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MyocardialInfarctionECGpedia

MyocardialInfarction
Contents[hide]
1RiskassessmentofCardiovasculardisease
2Riskassessmentofischemia

Author(s)

I.A.C.vanderBilt,MD

Moderator

I.A.C.vanderBilt,MD

Supervisor
somenotesaboutauthorship

3Diagnosisofmyocardialinfarction
4Thelocationoftheinfarct
5DevelopmentoftheECGduringpersistentischemia
6SubendendocardialIschemia
7References
8ExternalLinks

Ischemiaoccurswhenpartoftheheartmuscle,themyocardium,isdeprivedofoxygenand
nutrients.Commoncausesofischemiaare:
Narrowingorobstructionofacoronaryartery.
Arapidarrhythmia,causinganimbalanceinsupplyanddemandforenergy.
Ashortperiodofischemiacausesreversibleeffects:Theheartcellswillbeabletorecover.When
theepisodeofischemialastsforalongerperiodoftime,heartmusclecellsdie.Thisiscalled
aheartattackormyocardialinfarction.Thatiswhyitiscriticaltorecognizeischemiaonthe
ECGinanearlystage.
SevereischemiaresultsinECGchangeswithinminutes.Whiletheischemialasts,severalECG
changeswilloccuranddisappearagain.Therefore,itmaybedifficulttoestimatethedurationof
theischemiaontheECG,whichiscrucialforadequatetreatment.
Signsandsymptomsofmyocardialischemia:
Crushingpainonthechest(anginapectoris),behindthesternum,oftenradiatingtothelower
jawortheleftarm
Fearofdying
Nausea
Shock(manifestingaspaleness,lowbloodpressure,fastweakpulse)shock
Rhythmdisturbances(inparticular,increasingprevalenceofventricularectopia,ventricular
tachycardia,AVblock)

RiskassessmentofCardiovasculardisease
Narrowingofthecoronaryartery,leadingtoamyocardialinfarction,usuallydevelopsoverseveral
years.Anincreasedriskofcardiovasculardisease,whichmayleadtoamyocardialinfarctionor
cerebrovascularaccident,canbeestimatedusingSCOREsystem whichisdevelopedbythe
EuropeanSocietyofcardiology(ESC).Asshowninthefigure,themostimportantriskfactorsfor
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myocardialinfarctionare:
Malesex
Smoking
Hypertension
DiabetesMellitus
Hypercholesterolemia

Riskassessmentofischemia
Anexercisetestsuchasabicycleortreadmilltest,maybeusefulindetectingmyocardialischemiaafter
exercise.[1]Insuchatest,continuousECGmonitoringisperformedduringexercise.TheSTsegment,
bloodpressureandclinicalstatusofthepatient(i.e.chestcomplaints)aremonitoredduringandafter
thetest.
Anexercisetestispositiveformyocardialischemiawhenthefollowingcriteriaaremet:
HorizontalordownslopingSTdepressionof>1mm,60or80msaftertheJpoint
STelevationof>1.0mm

Diagnosisofmyocardialinfarction
Thediagnosisofacutemyocardialinfarctionisnot
onlybasedontheECG.Amyocardialinfarctionis
definedas:[2]
Elevatedbloodlevelsofcardiacenzymes
(CKMBorTroponinT)AND
Oneofthefollowingcriteriaaremet:
Thepatienthastypicalcomplaints,
TheECGshowsSTelevationordepression.
pathologicalQwavesdevelopontheECG
Acoronaryinterventionhadbeenperformed
(suchasstentplacement)
Sodetectionofelevatedserumcardiacenzymesis
moreimportantthanECGchanges.However,the
cardiacenzymescanonlybedetectedintheserum
57hoursaftertheonsetofthemyocardial

STelevationismeasuredatthejunctionalorJ
point

infarction.So,especiallyinthefirstfewhoursafter
themyocardialinfarction,theECGcanbecrucial.
ECGManifestationsofAcuteMyocardialIschaemia(inAbsenceofLVHandLBBB)are[3]:
STelevation
NewSTelevationattheJpointintwocontiguousleadswiththecutoffpoints:0.2mVinmenor
0.15mVinwomeninleadsV2V3and/or0.1mVinotherleads.
STdepressionandTwavechanges.
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NewhorizontalordownslopingSTdepression>0.05mVintwocontiguousleadsand/orT
inversion0.1mVintwocontiguousleadswithprominentRwaveorR/Sratio1
AstudyusingMRItodiagnosemyocardialinfarctionhasshownthatmoreemphasisonSTsegment
depressioncouldgreatlyimprovetheyieldoftheECGinthediagnosisofmyocardialinfarction
(sensitivityincreasefrom50%to84%).[4]
Myocardialinfarctiondiagnosisinleftorrightbundlebranchblockcanbedifficult,butitisexplainedin
theseseperatechapters:
MIdiagnosisinleftbundlebranchblockorpacedrhytm
MIDiagnosisinRBBB

Thelocationoftheinfarct
Theheartmuscleitselfisverylimitedinits

capacitytoextractoxygeninthebloodthatis
beingpumped.Onlytheinnerlayers(the
endocardium)profitfromthisoxygenrichblood.
Theouterlayersoftheheart(theepicardium)
aredependentonthecoronaryarteriesforthe
supplyofoxygenandnutrients.Withaidofan
ECG,theoccludedcoronarycanbeidentified.
Thisisvaluableinformationfortheclinician,
becausetreatmentandcomplicationsoffor
instanceananteriorwallinfarctionisdifferent
thanthoseofaninferiorwallinfarction.The
anteriorwallperformsthemainpumpfunction,
anddecayofthefunctionofthiswallwillleadto
decreaseofbloodpressure,increaseof

Anoverviewofthe

Overviewoftheseparate

coronaryarteries.LM=

ECGleads.Thelead

'LeftMain'=mainstem

withSTsegment

LAD='LeftAnterior

elevation'highlights'the

Descending'arteryRCX

infarct.Aninfarctionof

=RamusCircumflexus

theinferiorwallwillresult

RCA='RightCoronary

inSTsegmentelevation

Artery'.

inleadsII,IIIandAVF.A

heartrate,shockandonalongerterm:heart

lateralwallinfarctresults

failure.Aninferiorwallinfarctionisoften

inSTsegmentelevation

accompaniedwithadecreaseinheartrate

inleadsIandAVL.An

becauseofinvolvementofthesinusnode.

Anteriorwallinfarct

Longtermeffectsofaninferiorwallinfarctionare

resultsinSTsegment

usuallylessseverethanthoseofananteriorwall

elevationinthe

infarction.

precordialleads.

Theheartissuppliedofoxygenandnutrientsby
therightandleftcoronaryarteries.Theleft
coronaryartery(theLeftMainorLM)divides
itselfintheleftanteriordescendingartery
(LAD)andtheramuscircumflexus(RCX).
Therightcoronaryartery(RCA)connectsto
theramusdescendensposterior(RDP).With
20%ofthenormalpopulationtheRDPis
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suppliedbytheRCX.Thiscalledleft

dominance.
Belowyoucanfindseveraldifferenttypesof
myocardialinfarcation.Clickonthespecific
infarctlocationtoseeexamples.

Thecolouredfigure

TheSTsegment

showscontiguousleads

elevationpointsatthe

inmatchingcolors

infarctlocation.Inferior
MI=STsegment
elevationinredregions
(leadII,IIIandAVF).
LateralMI=STelevation
inblueleads(leadI,
AVL,V5V6).AnterioMI:
STsegmentelevationin
yellowregion(V1V4).
Leftmainstenosis:ST
elevationingrayarea
(AVR)

Thecoronaryblockade
cancauseconduction
block,onAVnodal,His
orbundlebranchlevel.

Helpwiththelocalisationofamyocardialinfarct
localisation
AnteriorMI

STelevation

ReciprocalSTdepression

coronary
artery

V1V6
V1V4,disappearanceof
septumQinleadsV5,V6

None

LateralMI

I,aVL,V5,V6

II,III,aVF

InferiorMI

II,III,aVF

I,aVL

PosteriorMI

V7,V8,V9

highRinV1V3withSTdepression
V1V3>2mm(mirrorview)

RCX

Right
VentricleMI

V1,V4R

I,aVL

RCA

SeptalMI

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none

LAD
LADseptal
branches
LCXorMO
RCA(80%)or
RCX(20%)

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AtrialMI

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PTainI,V5,V6

PTainI,II,orIII

RCA

Thelocalisationoftheocclusioncanbeadequatelyvisualizedusingacoronaryangiogram(CAG).On
theCAGreport,theplaceoftheocclusionisoftengradedwithanumber(forexampleLAD(7))using
theclassificationoftheAmericanHeartAssociation.[5]

DevelopmentoftheECGduringpersistentischemia
Thecardiomyocytesinthesubendocardiallayers
areespecciallyvulnerableforadecreased
perfusion.Subendocardialischemiamanifestsas
STdepressionandisusuallyreversible.Ina
myocardialinfarctiontransmural
ischemiadevelops.

TheevolutionofaninfarctontheECG.ST
elevation,Qwaveformation,Twaveinversion,
normalisationwithapersistentQwave

Inthefirsthoursanddaysaftertheonsetofa
myocardialinfarction,severalchangescanbe
observedontheECG.First,largepeakedT
waves(orhyperacuteTwaves),thenSTelevation,
thennegativeTwavesandfinallypathologicQ
wavesdevelop.
Wellenssyndromeorsign(seeimage)canbean
earlyECGwarningsignofcriticalanteriorischemia
beforethedevelopmentofovertmocardial
infarction.
ApathologicalQwave

Wellenssyndrome:symmetricalnegativeTwave
inprecordialleadswithoutRlossofRwavescan
regularlybeobservedinearlyanteriorischemia.Many
patientswithWellenssyndrome/signturnouttohave
acriticalproximalLADstenosis[6].

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TypicalnegativeTwavespostanteriormyocardial
infarction.ThispatientalsoshowsQTcprolongation.
Whetherthishasaneffectonprognosisisdebated.[7]
[8][9]

EvolutionoftheECGduringamyocardialinfarct
Timefrom
onsetof
symptoms
minutes

ECG
hyperacuteTwaves(tallTwaves),STelevation

Changesintheheart
reversibleischemicdamage
onsetofmyocardial
necrosis

hours

STelevation,withterminalnegativeTwaves,
negativeTwaves(thesecanlastfordaystomonths)

scarformation

days

PathologicQWaves

SubendendocardialIschemia
Subendocardialischemiaisischemiathatisnottransmural.Itismostlycausedbydemandischemia
whereenergysupplytocardiomyocytesisinsufficientfortheworkforce,e.g.duringextreme
hypertension,aorticvalvestenosis,extremeleftventricularhypertension,anemia,atrialfibrillationwith
rapidventricularresponse.OntheECGoftendiffuseSTdepressionispresent.Cardiacenzymes(CK
MB,Troponine)mayormaynotbeelevateddependingontheseverity.

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Anexampleofsubendocardialischemiawith
diffuseSTdepression

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