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ecg_ami

ECG diagnosis of AMI

introduction

  • ~45% of all AMI's on presentation to ED develop diagnostic ST elevation AMI, while the remainder are categorised as NSTEMI.
  • this is further compounded by the fact that most ST elevations on an ECG are not caused by AMI's.
  • a patient with acute chest pain consistent with ischaemia and with ST elevation consistent with AMI, or with new Left Bundle Branch Block (LBBB) should be immediately referred to cardiology for either urgent angioplasty or, if this is not available in a timely manner, and there are no contra-indications, early thrombolysis.
  • see Left Bundle Branch Block (LBBB) for suggestive features of AMI in patients with LBBB which may obscure the ECG diagnosis of AMI
  • Right Bundle Branch Block (RBBB) does not obscure changes of AMI.
  • “reciprocal changes” are located 180deg from the involved region

anatomic correlations

left anterior descending artery occlusions (LAD)

  • V3-4 = anterior wall
  • V1-4 = anteroseptal
  • NB. if anterior or anteroseptal + ST elevation in aVR > that in lead v1, then it may be occlusion of left main coronary artery
  • V5-6, I, and aVL = LAD distal to 1st septal perforator artery = lateral
  • V1-6, I, and aVL = proximal LAD = anteroseptal and lateral
  • V3-6, I, and aVL = LAD / LCX = anterolateral
  • II, III, aVF, I, aVL, V5-6 = LAD / LCX = inferolateral
  • V1,V2, V7-9, V5, V6, I, aVL = LAD / LCX = posterolateral

right coronary artery occlusions (RCA)

  • II, III, aVF = RCA/LCX = inferior
  • II, III, aVF, V1, V3R-6R = proximal RCA = inferior + RV
    • 25-30% of inf MI's are associated with RV infarction - check ST elevation lead III vs II and in V1!
    • ECG criteria for RV infarction:
      • presence of inf. MI, +
      • ST elevation in lead III > lead II
      • ST elevation in V1
      • ST depression in V2
      • ST elevation > 2mm in V4R
  • II, III, aVF, V1,V2, V7-9 = RCA/LCX = infero-posterior
  • V1,V2, V7-9 = RCA/LCX = posterior
    • differentiate from septal MI by R:S amplitude ratio of at least 1

occlusion of a dominant left circumflex artery

left main coronary artery occlusions (LMCA)

  • suggested in context of ischaemic chest pain, cardiogenic shock and:
    • widespread ST depression
    • ST elevation in aVR > 1 mm
    • ST elevation in aVR > V1
    • NB. the above ECG pattern may also occur in patents with rate related changes SVT, atrial flutter, and also in anaemia, hypoxia, patients with triple vessel disease, or in post VF arrest patents

typical ECG changes in ST elevation AMI

  • initial hyperacute T wave develops within 2-30 minutes but as it is usually transient is often not seen
  • ST elevation within minutes
    • ST segment changes from the usual concave state to straight then convex, however, the concave ST segment may persist in AMI
    • for ST elevation to be considered for thrombolysis or angioplasty in a patient with acute chest pain, the usual criteria is either:
      • presumed new ST elevation of 1mm or more in two or more contiguous limb leads, or,
      • presumed new ST elevation of 2mm or more in two or more contiguous precordial leads
    • subtle ST elevation changes may be easily missed, and thus repeated ECG looking for dynamic changes is important.
    • ST segment depression in V1-V4 may suggest a posterior ST elevation AMI as these leads reflect a reciprocal view of posterior aspect of the ventricle
    • reciprocal ST depression in leads opposite (aVL if inf. MI, II,III,aVF if anterior MI) those showing ST elevation further supports the diagnosis of AMI.
    • patients with inferior MI should be considered for right ECG leads to be performed to exclude an associated RV AMI which increases mortality and may mean alteration of clinical management.
  • Q wave formation may begin within 1 hour (particularly ant MI due to ischaemia of the conducting system) and be completed by 8-12hrs, although in 10%, Q waves do not develop until 3-11 days after MI.
    • abnormal Q wave criteria:
      • NB. normal people may have non-pathologic but still wide and deep Q waves in leads III, aVR and V1.
      • lead III: at least 0.04sec in duration or at least 25% the height of the accompanying R wave but width more significant than height.
      • lead aVL: at least 0.04sec in duration or at least 50% the height of the accompanying R wave.
      • lead V2: any Q wave
      • lead V3: almost any Q wave
      • lead v4: > 1mm deep or at least 0.02sec or more wide or larger than the Q wave in lead v5
      • other leads: any Q wave at least 0.03sec wide
    • Q waves occur in most patients with non-reperfused STEMI and may disappear in 15-30% after days-months post-MI.
  • stabilisation of ST segment usually within 12hrs
  • possible resolution of ST elevation and shallow T inversion forms within 72hrs
    • early resolution of ST elevation is a sign of successful re-perfusion after thrombolysis or angioplasty
  • ST elevation resolves within 2 weeks in 95% of inferior MI and 40% of anterior MI - persistence is associated with greater morbidity and may suggest development of a ventricular aneurysm.
  • T wave recovery over weeks-months

De Winter's waves

Wellen's syndrome

  • deep, prominent T wave inversion in leads V2-4 in the presence of persistent R waves
  • probably represents transient STEMI due to occlusion of the LAD that, before the ECG, spontaneously opened or received collateral flow.
  • this is associated with a high incidence of critical narrowing of the proximal LAD and thus high risk for reocclusion with recurrent STEMI and potential for sudden death.
  • these patients should be referred to cardiology urgently for angiography

inferior Wellen's syndrome

  • a similar scenario may occur with a very tight right coronary artery
  • the ECG shows upward bowing of the ST segments of the inferior leads with symmetrically inverted T waves
  • perhaps consider this next time you are looking for that S1 QIII TIII pattern of a PE

pseudo-infarction patterns

1)

hyperacute T waves

  • benign early repolarisation
    • usually concave upward slope, with steeper downward than upward stroke, tall R waves

ST elevation

  • ST elevation in aVR
  • benign early repolarisation
  • LV hypertrophy
    • ST elevation mainly V1-3 proportional with deep S waves
    • ST depression in lateral leads proportional with positive QRS
    • if ST changes out of proportion to QRS changes then consider infarct
    • see LVH
  • LV aneurysm:
    • ratio of T wave amplitude to QRS amplitude in V1-4 is low (<0.2)
    • QS or Qr waves, relatively low ST elevation, some T inversion
    • diffuse ST elevation easily confused with inf/lat MI
    • PR segment depression > 0.5mm
    • localised pericarditis may mimic AMI on ECG
  • ventricular pacing
    • unlike Left Bundle Branch Block (LBBB), all precordial leads normally have negative QR complex
    • like LBBB, ST elevation is discordant to QRS, look for pacemaker spikes
    • ST elevation and ST depression is discordant to most QRS
  • Brugada syndrome
    • ST elevation in V1-2 with RSR' pattern (ie. complete or incomplete Right Bundle Branch Block (RBBB) pattern) in young people
    • rare but important, often present as tachycardia or near syncope
    • 27% will develop VT or sudden cardiac death within 2-3 years without an implantable cardioverter-defibrillator being placed.

T wave inversion with normal QRS complex

non-pathologic
  • benign early repolarisation
    • leads V3-5, biphasic T waves, normal QTc
  • persistent juvenile T waves
    • leads V1-3 up to age 30 yrs, esp. women
  • hyperventilation
  • following SV or VT
pathologic

T wave inversion with abnormal QRS complex

ST depression with normal QRS

non-pathologic
pathologic

ST depression with abnormal QRS

abnormal Q waves

cardiac causes
non-cardiac causes
1)
Chan et al, ECG in Emergency Medicine and Acute Care. Mosby. 2005
ecg_ami.txt · Last modified: 2017/07/07 09:39 (external edit)