Saturday, November 27, 2021

A man in his 40s with epigastric pain and a dynamic ECG

 Case written and submitted by Dr. Arjun J V, peer reviewed by Meyers, Smith, Grauer

A 49 year male patient was brought to our ED at around 9 PM on with complaints of epigastric pain since that afternoon. The patient had the same complaints on and off for many years which would resolve on taking OTC antacids. However, this time the pain was persistent and included new diaphoresis, so he presented to an outside facility where this ECG was recorded:

What do you think?

There is sinus rhythm with a narrow QRS complex with normal axis. There is slight PR depression in III, followed by some STE with upright T wave. Lead aVL shows a negative QRS complex with a seemingly large negative T wave. Lead I also has a negative T wave. 

There is STE in the anterior leads but with reassuring large voltage QRS and reassuring morphology; to me it fits with normal variant anterior STE, not concerning for OMI. 

The question is: is this concerning for subtle inferior OMI? On on hand, the T wave in III is not definitively hyperacute, but the T wave in aVL may be fairly big for its QRS complex. We have shown many examples of this. 

At the outside hospital, the patient was given DAPT and was referred to a higher centre with Cath lab facilities. The providers were concerned for inferior OMI. The patient was hemodynamically stable but had persistent discomfort. An ECG was obtained at the receiving facility on arrival: 

What has changed compared to the first ECG? What does it mean?

Now the STE and T wave in III seem to be less elevated than before. The deep TWI in I and aVL are replaced by upright T waves. In the first ECG, aVR has a slightly upright T wave (a red flag for this condition, by the way), whereas now it is depressed.

Does it mean that the inferior OMI is starting to reperfuse? Does it mean that the high lateral area is showing pseudonormalization??


Neither of these are correct. All changes between the two ECGs are explained completely by reversal of the LA and RA electrodes on the first ECG.

Look at the differences:

 - Lead I (defined by RA negative, LA positive) is perfectly inverted between the two ECGs: in the first ECG (with lead reversal) we see qR then negative T wave. In the second ECG (with correct leads) we see rS with positive T.

 - Lead "aVL" in the first ECG is actually lead aVR, and it matches lead aVR of the second (correct leads) ECG

 - Lead "aVR" in the first ECG is actually lead aVL, and it matches aVL in the second (correct leads) ECG

 - aVR should not generally have a positive T wave if the leads are correct and the QRS is narrow and overall leftward

Below is Ken Grauer's excellent diagram showing the effects of LA/RA reversal:

Here they are side by side:

Here is the initial ECG before and after correcting the leads as per Dr. Grauer's diagram:

Unfortunately the lead reversal was not noticed by the treating team, who was still worried about OMI.

The patient’s ROS was unremarkable and POCUS did not show any RWMA. Both the ED team and Cardiology team were not completely convinced for the need for an emergent CAG but erred on the side of caution, possibly because of the following reasons:

 - Initial ECG showed perceived changes of inferior wall MI 

 - Young MIs can present with atypical changes

 - The recent & sudden death of a 45 year old male celebrity due to MI who was known to be extremely fit and health conscious. The untimely death shook the whole state to the core which witnessed an increase in the number of patients getting health check-ups[1]

Troponins were not awaited and emergent angiogram was done which was completely normal, with no evidence of CAD. No complications of the angiogram were experienced.

Labs were unremarkable. Troponin-I, Lipase & Amylase were negative.

CT abdomen showed possible changes of acute calculous cholecystitis. Patient was advised surgery but the patient did not go through with it. Patient was discharged against medical advice. Further follow up is unavailable.

Learning Points:

Lead reversal is common and can create scenarios like this one, in which a well meaning physician looking for signs of OMI can be fooled into concern for a dynamic ECG finding, leading to unnecessary concern and possibly an unnecessary angiogram. Learning the most common forms of lead reversal can help prevent this.

LA/RA reversal causes lead I to become inverted, and switches the places of leads II/III and aVL/aVR, while lead aVF remains unchanged.

When the QRS and T waves are otherwise normal, a positive QRS and/or T wave in aVR can be a red flag for lead misplacement.

Human factors and recency bias can affect patient management.




MY Comment by KEN GRAUER, MD (11/27/2021):


Lead misplacement is easy to overlook! This is because of the tendency to "assume" that routine normal placement of extremity electrode leads will automatically happen. And because it almost always does happen — we are not used to recognizing lead misplacement when it does occur. There are several additional reasons why the LA-RA lead reversal may have been missed in today's case:

  • This patient has RAD (Right Axis Deviation) on his baseline tracing — with a small amplitude QRS complex showing predominant negativity in lead I. LA-RA lead reversal is usually picked up because of the finding of "global negativity" (of the P wave, QRS and T wave) in lead I. But because of the RAD — the QRS complex in today's initial tracing was predominantly positive! (and therefore simulated a high lateral Q wave infarction with deep T wave inversion).
  • Global negativity (ie, negative P wave, QRS and T wave) is normally seen in lead aVR — because this most remote electrode lead normally views the heart's electrical activity as traveling away from its distant perspective (looking down from the right shoulder). But because of the baseline RAD — we did not see an all upright R wave as a "tip-off" to LA-RA lead reversal in lead aVR.
  • Small amplitude P wave activity in lead I on the initial tracing in today's case did not clearly suggest a negative P wave in lead I, that also would have been a "tip-off" to LA-RA lead reversal.
  • Finally — the P wave in lead II was upright, so that sinus rhythm was assumed.



The diagram Dr. Meyers credited me above, showing the effects of LA-RA lead reversal on the ECG is adapted from the LITFL ( = Life-In-The-Fast-Lane) web site — which is my "Quick GO-TO" reference for the most common types of lead misplacement. Simply put in, "LITFL lead reversal" in your on-line Search bar — and this KEY link comes up instantly!

  • LA-RA lead reversal is by far the most common technical mishap. It is usually EASY to recognize, because we are likely to see: i) Global negativity in lead I — which should never normally be seen — and which tells you there is either lead misplacement or dextrocardia; ii) The QRS in lead aVR is upright; andiii) The P wave in lead II will often be negative.
  • For another example of LA-RA Lead Reversal with more detailed discussion of this entity — CLICK HERE.


In Summary:

There are several reasons the LA-RA lead reversal was easy to overlook in today's case. The reason I immediately picked it up — is that today's initial ECG simply "looked funny" to me — because:

  • It is highly unusual to see a very wide Q wave with such disproportionately large T wave inversion in lead I (even when you have acute high lateral infarction).
  • We do not see global negativity in lead aVR (ie, the P wave is flat and the T wave is definitely positive).
  • Although positive — the P wave in lead II is smaller than the P wave in lead III (which would be unusual for normal sinus rhythm).
  • Lead aVL "looks funny" (ie, it shows "global negativity" — that is usually seen in lead aVR).
  • KEY Point: Whenever I see an ECG that "looks funny" — I verify lead placement and then immediately repeat that tracing (especially when my differential diagnosis is "Rule Out" acute MI)!



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