%inthoseolderthan80years.
AFcanoccurintheabsenceofunderlyingheartdiseaseormaybeassociatedwithanumberofconditions,
includingchronichypertension,valvulardisease,cardiomyopathy,myocardialischemia,myocarditis,pericarditis,
orcongenitalheartdisease.AFmayalsooccurinthepresenceofothersystemicdisorders,including
hyperthyroidism,pulmonaryembolism,hypoxia,andexcessconsumptionofalcoholorcaffeine.
PatientswithnonvalvularAFhaveapproximatelya5%annualincidenceofstrokeasaresultofathromboembolic
event.Thisriskincreasesfourfoldinpatientswithmitralstenosisandincreasesdramaticallyinolderpatients,
approaching30%inpatientsaged8089years.
Treatment
AcutemanagementofAFincludesventricularratecontrolandpreventionofthromboemboliccomplications.
Additionalmanagementconsiderationsincluderestorationandmaintenanceofsinusrhythm.
UNSTABLEPATIENTS
PatientsinAFwitharapidventricularresponsewhoarehemodynamicallyunstablerequireimmediate
synchronizedDCcardioversion.Recommendationsaretostartbetween100and200Jbiphasicandthento
increasethedoseinstepwisefashionasneededuntilsinusrhythmisrestored.
STABLEPATIENTS
Instablepatientswitharapidventricularresponse,theinitialgoalisratecontrol.Thiscanusuallybeachieved
withblockers,calciumchannelblockers,ordigoxin.blockersmayprovemosthelpfulinpatientswith
hyperthyroidismbutarerelativelycontraindicatedinpatientswithacutedecompensatedCHF.Diltiazemand
verapamilcanoftenslowtheventricularrateandhavetheaddedbenefitofantianginaleffectsandbloodpressure
controlinhypertensivepatients.Inmorethan90%ofpatients,areductioninheartrateofatleast20%isnoted.
DiltiazemappearstobesafeforuseinpatientswithmildCHF.Digoxincanalsohelpcontroltheventricularratein
patientswithAFandmaybeusefulinpatientswithleftventriculardysfunction.Itssloweronsetofactionas
comparedtootheragentsmakesitlessusefulforacuteratecontrol.InpatientswithmildtomoderateCHF,the
administrationofamiodaronemayproveuseful.Intravenousamiodaronecanalsobeconsideredanalternative
agentforratecontrolwhentheaboveagentsfail.Thespecificmedicationchoicewilloftenbedictatedbythe
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urgencyofthesituation,themedicationprofile,physicianpreference,andthepatient'sunderlyingcondition.
Anticoagulants
Prophylacticanticoagulationwithwarfarinhasbeenshowntosignificantlyreducetheincidenceofstrokein
patientswithAF.IfnewonsetAFisofundetermineddurationorgreaterthan48hoursduration,initiationof
anticoagulationisnecessary.Currentrecommendationsincludeanticoagulationfor3weeks,followedbyelective
cardioversionandthencontinuedoutpatientanticoagulationforfourmoreweeks.Analternativestrategyisinitial
anticoagulationwithunfractionatedorlowmolecularweightheparinfollowedbytransesophageal
echocardiographytoevaluatetheleftatrialappendageforthepresenceofclot.Ifnoclotisidentified,thepatient
maysafelyundergocardioversion,followedbyanticoagulationfor4weeks.Ifaleftatrialappendageclotis
identifiedbytransesophagealechocardiography,recommendationsincludeanticoagulationfor3weeks,followed
bycardioversionandthencontinuedanticoagulationforfouradditionalweeks.InpatientswithAFoflessthan48
hoursduration,anticoagulationisnotrecommended.
Antiarrhythmics
Variousantiarrhythmicagents,includingamiodarone,procainamide,andsotalol(classIII),areusedtochemically
convertAF.Pharmacologicorelectricalcardioversionmaybeconsideredinselectedstableemergency
departmentpatientswithAFoflessthan48hoursduration.Remodeling,bothanatomicallyandelectrically,
occurssoonaftertheonsetofAF.Postponingcardioversioncouldleadtoanincreasedresistancetoattemptsat
conversion.
Disposition
PatientswithchronicratecontrolledAFdonotrequirehospitaladmission.InpatientswithnewonsetAF,
hospitalizationisoftenrequiredforventricularratecontrol,initiationofanticoagulation,andsometimesfor
initiationofantiarrhythmictherapy.Ifapatientpresentswiththromboemboliccomplications,hospitaladmission
willalsobenecessary.
AtrialFlutter
ClinicalFindings
(SeeAppendix,Figure3514)Inatrialflutter,theatrialrateisusually250350beats/min.Itisthemostcommon
underdiagnosedtachyarrhythmia.SawtoothflutterwavesmaysometimesbeseenonECG,butshouldnotbe
reliedupon.Typically,atrialflutterwillpresentwith2:1AVconduction.Forthisreason,itisimportanttoconsider
atrialflutterinthedifferentialdiagnosisofaregulartachycardiaatapproximately150beats/min,eveninthe
absenceofflutterwaves.AtrialflutterismostcommonlyidentifiedasnegativewavesinII,III,andaVFwith
positiveflutterwavesinleadV1.
Ifatrialflutterissuspected,severaloptionsareavailabletobetteridentifyatrialactivity.Vagalmaneuversor
administrationofadenosinewitha12leadrhythmstripmayunmaskflutterwaves.
Treatment
Acutemanagementofatrialflutterincludesventricularratecontrolandpreventionofthromboembolic
complications.Additionalmanagementconsiderationsincluderestorationandmaintenanceofsinusrhythm.
UNSTABLEPATIENTS
Patientsinatrialflutterwitharapidventricularresponsewhoarehemodynamicallyunstablerequireimmediate
synchronizedDCcardioversion.Currentrecommendationsaretostartwithbetween50and100Jbiphasicand
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thenincreasetheenergydoseinstepwisefashionasneededuntilsinusrhythmisrestored.
STABLEPATIENTS
Instablepatientswitharapidventricularresponse,theinitialgoalisratecontrol.Adequateheartratecontrolcan
beachievedwiththeadministrationofeitherblockersorcalciumchannelblockers.Digoxinisoftenlesseffective
acutelybecauseofitsslowonsetofaction.Amiodaroneanddiltiazemarealternativesforratecontrolinthestable
patientwithimpairedcardiacfunctionorCHF.
ThestrokeriskforpatientsinatrialflutterislessthanthatofAF.Thesameanticoagulationguidelinesexistfor
atrialflutterasinAF.
Disposition
Patientswithchronicratecontrolledatrialflutterdonotrequirehospitaladmission.Inpatientswithnewonset
atrialflutter,hospitalizationisoftenrequiredforventricularratecontrol,initiationofanticoagulation,and
sometimesforinitiationofantiarrhythmictherapy.
MultifocalAtrialTachycardia
ClinicalFindings
(SeeAppendix,Figure3515)Inmultifocalatrialtachycardia(MAT)theheartrateistypically100130beats/min.
ThecharacteristicECGfindingisatleastthreedifferentPwavemorphologies.Therhythmoftenappearsirregular
andcanattimesbeconfusedwithAF.VaryingPRintervalsmayalsobenoted.Whentherateisslowerthan100
beats/min,thetermwanderingatrialpacemakerisapplied.Unlessunderlyingaberrantconductionispresent,the
QRScomplexesarenarrow.Severeunderlyingchronicobstructivepulmonarydiseaseaccountsforapproximately
6085%ofcases.Theophyllineanddigoxinlevelsshouldbecheckedsincetoxicityofthesedrugscancause
MAT.
Treatment
TheinitialtreatmentofMATisdirectedatcorrectingtheunderlyingcause.AswithAF,theinitialgoaloftherapyis
toachieveheartratecontrol.BecauseMATdoesnotrespondtoelectricalcardioversion,pharmacologic
interventionmayberequired.
MagnesiummaybeeffectiveinconvertingMATandcanbeadministeredasa2gintravenousbolusover1
minute.Thisisfollowedbya2g/hinfusionfor5hours.Magnesiumcanstillbeeffectiveifserummagnesium
levelsareinthenormalrange.Potassiumrepletionmaybehelpfulinpatientswhoarehypokalemic.
Amiodarone,digoxin,ordiltiazemmaybeconsideredasalternativeagentsforratecontrol,especiallywhenthe
patientexhibitsfindingsofCHF.
Disposition
PatientsmayrequirehospitalizationforMATiftheheartrateisdifficulttocontrolorforfurthermanagementofthe
underlyingcondition.
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.In
thiscase,thecardiacimpulsetravelsdowntheAVnode(antegradeconduction)andstimulatestheventricles
throughthenormalconductionpathways.TheaccessoryAVbypasstractservesastheretrogradelimbofthe
circuit.IntheabsenceofaberrantventricularconductionorafixedBBB,themorphologyoftheQRScomplexis
narrowwithoutevidenceofventricularpreexcitation(absentwave).Thebypasspathwayisconsidered
concealediftheshortPRandwavearenotpresentonthebaselineECG.
Rarely,antidromicAVRToccurswherebytheaccessoryAVpathwayactsastheantegradelimbofthecircuitand
theAVnodeastheretrogradelimb.AntidromicAVRTwillproduceawideQRScomplextachycardiaandmay
masqueradeasVT.Thetachycardiamaybeextremelyrapid(withventricularrate220300),leadingto
ventricularfibrillation(VF)asaresultofanRonTphenomenon.
AFisthesecondmostcommonarrhythmiaassociatedwithWPWsyndrome.AFwithventricularpreexcitationhas
ahighpotentialtoprecipitatehemodynamiccompromise.AFwitharapidventricularrateischaracterizedbyan
irregulartachycardiaandawideQRScomplexresultingfromventricularpreexcitation.
Treatment
PatientswithorthodromicAVRTwhoarehemodynamicallyunstablerequireimmediatesynchronizedDC
cardioversion.Currentrecommendationsaretostartbetween50Jand100Jbiphasicandthentoincreasethe
initialdoseinstepwisefashionasneededuntilsinusrhythmisrestored.InpatientswithknownWPWsyndrome
presentingwithanarrowcomplexregulartachycardia,orthodromicAVRTcanbeassumed.Instablepatients,the
medicaltreatmentwillbethesameasinAVNRT.Pharmacologictreatmentwithadenosine,adrenergicblocking
agents,orcalciumchannelblockerscanbeadministeredasdeemednecessaryandappropriatefortheindividual
case.Ingeneral,thetreatmentoforthodromicAVRTwithAVnodalblockingagentsissafe.Theriskofenhancing
antegradeconductiondownthebypasstractisverylow.
TreatmentofAFwithventricularpreexcitation(antidromicAVRT)isdifferentfromthatoforthodromicAVRT.Ifthe
patientishemodynamicallyunstable,immediatesynchronizedDCcardioversionstartingat100200Jis
warranted.TheuseofAVnodalblockingagents,specificallyblockers,calciumchannelblockers,anddigoxin,is
contraindicated.IfconductionthroughtheAVnodeisslowed,conductiondowntheaccessorypathwaymaybe
enhanced,possiblydegeneratingtoVF.BecauseprocainamidewillslowconductionthroughboththeAVnode
andtheaccessorypathway,itisthemedicationofchoicewhenAFwitharapidventricularresponseisassociated
withventricularpreexcitation.ProcainamideisalsothemedicationofchoiceinantidromicAVRT.Amiodaronecan
beusedasanalternativeagentintreatingAFwithventricularpreexcitationandfindingsofCHF.
Disposition
Hospitalizationisnotrequiredforpatientswhoareasymptomaticwithevidenceofventricularpreexcitationonthe
ECG(sinusrhythm,shortPR,andawave).Considerhospitalizingpatientswhohaveserioussignsand
symptomsorthoserequiringcardioversion.Inaddition,hospitalizationisrecommendedforpatientswithAFand
ventricularpreexcitationorantidromicAVRT.PatientswhopresentwithstableorthodromicAVRTmaybe
dischargedwithcloseoutpatientfollowupafterpharmacologicconversionintheemergencydepartment.
2005AmericanHeartAssociationGuidelinesforCardiopulmonaryResuscitationandEmergencyCardiovascular
Care.Circulation2005112:IV35IV46[PubMed:16314375].
DelacrtazE:Clinicalpractice.Supraventriculartachycardia.NEnglJMed2006354:10391051[PubMed:
16525141].
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InnesJA:Reviewarticle:Adenosineuseintheemergencydepartment.EmergMedAustralas200820:209215
[PubMed:18549383].
RaghavanAVetal:Managementofatrialfibrillationintheemergencydepartment.EmergMedClinNorthAm
200523:11271139[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)VentriculartachycardiaisthemostcommoncauseofwideQRS
complextachycardia.ThetermVTisusedwhensixormoreconsecutiveventricularbeatsoccur.Theventricular
rateisusually150220beats/min,althoughratesslowerthan120beats/minmayoccur.NonsustainedVTis
characterizedbyanepisodelastinglessthan30seconds.SustainedVTischaracterizedbyanepisodelasting
longerthan30seconds,associatedwithhemodynamiccompromise,orrequiringtherapeuticinterventionfor
termination.WCTreferstoaregulartachycardiawithaQRScomplexgreaterthan0.12seconds(120ms)in
duration.WCTmostoftenoccursasaresultofeitherVTorSVTwithaberrantconduction(underlyingorrate
dependentBBB).
Inmorethan75%ofpatientspresentingintheemergencydepartmentwithregularWCT,theunderlying
arrhythmiaisVT.Thepresenceofstructuralheartdisease,coronaryarterydisease,priormyocardialinfarction,or
CHFstronglysuggestsVT.CertainECGfindingsfavorVToverSVTwithaberrantconduction.Thesefindings
includeaQRScomplexwiderthan160ms,thepresenceoffusionbeats,andevidenceofAVdissociation.AV
dissociationoccursinabout20%ofpatientswithVTandconfirmsthediagnosis(thisisusuallyseenwith
ventricularrateslessthan150).AcommonclinicalerrorthatmustbeavoidedistoassumethatWCTisSVTwith
aberrantconduction.AllcasesofWCTofunknownoriginshouldbemanagedasVT.
Electricalstormisasomewhatrarebutwelldescribedentitythatconsistsofrecurrentventriculartahchycardia,
usuallywithanimplanteddefrillatorthatdischargesrepeatedly.Patientswiththisconditionhaveahighmortality
andwilllikelyneedsedationaswellassympatheticblockadetocontroltherecurrentdysrhythmias.Anti
arrhythmicsuseisusuallyrequiredandIVamiodaroneisthedrugofchoice.
TenTipsfortheDiagnosisofRegularWCT
1. AWCTismostlikelyVT.
2. Considertoxicityalwaysthinkofhyperkalemia,tricyclicantidepressants,anddigoxin.Treatmentisdifferent
andcardioversionisnothelpful.
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/S<1inV6.IfLBBBlike,thenlookfor
wideR(>30ms),onsetofRtonadirofS>100msinV1orV2,andQRorQSinV6.
8. IfstillunsuretreatforVT.
9. Besttreatmentiscardioversion.
10. Stabilizerhythmbeforeadmission.
Treatment
UnstablePatients
PatientswithVTorWCTofunknownoriginwhoarehemodynamicallyunstablewithserioussignsandsymptoms
requireimmediatesynchronizedDCcardioversion.Recommendationsaretostartwith50100Jandthen
increasetheinitialdoseby50Jasneededuntilsinusrhythmisrestored.
StablePatients
Traditionally,patientswithstableVTareadministeredanantiarrhythmicagentforchemicalcardioversion.A
numberofmedicationsareavailable.Thechoiceforaparticularpatientisoftenbasedonphysicianpreference
andexperience,findingsofpreservedorimpairedcardiacfunction,andtheunderlyingcauseoftheVT.
LIDOCAINE
LidocaineisaclassIbantiarrhythmicwithsodiumchannelblockingproperties.Becauseitcanbeadministered
rapidlywithfewsideeffects,someauthorsconsiderittheagentofchoiceforventriculararrhythmiasassociated
withacutemyocardialischemiaorinfarction.Therecommendedintravenousloadingdoseis1.01.5mg/kg.If
required,asecondbolusdoseof0.751.5mg/kgcanbeadministeredin510minutes.Ifventricularectopy
persists,anadditionalbolusdoseof0.50.75mg/kgcanbeadministeredevery510minutestoamaximum
doseof3mg/kg.Afterrhythmsuppression,startamaintenanceinfusionat24mg/min.Lidocainehasthelowest
incidenceoftoxicityofallcurrentlyusedantiarrhythmicmedications.
OTHERDRUGS
ProcainamideisanalternativeagenttolidocaineforthetreatmentofstablemonomorphicVT.Amiodaronemay
bepreferabletootherantiarrhythmicagentsforVTinpatientswithCHF.Althoughrecommended,amiodarone's
efficacymaynotbefastenoughforuseonanemergencybasis.
Disposition
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HospitalizationisrecommendedforallpatientswhopresentwithVT.
PolymorphicVentricularTachycardia(IncludingTorsadesDePointes)
ClinicalFindings
(SeeAppendix,Figure3518)PolymorphicventriculartachycardiaisaformofVTwithvaryingQRScomplex
morphology.Therhythmisoftenirregularandhemodynamicallyunstable,anditcandegeneratetoVF.
TorsadesdepointesisaformofPMVTassociatedwithaprolongedQTintervalonthebaselineECG.Therhythm
isoftendescribedashavingatwistingonpointappearanceandcanbeeitherparoxysmalorsustained.The
heartrateisusually200250beats/min.HereditarylongQTsyndromesassociatedwithtorsadesdepointes
includeLangeNielsensyndromeandRomanoWardsyndrome.Torsadesdepointesmayalsooccurasaresult
ofnumerousmedicationinteractions.AcompletelistofmedicationsthathavebeenreportedtoprolongtheQT
intervalisavailableatwww.qtdrugs.org.
PMVTcanalsooccurintheabsenceofaprolongedQTinterval.Inthiscase,cardiacischemiaorunderlying
structuralheartdiseaseisoftenthecause.
PatientswithPMVTwhoarehemodynamicallyunstablewithserioussignsandsymptomsrequireimmediate
cardioversionordefibrillation.Recommendationsaretostartwith200J.Topreventrecurrence,discontinueall
agentsthatcanprolongtheQTinterval.
Magnesiumisthemedicationofchoiceforthemanagementoftorsadesdepointesassociatedwithcongenital
andacquiredformsoflongQTsyndrome.Itmaybeeffectiveevenwhenserumlevelsarenormal.A2g
intravenousdosecanbeadministeredasaslowpushover5minutes.Followthebolusdosebyamaintenance
infusionof12g/h.Considersupplementalpotassiumasanadjunctivetherapytomaintainserumpotassium
levelsinthehighnormalrange.Temporarytransvenouspacingatratesaround100beats/minmaybeusefulto
preventrecurrences,especiallyinpatientswithbradycardiaorpauses.Hospitalizationisrecommendedforall
patientswhopresentwithPMVT.
VentricularFibrillation
ClinicalFindings
(SeeAppendix,Figure3519)Ventricularfibrillationischaracterizedbyanirregularventricularrhythmwithno
discernibledistinctionbetweentheQRScomplex,STsegment,andTwaves.VFisacommoncauseofsudden
cardiacdeathandremainsasignificantcontributortomortalityinthefirst24hoursafteranacutemyocardial
infarction.Intheabsenceofearlybystandercardiopulmonaryresuscitationandinitiationofadvancedcardiaclife
support,includingdefibrillation,survivalratesarepoor.
WitnessedVForpulselessVT,istreatedwithimmediatetreatmentisasynchronousdefibrillationfollowedbyCPR
for2minutesbeforerhythmcheck.IfVTorpulselessVTpersists,repeatdefibrillationfollowedbyeither
epinephrineorvasopressinandcontinuedCPRfor2minutes.IfVTorpulselessVTstillpersistsagainrepeat
defibrillationfollowedbyeitheramiodaroneorlidocaineandCPRfor2minutes.Allpatientswhohavebeen
successfullyresuscitatedfromVForpulselessVTshouldbestartedonadripofthelastantiarrhythmic
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administeredandadmittedtotheintensivecareunitforcloseobservation.Ifanacutecoronarysyndromeis
suspectedasthecauseofthearrest,thepatientmayrequirecardiaccatheterizationforevaluationandtreatment.
Chapter9offersamoreindepthdiscussionofthemanagementofcardiacarrest.
ACC/AHA/ESC2006Guidelinesformanagementofpatientswithventriculararrhythmiasandthepreventionof
suddencardiacdeathexecutivesummary.Circulation2006114:10881132[PubMed:16949478].
GoldbergerZD,RhoRW,PageRL:Approachtothediagnosisandinitialmanagementofthestableadultpatient
withawidecomplextachycardia.AmJCardiol2008101:14561466[PubMed:18471458].
HollowellH,MattuA,PerronAD,HolstegeC,BradyWJ:Widecomplextachycardia:beyondthetraditional
differentialdiagnosisofventriculartachycardiavssupraventriculartachycardiawithaberrantconduction.AmJ
EmergMed200523:876889[PubMed:16291445].
HuangDT,TraubD:Recurrentventriculararrhythmiastormsintheageofimplantablecardioverterdefibrillator
therapy:acomprehensivereview.ProgCardiovascDis200851:229236[PubMed:19026857].
MarrillKA,deSouzaIS,NishijimaDK,StairTO,SetnikGS,RuskinJN:Amiodaroneispoorlyeffectivefortheacute
terminationofventriculartachycardia.AnnEmergMed200647:217224[PubMed:16492484].
StahmerSA,CowanR:Tachydysrhythmias.EmergMedClinNorthAm200624:1140.[PubMed:16308111]
VohraJ:TheLongQTSyndrome.HeartLungCirc200716:S5S12[PubMed:17627884].
Bradyarrhythmias,ConductionDisturbances,andEscapeRhythms
Asintachycardiamanagement,ifabradycardicpatientishemodynamicallyunstable,immediateinterventionis
requiredregardlessoftheoriginoftheunderlyingarrhythmia(eg,SAblock,AVblock,andventricularescape
rhythm).Transcutaneouscardiacpacingfollowedassoonaspossiblewithtransvenouspacingistheinitial
interventionofchoiceforpatientswithserioussignsandsymptomsthatoccurasaresultofabradyarrhythmia.In
stablepatients,orinpatientswithmildsymptoms(eg,dizziness,lightheadedness),pharmacologictreatmentis
ofteninitiatedwithorwithoutstandbypacing.Medicalmanagementcanbeinitiatedinpatientswithsymptomatic
bradycardiaasabridgetocardiacpacing,ormaybeinitiatedifemergencycardiacpacingisunavailable.
Primaryconductionsystemdisturbancesaccountfor15%ofbradyarrhythmiasencounteredintheemergency
departmentsetting.Theremaining85%occurasaresultofvarioussecondarycausessuchasacutecoronary
ischemia(40%),medicationsortoxicologicalcauses(20%),metaboliccauses(5%),neurologicalcauses(5%),
permanentpacemakerfailure(2%),andothermiscellaneouscauses(13%).Symptomaticbradycardiaresulting
fromAVconductiondisturbancesorsicksinussyndromeismorecommonintheelderlythemajorityofpatients
presentatage65yearsorolder.
SinusBradycardia
ClinicalFindings
(SeeAppendix,Figure354)Sinusbradycardiaoccurswhenthesinusrateisslowerthan60beats/min.Usually
therateis4559beats/min,butonrareoccasionitmaybeasslowas35beats/min.Sinusbradycardiais
commonlyassociatedwithsinusarrhythmiaandisoftenanormalfindinginyoung,healthy,athleticindividuals.
Sinusbradycardiaisoftenbenignanddoesnotnecessarilyindicatesinusnodedysfunction.Althoughcommonly
physiologic,sinusbradycardiamaybepathologicwhenpatientsexperiencesymptomsofcerebralhypoperfusion
orwhentheheartratedoesnotincreaseappropriatelywithactivityorexercise.Certainunderlyingconditions
havebeenassociatedwithaslowingoftheheartrate,includinghypothermia,hypothyroidism,andincreased
intracranialpressure.Inaddition,anumberofdifferentmedications,includingblockers,calciumchannel
blockers,clonidine,digoxin,andlithium,cancausebradycardia.
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Usuallynotreatmentisrequiredforasymptomaticsinusbradycardia.Whenserioussignsandsymptomsare
present,medicalmanagement,pacemakerplacement,andhospitaladmissionareindicated.
SinusArrest
Sinusarrestisdefinedasafailureofsinusnodeimpulseformation.OntheECG,randomperiodsofabsent
cardiacactivitymaybenoted.Unlessescapebeatsoccur,lengthypausesarenoted.Whenpausesoccur,
patientsmaycomplainofdizzinessorlightheadednessormayhavesyncope.Ifuntreated,pauseslongerthan2.5
secondsmayprogresstoasystole.
SinoatrialBlock
SAblockdiffersfromsinusarrestinthatSAblockisaformofexitblockratherthanfailureofimpulseformation.
Likesinusarrest,SAblockmayoccurasaresultofanumberofconditions,includingacutemyocardialinfarction,
myocarditis,fibrosisoftheSAnode,excessivevagaltone,anddigoxintoxicity.AnalogoustoAVblock,SAblock
canbeclassifiedintofirst,second,andthirddegreeheartblock.
FirstdegreeSinoatrialBlock
FirstdegreeSAblockdoesnotproduceanyECGchanges.Thediagnosiscanbemadeonlythrough
electrophysiologictesting.
SecondDegreeSinoatrialBlock(MobitzTypeI)
(SeeAppendix,Figure3524)SeconddegreeMobitztypeISAblock,alsoknownasSAWenckebach,is
characterizedbyPPintervalsthatgraduallyshortenwhilethePRintervalremainsconstant.Thiscycleterminates
withablockedPwave.ThelengthofthepauseisshorterthantwicetheprecedingPPcycle.
SecondDegreeSinoatrialBlock(MobitzTypeII)
SeconddegreeMobitztypeIISAblockischaracterizedbyfixedpauses.OntheECG,thePPintervalremains
constantandisthenfollowedbyablockedPwave.ThePPinterval,includingtheblockedPwave,willbetwice
thelengthofthenormalPPinterval.
ThirdDegreeSinoatrialBlock
ThirddegreeSAblockmaybedifficulttodistinguishfromsinusarrest.Patientswitheitherconductiondisturbance
presentwithvariablepausesontheECGuntilanescaperhythmoccursorsinusrhythmisrestored.
SickSinusSyndrome
ClinicalFindings
Sicksinussyndromeisamanifestationofsinusnodedysfunction.Patientswiththesyndromemaypresentwitha
widerangeofbradyarrhythmias.Numerousarrhythmiasareassociatedwithsicksinussyndrome,including
markedsinusbradycardia,sinuspause,sinusarrest,andSAblock.Onoccasion,patientsmayalsopresentwith
ventricularoratrialtachyarrhythmias.
Treatmentmaybeindicatedwhenpausesofmorethan23secondsoccurorifthepatientissymptomatic.
Administrationofatropineorinitiationoftemporarycardiacpacingmayberequired.Symptomaticpatientswill
requirehospitaladmission,oftenforpermanentpacemakerplacement.
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AtrioventricularBlock
AVblockreferstoagroupofconductiondisturbanceswithintheAVjunctionaltissue.Ingeneral,AVblockis
characterizedbyprolongedconductiontimeorafailuretoconductimpulsesthroughtheAVnode.Theconduction
disturbancecanbepartial(firstorseconddegreeAVblock)orcomplete(thirddegreeAVblock).Ingeneral,the
hemodynamiceffectswilldependontheventricularrateandthepresenceofunderlyingheartdisease.AV
conductionblocksaretraditionallyclassifiedasfirst,second,orthirddegreeheartblock.
FirstDegreeAtrioventricularBlock
(SeeAppendix,Figure3525)FirstdegreeAVblockisthemostcommonconductiondisturbanceandis
characterizedbyaPRintervalthatisprolongedforgreaterthan0.2seconds.Ingeneral,thePRintervalis
constant,andeachatrialimpulseisconductedtotheventricles.FirstdegreeAVblockcanbeanormalvariantin
youngorathleticindividualsduetoexcessivevagaltone.FirstdegreeAVblockisalsocommoninelderlypatients
withoutunderlyingheartdisease.Itmayoccurinpatientswithmyocarditis,milddigoxintoxicity,andinferiorwall
myocardialinfarctionsecondarytoAVnodalischemia.
SecondDegreeAtrioventricularBlock(MobitzTypeI)
(SeeAppendix,Figure3526)SeconddegreeMobitztypeIAVblockisalsoknownasWenckebachAVblock.
ThistypeofblockischaracterizedbyaprogressivelengtheningofthePRintervalfollowedbyanonconductedP
waveleadingtoadroppedQRScomplex.Classically,thePPintervalremainsconstantexceptwhensinus
arrhythmiaispresent.TheRRintervalwillhaveacharacteristiccyclethroughouttheconductiondisturbance.The
RRintervalthatincludestheblockedPwaveisthelongestinduration.ThisisthenfollowedbyRRintervalsthat
subsequentlybecomeshorteruntilthenextPwaveisblocked.
Onarhythmstrip,groupedbeatingisoftenevidentandcanfurtherhelpdistinguishseconddegreefromthird
degreeAVblock.TheblockedPwavesmayoccurfrequentlyorperiodically,andmayormaynotoccurwith
regularity.BecauseMobitztypeIAVblockisattheleveloftheAVnode,theQRScomplexisnormalin
configurationunlessaberrantventricularconductionoranunderlyingBBBexists.Ingeneral,MobitztypeIAV
blockdoesnotusuallyproducehemodynamicallysignificantsymptoms.Itcanbeseeninpatientswithacute
myocardialinfarction(usuallyinferiorwall)anddoesnotcommonlyprogresstocompleteheartblock(CHB).If
CHBdoesoccur,theescaperhythmpacemakerisusuallylocatedintheAVjunctionaltissueandisoftenfast
enoughtomaintainanadequatecardiacoutput.
SecondDegreeAtrioventricularBlock(MobitzTypeII)
(SeeAppendix,Figure3528)SeconddegreeMobitztypeIIAVblockischaracterizedbyaconstantPRinterval,
eithernormalorprolonged,thatisfollowedbyanonconductedPwave.InMobitztypeIIAVblock,theQRS
complexisusuallywide.ThisoccursbecauseMobitztypeIIAVblockrepresentsaninfranodalblock.Attimes,
everyotherPwaveisblocked.Thisisdescribedas2:1AVconduction.Whenthisoccurs,onecannotdistinguish
betweenMobitztypeIortypeIIAVblock(seeAppendix,Figure3527).MobitztypeIIAVblockiscommonin
patientswithacutemyocardialinfarction(usuallyanteriorwall)andcansuddenlyprogresstoCHBresultingin
syncope.
ThirdDegreeAtrioventricularBlock(CompleteHeartBlock)
ClinicalFindings
(SeeAppendix,Figures3529,3530,and3531)ThirddegreeAVblock,orCHB,ischaracterizedby
independentatrialandventricularactivity.AsaresultofcompleteAVblock,noatrialimpulsesareconducted
throughtheAVnode.Theventricularrateisdeterminedbytheintrinsicescaperhythm,AVjunctionalescape
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(usually4560beats/min),oranidioventricularescaperhythm(usually3040beats/min).Theatrialratemaybe
sinusinoriginormaybefromanectopicatrialfocus.InCHBtheatrialrateistypicallyfasterthantheventricular
rate.AsnotedwithseconddegreeAVblock,thehemodynamicconsequencesdependontheventricularrateand
thepresenceofunderlyingheartdisease.SyncopeorCHFcommonlyaccompanyacuteacquiredCHB.Complete
AVblockismostcommonlycausedbycoronaryarterydiseaseorbydegenerationofthecardiacconduction
system.
Treatment
UNSTABLEPATIENTS
Emergencycardiacpacingisindicatedforpatientswithhemodynamicallyunstablebradycardia,especiallyfor
patientswhohavefailedmedicaltherapy,patientswithmalignantescaperhythms,andpatientsinbradyasystolic
arrest.Transcutaneouscardiacpacingistheinitialinterventionbecauseofitseaseofapplication,comparedto
temporarytransvenouspacing.Inunstablepatients,medicalmanagementcanbeinitiated,althoughattimesits
utilityisonlytemporary.
STABLEPATIENTS
Atropine
AtropineisananticholinergicmedicationwithparasympatholyticpropertiesleadingtoenhancedSAnode
automaticityandAVnodeconduction.Theinitialintravenousdoseofatropineis0.51.0mg,whichcanbe
repeatedevery5minutestoatotaldoseof0.04mg/kg(3mgfortheaverageadult).Themaximaldoseproduces
completevagalblockade.Atropineisrecommendedfor,butnotlimitedto,patientswithsymptomaticbradycardia
orrelativebradycardia,bradycardiawithmalignantescaperhythms,andasystole.
Rarely,aparadoxicreductioninheartratehasbeenobservedinpatientswithadvancedAVblockafter
administrationofatropine.Therefore,useatropinewithcautioninpatientswithinfranodalAVblock(MobitztypeII,
andCHBwithwideQRScomplexes).Otherrarelyencounteredsideeffectsofatropineadministrationinclude
worseningofcardiacischemiainpatientswithanacutemyocardialinfarction,orthedevelopmentofaventricular
tachyarrhythmia.Theseadverseeffectsareuncommon,butknowledgeofsuchresponsesmayassistwithproper
patientselection.Atropineisnoteffectiveinthemanagementofthehearttransplantpatientwithsymptomatic
bradycardiabecauseofsurgicaldenervationofthevagusnerve.
Isoproterenol
Isoproterenolisanonspecificadrenergicagonistthatcausesanincreaseinheartrateandcardiaccontractility.
Thecombinedeffectsleadtoincreasesincardiacoutputandsystolicbloodpressureanddecreasesinsystemic
andpulmonaryvascularresistanceanddiastolicbloodpressure.Asaresult,nosignificantchangeinmean
arterialpressureoccurs.Myocardialoxygendemandisincreasedasaresultoftheincreasedheartrateand
contractility.Inaddition,isoproterenolcausessmoothmusclerelaxationandbronchodilation.Isoproterenolmay
beusedtotreatsymptomaticbradycardiainhearttransplantpatients.Theinitialintravenousdoseof
isoproterenolis1g/min,titratedslowlyuntilthedesiredhemodynamiceffectsareachieved.Themaximum
infusionrateis4g/min.
Dopamine
Dopamineisanendogenouscatecholaminewithdoserelatedeffects.Atdosesof3.07.5g/kg/min,ithas
agonistpropertiesresultinginincreasedheartrateandcardiacoutput.Theagonisteffectsarelesspronounced
thanthoseofisoproterenol.Dopamineisthepreferredcatecholamineforsymptomaticbradycardiarefractoryto
atropine.
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Aminophylline
Aminophylline,amethylxanthinederivative,isacompetitiveantagonistofadenosine.Conductiondisturbances
duringanacutemyocardialinfarctionmaybepartiallymediatedbytheendogenousreleaseofadenosine.
Aminophyllinecanbeadministeredintravenouslyatadoseof56mg/kginfusedover5minutes.Amaintenance
infusionmayberequiredandcanbeinitiatedat0.5mg/kg/h.
Glucagon
Glucagonstimulatescyclicadenosinemonophosphateproduction.Itmaybebeneficialinthetreatmentof
bradycardiaassociatedwithblockerorcalciumchannelblockertoxicity.Aninitialintravenousdoseof0.050.15
mg/kgisrecommended,althoughoptimaldoseshavenotbeendetermined.
Disposition
Hospitalizeallpatientswhohavesymptomaticbradycardia.DiscontinuemedicationswithAVnodalblocking
properties.AlthoughsomepatientswithadvancedAVconductionblockswillbeasymptomatic,itisrecommended
thatallpatientswithnewlydiagnosedseconddegreeMobitztypeIIAVblockandCHBbehospitalized.
OftenpatientswithWenckebachAVblockwillbeasymptomatic.Treatmentisusuallynotnecessaryunless
symptomsoccur.Ingeneral,notreatmentisnecessaryforpatientswithfirstdegreeAVblock.Attimes,
hospitalizationwillbenecessarytotreattheunderlyingconditionsuchasmyocardialischemiaordigoxintoxicity.
IdioventricularRhythm
ClinicalFindings
Idioventricularrhythmreferstotheoccurrenceofsixormoreconsecutiveventricularescapebeats.Therateofan
idioventricularescaperhythmisusually3040beats/min.ThedurationoftheQRScomplexoftenexceeds0.16
seconds.ThemorphologyoftheQRScomplexissimilartothatinprematureventricularcontractions(PVCs)but
variesdependingonthelocationoftheectopicventricularfocus.Escaperhythmsoftendevelopinresponseto
severebradycardiaoranadvancedAVblock.Iftherateis50100beats/min,therhythmiscalledaccelerated
idioventricularrhythm(AIVR).AIVRcanalsobeseenafteradministrationofthrombolytictherapyforacute
myocardialinfarctionandmayserveasamarkerofreperfusion.
Treatmentmaybeindicatediftheventricularescaperhythmisunabletomaintainadequatecerebralperfusionor
ifthepatientisunstable.IfventricularescapebeatsoccurinresponsetoadvancedAVblock,itcouldbe
dangeroustoabolishtheescaperhythm.Inthiscase,theescaperhythmmaybehelpingtomaintainadequate
perfusion.ManagementisdirectedattreatingtheunderlyingAVblock.IfAIVRoccurssecondarytoreperfusion,
notreatmentisgenerallyneeded.Becauseanidioventricularescaperhythmoftenoccursasaresultofadvanced
AVblock,themajorityofpatientswillrequirehospitalization.
AtrioventricularJunctionalRhythm
ClinicalFindings
AVjunctionalescaperhythmreferstotheoccurrenceofsixormoreconsecutivejunctionalescapebeats.The
ventricularrateisusually4560beats/min.AVjunctionalrhythm,likeAVjunctionalprematurebeats,may
originatefromanylocationintheAVjunctionaltissue.BecausetheoriginoftherhythmistheAVjunctionaltissue,
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theQRScomplexisnarrowunlessthepatienthasapreexistingBBB.Ifthejunctionalescaperhythmisfasterthan
60beats/min,thetermAVjunctionaltachycardiaisapplied.Ifthisrhythmispresent,digoxintoxicityshouldbe
ruledout.
PatientswithsinusbradycardiaandoccasionalorintermittentAVjunctionalescapebeatsdonotgenerallyrequire
intervention.Treatmentincludinghospitalizationwilldependontheunderlyingcauseofthecardiacarrhythmia.
HaydenGE,BradyWJ,PollackM,HarriganRA:Electrocardiographicmanifestations:Diagnosisofatrialventricular
blockintheemergencydepartment.JEmergMed200426:95106[PubMed:14751485].
HoodRE,ShorofskySR:Managementofarrhythmiasintheemergencydepartment.CardiolClin200624:125
133[PubMed:16326262].
SherbinoJ,VerbeekPR,MacDonaldRD,SawadskyBV,McDonaldAC,MorrisonLJ:Prehospitaltranscutaneous
cardiacpacingforsymptomaticbradycardiaorbradyasystoliccardiacarrest:asystematicreview.Resuscitation
200670:193200[PubMed:16814446].
UfbergJW,ClarkJS:Bradydysrhythmiasandatrioventricularconductionblocks.EmergMedClinNorthAm
200624:19[PubMed:16308110].
PermanentCardiacPacemakersandImplantableCardioverter
Defibrillators
Itisestimatedthatmorethan100,000implantablecardioverterdefibrillators(ICDs)andmorethan200,000
permanentcardiacpacemakersareimplantedintheUnitedStatesannually.Thesedeviceshavedramatically
reduceddeathfromsuddencardiacdeathandotherarrhythmias.However,theyoccasionallyfailandemergency
medicinephysiciansshouldbefamiliarwithbothnormalpacemakerandAICDcommonmalfunctions.Itis
estimatedthatpermanentpacemakershavea6%yearlyincidenceofmalfunctionandalthoughmanyofthese
malfunctionswillbeidentifiedduringroutineevaluation,somemalfunctionswilloccurunexpectedly,resultinginan
emergencydepartmentvisit.
TypesofPacemakers
Pacemakersareeithersinglechamber(rightatriumorrightventricle)dualchamber(rightatriumandright
ventricle)orbiventricular(rightatrium,rightventricleandleftventricle)devices.Insinglechamberpacemakers,a
singleleadpacesandsensesinthesamechamber,mostoftentherightventricle.Indualchamberpacemakers,
onepacingandsensingleadisintherightatriumandtheotherisintherightventricle.Thebiventricular
pacemakerissimilartothedualchamberunitsexceptthatthereisalsoaleftventricuallead.Biventricularpacing
isusedwithincreasingfrequencytooptimizetreatmentofCHFwithconductiondelayordysynchrony.
Since1990,almostallpacemakerleadsarebipolar.Bipolarleadshavetwoelectrodesonthesamepacinglead,
adistalcathode,andaproximalanodelocatedapproximately1cmapartnearthedistaltipofthepacemaker
lead.Bipolarleadsproduceasmallelectricalfieldbetweenthetwoelectrodes.Thisproducesasmall,sometimes
barelynoticeable,pacingspikeontheECG.Olderpacemakerleadswereunipolarindesign.Thecathodewas
locatedatthedistalendoftheleadandthepulsegeneratorservedastheanode.Unipolarleadsproducealarger
electricalfieldandgiverisetolargerpacemakerspikesontheECG.Unipolarleadsaremorelikelytosense
noncardiacelectricaleventssuchaspectoralismuscleactivity.Thiscanresultininappropriateinhibitionof
pacemakeractivity(myopotentialinhibition).Theintroductionofbipolarleadshasvirtuallyeliminatedthistypeof
oversensingmalfunction.
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TypesofICDs
SincereceivingUSFoodandDrugAdministrationapprovalin1985,ICDshaveundergonesignificanttechnologic
advances.Initially,deviceswereimplantedintheabdominalwallandepicardialpatchesweresewninplaceviaa
mediansternotomy.Newerthirdgenerationdevicesaresmaller,andmostareimplantedinthesubpectoralfascia
usingatransvenousleadsystem,similartopermanentpacemakersystems.Ascomparedtoearliermodels,third
generationdeviceshavemoreadvancedtachycardiadetectionandterminationfeatureswithlongerbatterylife
(78years).Theadvancedtachycardiaterminationfeaturesincludeantitachycardiapacing(ATP),lowenergy
cardioversion,andhighenergydefibrillation.NewerICDsarealsocapableofrateresponsivedualchamberback
uppacing.
ComplicationsofImplantableCardiacPacemakersandICDs
VenousAccess
Althoughuncommon,themajorityofvenousaccesscomplicationsoccurearlyafterimplantation.Venousaccess
complicationsincludebleeding,pneumothorax,hemothorax,andrarelyairembolism.Venousthrombosisis
anotherrarecomplicationofpacemakerplacement.Patientsmaypresentwithunilateralupperextremitypainand
swelling.
PacemakerandICDPocketSite
Usuallyplacedintheleftsubclaviculararea,earlydevicepocketsitecomplicationsincludebleedingwith
hematomaformation,wounddehiscence,orinfection.Earlypocketsiteinfectionsareusuallycausedby
Staphylococcusaureus.Latecomplications(greaterthan30daysafterimplantation)canincludepacemakersite
erosion,keloidformation,pacemakermigration,andinfection.Lateinfectionsareusuallycausedby
Staphylococcusepidermidis.Approximately6%ofpatientswithpermanentpacemakersdeveloppocketsite
infections.
LeadComplications
AnumberofcomplicationscanoccurwithendocardialpacemakerandICDleads.Leaddislodgementis
uncommonforpacemakersratesarelessthan2%forventricularleadsandlessthan5%foratrialleads.ICD
leaddislodgementapproaches10%.Ifleaddislodgementissuspected,obtainposteroanteriorandlateralchest
radiographsandcomparethemwithpriorchestXray.Leadfractureorinsulationbreakmayalsooccur.Lead
fracturesgenerallyoccuratthreesites:(1)closetothepulsegenerator,(2)atthevenousentrysite,and(3)with
theheart.LeadfracturesmaybediagnosedbychestXrayorbypacemakerinterrogation.
Cardiacperforationisanotheruncommonbutpotentiallyseriousleadcomplication.Suspectperforationinthe
patientwithanewpacedrightbundlebranchblock(RBBB)patternonECG,intercostalmuscleordiaphragmatic
contractions(hiccups),pericardialeffusion,ortamponade.Cardiacperforationmayalsobeidentifiedbyaplain
chestradiographdemonstratingthetipofthepacemakerleadoutsidethecardiacsilhouette.Echocardiography
maybeinvaluableindiagnosingapericardialeffusion.Mostcases(80%)ofperforationoccurwithinthefirst4
daysofpacemakerinsertion.AnotheruncommonleadcomplicationisTwiddler'ssyndrome.Thisoccurswhena
patientwigglesorrotatesthepacemakergenerator,eventuallydislodgingthepacemakerleads.
DeviceMalfunction
GeneralConsiderations
Themostcommonpacemakermalfunctionsaresensingabnormalities.Sensingmalfunctionsarefurther
subdividedintoundersensingoroversensing.Undersensingoccurswhenthepacemakerfailstosenseintrinsic
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electricalcardiacactivity(PwaveorQRScomplex).OntheECG,apacingspikeisprecededbyanintrinsicP
waveorQRScomplex.Oversensingorcrosstalkmisinterpretationbyoneleadofthesignalgeneratedbythe
otherleadcancausethepacemakertoinappropriatelyinhibitapacingstimulus.OntheECG,thisisevidentby
apausethatislongerthantheprogrammedpacemakerrate.
Otherpacemakermalfunctionsincludefailuretopaceandfailuretocapture.Failuretopaceischaracterizedby
anabsenceofanappropriatepacingstimulus.Failuretocaptureoccurswhenapacingstimulusfailsto
depolarizethemyocardium.Physiologicfailuretocapturemayoccurifthepacingstimulusoccursduringthe
ventricularrefractoryperiod(within300msafteranativedepolarization).Thisisnotamalfunction,but
reprogrammingmaystillbenecessary.
Leadcomplicationsarecommoncausesofpacemakermalfunction.Anincreaseinthepacingthresholdmayalso
causesensingmalfunctionsandfailuretocapture.Thiscanoccurasaresultoffibrosisattheleadtip,
hyperkalemia,hypoxemia,myocardialischemia,andantiarrhythmicdrugtoxicity.Batterydepletionorcomponent
failuremayresultinfailuretopaceorundersensing.Electromagneticinterferencefromelectrocauteryor
magneticresonanceimaging(MRI)canleadtooversensing.Patientswithimplantablecardiacpacemakers
shouldnotundergoMRI.Variableeffectshavebeendocumented,includingpacemakermotion,function
modification,heatingofthepacemakergenerator,andinductionofvoltageorcurrentinthepacingleads.
Pacemakermediatedtachycardia(PMT)isanuncommoncomplicationthatcanoccurwithdualchamber
pacemakers.PMTcanbetriggeredbyaPVCwithventriculartoatrial(VA)conduction.Retrogradeatrialactivity
triggersaventricularpacedbeat.AstheventricularpacedbeatundergoesVAconduction,anotherventricular
pacedbeatistriggeredandthecyclecontinues.PMTwillbeevidentbysustainedpacingattheupperlimitofthe
programmedpacingrate(100140beats/min).TheECGwillcharacteristicallyrevealawidecomplexpaced
tachycardia.PMTisoftennotlifethreateningbecausetheheartratedoesnotusuallyresultinhemodynamic
instability.RunawaypacemakerisanotherrarecauseofawideQRScomplexpacedtachycardia.Inthiscase,the
malfunctioningpulsegeneratordischargesatarateaboveitspresetupperlimit.
ClinicalFindings
PatientsmaypresentwithanumberofsymptomssuggestiveofpacemakerorICDmalfunction.Theseinclude
dizziness,lightheadedness,nearsyncope,syncope,palpitations,shortnessofbreath,orchestpain.The
symptomsmostconcerningarethoseassociatedwithcerebralhypoperfusion.Patientsmaypresentafterblunt
chesttraumaorexternaldefibrillationleadingtopacemakermalfunction.Bradycardiamaybeanindicatoror
malfunctionbecausethelowerlimitoffixedratepacingistypically5060beats/min.Thismayoccurasaresultof
oversensingorfailuretopace.Theupperlimitofrateresponsivepacemakersisgenerally100140beats/min.A
pacedrhythmatthisratemayormaynotbepacemakermalfunction.
Althoughuncommon,frequentorrecurrentshocksmayrepresentanICDmalfunction.Anincreasedfrequencyof
shocksmaybecausedbyanumberofconditionsincludinganincreasedfrequencyofventriculararrhythmias,
deviceinefficacy,oranICDsensingmalfunction.ThemostcommoncauseofanincreasedfrequencyofICD
shocksisanincreasedfrequencyofVTorVF.Ventriculararrhythmiascanoccurasaresultofworseningleft
ventriculardysfunction,myocardialischemia,orchangesinantiarrhythmictherapy.AnICDsensingmalfunction
mayleadtodoublecountingoftheTwavesorinappropriaterecognitionofSVTasVT.Leadcomplicationsmay
alsocauseinappropriateICDshocks.
OccasionallyapatientmaypresentwithasustainedventriculararrhythmiawithoutICDintervention.Although
rare,thismayoccurasaresultofafailuretodetectthearrhythmiaorexhaustionoftherapies.Inpatientswith
ICDs,antibradycardiapacingmalfunctionswillbesimilartothoseexperiencedbypatientswithimplantable
cardiacpacemakers.
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EvaluationofthepatientsuspectedofhavingICDorpacemakermalfunctionincludesa12leadICGandrhythm
strip.Ifavailable,acomparisonECGmaybehelpful.Achestradiographshouldalsobeobtained.Labtesting,
specificallyofpotassium,magnesium,creatinine,thyroidscreening,andantiarrhythmiclevels,maybenecessary.
Asystematicapproachtotheevaluationofthe12leadECGandrhythmstripmayhelptoidentifypacemaker
malfunction.TheECGshouldbeevaluatedtodeterminethepresenceorabsenceofappropriatepacingspikes.A
normallyfunctioningpacemakershouldbeinhibitedfromfiringwhenthepatient'sintrinsicrateisfasterthanthe
programmedrate.Pacemakerfunctioncannotbeevaluatedwhentheintrinsicrateisfasterthantheprogrammed
rate.Whenproperlyinhibited,nopacingspikesareseenontheECG.
Magnetapplicationmayprovideinformationregardingbatterydepletionormalfunction.Whenappliedcorrectly
overapacemakerorICDgenerator,themagnettriggersareedswitch,whichinactivatesthesensingfunction.
Pacemakersshouldreverttoanasynchronouspacingmodeatarate(magnetrate)presetbythemanufacturer.
Amagnetratethatisslowerthanthemanufacturer'spresetratesuggestsbatterydepletion.Ifnopacemaker
spikesoccuraftermagnetapplication,leadfractureoranothermalfunctionmaybethecause.Whenappliedover
anICD,allantitachycardiafunctions(ATPandshocktherapies)aredisabled.Antibradycardiapacingfunctions
areunaffected.AlthoughmostpacemakersandICDsrespondimmediatelywhenamagnetisappliedcorrectly,
thereisnoindustrystandardandresponsesaresomewhatmanufacturerdependent.MRIiscontraindicatedin
patientswithbothimplantablepacemakersandICDs.Thestrongmagneticfieldmaydamagethegeneratorand
interferewithnormaldevicefunctioning.
MajorICDfunctionsincludesensing,detection,provisionoftherapytoterminateVTorVF,andpacingfor
bradycardia.Whenatachycardiaisdetectedtwotherapiesarepossible.First,ATP,whichcommonlyconsistsof
burstpacingatarate610beatsfasterthantheventricularrate,isusuallyattempted.ATPmaybefeltbutisnot
painful.Second,ifATPdoesnotterminatethetachyarrhythmia,thenhighenergyshocks(140J)willbe
deliveredbetweentherightventriclecoilelectrodeandtheICDcasingand/oranotherelectrode.Theseshocks
arepainfulifthepatientisconscious.
Treatvenousaccesscomplicationsaccordingly.Admitforparenteralantibioticsanypatientssuspectedofhaving
pocketsiteinfections.
Forpatientspresentingwithpacemakermalfunctionleadingtosymptomaticbradycardia,institutepharmacologic
treatmentoremergencypacingmeasures.Iftranscutaneouscardiacpacingisinitiated,placetheanteriorpacing
padasfarawayfromthepacemakergeneratoraspossible.Inthesettingofsymptomaticbradycardia,amagnet
canalsobeappliedtoreverttoasynchronouspacing.IfapatientrequiressynchronizedDCcardioversionor
defibrillation,placethepaddlesorpadsasfarfromthepulsegeneratoraspossible.
Intheemergencydepartment,treatmentofPMTmaybeundertakenbyanumberofdifferentmaneuvers.First,a
magnetmaybeappliedtoterminatethetachycardia.Ifamagnetisunavailableorunsuccessful,chestwall
stimulationusingatranscutaneouspacemakercanbeattempted.Therequiredstimulusisusually1020mA.
Thisislessthanthestimulusgenerallyrequiredfortranscutaneouspacing.Ifunsuccessful,isometricexercises
canbetried.Finally,chestthumpshavehadsuccessinterminatingPMTnomorethantwoarerecommended.
Eachofthementionedtechniquesisdesignedtoaffectthesensingfunctionofthepacemaker,inhibitventricular
pacing,andterminatePMT.Iftheseareunsuccessful,cardiologyconsultationforpacemakerinterrogationand
reprogrammingwillbenecessary.
Runawaypacemakerisararelyencounteredproblem.Pharmacologicinterventionormagnetapplicationcanbe
attemptedbutwillmostlikelybeunsuccessful.Definitivetreatmentmayrequiredisconnectingthepacemaker
leadsorremovalofthepulsegenerator.
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Obtaincardiologyconsultationforpatientssuspectedofhavingpacemakermalfunction.Unlessthepacemaker
canbeinterrogatedintheemergencydepartment,themajorityofpatientswithsuspectedpacemakermalfunction
willrequirehospitalization.ForICDmalfunctionresultinginfrequentinappropriateshocks,temporarydevice
deactivationmaybenecessary.Similartocardiacpacemakers,magnetapplicationshouldtriggeramagnetically
activatedreedswitch.Thisdisablesallantitachycardiafunctions(ATPandshocktherapies).Antibradycardia
pacingfunctionsareunaffected.AlthoughmostICDsareimmediatelydeactivatedwhenamagnetisapplied
correctly,responsesaresomewhatmanufacturerdependent.Deactivationisnotcommonlyperformed,however,
becausethemostcommonreasonforfrequentshocksisanincreaseinthefrequencyofVTorVF.
IfrecurrentventriculararrhythmiasresultinfrequentICDshocks,antiarrhythmicadministrationandsedationmay
benecessary.Iftheventriculararrhythmiaisincessant,externalcardioversionordefibrillationmaybeneeded.
PlacethedefibrillatorpadsorpaddlesasfarfromICDgeneratoraspossible.OlderICDswithepicardial
electrodeshavebeenreportedtoincreasethedefibrillationthresholdbypreventingexternallyappliedcurrent
frompassingintothemyocardium.Thismaydecreasethelikelihoodofsuccessfuldefibrillation.
CesarioDA,TurnerJW,DecGW:Biventricularpacinganddefibrillatoruseinchronicheartfailure.CardiolClin
200725:595603[PubMed:18063163].
ChanTC,CardallTY:Electronicpacemakers.EmergMedClinNorthAm200624:179194[PubMed:16308119]
.
GehiAK,MehtaD,GomesJA:Evaluationandmanagementofpatientsafterimplantablecardioverterdefibrillator
shock.JAMA2006296:28392847[PubMed:17179461].
HoodRE,ShorofskySR:Managementofarrhythmiasintheemergencydepartment.CardiolClin200624:125
133[PubMed:16326262].
StevensonWG,ChaitmanBR,EllenbogenKA,EpsteinAE,GrossWL,HayesDL,StrickbergerSA,SweeneyMO:
SubcommitteeonElectrocardiographyandArrhythmiasoftheAmericanHeartAssociationCouncilonClinical
CardiologyHeartRhythmSociety:Clinicalassessmentandmanagementofpatientswithimplantedcardioverter
defibrillatorspresentingtononelectrophysiologists.Circulation2004110:38663869[PubMed:15611390].
Appendix:CommonlyEncounteredCardiacArrhythmias
NormalSinusRhythm
(Figure352)Theheartrateis60100beats/min.ThereisaconstantandnormalPRinterval,andthePwave
willbeuprightinleadIIandinvertedinleadaVR.
FIGURE352.
Normalsinusrhythmatarateof90beats/min.
SinusTachycardia
(Figure353)Theheartrateisfasterthan100beats/min.Usuallytherateis101160beats/min.ThePwave
morphologyisthesameasinnormalsinusrhythm.
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FIGURE353.
Sinustachycardiaatarateof130beats/min.
SinusBradycardia
(Figure354)Theheartrateisslowerthan60beats/min.Usuallytherateis4559beats/min.Sinusbradycardia
iscommonlyassociatedwithsinusarrhythmia.ThePwavemorphologyisthesameasinnormalsinusrhythm.
FIGURE354.
Sinusbradycardiaatarateof45beats/min.
SinusArrhythmia
(Figure355)Theheartrateisusually45100beats/min.ThePwavemorphologyisthesameasinnormalsinus
rhythm.ThePPorRRcyclesvaryby0.16secondsormore.Mostcommonly,sinusarrhythmiaoccursinrelation
totherespiratorycycle.Thesinusratewillgraduallyincreasewithinspirationandslowwithexpiration.
FIGURE355.
Sinusarrhythmia.Theheartratevariesbetween60and80beats/min.
AutomaticAtrialTachycardia
(Figure356)Theheartrateisusually160250beats/minbutmaybeasslowas140beats/min.ThePwave
morphologyisusuallydifferentfromthatofnormalsinusrhythm.ThePPandRRcyclesareregularinmost
cases.Whentheatrialrateisslowerthan200beats/min,1:1AVconductioniscommonlynoted.Whentheatrial
rateisfasterthan200beats/min,theventricularrateisoftenhalftheatrialratebecauseoftherefractorinessof
theAVnode.
FIGURE356.
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Automaticatrialtachycardiaatarateof140beats/min.
AtrioventricularNodalReentrantTachycardia
(Figures357,358,359,and3510)Theheartrateisusually180200beats/min.ThePwavesoccur
concurrentwiththeQRScomplexandareoftendifficulttovisualizeontheECG.
FIGURE357.
Atrioventricularnodalreentranttachycardiaatarateof175beats/min.NotetheabsenceofclearlydiscernibleP
waves.
FIGURE358.
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A:AVnodalreentranttachycardiawithaleftbundlebranchblockatarateof155beats/min.B:Thebaseline
ECGinthesamepatientshowingsinusrhythmwithaLBBBatarateof95beats/min.Notethatthe11thbeatisa
prematureventricularcontraction.
FIGURE359.
A:AVnodalreentranttachycardiaatarateof150beats/min.B:Secondslateraftertheadministrationof
adenosine,thesamepatientconvertstosinusrhythm.
FIGURE3510.
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Paroxysmalsupraventriculartachycardiaatarateof150beats/mininapatientwhoishemodynamicallyunstable.
Aftertheseventhbeat,thepatientiscardiovertedwith50Jtosinusrhythm.
AtrioventricularReciprocatingTachycardia
(Figure3511)Theheartrateisusuallyfasterthan200beats/min.Becauseactivationoftheventricleoccurs
throughnormalconductionpathways,theaccessorypathwayisconcealedandtheQRSmorphologyisnormal.
FIGURE3511.
A:AVreciprocatingtachycardiaatarateof250beats/min.B:Thesamepatientafterpharmacologicconversion
showingsinusrhythmwithventricularpreexcitation.
AtrialFibrillation
(Figures3512and3513)Theatrialrateisdisorganizedandis400650beats/min.Theventricularrateis
irregularlyirregular.NoPwavesarediscernibleonECG.
FIGURE3512.
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A:Atrialfibrillationwithacontrolledventricularresponse.B:Atrialfibrillationataventricularrateof130beats/min.
FIGURE3513.
A:Atrialfibrillationwithventricularpreexcitation.B:Thesamepatientafterpharmacologicconversionshowing
sinusrhythmwithventricularpreexcitation.
AtrialFlutter
(Figure3514)Theatrialrateisusually250350beats/min.Characteristicsawtoothflutterwavesmaybeseen
ontheECG,particularlyinleadII.VariableAVconductionmaybenoted.Typically,2:1AVconductionoccurs,
resultinginaventricularrateofapproximately150beats/min.
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FIGURE3514.
A:Atrialflutterwith4:1AVconduction.B:Atrialflutterwith2:1AVconduction.Theventricularrateis145
beats/min.
MultifocalAtrialTachycardia
(Figure3515)Theheartrateistypically100130beats/min.ThecharacteristicECGfindingisatleastthree
differentPwavemorphologies.VaryingPRintervalsmayalsobenoted.
FIGURE3515.
Multifocalatrialtachycardiaatarateof145beats/min.NotethedifferentPwavemorphologies.
VentricularTachycardia
(Figures3516and3517)Theventricularrateisusually180250beats/min,althoughratesslowerthan160
beats/minmayoccur.TheQRScomplexiswide(greaterthan0.12sinduration)andoftenbizarreinappearance.
FusionbeatsorAVdissociationmaybenoted.IfAVdissociationispresent,thediagnosisofVTisconfirmed.
FIGURE3516.
Therhythmstripshowsarunofventriculartachycardiatherateis150beats/min.After16beatstheventricular
tachycardiaspontaneouslyconvertstosinustachycardia.
FIGURE3517.
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Ventriculartachycardiaatarateof145beats/min.
PolymorphicVentricularTachycardia(TorsadesDePointes)
(Figure3518)Theheartrateisusually200250beats/min.Torsadesdepointesisdescribedashavinga
twistingonpointappearance.
FIGURE3518.
Polymorphicventriculartachycardia.
VentricularFibrillation
(Figure3519)VFischaracterizedbyanirregularlyirregularventricularrhythmwithnodiscernibledistinction
betweentheQRScomplex,theSTsegment,andTwaves.
FIGURE3519.
Ventricularfibrillation.Aftersixbeats,sinusrhythmdegeneratesintoventricularfibrillation.
PrematureAtrialContractions
(Figure3520)Aprematureatrialcontraction(PAC)mayoriginatefromanywhereintheatriaexceptthesinus
node.ThePwavemorphologyisusuallydifferentfromthatofnormalsinusrhythm.Itiscommontoseea
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postectopicpauseafteraPAC.TheQRScomplexisnarrowunlessaberrantlyconducted.
FIGURE3520.
Sinusrhythmwithprematureatrialcontractionsinabigeminalpattern.TheconfigurationofthePwavesofthe
prematureatrialcontractionsaredifferentfromthatofnormalsinusrhythm.
PrematureVentricularContractions
(Figure3521)APVCmayoriginatefromanywhereintheventricles.TheQRScomplexis0.12secondorlonger
indurationandresembleseitheraLBBBorRBBB.UniformPVCsoriginatefromthesamefociandhavethesame
appearance.MultiformPVCshavedifferentmorphologybecausetheyoriginatefromdifferentventricularfoci.
FIGURE3521.
A:Sinusrhythmwithfrequentprematureventricularcomplexesinapatternofbigeminy.B:Sinusrhythmwith
frequentprematureventricularcomplexesinapatternoftrigeminy.
IdioventricularRhythm
(Figure3522)Theventricularrateisusually3040beats/min.ThemorphologyoftheQRScomplexeswillbe
similartoPVCsbutwillvarydependingonthelocationoftheventricularfoci.Iftheventricularrateis50100
beats/min,therhythmiscalledAIVR.
FIGURE3522.
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A:Atrialfibrillationwithanidioventricularescaperhythm.B:Acceleratedidioventricularrhythmatarateof50
beats/min.
AtrioventricularJunctionalRhythm
(Figure3523)Theventricularrateisusually4560beats/min.TheQRScomplexisnarrowunlessaberrantly
conducted.Ifthejunctionalrhythmisfasterthan60beats/min,thetermAVjunctionaltachycardiaisapplied.
FIGURE3523.
AVjunctionalrhythmatarateof40beats/min.
SinoatrialBlock
(Figure3524)SAblockischaracterizedbyblockedPwaves,evidentbyalongPPinterval.ThePPintervals
beforetheblockedPwavemaygraduallyshorten(SAWenckebach),orthePPintervalsmaybeconstant
(seconddegreeMobitztypeIISAblock).
FIGURE3524.
SinusrhythmwithseconddegreeMobitztypeISAblock.NotethatthePPintervalsgraduallyshorten,whereas
thePRintervalsremainconstant.ThecycleterminateswithablockedPwave.Thelengthofthepauseisshorter
thantwicetheprecedingPPcycle.
FirstDegreeAtrioventricularBlock
(Figure3525)ThePRintervalisconstantbutcharacteristicallyprolongedgreaterthan0.2second.
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FIGURE3525.
SinusrhythmwithfirstdegreeAVblock.ThePRintervalis0.44s.
SecondDegreeAtrioventricularBlock(MobitzTypeI)
(Figure3526)ThereisprogressivelengtheningofthePRintervalfollowedbyanonconductedPwaveleadingto
adroppedQRScomplex.Classically,thePPintervalremainsconstant.TheRRintervalthatincludestheblocked
Pwaveisthelongestinduration.
FIGURE3526.
SinusbradycardiawithseconddegreeMobitztypeIAVblock.NotetheprogressivelengtheningofthePRinterval
untilaQRScomplexisdropped.
SecondDegreeAtrioventricularBlock
(Figure3527)WheneveryotherPwaveisblocked,onecannotdistinguishbetweenMobitztypeIorMobitztype
IIAVblock.Thisisdescribedas2:1AVconduction.
FIGURE3527.
SinusrhythmwithseconddegreeAVblock.
SecondDegreeAtrioventricularBlock(MobitzTypeII)
(Figure3528)ThePRintervalisregularandcanbeeithernormalorprolonged.Periodically,aPwaveisnot
conducted,leadingtoadroppedQRScomplex.
FIGURE3528.
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SinusrhythmwithseconddegreeMobitztypeIIAVblock.NotethevariableAVconduction.
ThirdDegreeAtrioventricularBlock(CompleteHeartBlock)
(Figures3529,3530,and3531)ThePPinterval(atrialrate)isusuallyshorter(faster)thantheRRinterval
(ventricularrate).BecausenoatrialimpulsesareconductedthroughtheAVnode,norelationshipexistsbetween
theatrialandventricularactivity.
FIGURE3529.
ThirddegreeAVblock.Theatrialrateis92beats/minandtheventricularrateis50beats/min.
FIGURE3530.
FIGURE3531.
ThirddegreeAVblockwithanacceleratedidioventricularescaperhythmwithaventricularrateof60beats/min.
SingleChamberVentricularPacing
(Figures3532and3533)Whentheintrinsicheartrateisfasterthantheprogrammedpacemakerrate,the
pacemakerisinhibitedfromfiring.Whentheintrinsicrateisslower,thepacemakeristriggered,takingoverasthe
dominantpacemakeroftheheart.
FIGURE3532.
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Asynchronousventricularpacing.Inthiscase,theintrinsicheartrateisslowerthantheprogrammedpacemaker
rate.Whenthisoccurs,thepacemakeristriggered,takingoverasthedominantpacemakeroftheheart.
FIGURE3533.
VVIpacing.Althoughthepacemakerspikesaredifficulttoappreciate,beats38areventricularpacedbeats.
Whentheintrinsicheartrateisfasterthantheprogrammedrate,thepacemakerisinhibitedfromfiring.
DualChamberAtrioventricularPacing
(Figures3534and3535)Thepacemakeriscapableofpacingandsensingtheatriaandventricles.Depending
ontheintrinsicrate,thepacemakercaneitherbetriggeredorinhibited.
FIGURE3534.
AVsequentialpacinginadualchamberpacemaker.Inthiscase,thepacemakerwillpaceboththeatriaand
ventricleswhennointrinsiccardiacactivityissensed.
FIGURE3535.
DualchamberpacemakerfunctioningintheVATmode.Thepacemakerpacestheventriclesandsensesthe
atria.Ifintrinsicatrialdepolarizationsaresensed,aventricularpacingspikeistriggered.Thisisevidentonthe
ECGbythepresenceofatrialtracking.
FailuretoCapture
(Figure3536)Failuretocaptureoccurswhenanappropriatepacemakerdischargefailstodepolarizethe
myocardium.Physiologicfailuretocapturecanoccurifthepacingstimulusoccursduringtheventricularrefractory
period.
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FIGURE3536.
A:Singlechamberventricularpacemakershowingfailuretocapture.Theunderlyingrhythmisseconddegree
MobitztypeIAVblock.Aventricularpacingspikeoccursafterthefifthatrialcomplex(Pwave).Thispacingspike
failstodepolarizetheventricularmyocardium.B:Dualchamberpacemakershowingfailuretocapture.Beat3
showsanatrialpacingspikethatfailstodepolarizetheatrialmyocardium.Thepacemakerthenproceedstopace
theventricle.Beats1,2,and49showanatrialpacingspikewithcapturefollowedbynormalAVconduction.
(PartAreproduced,withpermission,fromGarsonA:StepwiseapproachtotheunknownpacemakerECG.Am
HeartJ1990119:924.)
FailuretoSense(Undersensing)
(Figure3537A)Undersensingoccurswhenthepacemakerfailstodetectintrinsicelectricalcardiacactivity.On
theECG,aPwaveorQRScomplexisinappropriatelyfollowedbyapacingspike.
FIGURE3537.
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A:Undersensing.Thefifthbeatisaprematureventricularcontraction(PVC).Thenextbeatisaventricularpaced
beat.NotethatthepacedbeatoccurssoonafterthePVC,indicatingafailuretosensetheprecedingcomplex.B:
ThefirstandsecondbeatsarepacedandthethirdandfourthbeatsshownormalAVconduction.Thereisa
longerthanexpectedpausebetweenthefourthandfifthbeats.Thisoccurssecondarytoventricularoversensing.
(Reproduced,withpermission,fromGarsonA:StepwiseapproachtotheunknownpacemakerECG.AmHeartJ
1990119:924.)
Oversensing
(Figure3537B)Oversensingistheinappropriateinhibitionofapacingstimulus.OntheECG,itisevidentbya
pausethatislongerthantheprogrammedpacemakerrate.
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NormalECG.
Normalsinusrhythmatarateof90beats/min.
Sinustachycardiaatarateof130beats/min.
Sinusbradycardiaatarateof45beats/min.
Sinusarrhythmia.Theheartratevariesbetween60and80beats/min.
Automaticatrialtachycardiaatarateof140beats/min.
Atrioventricularnodalreentranttachycardiaatarateof175beats/min.NotetheabsenceofclearlydiscernibleP
waves.
A:AVnodalreentranttachycardiawithaleftbundlebranchblockatarateof155beats/min.B:Thebaseline
ECGinthesamepatientshowingsinusrhythmwithaLBBBatarateof95beats/min.Notethatthe11thbeatisa
prematureventricularcontraction.
A:AVnodalreentranttachycardiaatarateof150beats/min.B:Secondslateraftertheadministrationof
adenosine,thesamepatientconvertstosinusrhythm.
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Paroxysmalsupraventriculartachycardiaatarateof150beats/mininapatientwhoishemodynamicallyunstable.
Aftertheseventhbeat,thepatientiscardiovertedwith50Jtosinusrhythm.
A:AVreciprocatingtachycardiaatarateof250beats/min.B:Thesamepatientafterpharmacologicconversion
showingsinusrhythmwithventricularpreexcitation.
A:Atrialfibrillationwithacontrolledventricularresponse.B:Atrialfibrillationataventricularrateof130beats/min.
A:Atrialfibrillationwithventricularpreexcitation.B:Thesamepatientafterpharmacologicconversionshowing
sinusrhythmwithventricularpreexcitation.
A:Atrialflutterwith4:1AVconduction.B:Atrialflutterwith2:1AVconduction.Theventricularrateis145
beats/min.
Multifocalatrialtachycardiaatarateof145beats/min.NotethedifferentPwavemorphologies.
Therhythmstripshowsarunofventriculartachycardiatherateis150beats/min.After16beatstheventricular
tachycardiaspontaneouslyconvertstosinustachycardia.
Ventriculartachycardiaatarateof145beats/min.
Polymorphicventriculartachycardia.
Ventricularfibrillation.Aftersixbeats,sinusrhythmdegeneratesintoventricularfibrillation.
Sinusrhythmwithprematureatrialcontractionsinabigeminalpattern.TheconfigurationofthePwavesofthe
prematureatrialcontractionsaredifferentfromthatofnormalsinusrhythm.
A:Sinusrhythmwithfrequentprematureventricularcomplexesinapatternofbigeminy.B:Sinusrhythmwith
frequentprematureventricularcomplexesinapatternoftrigeminy.
A:Atrialfibrillationwithanidioventricularescaperhythm.B:Acceleratedidioventricularrhythmatarateof50
beats/min.
AVjunctionalrhythmatarateof40beats/min.
SinusrhythmwithseconddegreeMobitztypeISAblock.NotethatthePPintervalsgraduallyshorten,whereas
thePRintervalsremainconstant.ThecycleterminateswithablockedPwave.Thelengthofthepauseisshorter
thantwicetheprecedingPPcycle.
SinusrhythmwithfirstdegreeAVblock.ThePRintervalis0.44s.
SinusbradycardiawithseconddegreeMobitztypeIAVblock.NotetheprogressivelengtheningofthePRinterval
untilaQRScomplexisdropped.
SinusrhythmwithseconddegreeAVblock.
SinusrhythmwithseconddegreeMobitztypeIIAVblock.NotethevariableAVconduction.
ThirddegreeAVblockwithanacceleratedidioventricularescaperhythmwithaventricularrateof60beats/min.
Asynchronousventricularpacing.Inthiscase,theintrinsicheartrateisslowerthantheprogrammedpacemaker
rate.Whenthisoccurs,thepacemakeristriggered,takingoverasthedominantpacemakeroftheheart.
VVIpacing.Althoughthepacemakerspikesaredifficulttoappreciate,beats38areventricularpacedbeats.
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Whentheintrinsicheartrateisfasterthantheprogrammedrate,thepacemakerisinhibitedfromfiring.
AVsequentialpacinginadualchamberpacemaker.Inthiscase,thepacemakerwillpaceboththeatriaand
ventricleswhennointrinsiccardiacactivityissensed.
DualchamberpacemakerfunctioningintheVATmode.Thepacemakerpacestheventriclesandsensesthe
atria.Ifintrinsicatrialdepolarizationsaresensed,aventricularpacingspikeistriggered.Thisisevidentonthe
ECGbythepresenceofatrialtracking.
A:Singlechamberventricularpacemakershowingfailuretocapture.Theunderlyingrhythmisseconddegree
MobitztypeIAVblock.Aventricularpacingspikeoccursafterthefifthatrialcomplex(Pwave).Thispacingspike
failstodepolarizetheventricularmyocardium.B:Dualchamberpacemakershowingfailuretocapture.Beat3
showsanatrialpacingspikethatfailstodepolarizetheatrialmyocardium.Thepacemakerthenproceedstopace
theventricle.Beats1,2,and49showanatrialpacingspikewithcapturefollowedbynormalAVconduction.
(PartAreproduced,withpermission,fromGarsonA:StepwiseapproachtotheunknownpacemakerECG.Am
HeartJ1990119:924.)
A:Undersensing.Thefifthbeatisaprematureventricularcontraction(PVC).Thenextbeatisaventricularpaced
beat.NotethatthepacedbeatoccurssoonafterthePVC,indicatingafailuretosensetheprecedingcomplex.B:
ThefirstandsecondbeatsarepacedandthethirdandfourthbeatsshownormalAVconduction.Thereisa
longerthanexpectedpausebetweenthefourthandfifthbeats.Thisoccurssecondarytoventricularoversensing.
(Reproduced,withpermission,fromGarsonA:StepwiseapproachtotheunknownpacemakerECG.AmHeartJ
1990119:924.)
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