3. coba terkontrol ataukomparatif,tidakadaobatpilihanyangbenaruntuksinkopvasovagal yangparah,
dan dokterdibiarkanmemilihagendanmenilai keefektifanklinispadapasienindividupadakasusper
kasus.dasar-case.
AtrioventricularBlock
Penundaanataupemblokirankonduksidapatterjadi di areamanapundari sistemkonduksi AV:simpul
AV,berkasHis,atau cabang berkas.BlokAV biasanyadikategorikanmenjadi tigajenisberdasarkan
temuanEKG (Tabel 39-11). BlokAV derajatpertamaadalah konduksi AV 1:1 denganinterval PRyang
lama.BlokAV derajatdua dibagi menjadi duabentuk:BlokAV MobitzI(periodisitasWenckebach)
kurangdari konduksi AV 1:1 denganinterval PRyangsemakinlamahinggakompleksventrikelterlepas;
BlokMobitzII AV secara intermitenmenurunkandenyutventrikelsecaraacaktanpa pemanjanganPR
yang progresif. BlokAV derajatketigaadalahblokjantunglengkapdi manakonduksi AV samasekali
tidakada (disosiasi AV).BlokAV derajatpertamabiasanyamenunjukkankonduksiberkepanjangandi
nodusAV.MobitzI, blokAV derajatkeduajugabiasanyadisebabkanolehkonduksi yangberkepanjangan
di simpul AV.Sebaliknya,MobitzII,blokAV derajatduabiasanyadisebabkanolehpenyakitkonduksi di
bawahAV node (yaitu,bundel His).BlokAV derajattigadapatdisebabkanolehpenyakitdi semua
tingkatsistemkonduksi AV:bloknodusAV lengkap,blokbundelnya,ataubloktrifasikular.Dalamsituasi
ini,ventrikel berdetaksecaraindependendari atrium(disosiasi AV),danlajuaktivasi ventrikel dan
konfigurasi QRSditentukanolehlokasi blokAV.Derajatotomatisitasalatpacujantungventrikel
menurunsecaraprogresif saattempatpembentukanimpulsbergerakke bawahsistemkonduksi
ventrikel.Olehkarenaitu,tingkatlolosventrikel dalamkasusbloktrifasikularakanjauhlebihkecil
daripadabloknodal AV lengkap.Akibatnya,bloktrifasikularadalahbentukblokAV yangjauhlebih
berbahaya.Misalnya,blokAV lengkappadatingkatnode AV biasanyamenghasilkanritme ventrikel yang
dikendalikanolehalatpacujantungAV yang stabil (kecepatannyakira-kira40denyut/ menit).
Sebaliknya,padablokAV lengkapkarenatrifasikularataublokbundel His,alatpacujantungyang jauh
lebihtidakdapatdiandalkandengankecepatanyanglebihlambatdi bawahlokasi blokmengontrol ritme
ventrikel.
atletatau selamatidurketikanadavagal tinggi.Juga,blokAV dapatbersifatsementaradi manaetiologi
yang mendasari adalahreversibel seperti padamiokarditis,iskemiamiokard,setelahoperasiCV,atau
selamaterapi obat.Betablocker,digoxin,atauCCBnon-DHPdapat menyebabkanblokAV,terutama di
area nodusAV.KelasIAADdapat memperburukpenundaankonduksi di bawahtingkatsimpul AV
(jaringanyangbergantungpadanatrium).Dalamkasuslain,blokade AV mungkintidakdapatdiubah,
seperti yangdisebabkanolehMIakut,penyakitdegeneratif yang jarangterjadi,penyakitmiokard
primer,ataupenyakitjantungbawaan.JikapasiendenganblokAV derajatduaatauderajatketiga
mengembangkantandaataugejalaperfusi yangburuk(misalnya,perubahanstatusmental,nyeri dada,
hipotensi,syok),atropin IV (0,5mgdiberikansetiap3-5menit,hingga3mg dosistotal) harusdiberikan.
92 Jikapasienini tidakmeresponatropin,pacingtranskutandapatdimulai.Infussimpatomimetikseperti
epinefrin(2-10mcg / menit) ataudopamin(2-10 mcg / kg / menit) jugadapatdigunakanjikaterjadi
kegagalanatropindansangat efektifpadabradikardia/henti sinusdanbloknodal AV.Infus
isoproterenol (2-10mcg / menit) dapatdipertimbangkanjikapasientidakmerespondopaminatau
epinefrin;Namun,obatini harusdigunakandenganhati-hati karenasifatvasodilatasi dan
kemampuannyauntukmeningkatkankonsumsi oksigenmiokard(terutamaselamaMIaktif).Seperti
4. yang diharapkan,obatini biasanyatidakmembantuketikalokasiblokAV beradadi bawahnode AV
(misalnya,MobitzIIataublokAV trifasikular) karenamekanisme utamanyaadalahuntukmempercepat
konduksi melalui nodusAV.JikapasiendenganbradikardiaataublokAV datangdengantanda dangejala
perfusi yangadekuat,tidakadaterapi akutselainobservasi ketatyangdirekomendasikan.Pasien
denganblokAV bergejalakronisharusdirawatdenganpemasanganalatpacujantungpermanen.112
Pasientanpagejalaterkadangdapatdiikuti tanpaperlualatpacujantung.PasiendenganMIakutdan
bukti blokAV baru atau gangguan konduksi seringkalimemerlukanpemasanganalatpacujantung
transvenoussementara.BlokAV lebihseringterjadisebagai komplikasiMIdindinginferiorkarena
persarafanvagal yangtinggi di tempatini,danalirandarah koronerke area nodal biasanyamenyuplai
dindinginferior.Namun,blokAV mungkinhanyasementara,meniadakankebutuhanakantempo
permanen.
SinusBradycardia
Sinusbradyarrhythmias(heartrate lessthan60 beats/min) are acommonfinding,especiallyinyoung,
athleticallyactiveindividuals,andusuallyare neithersymptomaticnorinneedof therapeutic
intervention.Onthe otherhand,some patients,particularlythe elderly,have SND.Thismaybe the
resultof underlyingSHDandthe normal agingprocessthat attenuate SA nodal functionovertime
resultinginsymptomaticsinusbradycardiaand/orperiodsof sinusarrest.112 SNDis usuallyreflective
of diffuse conductiondisease,andaccompanyingAV blockisrelativelycommon.Furthermore,
symptomaticbradyarrhythmiasmaybe accompaniedby alternatingperiodsof paroxysmaltachycardias
such as AF.In thisinstance,AFsometimespresentswitharatherslow ventricularresponse (inthe
absence of AV nodal blockingdrugs) because of diffuse conductiondisease.The occurrence of
alternatingbradyarrhythmiasandtachyarrhythmiasisreferredtoasthe tachy-bradysyndrome.The
occurrence of paroxysmal AFina patientwithSNDmaybe a resultof underlyingSHDwithatrial
dysfunctionoratrial escape inresponse toreducedsinusnode automaticity. Infact,because the rate of
impulse generationbythe sinusnode isgenerallydepressedormayfail altogether,otherautomatic
pacemakerswithinthe conductionsystemmay“rescue”the sinusnode.Theserescue rhythmsoften
presentasparoxysmal atrial rhythms(eg,AF) oras a junctional escape rhythm.The treatmentof SND
involveseliminatingthe symptomaticbradycardiaandpotentiallymanagingalternatingtachycardias
such as AF.In general,the longtermtherapyof choice ispermanentpacemakerimplantation.112 Dual-
chamber,rate-adaptive chronicpacingclearlyimprovessymptomsandoverall qualityof life and
decreasesthe incidence of paroxysmalAFandsystemicembolism.120 Drugs commonlyemployedto
treat supraventriculartachycardiasshouldbe used withcaution,if atall,inthe absence of a functioning
pacemaker.AADsprescribedtopreventAFrecurrencesmayalsosuppressthe escape orrescue rhythms
that appearinsevere sinusbradycardiaorsinusarrest.
Consequently,these drugsmaytransformanasymptomaticpatientwithbradycardiaintoasymptomatic
one.The additionof classI AADscan also affectpacemakerthresholdandresultinlossof capture if the
pacemakerisnot appropriatelyinterrogatedandadjusted.OtherdrugsthatdepressSA or AV nodal
function,suchas betablockers,non-DHPCCBs,andivabradine,mayalsosignificantlyexacerbate
bradycardia.Drugswithindirectsympatholyticactions,suchasmethyldopaandclonidine,mayalso
worsenSND.The use of digoxininthese patientsis controversial;however,inmostcases,itcanbe used
5. safely.Anotherreasonforparoxysmal bradycardiaandsinusarrest,notdirectlydue toSND,iscarotid
sinushypersensitivity.112Again,thissyndrome occurscommonlyinthe elderlywithunderlyingSHD,
and mayprecipitate fallsandhipfractures.Symptomsoccurwhenthe carotidsinusisstimulated,
resultinginanaccentuatedbaroreceptorreflex.Often,however,symptomsare notwell correlatedwith
the obviousphysical manipulationof the carotidsinus(inthe lateral neckregion).Patientsmay
experience intermittentepisodesof dizzinessorsyncope because of sinusarrestcausedbyincreased
vagal tone (the cardioinhibitorytype),adropinsystemicbloodpressure causedbysympathetic
withdrawal (the vasodepressortype),orboth(mixedcardioinhibitoryandvasodepressortypes).The
diagnosiscanbe confirmedbyperformingcarotidsinusmassage withECGandbloodpressure
monitoringinacontrolledsetting.Symptomaticcarotidsinushypersensitivity shouldbe treatedwith
permanentpacemakertherapy.
112 However,some patients,particularlythosewithasignificantvasodepressorcomponent,still
experience syncopeordizzinessevenafterpacemakerimplantation.The choice of definitive drug
therapyinthissituationismarredbythe lackof controlledtrials,althoughalpha-adrenergicstimulants
such as midodrine are oftentriedinadditiontothe pacemaker.120 Vasovagal syndrome,bycausing
bradycardia,sinusarrest,and/orhypotension,isthe cause of syncope inmanypatientswhopresent
withrecurrentfaintingof unknownorigin.112 By history,manyindividualscanrecountrare instancesof
faintingspellsattimesof duressorfear.These episodesare mostoftencausedbyvasovagal syncope.
However,some patientshave extremelyfrequent,unexpectedsyncopal episodesthatinterfere withthe
patient’squalityof life andcause physical danger(sometimesreferredtoasneurocardiogenicsyncope
syndrome ormalignantvasovagal syndrome).Vasovagal syncopeispresumedtobe a neurallymediated,
paradoxical reactioninvolvingstimulationof cardiacmechanoreceptors(ie,Bezold-Jarischreflex).
Forceful contractionof the ventricle (eg,aswithadrenergicstimulation) coupledwithlow ventricular
volumes(eg,withuprightposture ordehydration) providesapowerfulstimulusforcardiac
mechanoreceptors.Syncope resultsfromthe spontaneousdevelopmentof transienthypotension
(sympatheticwithdrawal) andbradycardia(vagotonia).However,the true mechanismof vasovagal
syncope remainstobe definitivelydetermined.Forinstance,patientswithdenervatedhearts(eg,heart
transplantrecipients) canstill experiencethisformof syncope.Regardless,patientsbelievedtohave
frequentepisodesof vasovagal syncope have beenevaluatedanddiagnosedusingthe uprightbody-tilt
test,a potentstimulusforthe developmentof vasovagal symptoms.121 Althoughcommonlyused,the
sensitivityandreproducibilityof thistesthave beenquestioned.122Traditionally,betablockers,suchas
metoprolol,were frequentlychosenasthe drugsof choice inpreventingepisodesof vasovagal syncope.
Althoughthese drugsmayseeminappropriate totreata syndrome resultingfromvasodilationand
bradycardia,the therapeuticapproachis designedtoblockan inappropriate vasovagal reaction(ie,they
inhibitthe sympatheticsurge thatcausesforceful ventricularcontractionandprecedesthe onsetof
hypotensionandbradycardia).
To most clinicians’surprise,mostcontrolledtrialsof the use of betablockersinpatientswithsevere
vasovagal syncope have shownnoeffectcomparedwithplaceboinpreventingsyncopal episodes.123
Some trialshave suggestedthatbetablockersare more effective andshouldbe usedinolderpatients
(olderthan 40 yearsof age) withvasovagal syncope ratherthanthe relativelyyoung.124Otherdrugs
that have beenusedsuccessfully(withorwithoutbetablockers) include mineralocorticoidsasvolume
expanders(fludrocortisone),anticholinergicdrugs(scopolamine patches,disopyramide),alpha-
adrenergicagonists(midodrine),adenosine analogs(theophylline,dipyridamole),andselective
6. serotoninreceptorantagonists(sertraline,paroxetine).125 Permanentpacinghasbeenusedwithsome
successbut shouldbe reservedfordrug-refractorypatients.112 Because of the questionable
effectivenessof betablockersandthe paucityof controlledorcomparative trials,there isnota true
drug of choice for severe vasovagal syncope,andcliniciansare leftwithchoosingagentsandjudging
clinical effectivenessinindividualpatientsona case-by-case basis.
AtrioventricularBlock
Conductiondelayorblockmay occur inany area of the AV conductionsystem:the AV node,the His
bundle,orthe bundle branches.AV blockisusuallycategorizedintothree differenttypesbasedonECG
findings(Table 39-11).First-degree AV blockis1:1AV conductionwitha prolongedPRinterval.Second-
degree AV blockisdividedintotwoforms:MobitzIAV block(Wenckebachperiodicity) islessthan1:1
AV conductionwithprogressivelylengtheningPRintervalsuntilaventricularcomplex isdropped;
MobitzII AV blockis intermittentlydroppedventricularbeatsinarandomfashionwithoutprogressive
PR lengthening.Third-degreeAV blockiscompleteheartblockwhere AV conductionistotallyabsent
(AV dissociation).First-degree AV blockusuallyrepresentsprolongedconductioninthe AV node.Mobitz
I, seconddegree AV blockisalsousuallycausedbyprolongedconductioninthe AV node.Incontrast,
MobitzII, second-degree AV blockisusuallycausedbyconductiondisease belowthe AV node (ie,His
bundle).Third-degreeAV blockmaybe causedbydisease atany level of the AV conductionsystem:
complete AV nodal block,Hisbundle block,ortrifascicularblock.Inthissituation,the ventricle beats
independentlyof the atria(AV dissociation),andthe rate of ventricularactivationandQRSconfiguration
are determinedbythe site of the AV block.The usual degree of automaticityof ventricularpacemakers
progressivelydeclinesasthe site of impulse generationmovesdownthe ventricularconductionsystem.
Therefore,the ventricularescape rate incasesof trifascicularblockwill be significantlylessthan
complete AV nodal block.Consequently,trifascicularblockisa muchmore dangerousformof AV block.
For instance,completeAV blockatthe level of the AV node usuallyresultsinthe ventricularrhythm
beingcontrolledbythe stable AV junctional pacemaker(rate approximately40beats/min).Incontrast,
incomplete AV blockdue totrifascicularorHis bundle block,amuchlessreliable pacemakerwith
slowerratesbelowthe site of blockcontrolsventricularrhythm.
athletesorduringsleepwhenvagal tone ishigh.Also,AV blockmaybe transientwhere the underlying
etiologyisreversible suchasinmyocarditis,myocardial ischemia,afterCV surgery,orduringdrug
therapy.Betablockers,digoxin,ornon-DHPCCBsmaycause AV block,primarilyinthe AV nodal area.
ClassI AADsmay exacerbate conductiondelaysbelow the levelof the AV node (sodium-dependent
tissue).Inothercases,AV blockmaybe irreversible,suchasthatcausedby acute MI, rare degenerative
diseases,primarymyocardial disease,orcongenital heartdisease.If patientswithsecond-degree or
third-degreeAV blockdevelopsignsorsymptomsof poorperfusion(eg,alteredmental status,chest
pain,hypotension,shock),IV atropine (0.5mggivenevery3-5 minutes,upto3 mgtotal dose) shouldbe
administered.92If these patientsdonot respondtoatropine,transcutaneouspacingcanbe initiated.
Sympathomimeticinfusionssuchasepinephrine(2-10mcg/min) ordopamine (2-10mcg/kg/min) can
alsobe usedinthe eventof atropine failure andare particularlyeffectiveinsinusbradycardia/arrestand
AV nodal block.Anisoproterenolinfusion(2-10mcg/min) maybe consideredif the patientdoesnot
respondtodopamine orepinephrine;however,thisdrugshouldbe usedwithcautionbecauseof its
vasodilatingpropertiesandabilitytoincrease myocardial oxygenconsumption(particularlyduringactive
MI). Aswouldbe expected,these drugsusuallydonothelpwhenthe site of AV blockisbelow the AV
node (eg,MobitzII or trifascicularAV block) because theirprimarymechanismistoaccelerate
7. conductionthroughthe AV node.If patientswithbradycardiaorAV blockpresentwithsignsand
symptomsof adequate perfusion,noacute therapyotherthanclose observationisrecommended.
PatientswithchronicsymptomaticAV blockshouldbe treatedwiththe insertionof apermanent
pacemaker.112 Patientswithoutsymptomscansometimesbe followedcloselywithoutthe needfora
pacemaker.Patientswithacute MIand evidenceof new AV blockorconductiondisturbanceswill often
require the insertionof atemporarytransvenouspacemaker.AV blockmore commonlyoccursasa
complicationof inferiorwall MIsbecause of highvagal innervationatthissite,andthe coronary blood
flowtothe nodal areasusuallysuppliesthe inferiorwall.However,the AV blockmayonlybe transient,
obviatingthe needforpermanentpacing.
