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Posterior ST Elevation MI in the Setting of Right Bundle Branch Block, with Posterior Leads V7-V9

Posted Dec 05 2009 10:57am 1 Comment
This is a 68 year old man who had a resuscitated cardiac arrest. His prehospital ECG looks identical to this one which was recorded upon arrival to the ED

There is sinus rhythm with a wide QRS, with rSR' in V1 and a wide S-wave in lateral leads, consistent with right bundle branch block (RBBB). ST elevation or depression in RBBB is not difficult to find if you identify the end of the QRS. In this case, the QRS duration is about 135 ms, and in V2 and V3 there are 2 small S-waves; only after these S-waves does the ST segment begin. There is also almost 4 mm of ST depression in right precordial lead V3. Some ST depression (up to 1 mm) in the opposite direction (discordant) to the positive QRS is normal in RBBB, as in V1 here. This much ST depression (V2 and V3) is always abnormal (ischemia).

Most posterior STEMI is in conjunction with either inferior STEMI, lateral STEMI, or both. Only 3-11% of all MI are isolated posterior. In this case, there is no ST elevation elsewhere on the ECG. Marked isolated ST depression in the right precordial leads in a clinical scenario consistent with STEMI is usually posterior STEMI. Such ST depression can also (much less likely) be due to subendocardial ischemia. Two modalities that can help are: 1) recording posterior leads V7-V9 and 2) echocardiography with a posterior wall motion abnormality. In this case, both were done. The posterior ECG is shown here and was done 31 minutes later. Leads labelled V4-V6 were actually recorded on the back as leads V7-V9 (V7 at posterior axillary line, even with tip of scapula; V9 paraspinal at same level; V8 between them).

There is only one lead with ST elevation, lead V9 (labelled V6). There is approx 0.75 mm of ST elevation. Up to 0.5 mm is within normal limits, but any amount in even one lead >/= 0.5 is abnormal and very sensitive and specific for posterior STEMI (Matetzky S. et al. JACC 1998;31:506-511. Matetzky S et al. JACC 1999;34:748-753. Taha B et al. J Electrocardiol 1998;31(Suppl):178-9. Wung SF et al. Am J Cardiol 2001;87:970-974;A4.) Moreover, the QRS amplitude in V9 is tiny, and the ST elevation is very high in proportion. Similarly, there is also now a small amount of ST Elevation (< 1 mm in context of very small QRS) in aVL, suggestive of lateral STEMI.

Emergency physician performed bedside echocardiogram showed evidence of posterior wall motion abnormality and no anterior WMA. Immediate angiography showed a thrombotic occlusion of the mid circumflex, as well as disease in the RCA and LAD. Formal Echo the next day confirmed posteriorlateral WMA. Max troponin I was 12 ng/ml.

Approximately 75% of posterior STEMI will manifest at least 1 mm of anterior ST depression. (Matetzky S et al. JACC 1999;34:748-753. Wung SF et al. Am J Cardiol 2001;87:970-974;A4.)
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In the 2nd ECG the left and right arm electrodes have been transposed! Lead I has turned upside down and leads II and II have swapped places. Leads aVR and aVL have also swapped places, while aVF remains unchanged.
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