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ARRHYTHMIA
(General)OutlineArrhythmia
isanyofagroupofconditionsinwhichtheelectricalactivityoftheheartisirregularorisfasterorslowerthannormal.
Theheartbeatmaybetoofast(over100beatsperminute)ortooslow(lessthan60beatsperminute),andmayberegularorirregular.Aheartbeatthatistoofastiscalledtachycardiaandaheartbeatthatistooslowiscalledbradycardia.Althoughmanyarrhythmiasarenotlife-threatening,somecancausecardiacarrest.2023/11/62DefinitionTheOrigin,Rate,Rhythm,Conductvelocityandsequenceofheartactivationareabnormally2023/11/63Arrythmiarelated
CardioanatomyThecardiacmusclemajorityiscomposedoftheordinarycardiacmuscletextilefiber,thesmallpartforthecardiacmuscletextilefiberofspecialdifferentiation,lattercomposesthecardiac
pacing-conductionsystem2023/11/64Cardiac
Conduction
SystemSAN
Internodal
pathways
AVN
His
bundle
L./R.
bundle
branch
Purkinje
fibers2023/11/65Pacing
conduction
system2023/11/66PathogenesisandInducement
ofArrhythmiaSomephysicalconditionPathologicalheartdiseaseOthersystemdiseaseElectrolytedisturbanceandacid-baseimbalancePhysicalandchemicalfactorsortoxicosis2023/11/67MechanismofArrhythmiaAbnormalheartpulseformationSinuspulseEctopicpulseTriggeredactivityAbnormalheartpulseconductionReentryConductblock2023/11/68Phase1快速復(fù)極初期:鉀離子外流Phase0
快速或上升鈉離子內(nèi)流入進(jìn)入細(xì)胞進(jìn)行除極Phase2平臺期:持續(xù)的鈉離子內(nèi)流和緩慢鈣離子內(nèi)流和鉀離子外流Phase3快速復(fù)極末期:鉀離子外流Phase4靜息期5Phases心肌細(xì)胞的動作電位AbnormalheartpulseformationAutomaticityTriggered
activity觸發(fā)機(jī)制后電位產(chǎn)生于動作電位的第3相(早期)或第4相(晚期)可觸發(fā)心律失常2023/11/610AutomaticityHeartcellsotherthanthoseoftheSAnodedepolarizefasterthanSAnodecells,andtakecontrolasthecardiacpacemaker.Factorsthatenhanceautomaticityinclude:
SANS,
PANS,
CO2,
O2,
H+,
stretch,hypokalemiaandhypocalcaemia.Examples:EctopicatrialtachycardiaormultifocaltachycardiainpatientswithchroniclungdiseaseORventricularectopyafterMI2023/11/611Triggeredactivity…islikeadominoeffectwherethearrhythmiaisduetotheprecedingbeat.Delayedafter-depolarizationsariseduringtherestingphaseofthelastbeatandmaybethecauseofdigitalis-inducedarrhythmias.Earlyafter-depolarizationsariseduringtheplateauphaseortherepolarizationphaseofthelastbeatandmaybethecauseoftorsadesdepointes(ex.Quinidineinduced)2023/11/612Abnormalheartpulseconduction:Reentry:mostcommon2023/11/613FastConductionPathSlowRecoverySlowConductionPathFastRecoveryReentryRequires…ElectricalImpulseCardiacConductionTissue2distinctpathwaysthatcometogetheratbeginningandendtoformaloop.Aunidirectionalblockinoneofthosepathways.Slowconductionintheunblockedpathway.
2023/11/614FastConductionPathSlowRecoverySlowConductionPathFastRecoveryThe“Re-Entry”MechanismofEctopicBeats&RhythmsElectricalImpulseCardiacConductionTissueTissueswiththesetypeofcircuitsmayexist:
inmicroscopicsizeintheSAnode,AVnode,oranytypeofhearttissue
ina“macroscopic”structuresuchasanaccessorypathwayinWPW2023/11/615FastConductionPathSlowRecoverySlowConductionPathFastRecoveryPrematureBeatImpulseCardiacConductionTissue1.AnarrhythmiaistriggeredbyaprematurebeatThebeatcannotgainentryintothefastconducting
pathwaybecauseofitslongrefractoryperiodand
thereforetravelsdowntheslowconductingpathway
onlyRepolarizingTissue(longrefractoryperiod)The“Re-Entry”MechanismofEctopicBeats&Rhythms2023/11/6163.Thewaveofexcitationfromtheprematurebeatarrivesatthedistalendofthefastconductingpathway,whichhasnowrecoveredandthereforetravelsretrogradely(backwards)upthefastpathwayFastConductionPathSlowRecoverySlowConductionPathFastRecoveryCardiacConductionTissueThe“Re-Entry”MechanismofEctopicBeats&Rhythms2023/11/6174.Onarrivingatthetopofthefastpathwayitfindstheslowpathwayhasrecoveredandthereforethewaveofexcitation‘re-enters’thepathwayandcontinuesina‘circular’movement.Thiscreatesthere-entrycircuitFastConductionPathSlowRecoverySlowConductionPathFastRecoveryCardiacConductionTissueThe“Re-Entry”MechanismofEctopicBeats&Rhythms2023/11/618AtrialRe-entryatrialtachycardiaatrialfibrillationatrialflutterAtrio-VentricularRe-entryWolfParkinsonWhitesupraventriculartachycardiaVentricularRe-entryventriculartachycardiaAtrio-VentricularNodalRe-entrysupraventriculartachycardiaRe-entryCircuitsasEctopicFociandArrhythmiaGenerators2023/11/619BRADYCARDIASAslowrhythm(lessthan60beats/min)MaybecausedbyaslowedsignalfromtheSAN,
apauseinthenormalactivityoftheSAN,orbyblockingoftheelectricalimpulseonitswayfromtheatriatotheventricles(AVblockorheartblock)Mayalsobepresentinthenormallyfunctioningheartofenduranceathletesorotherwell-conditionedpersons2023/11/620MECHANISM
OF
BRADYCARDIAS竇房結(jié)自律性受損如因炎癥、缺血、壞死或纖維化可致竇房結(jié)功能衰竭,起搏功能障礙,引起竇性心動過緩,竇性停搏傳導(dǎo)阻滯SAN及A病變,可引起S-A阻滯等AVB是由于AVN或房室束的傳導(dǎo)功能降低,SAN的興奮激動不能如期向下傳導(dǎo)而引起,可分為生理性和病理性兩種病理性常見于風(fēng)濕性心肌炎、白喉及其他感染、冠心病、洋地黃中毒等生理性多系迷走神經(jīng)興奮性過高2023/11/621ClassificationofArrhythmiaAtrialJunctional
arrhythmiaVentricularHeart
blocksSuddenarrhythmicdeathsyndromeArrhythmiamaybeclassifiedbyrate(normalsinusrhythm,tachycardia,bradycardia)ormechanism(automaticity,reentry,junctional,fibrillation).Itisalsoappropriatetoclassifybysiteoforigin:2023/11/622Diagnosis
of
ArrhythmiaMedical
HistoryPhysical
ExaminationLaboratory
Test2023/11/6232023/11/6242023/11/6252023/11/626ELECTROCARDIOGRAM“5”stepsapproachtoarrhythmiasStep1:Istherea“QRS”Step2:Istherea“P”WaveStep3:WhatistherelationshipbetweenthePwavesandtheQRScomplexes?Step4:CalculaterateStep5:
Miscellaneous2023/11/627Step
1:
Istherea
“QRS”
(Nopulse)YESNOCHAOTICFLATLINEWIDENARROWPEAVFAsystoleVT2023/11/628Step
2:
Istherea“P”WaveYESNOVARYCONSTANTMORPHOLOGYRATE220to350AFJUNCTIONALInvertedRRIntervalJUNCTIONALAtrialFlutter2023/11/6292023/11/6302023/11/631Step
3:
WhatistherelationshipbetweenthePwavesandtheQRScomplexes?2023/11/632<0.2Normal>0.2IoAVBConstant?YesIIo
AVBtype2NoRRintervalYesIIIoAVBNoType1IIoPRintervalPRintervalHEARTBLOCKn“P”=n“QRS”?NoYesConstant?2023/11/6331stDegreeblock
(AVNodalDelay)2023/11/6342023/11/6352023/11/636EventMonitorsHoltermonitoring:Documentsymptomaticandasymptomaticarrhythmiasover24-48hours.Canalsoevaluatetreatmenteffectivenessina-fib,pacemakereffectivenessandidentifysilentMIs.Trans-telephoniceventrecording:patienteitherwearsmonitorforseveraldaysorattachesitduringsymptomaticeventsandanECGisrecordedandtransmittedforevaluationviatelephone.Only20%arepositive,butstillhelpful.2023/11/637ExercisetestingSymptomsonlyappearorworsenwithexercise.Alsousedtoevaluatemedicationeffectiveness(esp.flecanide&propafenone)
YoucanassessSAnodefunctionwithexercisetesting.
Mobitz1(Wenkebach)isblockageattheAVnode,socatecholaminesfromexerciseactuallyhelp!
Mobitz2isblockageatbundleofHis,soitworsensascatecholaminesfromexerciseincreaseAVnodeconduction,thusprognosisisworse.*PVCsoccurin10%withoutand60%ofpatientswithCAD.*PVCsDONOTpredictseverityofCAD(neitherfornoragainst)!2023/11/638SignalAveragedECGUsedonlyinpeoplepostMItoevaluateriskforv-fiborv-tach.Damagearoundtheinfarctisvariable,sothismeasureslatepotentials(low-signal,delayedactionpotentials)astheypassthroughdamagedareas.Positivepredictivevalueis25%-50%butnegativepredictivevalueis90%-95%,thusiftestisnegative,patientisatlowrisk.2023/11/639ElectrophysiologicTesting…CathetersareplacedinRA,AVnode,BundleofHIS,rightventricle,andcoronarysinus(tomonitorLAandLV).Usedtoevaluatecardiogenicsyncopeofunknownorigin,symptomaticSVT,symptomaticWPW,andsustainedv-tach.*AblativetherapyisbeneficialinAVnodereentry,WPW,atrialtachycardia,a-flutter,andsomev-tach.Complicationis1%2023/11/640ManagementPhysicalmaneuvers,Medications,Electricityconversion,orElectro-orcryo-cautery.Themethodofcardiacrhythmmanagementdependsfirstlyonwhetherornottheaffectedpersonisstableorunstable2023/11/641TherapyPrincipalPathogenesistherapyStopthearrhythmiaimmediatelyifthehemodynamicwasunstableIndividualtherapy2023/11/642Physicalmaneuvers
(vagalmaneuvers)Anumberofphysicalactscanincreaseparasympatheticnervoussupplytotheheart,resultinginblockingofelectricalconductionthroughtheAVnode.ThiscanslowdownorstopanumberofarrhythmiasthatoriginateaboveorattheAVnode2023/11/643Anti-arrhythmiaAgentsAnti-tachycardiaagentsAnti-bradycardiaagents2023/11/644Anti-tachycardiaagentsModifiedVaughamWilliamsclassificationIclass:NatriumchannelblockerIIclass:?-receptorblockerIIIclass:PotassiumchannelblockerIVclass:CalciumchannelblockerOthers:Adenosine,Digital2023/11/645Phase1快速復(fù)極初期:鉀離子外流Phase0
快速或上升鈉離子內(nèi)流入進(jìn)入細(xì)胞進(jìn)行除極Phase2平臺期:持續(xù)的鈉離子內(nèi)流和緩慢鈣離子內(nèi)流和鉀離子外流Phase3快速復(fù)極末期:鉀離子外流Phase4靜息期5Phases心肌細(xì)胞的動作電位Classification
of
AADs類別亞類電生理效應(yīng)代表制劑新制劑傳導(dǎo)速度不應(yīng)期Ap時限ⅠⅠa↓↑多↑奎尼丁Ajmaline、Pirmenol、AprindinⅠb↓/↑↓↓利多卡因Maxiletine、TocainideⅠc↓↑=EncainidePropafenone、Flecainide、Lorcainide、EthmozideⅡ↓=↑心得安Ⅲ↓=↑↑胺碘酮SotablⅣ↓↑異搏定硫氮唑酮Bepridi其它藥物包括:洋地黃類(臨床上稱之為第五類)以及新斯的明、甲氧胺、氯化鉀、硫酸鎂、ATP等抗緩慢心律失常的藥物,包括:擬交感胺類、阿托品類、堿性藥物等
2023/11/647Clinicalusage:
IaclassGuinidineProcainamideDisopyramide:Sideeffect:likeM-cholinergicreceptorblockerLessuseinclinic
2023/11/648Clinicalusage:
IbclassLidocaineMexiletinePerfecttoventriculartachyarrhythmia2023/11/649Clinicalusage:
IcclassMoricizinePropafenoneCanbeusedinventricularand/orsupra-ventriculartachycardiaandextrasystole.2023/11/650Clinicalusage:
IIclassPropranolol:Non-selectiveMetoprolol:Selective?1-receptorblocker,Perfecttohypertensio
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