内科学精品教学课件（时国朝）07 心律失常 8年制2015

心律失常 CardiacArrhythmia Dr WeiMeng MD FACCDepartmentofcardiology affiliated6thpeople shospital ShanghaiJiaoTongUniversity Mechanismofarrhythmia Propertyofcardiacelctrophysiology兴奋性 Excitability 自律性 automaticity 传导性 Conductivity Excitability ExcitabilityindicatesthatmyocardialcellhaselectricalactivitywhenitisstimulatedElectricalactivityofsinglemyocardialcelliscalledactionpotential AP ElectricalactivityofwholeheartmakesECG 0 60 90 20 Thresholdvoltage mv 0 1 2 3 4 ARP ERP RRP Super conductiveperiod ARP AbsoluteRefractoryperiod ERP EffectiveRefractoryperiod RRP RelativeRefractoryperiod Conductivity ElectricalimpulsecanconductinmyocardialtissuebidirectionallyNormalconductionpathway sinusnode intranodebundle atrioventriculanodeandintraatrialbundle Hisbundle rightandleftbundlebranch includingleftanterosuperiorandposteroinferior Purkinjefiber myocardium automaticity Cellsspontaneouslydischarging spontaneousAP diastolicdepolarization Automaticityincreasesfromhightolowasfollows Physiologicalstatus SN AVN HIS Purkinjepathological diseasedmyocardialandconductivetissue etc Propertyofnormalrhythm ImpulsefromSNHeartrateiswithin60 100 minRegularrhythm PPinterval 0 12sPRintervalisbetween0 12 0 20s QRScomplexduration 0 10sFrontalaxiswithin 30 110 Itisconsideredasarrhythmiaifanyitemaboveisnotmatched Mechanismsofarrhythmogenesis EnhancedautomaticityTriggeredactivityAutomaticcellsdiminishormalfunction DysfunctionofconductivetissuesReentry Mechanismsofarrhythmogenesis 1 EnhancedautomaticityEndogenousorexogenouscatecholamineincreasingAbnormalityofacid basic electrolytebalanceIschemia hypoxiaMechanicalstretchdrugsDisturbanceofnerveandliquidmodulation Mechanismsofarrhythmogenesis 2 TriggeredactivityDepolarizingoscillationsofmembranevoltageinducedbyabnormalinwardNa current oneormoreprecedingAP duringearlierorlaterreporlarization ie AfterdepolarizationEarlydepolarizationDelayeddepolarization Mechanismsofarrhythmogenesis 3 Automaticcellsdiminishormalfunction suchassicksinussyndromeDysfunctionofconductivetissues suchassinoatrialblock atrioventricularblockorbundlebranchblockaswellasabnormalpathway Mechanismsofarrhythmogenesis 4 ReentryprerequisiteofreentryConductioninconsistencyofanatomyorphysiologySingledirectionalconductionblockingDelayedconductionInitialblockingarearecoversexcitability reentrycyclelengthgreatthanrefractoryperiodoftheblocking Classificationofcardiacarrhythmias ClassifiedonpropertyofelectricalactivityAbnormalityofimpulseandconductionClassifiedonheartrate rapidorslowRapidorslowarrhythmiasClassifiedonclinicalmanifestation mildorseverFatalornonfatalHighriskorlowriskClassifiedonoriginofarrhythmias Methodofdiagnosingarrhythmiaanditsevaluation SymptomCausedbyabnormalcontractile palpitation discomfort beatingstop etc Inducedbycardiacoutputdecreasing chestcompressingandpain dizziness presyncope syncope shortofbreathlessFactorsrelatedtosymptom medications diet emotion infection etc Methodofdiagnosingarrhythmiaanditsevaluation SignChangingofrhythm sloworfast regularorirregularIntensityofheartsound S1muffleorloud cannonsoundRelationbetweencarotidveinwavepulseandheartrate andchangingofbloodpressure Methodofdiagnosingarrhythmiaanditsevaluation ElectrocardiogramMostvaluable evaluatingarrhythmiatype property prognosis etc DynamicElectrocardiogram Holter Mostvaluable assessingarrhythmiatype numbers distribution property prognosis Evaluatingclinicalsignificance effectsoftreatment etc Methodofdiagnosingarrhythmiaanditsevaluation EsophaguselectrocardiogramDifferentiatingSVTfromVT understandingmechanismofSVT Semi invasive Methodofdiagnosingarrhythmiaanditsevaluation Electrophysiologicstudy EPS Classicalwayofresearchingarrhytnmias InvasiveAssessingfunctionofSNSinusnoderecoverytime SNRTSinoatrialconductiontime SACTAssessingAVconductionAnalyzingmechanisimoftachyarrhythmiasEvaluatingunknownsyncope Methodofdiagnosingarrhythmiaanditsevaluation ExerciseElectrocardiogramSuitableforsomeofarrhythmias suchasVTOthersAveragesignaltechnique suchaslatepotential LP QTdispersion Twavealterationusedforevaluatingprognosisofventriculararrhythmia Specificarrhythmias RapidarrhythmiasPrematurecontractionAtrial junctional ventricularTachyarrhythmiasSinus atrial supraventricular junctional ventricular atrialflutterandfibrellationBradyarrhythmiasDiseaseofsinus AVnodeorbundlebranch Specificarrhythmias TwosyndromesPreexcitingsyndromeRelatedwithrapidarrhythmiasSicksinussyndrome SSS Relatedwithslowarrhythmias sinusarrhythmias Sicksinussyndrome FeaturesofECG 1 Seriouspersistentbradycardia often 50bpm Brady tachysyndrone recurrentepisodeofbothbradyarrhythmiaandsupraventriculartachycardia AF AFL SVT underbasisofbradyarrhythmia thereisoftenlongasystoleafterrapidarrhythmiasstop whichcancausesyncopeorpresyncope Sicksinussyndrome FeaturesofECG 2 FrequentsinusarrestorexitblockwithslowHRBothofsinoatrialandAVnodearediseasedescapeinterval 2s orslowandpersistentAF AFL orslowescaperhythm Sicksinussyndrome EtiologyIntrinsic sinusnodeitselfisinvolved e g ischemia regressivedegeneration infiltrationofothercellsortissuesExtrinsic highvagaltone hyperkalemia antiarrhythmicsmostfrequentetiologyareregressivedegenerationandCHD Sicksinussyndrome SymptomsIschemiaofbrain heart kidneyAdams StokessyndromeDiagnosisTypicalECGpatternsSymptomsisrelatedwithECGchangingsHolter provokingtest treadmillandfinallyelectrophysiologicalstudyforthesuspected Holterismostvaluable Sinusstandstill FeaturesPPintervalelongatesabruptly basicallyatsinusbradycardia whichisnotcommonmultiplesofbasicPPintervalEscapebeatorrhythmiscommonseenSymptomsisdependondurationofstandstillSymptomatictreatment pacemakerisultimatechoice sinoatrialblock ClassificationofECGFirstdegreeSABcan tbeseenonECGThirddegreeSABcan tbedifferentiatedfromsinusstandstillSeconddegreeSABisdividedintotwosubtype i e typeIandtypeIIseconddegreeSABSymptomsandtherapyaresameassinusstandstill TypeISeconddegreeSAB FeaturesofECGPPintervalprogressivelyshortensuntilnextPwavefailstooccurThelongPPintervalthat normalregularPPinterval Type secondarydegreeSAB FeaturesofECGPwaveislostabruptly followedbylongpauseThedurationofthepausetakestheformof2 1 3 1AVconductionEscapebeatorrhythmcanbeenseen Sinustachycardia ClinicalfeaturesVerycommon Etiologyincludingsympatheticexecitation excise avtiveinfection bloodloss hypoxia heartfailure etc PalpitationorchestdiscomfortareoftencomplainedEtiologicaltreatment Atrialarrhythmias Prematureatrialcontraction FeaturesofECGPrematurePwavefollowedbynearnormalQRScomplexQRScomplexissimilartoitfromsinusnodewithincompletecompensatorypauseSometimes PRintervalisprolonged PrematurePwavenotconducttotheventricles oraberrationinventricle fullcompensatorypausecanbeseen Prematureatrialcontraction ClinicalfeaturesCommonseen provokedbyvarietyoffactors e g infection inflammation ischemia tobacco alcoholetc itismorecommonintheelderlySymptomisrelatedtoprolongedcompensatorypause increasedcontraction frequentPACandsensitivityofpatientsOnauscultation irregularbeating longerinterval increasedS1Treatmentaimforetiologyexceptobvioussymptomantiarrhythmicscanbegiven Automaticatrialtachycardia FeaturesLesscommon Mosthaveunderlyingdiseases HRisaround130bpm 200bpmlessseenPwaveisnotassameassinusone PRintervalchangingwithslightlyirregularrhythmAVblockwithdifferentratiocanbeseen Warm up canbeseenatitsinitialattackEtiologicalorsymptomatictreatment RFalsoplaysarole chaoticatrialtachycardia FeaturesRare mosthavingbasicdiseaseHRisbetween100 130bpm atlesttwokindPwavecanbeseenPRandPPintervalarechanging Pnotconductingsometimes isoelectricallinebetweenPPintervalcanbeseen precursorofatrialfibrillationEtiologicalorsymptomatictreatment antiarrhythmicswithcaution Atrialflutter AFL FeaturesofECGPwavedisappears substitutedbyregularsaw likeFwavewithitsratebetween220 350bpmVentricularresponse AVratio isusually2 1 sometimes4 1orirregularStimulationofvagusnerveorexercisemaydecreaseorincreaseAVratiowithmultipleUsuallyAFLisduetoreantryaroundtricuspidring andtendtobecomeAF Atrialflutter AFL ClinicalfeaturesHRisusuallyaround150bpmwhichrepresentsAVratiois2 1 mayhavingunderlyingdiseasesTinyandrapidjugularpulsescanbeseenwithitsratebeyond300bpmSimilarmanifestationtoitinatrialfibrillation AF Rateorrhythmcontroldependsonclinicalpresentation Atrialfibrillation AF FeaturesofECGNoPwave replacedbyrapid chaoticandtinyatrialwaveswithitsrateof350 600bpmVentricleresponseisirregularlyduetoAVdelay irregularrateswithnormalQRScomplex butindividualQRScomplexmayslightlydifferent Etiologiesofatrialarrhythmias CardiacDegeneration ischemic myocarditis enhancedloadduetovarietyofheartdiseases hypertension postCABG preexcitingsyndrome loneAFNoncardiacAlcoholabuse hyper orhypothyroidism alterationofvagalorsympathetictone COPD pulmonaryembolism diabetes sepsis Atrialfibrillation ClinicalfeaturesCommonwithagingaswellasthosewithunderlyingdiseasesSymptomaticseveritydependsonHR AFduration underlyingheartdiseaseTendtoembolismbecauseofthrombosisinatriaMayhavelongcardiacarrestafterparoxysmalAFstops Atrialfibrillation ClinicalfeaturesWithstethoscope palpatingarterypulseandwatchingjugularpulse nearallmostofAFcanbediagnosedwithconfidenceAmphasisngpreventionembolismRateorrhythmcontroldependsonclinicalpresentation AFClassificationbasedonfeaturesofepisode NewclassificationFirst detectedepisodeRecurrentparoxysmal self terminating 7d permanentOldclassificationparoxysmal persistentandpermanentAF Junctionalarrhythmias Junctionalprematurecontraction FeaturesofECGPrematureretrogradePwave maynotseen ThePusuallyinfrontofQRScomplex mayfollowsQRSone PR 0 10s RP 0 20sMostofthemwithcompletecompensatorypause QRScomplexnormalorinaberration Junctionalprematurecontraction ClinicalfeaturesRathercommon MostoccurredwithorganicheartdiseaseSimilarfindingstoatrialoneonauscultationSymptomissimilartothatofatrialonesTreatmentisnotnecessaryunlessobvioussymptom Nonparoxysmaljunctionaltachycardia FeaturesLesscommon Mosthaveunderlyingdiseases digitalissideeffectAttackgradually AVdissociationcommon QRScomplexusuallynormalHRbetween70 130bpm hemodynamicsrelativelychanginglessEiologicaltreatment antiarrhythmicsisnotrecommended Supraventricularparoxysmal AVnodalreantrant tachycardia FeaturesofECGHRbetween160 250bpm absoluteregular QRScomplexnarrowing exceptionofaberration Occasionally retrogradePwaveseenReentry AVnode AV ismajorityofmechanism Supraventricularparoxysmaltachycardia ClinicalfeaturesMostwithoutorganicheartdisease commonseenAttackwithsuddeninitiationandtermination maintainingshortforminutesorlongforhours PalpationismainstreamofsymptomHypotension collapseisfarlessthanVTGoodreactiontotreatment e g vagalmaneuvers antiarrhythmics Radiofrequaceisbestwayforradicalcure Pre excitationorWolf Parkinson white WPW syndrome FeaturesofECGPRinterval 0 12sornormal waveinonsetofQRScomplexwhichresultinwidenedQRScomplexfollowedbysecondaryST TchangePRintervalis 0 12s butQRScomplexisnormal shortPRsyndromeorLGL lown Ganong Levinesyndrome FeaturesofPreexcitationsyndrome P R 0 12s wave SecondaryST Tchange STVoftenseen Preexcitationsyndrome ClnicalfeaturesPartofpatientshaveonsetofSVT AF AFL itsmechanismisreentryThereareseveraltypesofpreexcitation e g persist intermittent latent concealedItispredisposedtosuddendeathifrefractoryperiodofaccessorypathwayis 270msTherapyisassameasitinSTV butdigitalis varapamil blockerareforbiddeninAFattack Ventriculararrhythmias Ventricularprematurecontraction FeaturesofECGPrematureQRScomplexwithnoprecedingrelatedPwaveQRScomplexisbizarreinshapewithfullcompensatorypause insertoneexception AVdissociationcanbeseen Ventricularprematurecontraction ClinicalfeaturesMostcommon Seenatorganicheartdiseases someofitinAMIormyocardiopathycaninducefatalarrhythmiaSimilarfeaturestootherprematurecomplexonauscultation PalpitationisacommoncomplainTreatmentregimenonbasisofclinicalmanifestation Ventricularparoxysmaltachycardia FeaturesofECGHRbetween150 200bpm regularrhythmQRScomplexbizarreandwidenAVdissociation ventricularfusionandcapture Ventricularparoxysmaltachycardia ClinicalfeaturesOftenwithorganicdiseases inducinghemodynamicsdeteriorationcausingremarkablesymptomsBothsustainedandnon sustainedVTseeninclinicalItshouldbestoppedassoonaspossible withantiarrhythmicsorDCcardioversion Varapamil adenosine blockerareeffectiveforsomespecificVT Torsadedepointes TDP FeaturesCongenital recurrentsyncope deafness longQT i elongQTsyndrome Acquired drugse g quinidine electrolytedisturbance highdegreeAVB etc atleast80 isacquiredinclinicalLongQTiscommon oftenVPCatlatediastoleinducingTDPTDPdisplaysaspeakofQRScomplexreversesalongisoelectricline causingpatientssyncopeTDP mostofit terminatingspontaneouslywithseveralsec Torsadedepointes TDP TreatmentDuringattackIncreasingHR atropine pacing isoproterenolInfusionofmagnesium potassium lidocaineusefulonlyinafewpatientsDuringreliefe blocker calciumantagonist antiepilepticdrugsLeftsidecervicothoracicsymppatheticganglionectomyorimplantationofcardioverter defibrillatorinsomerefractorycases Acceleratedidoventricularrhythm FeaturesCommoninAMI myocarditis digitalisintoxicationHRbetween60 120bpm regular QRScomplexbizarreBothonsetandceasingaregradualMildeffectonhemodynamicschangingEtiologicaltreatment antiarrhythmicswithcaution Heartblocking atrioventricularblock AVB ClassificationAcuteandchronicAVBTheacuteismainlyduetomyocarditis AMI electrolyteabnormalityandsomedrugsimpactThechronicismainlycausedbyregressivedegenerativefibrosisorconsequenceoftheacuteone 1stdegreeAVB FeaturesofECGPRinterval 0 20sinadultsor 0 18sinchildrenMostofitisin0 21 0 35s 2nd type AVB Wenchebachblock FeaturesofECGProgressivePRintervalprolongationoccurs resultinginanonconductionPwave thepause thedurationofthepauseis twobasicRRcyclesRRintervalprogressivelyshortensFirstPRintervalafterthepauseisshortest AVconductionratiosusuallyare3 2or4 3 2nd type AVB FeaturesofECGPRintervalisusuallynormalandnochangePwavedonotconductsuddenlyorperiodically makingthelongpauseThelongpauseismultiplesofbasiccycles 3rddegreeAVB FeaturesofECGAVconductionfailscompletelywithAVdissociationVentricularactivityismaintainedbyanescaperhythmarisingfromsitedistaltoHisbunduleAtrialrate ventricularrateQRScomplexisbroadifpacesitedistaltoHis otherwiseitisnearlynormalAdvancedAVBrefertothatonlyafewPwaveconductstotheventricles gettingitssameclinicalsignificantasitinIII AVB FeaturesofAVB firstdegreeAVBSeenatinflammation myocarditis AMI drugs trauma fibrosis increasedvagustone etc Nosymptoms ManifestationofAVB Seconddegreetype AVBSeenathighvagaltone drugsmyocarditis AMI etc Noremarkablehemodynamicschange mayhavewildsymptomsAfewcasesmayprogressworseintosevereAVB ManifestationofAVB SeconddegreetypeIIAVBAlmosthasunderlyingheartdiseasesHRisslowandsometimesunstableThosewhoseblockinglevelisdistaltoHisbundlearepredisposedtoprogressintothirdAVBSymptomsareprominent ManifestationofAVB ThirddegreeAVBAlmosthasunderlyingheartdiseasesHRisslowandunstableThosewhoseblockinglevelisdistaltoHisbundlearepredisposedtoturnintocardiacasystoleorTDP whichcouldcauserecurrentsyncopeorAdams Stokes syndrome ManifestationofAVB ThirddegreeAVBOnauscultation intensityofS1variesduetolossofAVsynchrony cannonsound wave S3 S4canbeheardSyncope presyncope chestcompressionheartfailure etc areseenfrequently Withhighriskofsuddendeath ManagementofAVB FirstorseconddegreetypeIAVBAimforetiologyandsymptoms followupAVconductionchangingSeconddegreetype AVBAimforetiologyandsymptoms closeinvestigationofclinicalmanifestationPatientswithsymptomaticbradyarrhythmiashouldreceiveapermanentpacemaker ManagementofAVB ThirddegreeAVBThereisevidencethatpacingcanimproveprognosisinthesepatientnomattersymptomaticorasymptomatic inacutestage temporarypacemaker chronicpermanent Bundlebranchblock BBB RightBBB complete incomplete LeftBBB complete incomplete LeftanteriorfascicularblockRBBBplusLeftanteriorfascicularblockIntraventricularblock nonspecificintraventricularconductiondefect Leftposteriorfascicularblock Rightbundlebranchblock FeaturesofECGDurationofQRScomplex 0 12sVAT ventricleactivitytime atrightprecordialleads 0 07sQRScomplexinleadV1isinpatternofrSR inV5withablunt prolongedandshallowSwave withsecondaryST TchangingQRScomplexmeasuredis 0 12sisrecognizedasincompleteRBBB Lefttbundlebranchblock FeaturesofECGDurationofQRScomplex 0 12sVAT ventricleactivitytime atleftprecordialleads 0 07sQRScomplexinleadV1isinpatternofrS inV5isahigh blunt widenRwave withsecondaryST TchangingQRScomplexmeasuredis 0 12sisrecognizedasincompleteLBBB ClinicalsignificanceofBBB BBBpersehavenosignificanteffectonhemadynamicsBBBmaynotdeteriorateatlongtermfollow upinpatientswhohavenounderlyingheartdiseasesNewBBBinAMIormyocarditissignifiesclinicaldeterioration ClinicalsignificanceofBBB MostofbilateralBBBwilldevelopcompleteheartblockNoparticulartreatmentunlessthereisindicationofpacing Managementofarrhythmias MedicationNonmedicationCatheterbasedAblation electric radiofrequecy cryoablation Chemo ablation laser Programmedelectricstimulation Managementofarrhythmias NonmedicationpacemakerForbradycardiaFortachycardiaSurgicaloperationCutoff excision Foxoperation CABG etc othersDCcardioversion stimulationofvagusnerve transesophagealpacing Strategy EvaluatingriskofarrhythmiasDecidingtoTreatingitornotWhichtherapyshouldbechosenWhatistheendpointoftherapy Evaluationofrisk RecognitionofmalignantarrhythmiasVentricularflutterorfibrillationSustainedornonsustainedVTAdvancedorcompleteAVB Evaluationofrisk RecognitionofmalignantarrhythmiasAForAFLwithrapidventricleresponseVPCareMultilocal polymorphic couplet tripletandRonTSevereSSS Evaluationofrisk SeriousheartdiseasesAMI seriousmyocarditis myocardiopathy hearfailure takingdigitalisHemodynamicsunstableBloodpressuredecrease shock heartfailureorheartfailuredeteriorationwhenononsetofarrhythmias Evaluationofrisk Lifequalityisdecreased whichiscausedbyarrhythmiasSuggestworseprognosiswhenthearrhythmia Attitudeofmamagement EmergencyUrgentactivePalliative Emergencytreatment FatalarrhythmiasSustainedVT VFL VFExtremelyslowandunstablebradycardia asystolewillhappenatanytimeHemodynamicsdeteriorationorshockVT rapidAForAFL extremeand orbradycardias etc Urgentmam