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Definition
Nonsustained ventricular tachycardia (NSVT): Three or more consecutive ventricular complexes
(>100bpm)thatterminatespontaneouslywithin30seconds.
Sustained monomorphic ventricular tachycardia (SMVT): Tachycardia of ventricular origin with
singleQRSmorphologylastinglongerthan30secondsorrequiringcardioversionduetohemodynamic
compromise.
Polymorphicventriculartachycardia(PMVT): VT is characterizedby evolving QRSmorphology.
TdP isa variantofPMVTtypicallyprecededbyprolongedQTinterval inSR.PMVT isassociated
withhemodynamiccollapseorinstability.
VF: Associatedwith disorganizedmechanical contraction of ventricles, hemodynamic collapse, and
sudden death. ECG reveals irregular and rapid oscillations (250–400 bpm) of highly variable
amplitudewithoutclearlyidentifiableQRScomplexesorTwaves.
Ventriculararrhythmias—majorcauseofsuddencardiacdeath(SCD).
SCD—unexpecteddeaththatgenerallyoccurswithin1hourofonsetofsymptomsinpersonwithout
prior condition that would appear fatal. In the US, approximately 350,000 cases of SCD occur
annually.
AmongpatientswithabortedSCD,ischemicheartdiseaseis mostcommonlyassociatedcardiac
structuralabnormality.MostcardiacarrestsurvivorsdonothaveevidenceofacuteMI;however,
>75%haveevidenceofpreviousinfarcts.
Nonischemiccardiomyopathy(NICM)isalsoassociatedwithanelevatedriskforSCD.
15
Etiology
VTassociatedwithstructuralheartdisease
Mostventriculararrhythmiasareassociatedwithstructuralheartdisease,typicallyrelatedtoactive
ischemiaorpriorinfarct.
Scarandtheperi-infarctareaprovidesubstrateforreentrythatproducesSMVT.
PMVT and VF—commonly associated with ischemia and are presumed cause of most out-of-
hospitalSCD.
NICM typically involves progressive dilation and fibrosis of ventricular myocardium, providing
arrhythmogenicsubstrate.
Infiltrativecardiomyopathies(secondarytosarcoidosis,hemochromatosis,amyloidosis,etc.)affect
smaller patient population that is at significant risk for ventricular arrhythmias and whose
managementislessclearlydefined.
AdultswithpriorrepairofcongenitalheartdiseasearecommonlyafflictedwithbothVTandSVT.
Arrhythmogenic right ventricular dysplasia (ARVD) or cardiomyopathy—marked by fibrofatty
replacement of the RV (and sometimes LV) myocardium giving rise to left bundle branch block
(LBBB)morphologyVTandisassociatedwithsuddendeath,particularlyinyoungathletes.
Bundlebranch reentryVT—form ofventriculartachyarrhythmiathatuses His–Purkinjesystemina
reentrantcircuitandistypicallyassociatedwithcardiomyopathyandabnormalconductionsystem.
VTintheabsenceofstructuralheartdisease
Inheritedionchannelopathies,suchasthoseseeninBrugadasyndromeandLQTS,canleadtoPMVT
andsuddendeathinpatientswithoutevidenceofstructuralheartdisease.
Catecholaminergic PMVT involves inherited, exercise-induced VT related to irregular calcium
processing.
IdiopathicVT—diagnosisofexclusionthatrequiresdocumentedabsenceofstructuralheartdisease,
geneticdisorders,andreversibleetiologies(i.e.,ischemia,metabolicabnormalities).
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MostoriginatefromRVoutflowtract(RVOT)andareamenabletoablation.
LVoutflowtract(LVOT)VTs, arisingfromnearthe coronary cuspsoraortomitralcontinuity,or
fascicularVTs(usinganteriorandposteriordivisionsoftheleftbundlebranch)arelesscommon
formsofidiopathicVT.
Tachycardia-mediatedcardiomyopathycanresultifleftuntreated.
DIAGNOSIS
ClinicalPresentation
Evaluation of WCTs should always begin with prompt assessment of vital signs and symptoms. If
arrhythmiaispoorlytolerated,postponefurtherevaluationandproceedtoacutemanagementperACLS
guidelines.If patientis clinicallystable, rhythm should be carefullyanalyzedtodistinguishVTfrom
SVT.Acommonmistake isthe assumptionthat hemodynamicstabilitysupportsthe diagnosisofSVT
overVT.
VT represents the majority of WCT seenin the inpatient setting withreported prevalence of 80%.
Eliciting historical points of emphasis and closely assessing ECG properties can help delineate
mechanismofunderlyingrhythmdisturbance.Beginwiththefollowingquestions:
Doespatienthavehistoryofstructuralheartdisease?
Patientswithstructuralheartdisease are muchmore likely tohaveVTthan SVTas etiology of
WCT.Inoneanalysis,98%ofpatientswithWCTonECGwhohadpriorMIprovedtohaveVT.
16
Doespatienthaveimplanteddevice(PPMorICD)orwideQRSatbaseline?
PresenceofeitherpacemakerorICDshouldraisesuspicionfordevice-mediatedWCT.
Device-mediatedWCTcanoccurfromventricularpacingatrapidrateeithercausedbytracking
of an atrial tachyarrhythmia or alternatively by “endless loop tachycardia” from tracking of
retrogradeatrialimpulsescreatedbyprecedingventricularpacedbeat.Ineithercase,tachycardia
rateisacluetomechanismbecauseitistypicallyequaltoprogrammedupperratelimit(URL)of
the device.AcommonlyprogrammedURL is120 bpm.TachycardiarateaboveURLeffectively
excludesdevice-mediatedWCT.
Presenceofanimplantabledevicecanbeconfirmedbyinspectionofthechestwall(usuallyleft
chestforright-handedpatients),CXR,orappearanceofpacingspikesonECGortelemetry.
Patients with known right bundle branch block (RBBB), LBBB, or intraventricular conduction
delay(IVCD)atbaselinepresentingwithWCTwillhaveQRSmorphologyidenticaltobaseline
in the presence ofSVT. In contrast, some patients with narrow QRS at baseline will manifest
WCTduetoSVTwhenarate-relatedbundlebranchblockispresent(SVTwithaberrancy).
Whatarepatient’shomemedications?
Homemedicationlistshouldbecarefullyreviewedforanydrugswithproarrhythmicsideeffects,
especially those that can prolong the baseline QT interval—including many class I and III
antiarrhythmics,certainantibiotics,andantipsychotics.
Medications that can lead to electrolyte derangements, such as loop and potassium-sparing
diuretics,ACE-I,ARB,anddigoxintoxicity,ifapplicable,shouldbeconsideredinsettingofany
arrhythmia.
DifferentialDiagnosis
WCTissecondarytoeitherSVTwithaberrantconductionorVT.Differentiationbetweentheserhythm
abnormalitiesisofutmostimportance.ThepharmacologicagentsusedinthemanagementofSVT
(i.e.,adenosine,β-blockers,calciumchannelblockers)maycausehemodynamicinstabilityifused
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inthesettingofVT.Therefore,allWCTsareconsideredventricularinoriginuntilprovenotherwise.
Other less common mechanisms of WCT include A-AVRT, hyperkalemia-induced arrhythmia, or
pacemaker-inducedtachycardia.
Telemetryartifact from poor lead contact or repetitive patient motion (tremor, shivering, brushing
teeth,chestphysicaltherapy,etc.)canmimicVTorVF.
DiagnosticTesting
LABORATORIES
BasicstudiesshouldincludeCBC,completemetabolicpanel,magnesiumlevel,andserialtroponins.
Additionallabsbasedonclinicalsuspicionshouldalsobeobtainedduringinitialworkup.
ELECTROCARDIOGRAPHY
DifferentiationofSVTwithaberrancyfromVTbasedonECGanalysisiscriticalfordetermination
of appropriate therapy. Features diagnostic of VT: AV dissociation, capture or fusion beats, an
absenceofRS morphology inall precordial leads (V1–V6), and LBBBmorphology with right axis
deviation.Inabsenceofthesefeatures,examinationofanRScomplexinaprecordialleadforanRS
interval >100 ms is consistent with VT. In addition, characteristic QRS morphologies that are
suggestiveofVTmaybesought,asshowninFigure7-2.
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Figure 7-2 A and B,Brugada criteria for distinguishing ventricular tachycardia fromsupraventricular tachycardia with
aberrancy in wide-complex tachycardias.LBBB, left bundle branch block; RBBB, right bundle branch block; SVT,
supraventriculartachyarrhythmia;VT,ventriculartachycardia.(ReprintedwithpermissionfromSharmaS,SmithT.Advanced
electrocardiography. In:CuculichPS,KatesAM,eds. TheWashington ManualofCardiologySubspecialtyConsult.3rd
ed.Lippincott,Williams&Wilkins;2014.)
ECGpearls
BrugadasyndromeECGpatterns
Type1:characterizedbySTsegmentelevationofatleast2mmwithacovedmorphologyinleads
V1 and V2, associated with an incomplete or complete RBBB, and followed by descending T
wave.
Type2(alsoreferredtoas“saddleback”pattern):characterizedbySTsegmentelevationof2mm
followedbyatroughwithintheSTsegmentwithcontinuedSTelevationof≥1mmandpositiveor
biphasicTwave.
Patternsmaybeobservedspontaneouslyorunmaskedafterfever,drugadministration,stress,etc.
Onlytype1patternisdiagnosticofBrugadasyndrome,whiletype2issuggestivebutnotspecific.
ARVD
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NSRECGatbaselinewiththepresenceofanepsilonwave(latepotentialjustafterQRS)and/or
TwaveinversionsintherightprecordialleadsisadiagnosticcriterionforARVD.
VT in ARVD generally arises from an RV origin and is therefore likely to have LBBB
configuration;patientsmaypresentwithNSVTorPMVT.
BundlebranchreentrantVT
BaselineECGoftenshowsIVCD.
InVT,ECGtypicallypresentswithLBBBmorphologywithelectricalimpulsetraveling“down”
therightbundleand“up”theleftbundle.
FascicularVT
ECGinVTshowsRBBBmorphologywithsuperioraxis.
LQTS
AbnormalprolongationofQTintervalonECGatbaseline(ideallymeasuredinleadsIIandV5or
V6).
QTc≥450msinmenand460msinwomen.
ECGinVToftenshowsTdPdegeneratingintoVF.
OutflowtractVT
ECGcharacteristicallyhasinferioraxiswithLBBBmorphology.
R/Stransitioninprecordial leadscanaidinlocalization:earlytransition(V1or V2) suggestsan
LVOTorigin,whereaslatertransition(V4orafter)issuggestiveofanRVOTorigin.
IMAGING
PresenceorabsenceofstructuralheartdiseaseshouldbeinitiallyevaluatedbyTTE.
Further imaging (cardiac MRI,noninvasivestress test,coronaryangiogram, etc.)shouldbe obtained
basedonsuspectedetiology.
TREATMENT
DifferentiationofSVTwithaberrancyfromVTbasedonanalysisofsurfaceECGiscriticalinthe
determinationofappropriatetreatment.
For acute therapy of SVT, IV medications such as adenosine, calcium channel blockers, or βblockersareused(see“Treatment”of“SupraventricularTachyarrhythmias”earlierinthischapter).
However,calciumchannelblockersandβ-blockerscanproducehemodynamicinstabilityinpatients
withVT.
ImmediateunsynchronizedDCCVistheprimarytherapyforpulselessVTandVF.
NonpharmacologicTherapies
ICDs provide automatic recognition and treatment of ventricular arrhythmias. ICD implantation
improvessurvivalinpatientsresuscitatedfromventriculararrhythmias(secondarypreventionofSCD)
andinindividualswithoutpriorsymptomswhoareathighriskforSCD(primarypreventionofSCD).
Idiopathic VT is thought to be benign in the absence of structural heart disease. Therefore, ICD
implantationisnotappropriate.
Secondaryprevention of SCDwithICD implantationis indicatedformostpatientswhosurvive
SCDoutside ofthe peri-MIsetting.ThesuperiorityofICDtherapytochronic antiarrhythmic drug
therapyhasbeendemonstrated.
17
PrimarypreventionofSCDwithICDimplantationisindicatedforpatientswhoareathighriskof
SCD. The efficacy of ICD implantation for primary prevention of SCD in the setting of
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cardiomyopathyhasbeenestablishedinmultiple prospectiveclinicaltrials.
18-20
Mostpatientswith
LVejectionfractionof<35%formorethan3monthsonoptimalmedicaltherapyforcardiomyopathy
meetindicationsforprophylacticICDimplantation.
AlternativeindicationsforICDplacement
Phenotypes associated with HCM, ARVD, cardiac sarcoid, congenital LQTS, or Brugada
syndrome have higher risk of SCD. ICD implantation indicated if patients withone of these
syndromes have had resuscitated cardiac arrest or documented ventricular arrhythmia.
ProphylacticICDimplantationisbasedondisease-specificriskfactors.
PatientsawaitingcardiactransplantationareathighriskforSCD,especiallyiftheyarereceiving
an IV inotrope. Prophylactic ICD implantation is reasonable to protect against SCD prior to
transplantation.
ICDs are contraindicated in patients who have incessant VT, recent MI <40 days or
revascularization<3monthsinthecaseofprimaryprevention,significantpsychiatricillnesses,or
lifeexpectancyof<12–24months.
RFAofVT—mostsuccessfullyperformedinpatientswithhemodynamicallystableformsofidiopathic
VTnotassociatedwithstructuralheartdisease.Long-termcureratesaresimilartothoseforcatheter
ablationofSVT.Instructuralheartdisease,catheterablationhasalowerefficacyandhighermorbidity
butisanimportanttreatmentoption,particularlyindrugrefractoryVTleadingtoICDtherapy.
IdiopathicVTisamenabletotreatmentwithRFAordrugtherapy.
VTassociatedwithischemicheartdiseasecanalsobetreatedbycatheterablationtargetingscar-
based substrate. Emergent catheter ablation in setting of frequent hemodynamically unstable VT
requiring defibrillation (VT storm) can be life-saving. Ablation has been shown to reduce ICD
therapyandtoimprovequalityoflife.
AblationofVTinNICM—reasonableoption,particularlyindrugrefractorypatients.However,VT
circuits may be intramyocardial or epicardial. As a result,success rates are typicallylower than
with ischemic VT. Referral to a center that routinely performs both endocardial and epicardial
ablationsshouldbeconsidered.
Medications
OutflowtractVTcanberesponsivetoβ-adrenergicblockers,diltiazem,verapamil,and/oradenosine.
VTorVFresistanttoexternaldefibrillationrequiresadditionofIVantiarrhythmicagents.
IVlidocaineisfrequentlyused;however,IVamiodaroneappearstobemoreeffectiveinincreasing
survivalofVFwhenusedinconjunctionwithdefibrillation.
21
Aftersuccessfuldefibrillation,continuousIVinfusionofeffectiveantiarrhythmictherapyshouldbe
maintaineduntilreversiblecauseshavebeencorrected.
Chronic antiarrhythmic drug therapy is indicated for treatment of recurrent symptomatic ventricular
tachyarrhythmias.InsettingofhemodynamicallyunstableventriculararrhythmiastreatedwithanICD,
antiarrhythmicdrugtherapyisoftennecessarytopreventfrequentshocks.
ACUTEDRUGTHERAPY
Amiodarone—safeandwell-tolerated foracutemanagement ofventricular arrhythmias. Amiodarone
has complex pharmacokinetics and is associated with significant toxicities arising from chronic
therapy.
After loading, amiodarone prevents recurrence of sustained VT or VF in up to 60% of patients.
Therapeuticlatencyofmorethan5daysexistsbeforebeneficialantiarrhythmiceffectsareobserved
withoraldosing,andfullsuppressionofarrhythmiasmaynotoccurfor4–6weeksaftertherapyis
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initiated. Unfortunately, recurrence of ventricular arrhythmias during long-term follow-up is
common.
Lidocaine—classIb agent available onlyin IV form with efficacyin management ofsustained and
recurrentVT/VF.ProphylacticuseforsuppressionofprematureventricularcontractionsandNSVTin
otherwiseuncomplicatedpost-MIsettingshouldbeavoided.
Toxicities canincludecentral nervous system (CNS) effects (convulsions, confusion,stupor, and,
rarely,respiratoryarrest),allofwhichresolvewithdiscontinuationoftherapy.
Serumlevelsshouldbemonitoredduringprolongeduse.
Class II agents, β-adrenergic antagonists, are the only class of antiarrhythmic agents to have
consistentlyshownimprovedsurvivalinpost-MIpatients.
β-adrenergicblockersreducepostinfarctiontotalmortalityby25%–40%andSCDby32%–50%.
22-
25
AfteracutetherapyofVT/VFandstabilization,β-adrenergicblockersshouldbeinitiatedandtitrated
asbloodpressureandheartrateallow.
CHRONICDRUGTHERAPY
Sotalol—class III agent indicated for chronic treatment of VT/VF. Sotalol prevents recurrence of
sustainedVTandVFin70%ofpatientsbutmustbeusedwithcautioninindividualswithCHF.
ClassIagentshavenotbeenshowntoreducemortalityinpatientswithVT/VF.Infact,classIcagents,
flecainide and propafenone, are associated with increased mortality in patients with ventricular
arrhythmiasafter MI.12Mexiletine is similar to lidocaine(also anIbagent) butis available inoral
form.Mexiletineismostoftenusedincombinationwitheitheramiodaroneorsotalolforchronic
treatment of refractory ventricular arrhythmias. CNS toxicity includes tremor, dizziness, and
blurredvision.Higher levelsmayresultindysarthria, diplopia,nystagmus,andanimpairedlevelof
consciousness.Nauseaandvomitingarecommon.
Phenytoin can be used in the treatment of digitalis-induced ventricular arrhythmias. It may have
limitedrole intreatmentof ventricular arrhythmias associatedwith congenital LQTS and those with
structuralheartdisease.
SPECIALCONSIDERATIONS
ClassIVagentshavenoroleinchronicmanagementofVTassociatedwithstructuralheartdisease.
Primary therapy for VF that occurs secondary to ischemia in the setting of an MI is complete
revascularization. In the absence of complete revascularization, patients remain at high risk for
recurrentVT/VF.
InTdPassociatedwithLQTS,acutetherapyisimmediatedefibrillation.
Bolusadministrationofmagnesiumsulfatein1-to2-gincrementsupto4–6gIViseffective.
IncasesofacquiredlongQT,identificationandtreatmentofunderlyingconditionshouldbeperformed,
ifpossible.
Eliminationoflong–shorttriggering sequences andshortening ofthe QTintervalcanbe achieved by
increasingtheheartratetotherangeof90–120bpmbyeitherIVisoproterenolinfusion(initialrateat
1–2µg/min)ortemporarytransvenouspacing(TVP).
AlternativeTherapies
For patients with ventricular arrhythmias that persist despite antiarrhythmic drug therapy and/or
catheterablation,considerationcanbe giventocervicalsympathectomyortargetedstereotacticbody
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radiationtherapy(SBRT)atcapablecenters.
Cervicalsympathectomyisperformedeitherunilaterally(ontheleft)orbilaterallyforthepurposesof
reducingICDshocks.Sympathectomyisgenerallyprecededbystellateganglionblocktoevaluatethe
short-termresponsetoneuromodulation.
26
SBRTforthemanagementofrefractoryVTisarelativelynovelmodalitythathasbeenshowntoreduce
boththeburdenofVTandICDshocksintreatedpatients.
27
Bradyarrhythmias
GENERALPRINCIPLES
Bradyarrhythmiascanbeencounteredinboththeinpatientandoutpatientsettings.
Clinicaldecision-makingisguidedbypatientsymptomsandsignsofhemodynamicstability.
Definition
Cardiacrhythmswhoseventricularrateisbelow60bpm.
Anatomyoftheconductionsystem
TheSAnode—collectionofspecializedpacemakercellslocatedinhighrightatrium.Undernormal
conditions, a wave of depolarization spreads inferiorly and leftward via atrial myocardium and
intranodaltracts,producingatrialsystole.
Waveofdepolarizationthenreachesanothergroupofspecializedcells,theAVnode,locatedinthe
lowerrightatrial sideoftheinteratrialseptum.Normally,AVnodeshouldserveasloneelectrical
connectionbetweentheatriaandventricles.
FromtheAVnode,waveofdepolarizationtravelsdowntheHisbundle,locatedinthemembranous
septum,andintorightandleftbundlebranchesbeforereachingthePurkinjefibersthatdepolarize
theremainingventricularmyocardium.
Etiology
CommoncausesofbradycardiaarelistedinTable7-6.
TABLE7-6
CAUSESOFBRADYCARDIA
Intrinsic
Congenitaldisease(maypresentlaterinlife)
Idiopathicdegeneration(aging)
Infarctionorischemia
Cardiomyopathy
Infiltrativedisease:sarcoidosis,amyloidosis,hemochromatosis
Collagenvasculardiseases:systemiclupuserythematosus,rheumatoidarthritis,scleroderma
Surgicaltrauma:valvesurgery,transplantation
Infectiousdisease:endocarditis,Lymedisease,Chagasdisease
Extrinsic
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Autonomicallymediated
Neurocardiogenicsyncope
Carotidsinushypersensitivity
Increasedvagaltone:coughing,vomiting,micturition,defecation,intubation
Drugs:β-blockers,calciumchannelblockers,digoxin,antiarrhythmicagents
Hypothyroidism
Hypothermia
Neurologicdisorders:increasedintracranialpressure
Electrolyteimbalances:hyperkalemia,hypermagnesemia
Hypercarbia/obstructivesleepapnea
Sepsis
DIAGNOSIS
ClinicalPresentation
Whenevaluatingsuspectedbradyarrhythmia,history,physicalexamination,andavailabledatashould
beusedtoaddressstability,symptoms,reversibility,siteofdysfunction,andtheneedfortemporaryas
wellaspermanentpacing.
If patient demonstrates signs of poor perfusion (hypotension, confusion, decreased consciousness,
cyanosis,etc.),immediatemanagementperACLSprotocolshouldbeinitiated.Clinicalmanifestations
ofbradyarrhythmiasarevariable,rangingfromasymptomatictononspecific(lightheadedness,fatigue,
weakness,exerciseintolerance)toovert(syncope).
Emphasis should be placed on determining if presenting symptoms have a direct temporal
relationshiptounderlyingbradycardia.Otherhistoricalpointsofemphasisincludethefollowing:
Ischemicheartdisease,particularlyinvolvingrightcoronarycirculation,canprecipitateanumberof
bradyarrhythmias.Therefore,signsandsymptomsofacutecoronarysyndromeshouldbethoroughly
investigated.
Precipitating circumstances (micturition, coughing, defecation, noxious smells) surrounding
episodesmayhelpidentifyneurocardiogenicetiologyofbradycardia.
Tachyarrhythmias,particularlyinpatientswith underlyingsinusnodedysfunction, canbefollowed
bylongpauses(conversionpauses)becauseofsinusnodesuppressionduringtachycardia.
History of structural heart disease, hypothyroidism, OSA, collagen vascular disease, infections
(bacteremia, endocarditis, Lyme, Chagas), infiltrative diseases (amyloid, hemochromatosis, and
sarcoid),neuromusculardiseases,andpriorcardiacsurgery(valve replacement,congenitalrepair)
shouldbeelicited.
Medications should be reviewed with emphasis on those that affect the SA and AV nodes (i.e.,
calciumchannelblockers,β-adrenergicblockers,digoxin).
After hemodynamic stability is confirmed, a more thorough examination with emphasis on the
cardiovascularsystemandanyfindingsconsistentwiththeabovecomorbiditiesisappropriate(Figure
7-3).
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