ST depression limited to Inferior leads is reciprocal to high lateral wall and represents STEMI

When there is inferior ST depression, one is tempted to diagnose "inferior ischemia". However (paradoxically and mysteriously) there is no correlation between location of subendocardial ischemia on the ECG and the location of the ischemia in the heart. When there is subendocardial ischemia, the ST depression tends to be diffuse.

So what does "inferior" ST depression represent? It is reciprocal to high ST elevation until proven otherwise.

Here is the EKG of a 50 year old man with epigastric discomfort:


Notice the very subtle ST depression in III and aVF. aVF (circled) has 0.5 mm of ST depression in the context of a 1 mm QRS (ST depression should be considered with proportionality in mind). Lead III also shows ST depression. These should be interpreted as reciprocal to aVL, the opposite lead. As in this case, the reciprocal ST depression is often much more evident than the ST elevation in aVL, which is only 0.5 mm in the context of a 5 mm R-wave. This inferior ST depression is most likely to be due to poor flow in the diagonal or circumflex arteries.

This was interpreted as normal, but it is not normal. This is very subtle and easily missed, but the prepared mind can see it.

The patient was sent home. He suffered a cardiac arrest and was resuscitated, underwent therapeutic hypothermia for coma, and had his occluded circumflex opened with PCI. He had a prolonged but nearly complete recovery and is able to go back to work part time.

If there is high suspicion for ischemia, do serial EKGs and pay attention to them!

Case 1)
This is the initial EKG of a 60 yo male with a couple days of stuttering chest pain. He is pain free at the time of the EKG at 2100.

At 2140, the patient had recurrent pain, and the following EKG was recorded:

If seen alone, this EKG would not look terribly abnormal. But compared to 40 minutes prior, there is ST elevation now where there was none before, and the T-waves are much taller.

This was not appreciated by the treating physician. Even with no change in the EKG, the patient should have at least been admitted for observation. Unfortunately, the patient was discharged and suffered significant loss of the anterior wall.

Case 2)
This is the initial ECG of another 60 yo man with chest pain that is now resolved.

There is left bundle branch block (LBBB) without any ST segment shift that would be suggestive of acute coronary occlusion (of LBBB with STEMI). Such shifts would be 1) concordant (same direction as QRS) ST elevation in inferior or lateral leads 2) concordant ST depression in leads V1-V3 (where the QRS is negative, ST depression would be concordant and this would be posterior STEMI) or 3) excessive ST elevation in leads with a negative QRS; excessive is greater than or equal to 20% of the preceding S-wave. This EKG has some T-waves that are suspicious for NSTEMI: in the presence of an upright QRS, these are positive T-waves in II and V6 and also biphasically positive (terminal portion upright) in I and aVL. T-waves, like the ST segment, should be opposite the QRS in LBBB without ischemia.

The patient was admitted to the CCU and had recurrent chest pain. The following ECG was recorded:

Now there is definite ST elevation, concordant with the QRS, in lead V5. There is also excessively discordant ST elevation in lead V2 (=25% the depth of the preceding S-wave). More importantly, these are all changes from the initial ECG. The patient's cardiologist did not see this change and the anterior wall was lost.