Dawn's picture

This is from a Cardiac Alert patient, with chest pain, in the Emergency Department.  The ECG shows ST elevation in the inferior leads (II, III, and aVF), and in the low lateral leads (V5 and V6).  There is reciprocal depression in V1 and V2, indicating injury in the posterior wall.  One could argue that "inferior" is just the term we use for the lower part of the posterior wall - the part that faces the floor in a standing person.  So, "inferior-posterior" reflects a more proximal occlusion of the culprit artery.

The high lateral wall is represented by I and aVL.  These leads would usually show marked reciprocal ST depression when II, III, and aVF have elevation.  However, in this ECG, aVL is depressed, but not as much as expected, and Lead I almost looks elevated!  This could represent even more extensive lateral wall involvement.  A dominant right coronary artery could be the culprit, but it seems more likely that a dominant circumflex artery is to blame, as it could perfuse the entire lateral wall before joining with the posterior descending artery and perfusing the inferior wall.  Unfortunately, we do not have the cath results on this patient.

The ST elevation in this ECG has the classic appearance of acute M.I., and will be interesting to both beginner and advanced students.

Often, one ECG can provide a wealth of teaching opportunities, no matter what the level of your students.  For the student learning to monitor the rate and rhythm, you might crop this image to only show the Lead II rhythm strip at the bottom, for a good example of normal sinus rhythm with a borderline PRI of .20 sec.   For the student learning about ST elevation M.I., this is a good example of inferior-posterior and lateral injury.  Leads aVL, V1 and V2 demonstrate reciprocal ST depression.  When an observant student notices the slight ST elevation in V6, a discussion of coronary artery distribution can occur.  

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ekgpress@mac.com's picture


As per Dawn  this ECG shows normal sinus rhythm with acute infero-postero-lateral STEMI. Although the RCA (Right Coronary Artery) is "dominant" in ~80-15% of individuals  this is one case in which my bet would be on a dominantLCx (Left Circumflex) as the "culprit"coronary artery. My reasons for this impressions are the following:
  • The amount of ST elevation in lead III is not clearly more than in lead II as is usually the case when there is acute RCA occlusion. The J-point appears to be equally elevated in these 2 leads but if anything, the T wave in lead II is more hyperacute.
  • With acute RCA occlusion there is usually marked reciprocal ST depression in lead aVL that usually looks like the "mirror image" of lead III. Instead there is relatively minimal ST depression in aVL (and not nearly enough to "mirror" the ST elevation we see in lead III). Furthermore the other high lateral lead ( = lead I) shows subtle-but-real ST elevation instead of depression. This is typical for a circumflex occlusion.
  • There is significant ST elevation in lead V6 which also goes along with a LCx occlusion.
  • There is no indirect evidence of acute RV (right ventricular) involvement. When there is acute RV infarction this will commonly counterbalance some of the ST depression seen in lead V1 from acute posterior involvement such that if ever the ST segment is either isoelectric or slightly elevated in lead V1 in a patient with acute infero-postero stemi think acute RV involvement. The LCx does not supply the right ventricle ...
NOTE: Having said all of the above  some patients "do not read the textbook"  so the final arbiter is the cath report (which we unfortunately don't have for this case).
  • For more on discussion re distinguishing between the RCA vs a dominant LCx as the "culprit artery" — Please check out my ECG Blog #80 -
  • This case is linked to my ECG Blog #103

 

Ken Grauer, MD  www.kg-ekgpress.com   [email protected] 

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