ECG in Acute Myocardial ECG in Acute Myocardial infarctioninfarction

& & culprit artery localisationculprit artery localisation

Dr.Nagaraj MoorthyDr.Nagaraj Moorthy

SJICSJIC

04-04-0804-04-08

IntroductionIntroduction

► The ECG is considered an essential part of the diagnosis and initial evaluation of patients with chest pain.

► The information that can be obtained from the admission ECG in patients with STEMI,

► (1) prediction of infarct size, (2) estimation of prognosis, and (3) Various electrocardiographic patterns and the

localisation of the infarct and the underlying coronary anatomy.

► ECG without extra costs or time

IntroductionIntroduction ► The ECG remains a crucial tool in the identification and The ECG remains a crucial tool in the identification and

management of AMI.management of AMI.► A detailed analysis of patterns influence decisions A detailed analysis of patterns influence decisions

regarding the use of reperfusion therapy. regarding the use of reperfusion therapy. ► Early and accurate identification of the IRA on the ECG Early and accurate identification of the IRA on the ECG

can help predict the amount of myocardium at risk.can help predict the amount of myocardium at risk.► ECG signs of reperfusion represent an important ECG signs of reperfusion represent an important

marker of microvascular blood flow and consequent marker of microvascular blood flow and consequent prognosis. prognosis.

► Crucial for identifying new conduction abnormalities Crucial for identifying new conduction abnormalities and arrhythmias that influence both short- and long-and arrhythmias that influence both short- and long-term outcome.term outcome.

ECG changes in AMIECG changes in AMI

► In the early stages of AMI the ECG may be normal

► <50% of patients with AMI have clear diagnostic changes on their first trace.

► About 10% of patients with a proved acute myocardial infarction fail to develop ST segment elevation or depression.

► In most cases, however, serial ECG’s show evolving changes that tend to follow well recognised patterns.

ECG manifestations of AMIECG manifestations of AMI

ST Elevation:ST Elevation:

New ST elevation at the J-point in two contiguous New ST elevation at the J-point in two contiguous leads with the cut-off points:leads with the cut-off points:

≥ ≥ 0.2 mV in men0.2 mV in men

≥ ≥ 0.15 mV in women in leads V0.15 mV in women in leads V22-V-V33

and /orand /or

≥ ≥ 0.1 mV in 0.1 mV in other leadsother leads► sensitivity of 56% and a specificity of 94%.

► The addition of multiple QRST variables (Q waves, ST depression, T wave inversion, bundle branch block, axes deviations, and LVH) increased specificity.

ECG changes associated with Prior ECG changes associated with Prior MIMI

Any Any Ǫ wave in leads VǪ wave in leads V22-V-V3 3 ≥0.02 s or QS ≥0.02 s or QS complex in leads Vcomplex in leads V22-V-V33

Ǫ wave ≥ 0.03 s and ≥ 0.1 mV deep or QS Ǫ wave ≥ 0.03 s and ≥ 0.1 mV deep or QS complex in leads I , II, aVL, aVF or Vcomplex in leads I , II, aVL, aVF or V44 – V – V66

in any two contiguous leadsin any two contiguous leads

R-wave ≥ 0.04 s in VR-wave ≥ 0.04 s in V11-V-V22 & R/S ≥ 1 with a & R/S ≥ 1 with a concordant positive T-wave in the absence concordant positive T-wave in the absence of a conduction defect. of a conduction defect.

Re infarction by ECGRe infarction by ECG

ST elevation of ST elevation of ≥ 0.1 mV re-occurs in a ≥ 0.1 mV re-occurs in a

patient having a lesser degree of ST patient having a lesser degree of ST

elevation or new pathological elevation or new pathological

Q waves in at least two contiguous leads,Q waves in at least two contiguous leads,

particularly when associated with ischemicparticularly when associated with ischemic

symptoms.symptoms.

AMI-Early Hyperacute PhaseAMI-Early Hyperacute Phase

► Increased VATIncreased VAT► amplitude of R wareamplitude of R ware► Straightening of the normal upward Straightening of the normal upward

concavityconcavity► ST – T merge not to separateST – T merge not to separate► T remains upright,amplitude increases, T remains upright,amplitude increases,

widenswidens

Hyperacute T waves

Grading of ischemia-Grading of ischemia-Sclarrovsky Sclarrovsky BirnbaumBirnbaum

Reciprocal and Indicative Reciprocal and Indicative ChangesChanges

Early repolarisation patternEarly repolarisation pattern

PericarditisPericarditis

L V aneurysmL V aneurysm

Hypertrophic cardiomyopathyHypertrophic cardiomyopathy

Reciprocal ST segment depression

Chronic Stable MIChronic Stable MI

Resolution of changes in ST segment

and T waves

RVMIRVMI

Posterior wall MIPosterior wall MI

Ischemia and Ischemia and InfarctionInfarction

► ST segment depressionST segment depression may identify ischemia but non-localizingmay identify ischemia but non-localizing► ST segment elevationST segment elevation identifies epicardial injury – localizingidentifies epicardial injury – localizing► T wave inversionT wave inversion not good for identifying ischemia not good for identifying ischemia

(nonspecific) but highly localizing if injury (nonspecific) but highly localizing if injury presentpresent

►Q wavesQ waves good for diagnosis of MI and highly localizinggood for diagnosis of MI and highly localizing

Transmural and subendocardial Transmural and subendocardial MIMI

Q-MI does not always Q-MI does not always correlate with correlate with transmural MItransmural MI

Non-Q-MI does not always Non-Q-MI does not always correlate with correlate with subendocardial subendocardial

MIMI

Q-wave Myocardial Infarction (1)Q-wave Myocardial Infarction (1)

►Genesis of Q waveGenesis of Q wave Death cells => loss of electrical Death cells => loss of electrical

forces => redirection of electrical forces => redirection of electrical forces from that area, it occurs forces from that area, it occurs during initial 0.04-.06 sec of QRS => during initial 0.04-.06 sec of QRS => Q wave in leads overlying infarction Q wave in leads overlying infarction

Small amount of death issue => Small amount of death issue => reduce the magnitude of normal reduce the magnitude of normal mean force => reduction of R wave mean force => reduction of R wave voltagevoltage

Sampling through electrically “silent” area into the cavity.

In the cavity, all initial wavefronts aredirected away Q wave

Transmural Injury

Q wave

Q-wave Myocardial Infarction (2)Q-wave Myocardial Infarction (2)

► Q wave criteria:Q wave criteria: 0.04 sec wide0.04 sec wide 25% of the height of R wave in a given lead25% of the height of R wave in a given lead

► Exceptions:Exceptions: Q wave is confined to lead IIIQ wave is confined to lead III Q wave is confined to lead aVL and there Q wave is confined to lead aVL and there

are no other ECG abnormalities are no other ECG abnormalities

Regions of the MyocardiumRegions of the Myocardium

InferiorII, III, aVF

LateralI, AVL, V5-V6

Anterior / SeptalV1-V4

Posterior wall MIPosterior wall MI

►Difficult to diagnose Difficult to diagnose by Surface ECGby Surface ECG

►Manifested by ST Manifested by ST segment depression segment depression and upright T waves and upright T waves in V1 and V2 ( Just in V1 and V2 ( Just opposite to MI)opposite to MI)

► Posterior leads my Posterior leads my show ST segment show ST segment elevation elevation

Posterior Myocardial Posterior Myocardial InfarctionInfarction

recent or probably acuterecent or probably acute

► Initial R wave in V1 and V2 Initial R wave in V1 and V2 > > 0.04 sec 0.04 sec with:with: R>S R>S and and ST depression with upright ST depression with upright

T wavesT waves usually in setting of acute inferior MIusually in setting of acute inferior MI RVH, WPW and RBBB interfere with RVH, WPW and RBBB interfere with

diagnosis of posterior MIdiagnosis of posterior MI

RVMIRVMI

►Right leads show ST segment Right leads show ST segment elevation( V3 and V4)elevation( V3 and V4)

► ST elevation in V1 in presence of ST elevation in V1 in presence of IWMI, suspect RVMIIWMI, suspect RVMI

►ST segment elevation in V1 > V2 in ST segment elevation in V1 > V2 in AWMI, suspect RVMIAWMI, suspect RVMI

► In presence of IWMI, ST elevation in In presence of IWMI, ST elevation in lead III>II suspect RVMIlead III>II suspect RVMI

Localisation of culprit vessel in Localisation of culprit vessel in AMIAMI

► CAG identifies vessel anatomy whereas the ECG reflects

the physiology of the myocardium during acute

ischaemia.

► It is possible to observe restored vessel patency upon

angiography with ECG evidence of ongoing ischaemia

due to “no-reflow”, reperfusion injury, or myocardial

damage that has already developed before reperfusion

occurs.

► While CAG remains the “gold standard” for identifying

the infarct related artery, the ECG remains the gold

standard for identifying the presence and location of

acute myocardial ischaemia.

Coronary Artery CirculationCoronary Artery Circulation

Coronary Artery CirculationCoronary Artery Circulation

Right Coronary ArteryRight Coronary Artery► right atriumright atrium► right ventricleright ventricle► inferior wall of left inferior wall of left

ventricleventricle► posterior wall of left posterior wall of left

ventricleventricle► 1/3 interventricular 1/3 interventricular

septumseptum

Coronary Artery CirculationCoronary Artery Circulation

Left Anterior Left Anterior Descending ArteryDescending Artery

► antero-lateral surface antero-lateral surface of left ventricleof left ventricle

► 2/3 interventricular 2/3 interventricular septumseptum

Circumflex ArteryCircumflex Artery► left atriumleft atrium► lateral surface of left lateral surface of left

ventricleventricle

Lesions in LADLesions in LAD

D1

S1D1

Proximal LADProximal LAD

TerminologyTerminology

►Proximal LAD – origin to S1Proximal LAD – origin to S1►Mid LAD – S1- S2Mid LAD – S1- S2►Distal LAD – Beyond S2Distal LAD – Beyond S2

Proximal LAD before S1Proximal LAD before S1

►ST ↑ in lead aVRST ↑ in lead aVR►Complete RBBBComplete RBBB►ST ↑ in V1 > 2.5 mmST ↑ in V1 > 2.5 mm►ST ↓ in V5ST ↓ in V5►ST ↓ in lead II, lead III > 1mmST ↓ in lead II, lead III > 1mm►ST ↓ in lead aVF > 2 mmST ↓ in lead aVF > 2 mm

Proximal to D1Proximal to D1

Proximal to D1Proximal to D1

►Lateral wallLateral wall►Q in aVLQ in aVL►ST ↓ in lead II, lead III, lead aVF > ST ↓ in lead II, lead III, lead aVF >

1mm1mm

Distal LADDistal LAD

Distal to D1Distal to D1

►ST ↓ in aVLST ↓ in aVL►Absence of ST ↓ in lead II, lead III ,aVFAbsence of ST ↓ in lead II, lead III ,aVF

Localisation in IWMILocalisation in IWMI

Right coronary arteryRight coronary artery

►Lead 3 ST elevation > Lead 2 ST elevationLead 3 ST elevation > Lead 2 ST elevation►AV nodal block AV nodal block

►ST-segment vector is directed toward the ST-segment vector is directed toward the right (lead III). right (lead III).

►ST-segment elevation in lead V1 -proximal ST-segment elevation in lead V1 -proximal occlusion of RCA with associated RVMIocclusion of RCA with associated RVMI

Left circumflex arteryLeft circumflex artery

► Lead 2 ST elevation > lead 3 ST elevationLead 2 ST elevation > lead 3 ST elevation

► ST-segment vector directed toward the left ST-segment vector directed toward the left (lead II). (lead II).

► There is an isoelectric or elevated ST There is an isoelectric or elevated ST segment in lead aVL segment in lead aVL

► Zimetbaum PJ, Josephson ME. Use of the Zimetbaum PJ, Josephson ME. Use of the electrocardiogram electrocardiogram inin acute myocardial infarction. acute myocardial infarction. N Engl J Med 2003;348:933-940N Engl J Med 2003;348:933-940

Value RV4Value RV4

AMI with LBBBAMI with LBBB

►LBBB can obscure the LBBB can obscure the electrocardiographic diagnosis of AMI. electrocardiographic diagnosis of AMI.

LBBB with MILBBB with MI

Sgarbossa’s criteriaSgarbossa’s criteria

► Sgarbossa et al NEJM 1996, 334: 481Sgarbossa et al NEJM 1996, 334: 481► Ecg diagnosis of evolving AMI in the presence of Ecg diagnosis of evolving AMI in the presence of

LBBBLBBB

LBBB with AMILBBB with AMI

WELLEN’S SYNDROMEWELLEN’S SYNDROME

► Clinical UA with:Clinical UA with: Inverted Inverted or or biphasicbiphasic T-waves in V2 and V3 T-waves in V2 and V3 T wave changes may also be present in V1, V4-V6T wave changes may also be present in V1, V4-V6 Changes appear when Changes appear when pain freepain free Little to no ST changeLittle to no ST change No loss of precordial R wavesNo loss of precordial R waves No pathologic Q wavesNo pathologic Q waves

► Concern:Concern: Highly specific for LAD lesionsHighly specific for LAD lesions At risk for extensive AMI or sudden deathAt risk for extensive AMI or sudden death

WELLEN’S SYNDROMEWELLEN’S SYNDROME

WELLEN’S SYNDROMEWELLEN’S SYNDROME

? RVMI? RVMI

?RVMI?RVMI

Localisation of culprit vesselLocalisation of culprit vessel

► Identification of the IRA is excellentIdentification of the IRA is excellent► The specificity of the ECG in AMI is limited The specificity of the ECG in AMI is limited by large individual variations in coronary by large individual variations in coronary

anatomyanatomyby the presence of preexisting coronary artery by the presence of preexisting coronary artery

disease, disease, ► collateral circulation, collateral circulation, ► previous CABG.LBBB,Pre-exitation,V pacing previous CABG.LBBB,Pre-exitation,V pacing ► The ECG is also limited by its inadequate The ECG is also limited by its inadequate

representation of the posterior, lateral, and representation of the posterior, lateral, and apical walls of the left ventricle. apical walls of the left ventricle.

FACTORS THAT DETERMINE PROGNOSISIN ACUTE MYOCARDIAL INFARCTION

►The immediate prognosis in patients with AMI is inversely related to the amount of myocardial reserves.(ischaemic area at risk),

ESTIMATION OF THE SIZE OF THE ISCHAEMIC

MYOCARDIUM AT RISK►ST elevation scoreST elevation score►Sclarovsky-BirnbaumSclarovsky-Birnbaum►Aldrich score:Aldrich score:► % of myocardium at risk=3[0.6(# ST elevation % of myocardium at risk=3[0.6(# ST elevation

II,III,aVF)+2]II,III,aVF)+2]

► % of myocardium at risk=3[1.5(#leads with of ST % of myocardium at risk=3[1.5(#leads with of ST elevation)-0.4]elevation)-0.4]

ESTIMATION OF THE SIZE OF THE ISCHAEMICMYOCARDIUM AT RISK

► 2D echo,ventriculography2D echo,ventriculography► ECG:ECG:► Aldrich et al studied patients with AMI who did not receive

thrombolytic therapy.The best correlation between the final ECG Selvester QRS scoring system(an estimation of infarct size) and the admission ECG was found using the magnitude of ST elevation in leads II, III, and aVF in IWMI and the number of leads with ST elevation in AWMI.

► However,in patients who received reperfusion therapy there was only week correlation between the Aldrich score and either the ischaemic area at risk or final infarct size, as measured by pretreatment and predischarge technetium 99m (99mTc) sestamibi

► Clemmensen et al reported a good correlationbetween the final Selvester score and the number of leads with ST elevation (r=0.70) in anterior myocardial infarction.

► Clements et al also reported only a weak correlation between myocardial area at risk (as assessed by 99mTc sestamibi scan) and either the number of leads with ST deviation, total ST deviation, total ST elevation, or total ST depression.The myocardial area at risk correlated modestly (r=0.58) with total ST deviation in anterior myocardial infarction, and with total ST depression normalised to the R wave (r=0.70) in inferior myocardial infarction.

►LimitationsLimitations:: ►12-lead ECG does not equally represent all

myocardial regions. ► Ischaemia in opposed regions may attenuate

or augment ST deviation►Many variables such as width of the chest

wall, the distance of the electrode from the ischaemic zone, the myocardial mass, and presence of “ischaemic preconditioning” and collateral circulation have a major influence.

ECG Predictors of ReperfusionECG Predictors of Reperfusion

► The presence of normal epicardial blood flow does The presence of normal epicardial blood flow does not always correlate with microvascular perfusion not always correlate with microvascular perfusion of the myocardial tissue.of the myocardial tissue.

► The absence of tissue perfusion is the most potent The absence of tissue perfusion is the most potent predictor of impaired ventricular function and the predictor of impaired ventricular function and the risk of death after myocardial infarction.risk of death after myocardial infarction.

► Resolution of ST-segment elevation-excellent Resolution of ST-segment elevation-excellent marker of reperfusion, marker of reperfusion,

► ST-segment resolution is also useful for guiding ST-segment resolution is also useful for guiding reperfusion therapy.reperfusion therapy.

► A reduction in ST-segment elevation by more than A reduction in ST-segment elevation by more than 70 percent in the leads with maximal elevation is 70 percent in the leads with maximal elevation is associated with the most favorable outcomes.associated with the most favorable outcomes.

►Other ECG markers of reperfusion include Other ECG markers of reperfusion include T-T-wave inversion within four hourswave inversion within four hours after after myocardial infarction. myocardial infarction.

► An An accelerated idioventricular rhythmaccelerated idioventricular rhythm is a is a highly specific marker of reperfusion.highly specific marker of reperfusion.

► This rhythm is benign and should not be This rhythm is benign and should not be suppressed with medication. Isolated suppressed with medication. Isolated ventricular premature depolarizations may ventricular premature depolarizations may also be seen with reperfusion. also be seen with reperfusion.

► Polymorphic VT and VF may be seen with Polymorphic VT and VF may be seen with reperfusion but are rare and should raise the reperfusion but are rare and should raise the suspicion of ongoing arterial occlusion. suspicion of ongoing arterial occlusion.

Arrhythmias and Conduction Disease in Arrhythmias and Conduction Disease in AMIAMI

►Conduction abnormalities AMI Conduction abnormalities AMI associated with a poor prognosis associated with a poor prognosis

Inferior Myocardial InfarctionInferior Myocardial Infarction

► Can occur immediately or hours or days after MI Sinus Can occur immediately or hours or days after MI Sinus bradycardia or varying degrees of atrioventricular block bradycardia or varying degrees of atrioventricular block including CHB can occur within the first two hours after including CHB can occur within the first two hours after an AIWMI as a result of heightened vagal tone.an AIWMI as a result of heightened vagal tone.

► The AVN is the site of conduction disturbances in AIWMIThe AVN is the site of conduction disturbances in AIWMI► CHB is generally associated with a narrow complex CHB is generally associated with a narrow complex

escape rhythm of between 40 and 60 beats per minute .escape rhythm of between 40 and 60 beats per minute .► Usually asymptomatic but may be associated with Usually asymptomatic but may be associated with

hemodynamic instability due to loss of atrioventricular hemodynamic instability due to loss of atrioventricular synchrony. synchrony.

► Generally transient and resolves within five to seven Generally transient and resolves within five to seven days but may persist for up to two weeks.days but may persist for up to two weeks.

Anterior Myocardial InfarctionAnterior Myocardial Infarction

► Due to necrosis of the intramyocardial conduction Due to necrosis of the intramyocardial conduction

system. system.

► Occurs almost exclusively in the presence of proximal Occurs almost exclusively in the presence of proximal

occlusion of the LAD and septal necrosis. occlusion of the LAD and septal necrosis.

► Second-degree atrioventricular block with AWMI is Second-degree atrioventricular block with AWMI is

usually Mobitz type II block secondary to block in the usually Mobitz type II block secondary to block in the

His–Purkinje system.His–Purkinje system.

► CHB results from extensive necrosis of the IVS. It CHB results from extensive necrosis of the IVS. It

usually occurs abruptly during the first 24 hours after usually occurs abruptly during the first 24 hours after

myocardial infarction.myocardial infarction.

►The development of bifascicular block The development of bifascicular block with anteroseptal infarction is with anteroseptal infarction is associated with as much as a 30 associated with as much as a 30 percent excess risk of complete heart percent excess risk of complete heart block. block.

►The mortality associated with CHB in The mortality associated with CHB in AWMI, with or without preceding right AWMI, with or without preceding right bundle-branch block and left fascicular bundle-branch block and left fascicular block, may be as high as 80 percent. block, may be as high as 80 percent.

Post MI Risk StratificationPost MI Risk StratificationRole of ElectrocardiogramRole of Electrocardiogram

At The Time of PresentationAt The Time of Presentation

► Predictors of size of MIPredictors of size of MI Presence of Q waves with ST elevationPresence of Q waves with ST elevation Number of leads with ST ElevationNumber of leads with ST Elevation Sum of ST Elevation in 12 leadsSum of ST Elevation in 12 leads ST elevation in V4 with Inferior MIST elevation in V4 with Inferior MI Abnormal R in V1 (R/S>1) with inferior MIAbnormal R in V1 (R/S>1) with inferior MI Conduction disturbancesConduction disturbances

► Predictors of in hospital mortalityPredictors of in hospital mortality Anterior location of MIAnterior location of MI ST elevation in anterior and inferior leadsST elevation in anterior and inferior leads Evidence of earlier remote MIEvidence of earlier remote MI Marked ventricular ectopic activityMarked ventricular ectopic activity

Conclusion Conclusion

► 12 lead ECG is of great value in Diagnosis of AMI12 lead ECG is of great value in Diagnosis of AMI

1.1. Site of occlusion of culprit arterySite of occlusion of culprit artery

2.2. Decision regarding reperfusionDecision regarding reperfusion

3.3. Recognising reperfusionRecognising reperfusion

4.4. Recognising RV involvementRecognising RV involvement

5.5. Identify risk of conduction blockIdentify risk of conduction block

6.6. Risk stratificationRisk stratification

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clinics.2006:24clinics.2006:24► Robert roberts,prognosis after myocardial infarction,cardiology Robert roberts,prognosis after myocardial infarction,cardiology

clinics.1984:2clinics.1984:2► SS Barold,Advanced 12 lead electrocardiogram,cardiology SS Barold,Advanced 12 lead electrocardiogram,cardiology

clinics.1987:5clinics.1987:5► Francis Morris, William J Brady, ABC of clinical electrocardiography► Acute myocardial infarction—Part I, BMJ VOLUME 324 6 APRIL

2002► Peter J. Zimetbaum, Mark E. Josephson, Use of the Peter J. Zimetbaum, Mark E. Josephson, Use of the

Electrocardiogram in Acute Myocardial Infarction.nejm,2003: Electrocardiogram in Acute Myocardial Infarction.nejm,2003: 348:933-940 348:933-940

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