ECG 导联.ppt

导联的连接 I右上 左上avR正极连右上II右上 左下avL正极连左上III左上 左下avF正极连左下胸导V14肋间胸骨右V24肋间胸骨左V3V2 V4中点V45肋间左锁骨中线V5腋前线V4水平V6腋中线V4水平 Einthoven三角与六轴系统 Einthoventriangle LeadI LA RALeadII LF RALeadIII LF LALeadI LeadIII LeadII theleftarm rightarm andleftlegformtheapexesofanequilateraltriangle whiletheheart anelectricalpoint isassumedtobethecenterofthetriangle Thesidesofthetriangleareanalogoustothethreestandardlimbleadsandcalledleadaxes Transposingthethreesideofthetriangle leadI II III toacommoncentralpointofzeropotentialformsthetriaxialreferencesystemofBayley TheConceptofa Lead LeadsIIIIII RA RA LL LA LL LA LEADII LEADI LEADIII Remember theRLisalwaystheground Thehorizontalortransverseplane hexaxialfrontalplane额面六轴系统 horizontalplane 心室肥厚 High amplitudeRwaveinleftchestleads V5 V6 DeepSwaveinrightchestleads V1 V2 TallRwaveinleadV1 DeepSwaveinV5 V6 左室肥大 左室的位置及特点左后方厚于右侧ECG表现 QRS电压增高胸导 Rv5 v6 2 5mvRv5 Sv1 4 0 男 或3 5mv 女 肢导 R 1 5mvRaVL 1 2mvRaVF 2 0mvR S 2 5ml 电轴左偏 QRS时间延长0 10 0 11s 但 0 12s 以R波为主的导联可出现ST T的改变QRS电压高 同时有ST T改变 称为左室肥大合并劳损 右室肥大 特点1 3左室厚ECG改变 V1导联R S 1 V5R S 1或S波加深 重者V1为qR型 Rv1 Sv5 1 05mV avRR q或R S 1 R 0 5mv 电轴右偏 90 ST T改变 双侧心室肥大 大致正常心电图向量相抵 单侧心室肥大一侧掩盖另侧 双侧心室肥大 TheECGofbiventricularhypertrophy TallRwaveinleftchestleadsplusRightaxisdeviation TallRwaveinV1 Outline 4 IschemiaandST Tchanges5 Myocardialinfarction 4 Myocardialischemia andST Tchanges心肌缺血与ST T改变 Inferiorportionoftheheartandtherightventricle theventricularseptumandalargepartoftheleftventricularfreewall lateralwalloftheleftventricle Theocclusionofthecoronaryarteryinexperimentalcaninestudies Afterclampingcoronaryartery theinitialECGchangeswasaninversionofTwave Ischemiaisareversibleprocessunassociatedwithhistologicchanges Theclampwasleftonthecoronaryartery theischemiapatternpersistedandtheSTsegmentbecomeelevated Theclampwasnotreleasedaftertheappearanceoftheinjurystage theelevatedSTsegmentpersisted andtheRwavedisappearedandwasreplacedbyQwave 心肌缺血 myocardialischemia 心肌缺血主要影响心室复极 ST T ST T的改变起决于缺血程度 持续时间和部位 表现为缺血型和损伤型 缺血型 波改变 心内膜下缺血 波高尖机理缺血使心内膜复极更慢 心内膜向量减弱 心外膜 波向量相对增加 心外膜下心肌缺血 含透壁 波倒置冠状 波机理心外膜缺血时 外膜复极缓慢 内膜相对较早复极 故复极顺序发生变化 由内向外 故 波方向与正常相反 缺血导联记录到倒置 波 TheischemiaECG Twavechange SubendocardialischemiatallanduprightTwavewithprolongedQ Tinterval SubepicardialischemiadeeplyandsymmetricallyinvertedTwave Transmuralischemia bothsubendo andsubepicardial thesameassubepicardialischemia 缺血引起T波改变的机制 损伤性ECG ST段改变 心内膜ahorizontaldepressionoftheSTsegmentSubepicardialinjurytheSTsegmentelevation Transmuralinjury bothsubendo andsubepicardialinjury thesameasthesubepicardialinjure 损伤型表现为ST段压低或抬高 心内膜损伤 ST段压低机理轻度损伤 钾内流增加 细胞内外钾浓度差加大 细胞过度极化 静息时损伤部电位较高 T P上抬 除极后损伤与正常部位无电位差 恢复等电位线 相对地ST段压低 心外膜损伤 ST段抬高机理心肌损伤较重 细胞膜通透性增加 钾外逸 细胞内外钾浓度差减小 细胞极化不足 静息时损伤部电位较低 T P下移 除极后损伤与正常部位无电位差 恢复等电位线 相对地ST段抬高 Interpretationofinjurypattern Theinjury ST vectorpointsfromnormalareatowardtheinjuryarea SubendocardialinjuryTheSTvectorpointsfromtheepicardialtowardtheendocardialsurfacewithSTsegmentdepression SubepicardialinjuryTheSTvectorpointsfromtheendocardialtowardtheepicardiumsurfacewithSTsegmentelevation endocardium epicardium Exploringelectrode 损伤型ECG ST改变 Theacutephase STelevationsandsometimestallpositive hyperacute Twavesincertainleads ST T改变的临床意义 冠脉灌注不足心绞痛的发作 短时间ST T改变通常为压低 慢性冠脉缺血 持续性ST T改变 变异性心绞痛 ST段抬高 ST段抬高与压低相比 可能提示更为严重的缺血鉴别诊断非特异性 继发性 ST T改变原发性ST T改变 缺血 Anginapectoris心绞痛 apatientwhocomplainedofchestpainwhilebeingexamined Fiveminuteslater afterthepatientwasgivensublingualnitroglycerin theSTsegmentshaverevertedtonormal withreliefofangina theECGwithclassicortypicalanginaoftenshowsthepatternofsubendocardialischemiawithSTsegmentdepressions Anginapectoris心绞痛 ABaselinerhythmstripfromthepositiveexercisetestofapatientwithcoronaryarterydisease NoticethemarkedSTdepressionswithincreasedheartrate Variantanginapectoris变异性心绞痛 Theiranginaisatypicalbecause theyhaveSTsegmentelevations OtherconditionscanproduceST Tchanges SecondaryTwavechange myocarditis cardiomyopathy pericarditis electrolyteimbalance druguse ventricularhypertrophy bundle branchblock W P Wsyndrome etal PrimaryTwavechange characteristicECGfindingsofmyocardialischemia OtherconditionscanproduceST Tchanges STsegmentelevation usuallymostmarkedinthechestleads issometimesseenasanormalvariant Thisso calledearlyrepolarizationpatternmaybeconfusedwiththeSTsegmentelevationsofacutemyocardialinfarctionorpericarditis CharacteristicmorphologicfeaturesofsecondaryandprimaryTwavechanges Jpoint Myocardialinfarction心肌梗死 心肌梗死 myocardialinfarction 心肌梗死是冠心病的严重类型 为心肌的缺血性坏死 其发生包括缺血 损伤和坏死三个类型 在ECG上有特征性的演变过程 缺血型改变表现为T波的高尖 内膜 或倒置 外膜 机理同前损伤型改变由于损伤严重 故表现为ST段上抬机理 舒张期损伤电流学说 同前 除极波受阻学说损伤除极不完全 表面电位为正 而此时正常心肌表面电位为负 损伤部电位较高 面对损伤部的电极出现ST抬高 损伤型ECG ConvexupwardSTelevationIntransmuralAMI STchangeisthesamefindingasapuresubepicardialinjury monophasicwave PlateaushapeDomeshape Monophasicwave Interpretationofinjurypattern Systoliccurrentofinjury收缩期损伤电流 Diastoliccurrentofinjury舒张期损伤电流 TwotheoriestoexplainSTelevation 1 舒张期损伤电流学说 therestingstate diastoliccurrentofinjury Thenormalareaofcompletedpolarization Theinjuredareaofincompletepolarization Theexploringleadfacingoppositetotheinjuryvector Injurydeflectionbelowthebaseline 2 除极受阻学说 去极化 systoliccurrent Thenormalareaofcompletedepolarization Theinjuryareaofblockingofdepolarization TheSTvectorpointstotheexploringlead anelevatedSTisproduced ReciprocalSTdepressionscanappearinleadssensingthecontralateralsurfaceoftheheart Restingdepolarizationrepolarization Restingdepolarizationrepolarization Baseline Baseline 坏死型改变 MI诊断的标志abnormalQwaveanddiminishedamplitudeorabsenceoftheRwaveintheleadsfacingthenecroticorscarredmyocardium 坏死型Q波的诊断标准WidthofQwave 0 04secDepthofQwave Rwave 坏死型Q波的发生机理 infractedQwaveistheresultantvectorofbothinfractedanduninfractedmyocardium MostMIarelocatedintheLVfreewallandtheventricularseptum Theinitialvectorofmyocardialdepolarizationchanges Sequenceofdepolarizationinthenormalmyocardium Sequenceofdepolarizationininfarctedmyocardium Aninitialqwave septaldepolarization ispartofthenormalLVmorphology Resultantvectorofthefreebothventricularwall Necroticzonebecomeselectricallyinactive theresultantvectorpointsawayfromthenecroticzone q Q和QR 取决于记录电极的位置 Theexploringelectrodeisplaceddirectlyoveratransmuralinfarctedarea noRwave butQSwave Theexploringelectrodeisplacedoveranareawheretheendocardialsurfaceisinfarcted butepicardialsurfaceisnot SoaQRwaveispresent andtheamplitudeoftheRwaveissmall 直接的心表电极记录 胸导联记录 Precordialleadclosetoischemicandinjuredzone Precordialleadclosetonecrotic injuredandischemiczone 心肌梗死ECG的演变及分期 分期时间心电图表现早期 超急性期 数分ST抬高T高大无Q急性期小时 日 周T下降 倒置ST抬高 下降Q波出现近期 亚急期 数周 月ST段正常Q波T波改变陈旧期 愈合期 3 6月后ST T正常或T稍异常Q波 EvolutionofMI心肌梗死的演变 Minuteslater perisitinghoursTall peaked broadTwave STelevation Hoursordayslater perisitingweeksAbnormalQorQs STelecvation invertedT weeksmonthsAbnormalQorQS STretuningtobaseline DeeplyinvertedT 3 6monthsafterMI Qmayormaynotdisappear Tnormalorinverte OnsetofAMI Normalhyperacuteacutestagesubacute recent stageoldstage ClinicalsignificanceofevolutionofMI ThecharacteristicQ ST andTchangesofMIfrequentlydonotoccursimultaneouslyinthesameECGandshouldbefollowedbythemeansofserialtracings whichareextremelyimportantforaccuratediagnosisofAMI ProgressivechangesintheST T QRSconfigurationarethehallmarkofAMI 心肌梗死的定位 根据Q波出现的导联定位 Inferiorportionoftheheartandtherightventricle theventricularseptumandalargepartoftheleftventricularfreewall lateralwalloftheleftventricle theanteriorportionoftheleftventricle theinferiorportionoftheleftventricle Localizationofinfarction Localizationofinfarction Determinedbyrecognizingabnormalities abnormalQorQS intheleadsfacingthedamagedarea ExpressedforthediagnosisofMIthreemajorlocations anterior 前壁 inferior diaphramatic 下壁 posterior 后壁 anteriorMIfurtherdividedinto anteroseptal 前间壁 localizedanterior 前壁 anterlateral 前侧壁 extensiveanterior 广泛前壁 TheelectrocardiographiclocationsofMIdonotcorrelatepreciselywithpathologicfindings 导联前间壁前壁前侧壁高侧壁广泛前壁下壁后壁右室V1 V2 V3 V4 V5 V6 V7 V8 V9 avL aVF V3R V4R V5R V6R Localizationofanteriorinfarctions aVL AnteroseptalMI前间壁V1 3Anterior localized MI前壁V2 4AnterolateralMI前侧壁I aVL V4 6HighlateralMI高侧壁I aVLExtensiveanteriorMI广泛前壁I aVL V1 6 ECGsequencewithanteriorwallQwaveinfarction ECGsequencewithinferiorwallQwaveinfarction EvolutionofacuteanteriorwallMI EvolutionofacuteextensiveanteriorMI EvolutionofacuteinferiorMI 12Hoursafteronsetofchestpain 24Hourslater 5Dayslater MarkedlyelevatedSTinleadsII III aVF ReciprocalSTdepressioninleads I aVR aVL V1 4 facingtheundamagedareaduringtheacutephase QwaveandinvertedTwavesinII III aVF RecentinferiorMI Thispatientsustainedamyocardialinfarction1monthpreviously OldinferiorMI NoticetheprominentQwavesinleadsII III andaVFfromapatientwhohadamyocardialinfarction1yearpreviously TheST Tchangeshaveessentiallyrevertedtonormal AnteriorwallandinferiorMI NoticetheslowRwaveprogressionandQScomplexesinchestleadsV1toV5 aswellastheQSwavesinleadsII III andaVF Non Qwavemyocardialinfarction TheECGchanges STelevationordepression Twaveinverted withoutabnormalQwave ST Tevolution Non Qwaveinfarctioninapatientwhocomplainedofseverechestpain Subsequently thepatient scardiacenzymelevelswereelevated Noticethemarked diffuseSTdepressionsinleadsI II III aVL aVF andV2toV6 inconjunctionwiththeSTelevationinleadaVR Thesefindingsareconsistentwithseveresubendocardialischemia MIcomplicatedbyventricularaneurysm室壁瘤 NoticetheprominentQwavesinleadsV1toV3andaVL thepersistentSTelevationsintheseleads andthereciprocalSTdepressionsintheinferiorleads II III andaVF Thediagnosisisconfirmedbycardiaccatheterization MIwithrightbundle branchblock Twoabnormalities MIcomplicatespreexistingRBBB RBBBoccursasacomplicationofAMI Diagnosingbothabnormalitiesarenotaffected reasons 1 RBBBaffectsthemidandterminalportionsoftheQRScomplex 2 MIaffecttheinitialpartoftheQRSc