Infart ECGs
Ischemic, injury & necrosis
Phases of Evolution of an acute transmural MI
Phase 1 - importance of rapid intervention
Phase 2 - importance of rapid intervention
Ischemia
ST depression
•Upward sloping = non specific for ischemia
•Downward sloping/horizontal >1mm in 2+ leads
•Widespread ST depression may reflect reciprocal changes
T wave inversion
•1mm deep inversion in 2+ leads which have dominant R waves
•Dynamic: previously not seen on other ECGs
•Caused by delay or change in direction of repolarisation of the myocardium due to hypoxia.
•They may be abnormally tall/peaked or deeply inverted
•QT intervals may also be prolonged
Wellens syndrome
A pattern of inverted or biphasic T waves in V2-V4 highly specific for critical LAD stenosis
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Type A – biphasic (~25% of cases)
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Type B (~75% cases)
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Wellens type A
Wellens type B
De winter T wave
ST depression (can be upsloping, but >1mm)
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Peaked T waves in precordial leads
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~2% of acute LAD occlusions
Injury
ST elevation and reciprocal depression
•ST elevation is “the current of injury” an electrical manifestation of the inability of cardiac cells “injured” by severe ischemia to maintain a normal resting membrane potential in diastole
•Reciprocal ST depression reflect the myocardium directly opposite the are of ischemia
Necrosis
•Q wave development - ~50% of pts
•Usually develop ~8-12hrs after MI onset- max size ~24-48 hrs
•“window” through to opposite non infarcted wall (electrically inert)
Regional pattern changes on ECG
Anterior infarct
Acute anterior infarct
Old anterior infarct
Extensive anterior infarct
Old extensive anterior infarct
Antero-septal
Septal
Lateral
high lateral
Antero-lateral
LMCA
Inferior
Acute inferior infarct
Old inferior infarct
Posterior
RV
Arrhythmias in infarcts
Bradyarrhythmias
Sinus node dysfunction
•Atrial branch of RCA (~55% of pts)
•Proximal branch of LCx (~45% of pts)
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AV blocks
•RCA (AVN and proximal HIS)
•LAD (distal HIS)
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Bundle branch blocks
•LAD (LPF, LAF, RBB)
•RCA (LPF)
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Occurs in ~0.3% - 18% of AMI pts
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May also be vagally mediated
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May require temporary pacing
Sinus bradycardia
Wenckebach
2nd degree AV block (2:1 pattern)
sinus with CHB - junctional escape
Sinus with CHB - ventricular escape
High grade AV block - ventricular escape
AF with CHB
Tachyarrhythmias
Sinus tachycardia
•May be due to elevated sympathetic nervous activation
•May be a result of cardiogenic shock (overcompensating hypotension)
•Response to administered medications (adrenaline/atropine)
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Ventricular arrhythmias
•May require defibrillation or Amiodarone infusion
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Atrial fibrillation
•Between 6-20% of AMI
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Reperfusion Arrhythmia –accelerated idioventricular/VPBs
•Consequence of cellular humoral reactions resulting from opening of coronary artery
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Sinus tachycardia
Ventricular tachycardia
Torsades / Polymorphic VT
Ventricular fibrillation
Reperfusion arrhythmia
Reperfusion arrhythmia
