Monday, April 22, 2019

A 40 yo with Chest pain. Only ECG abnormality is minimal ST depression in I and aVL (computer interpretation: normal)

A former resident sent this.

He asked: "Hey Steve, Wanted to get your thoughts on this EKG:"
What do you think?
The computer called it a normal ECG

Algorithm unknown

Aside: [There is some "sinus arrhythmia", which is indeed a normal finding.  Sinus arrhythmia is sinus rhythm whose rate varies with respiration.  If the longest P-P interval is 120 ms greater than the shortest, it is sinus arrhythmia.  In this case, the longest P-P interval is 1020ms, and the shortest is 740 ms, for a difference of 280 ms.]

Here was my response: "Leads I and aVL bother me (some ST depression), but the rest of it looks totally normal."

He then went on to say: "40-something with chest pain for one hour.  Had episode of nausea and dizziness when it started.  Burning pain subxiphoid and into throat."

Sounds like reflux, right?

But ST depression in I and aVL is abnormal.  It does not usually represent subendocardial ischemia, but rather it is usually reciprocal ST depression, reciprocal to inferior ST elevation.  There is no ST elevation in inferior leads, but it may just be too early to manifest.

So he obtained a second ECG 40 minutes later:
Now there is new STE in inferior leads and much more obvious ST depression in I and aVL.
Still does not meet STEMI criteria, but it is an obvious OMI

And then another one became more obvious:

Cath lab was activated and a 100% RCA occlusion was found.

Learning Points:

1. Beware ST depression in I and aVL.  It may be the first sign of inferior ST elevation.

2. Also beware isolated T-wave inversion in aVL.  This also may be a soft sign of acute inferior MI, before ST elevation.  (But remember that a negative T-wave in aVL is only "inverted" if the QRST angle is wide; in other words, if the QRS is negative, then a negative T-wave has much less significance.  This is also true in lead III.)

Comment by KEN GRAUER, MD (4/22/2019):
I liked this case — because it provides unique insight on recognition of a subtle abnormality. It also provides me a forum to reflect on when Q waves, ST depression and T wave inversion may be unassociated with pathology.
  • For clarity — I’ve reproduced the first 2 ECGs that were done in this case in Figure-1. It should be noted that the initial ECG is angled — though this does not impair interpretation.
Figure-1: The first 2 ECGs shown in this case (See text).
BEFORE Knowing the History:
We were shown ECG #before being told the history. My interpretation was similar to that of Dr. Smith: There is a fairly marked sinus arrhythmia — there is slightly early transition in the chest leads (lead V3 abruptly becoming all positive) — there are small and narrow q waves in the inferior leads, and in the lateral chest leads — and, there is very subtle but definitely not normal ST segment straightening and slight ST depression in leads I and aVL. Other than nondiagnostic reduced T wave amplitude in leads III and aVF — I saw nothing else that was clearly abnormal.
  • I interpreted the ST-T wave abnormalities in leads I and aVL as nonspecific” — with the KEY point being that these findings are present in both of the high lateral leads ( = leads I and aVL).
  • Regarding the small waves — these are most probably not abnormal. It is common and normal to see small and narrow q waves in one or more of the 5 lateral leads (I, aVL; V4, V5, V6) — that simply reflect normal left-to-right septal activation. It is also common and normal to see small septal q waves in 2 or 3 of the inferior leads in patients with a relatively vertical axis (which is estimated to be between +75-80 degrees in Figure-1).
  • BOTTOM Line — Clinical Correlation is needed for interpretation: iIF a prior ECG on this patient was available — It might tell us if these ST-T wave changes are new or old; iiIF the patient was without cardiac-sounding chest pain — then the above findings might reflect any of the many potential causes of nonspecific ST-T wave abnormalities; iiiST segment flattening and/or slight ST segment depression (especially in leads like lead I and aVL that do not usually show ST depression) — may be a sign of chronic or acute cardiac ischemia; and, ivIF this patient was having new-onset chest pain — then acute cardiac ischemia moves to #on our list of differential possibilities! As per Dr. Smith — it could be early in the course of an acute cardiac event, such that other leads aren’t yet showing definite abnormality.
At this point — We were told that the patient did have new-onset chest pain  and, “the Answer” was then forthcoming 40 minutes later once the 2nd ECG was obtained (Figure-1):
  • I find it instructive whenever possible to practice Lead-by-Lead Comparison of serial tracings — especially in cases like this, in which an acute cardiac event is evolving in front of our eyes!
  • First — Note that there is virtually NO change in frontal plane axis between ECG #1 and ECG #2 — and NO change is seen in R wave progression (or in QRS morphology) as we move across the chest leads. This is important to note — because it tells us that any difference in QRST morphology that we might see between ECG #1 and ECG #2 is a real change, and not due to an axis shift or lead malposition!
  • Second — It is interesting to note that the heart rate is faster and much more regular in ECG #2. As noted by Dr. Smith — the marked sinus arrhythmia that we saw in ECG #1 of this 40-something patient was not necessarily an abnormal rhythm. That said, I’ll speculate ( = purely academic to satisfy my intellectual curiosity) — by commenting that sinus arrhythmia in a younger adult often reflects increased vagal tone — and perhaps (I wasn’t there …) the patient was now having increased symptoms at the time ECG #2 was obtained, leading to a relative increase in sympathetic tone (with as a result, a faster and more regular heart rate).
  • Other than lead aVR — all of the limb leads have shown similar evolution in ECG #2. That is — each of the inferior leads (II, III, aVF) now clearly shows ST elevation — with reciprocal ST depression in both of the high lateral leads (ie, leads I and aVL). It should be apparent that the “magical” reciprocal (ie, mirror-image) relationship between leads III and aVL is now evident. So despite lack of meaningful evolution in the chest leads (I don’t think the slight decrease in T wave amplitude in lead V2 of ECG #2 is clinically meaningful) — the evolution we see between ECG #1 and ECG #2 in this patient with new-onset chest pain is diagnostic of acute OMIregardless whether or not numeric criteria for a STEMI have been satisfied.
Figure-2: On Q waves and T wave inversion ... (See text).
WHEN may Waves and Wave Inversion be Normal?
I’ve excerpted the illustration and text in Figure-2 from HERE. I’ll emphasize that the generalities stated here may not pertain early on in the process in a patient with a worrisome history of new-onset chest pain.
  • There are many potential causes of ST-T wave abnormalities (ie, LV “strain” from LVH; medication effect; electrolyte disturbance; pulmonary embolus, etc.). The generalities stated here for predicting ischemia are much more likely to apply when other factors are minimal.
  • Because 2 of the 3 inferior leads (leads III and aVF) may normally manifest even large Q waves and/or deep T wave inversion — the 3rd inferior lead ( = lead II) exerts an important role in decision-making. Thus, it becomes more likely that inferior ST-T wave changes and Q waves of at least moderate size are significant when such changes are seen in all 3 inferior leads. It is less likely that such changes are significant when they are not seen in lead II.
  • Isolated T wave inversion in lead III, lead aVF and/or in lead aVL is less likely to be ischemic when the QRS complex in the same lead is predominantly negative. This is because the T wave axis often follows relatively close behind the QRS axis. That said, even when the QRS is predominantly positive — shallow T wave inversion in one of these leads is not necessarily ischemic.
  • BOTTOM Line: No criteria for LVH are met in ECG #1 — so LVH is not a confounding factor. The principal ST-T wave abnormality in this tracing is ST segment straightening and slight ST depression in leads I and aVL. Although isolated T wave inversion in lead aVL would not necessarily be abnormal (especially given the predominantly negative QRS complex in this lead) — there should not be ST flattening with ST depression in both of these high lateral leads. Given the history of new-onset chest pain — this ECG finding is ischemic until proven otherwise. The evolution seen in ECG #2 confirmed our suspicion.


  1. I see his rate picked up a little bit on the second then dropped markedly by the third. Sinus arrhythmia is gone by then too. Why?

    1. Hard to say. Sometimes when patients show up in the emergency dept they have been walking, running etc. and heart rates are often faster on arrival than after the patient has lain in bed for a while. Also, inferior MI can cause sinus bradycardia.

  2. ST is also depresses in lead I in this Pt indicating the ST vector is pointing down and shifted to the patient's right. Why to the right?, because the right ventricle is also involved. ST elevation in V1 also supports RV involvement. One can predict the thrombus is in the proximal RCA before the RV branch takes off. Why is it important whether the RV is involved or not? If the BP is around 80 and if RV is involved, the BP can considerably improve with fluid alone.
    So, I always pay attention to Lead I in inferior STEMI.
    K. Wang.


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