ECG Blog #167 (Reciprocal-OMI-Normal)

You are “On” for interpreting a series of tracings from your local hospital. The ECG in Figure-1 was in your “pile” of tracings to interpret. No clinical information is provided.

• How would you interpret this ECG?
• Clinically — What should you do?

Figure-1: 12-Lead ECG in your “pile” of tracings to interpret. No clinical information is provided (See text).

COMMENT: Having worked in a clinical outpatient setting for 30 years, during which time I was charged with overreading all ECGs that were ordered by 35 medical providers — I am well familiar with the assignment of having a “pile” of tracings to review on patients I did not know, and about whom little or no clinical information was provided on the tracing.

• As is “usual” in such cases — the clinician who ordered the ECG will have already examined the patient and interpreted the ECG. But written documentation of HOW they interpreted the ECG usually would not appear on the tracing given to me for review.
• The TASK of the OVER-READER: To determine if there is anything important on the ECG that may have been overlooked — and to follow-up on this as appropriate. With time always at a premium — one obviously must be selective in deciding which tracings mandate follow-up ...

Descriptive Analysis of the ECG in Figure-1: There is a fairly regular sinus rhythm at ~85/minute. Overall voltage is reduced in both the limb and chest leads (although criteria for “low voltage” are not technically reached — since QRS amplitude in at least one of the limb leads [lead I] is >5 mm).

• Intervals — The PR interval is normal (ie, not more than a large box in duration). The QRS is narrow. The QTc is probably at the upper limits of normal.
• Axis — The mean QRS axis is normal (about +15 degrees).
• Chamber Enlargement — None.

Looking next at Q-R-S-T Changes:

• Q Waves — A definite Q wave is seen in lead III. Given tiny amplitude of the R wave in this lead — this is a large Q wave in lead III. I believe a tiny q wave is also seen in lead aVF (though this is admittedly difficult to discern given how tiny the QRS complex is in this lead).
• R Wave Progression — Transition is slightly delayed in the chest leads (ie, the R wave does not become taller than the S wave is deep until between V4-to-V5).

Regarding ST-T Wave Changes: 
Because of the small amplitude of the QRS complex in all limb leads (especially in lead aVF) — ST-T wave deviations are correspondingly small. As a result — assessment of ST-T wave deviation must be considered in proportion to QRS amplitude in the lead being assessed!

• There is ST elevation in each of the inferior leads! Relative to the R wave — the amount of ST elevation in lead III is more than 50% of R wave height, and 100% of R wave height in lead aVF! In addition — there is beginning T wave inversion in both of these leads, and probably also in lead II. As noted previously — there is a large Q in III, and a small-but-present q in aVF.
• There is mirror-image (reciprocal) ST depression in lead aVL when one compares this to the SHAPE of the ST elevation in lead III. This mirror-image relationship is best appreciated in Figure-2, in which I have superimposed the mirror-image of lead III (in GREEN) to the right of upright lead aVL (in RED). I’ve superimposed the mirror-image of lead aVL below upright lead III. 
• PEARL: There is an almost "magic" mirror-image relationship between leads III and aVL in many (if not, almost all) cases of acute inferior MI.
• Otherwise — there are some non-specific ST-T wave changes in the chest leads (ie, relative flattening of the T wave in most chest leads), and perhaps slight ST coving (but not elevation) of the ST segment in leads V4, V5 and V6. That said, there is really no anterior ST depression.

Figure-2: Blow-up of the 6 limb leads from Figure-1. Mirror-image blow-ups of leads III and aVL have been added (See text).

Clinical Impression / Clinical Notes on the ECG in Figure-1:

The ECG in Figure-1 is virtually diagnostic of recent, if not acute inferior MI. The presence of ST elevation in each of the inferior leads — in association with mirror-image ST depression in lead aVL — tells us to assume acute MI is ongoing until proven otherwise.

• As suggested above — given tiny QRS amplitude in the limb leads, the relative amount of ST elevation in the inferior leads is considerable!
• The Q wave in lead III is large! That said, it has been shown that even “large” Q waves may form within the first 1-2 hours of acute MI — so definitive information regarding the “age” of this MI is not forthcoming based on the size of the inferior Q waves seen here.
• There is beginning T wave inversion in the inferior leads. This suggests that this acute MI may not have just happened (ie, within the past 1-to-a-few hours) — though, on the other hand, this MI could be quite recent, because depth of these inferior T waves is minimal.
• Persistence of reciprocal ( = mirror-image) ST depression in lead aVL that is as deep as the ST elevation in lead III is tall (as we see in Figure-2) — is usually an acute finding.
• Most cases of acute inferior MI are associated with acute posterior involvement. However, none of the anterior ST depression usually associated with acute posterior involvement is seen here.

BOTTOM LINE: Clinical correlation is impossible without some history. That said, the ECG in Figure-1 is diagnostic of inferior MI, that could be quite recent in what may be an ongoing process.

• NOTE: The most likely “culprit artery” is the RCA (Right Coronary Artery) because: i) 80-90% of patients have a dominant right circulation, in which the RCA provides the primary blood supply to the inferior wall of the left ventricle; ii) The presence of more ST elevation in lead III than lead II (as is seen here) suggests the RCA rather than the LCx (Left Circumflex) as the “culprit” artery; and, iii) The presence of marked reciprocal ST depression in lead aVL also suggests the RCA (rather than the LCx) as the culprit artery. (For more on determining the likely “culprit" artery — See ECG Blog #80).

WHAT To Do in this Case? Unfortunately — NO historical information has been provided. By far, the BEST way to judge probable “age” of an acute MI is by correlating the history to ECG findings.

• As the clinician assigned to overread this ECG — the 1st thing I would do is immediately find the chart on this patient to see what was going on clinically. If the chart could not be quickly found, or if information on the chart was incomplete — I would call the medical care provider. We simply need to find out some History on this patient.
• IF the medical provider was not available — I’d call the patient.
• BOTTOM Line: IF the history in this case was at all suggestive of recent onset of symptoms — then acute intervention (ideally by cardiac catheterization with angioplasty as appropriate) would be indicated.

Follow-up of this Case:

• It turned out that this patient was seen for symptoms. Unfortunately, the possibility of an MI that was ongoing was not recognized. The patient died before referral was made ...

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Acknowledgment: This case was sent to me from Malaysia.

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