Tuesday, November 10, 2020

A 30-something Man with Chest Pain and this ECG

 

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MY Comment by KEN GRAUER, MD (11/10/2020):

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A 30-something man presented in agony holding his chest. He thought the pain was due to esophageal reflux. The patient’s initial ECG in the ED is shown in Figure-1.

  • The rhythm is sinus. There appears to be ST elevation in each of the inferior leads. (The computer interpretation said, "Marked ST elevation; Consider inferior Injury" ... ).

  • QUESTION: Would YOU activate the cath lab? 


Figure-1: The initial ECG in this case (See text).



Dr. Smith: I saw this patient when he arrived at triage, ordered the ECG — and placed the patient in a room. Then I went back to triage.  One of my partners was in the room when the ECG was recorded — and he was immediately concerned about possible inferior OMI.  He asked my opinion:

  • Dr. Smith's Thoughts: "This just does not look right.  I don't think it is OMI. There is very strange morphology — and there is no reciprocal ST depression in lead aVL. It is some sort of artifact — but I don't know what kind.  I would order serial ECGs and rule out with troponin."



The Case Continued:

Being comfortable that ECG #1 did not represent OMI, but instead had to be some type of artifact — Dr. Smith repeated the ECG 15 minutes later (Figure-2). He sent both tracings in Figure-2 to me.

  • WHAT has happened in the 15 minutes since ECG #1 was recorded?



Figure-2: Both ECGs in this case. For clarity — I’ve placed the repeat ECG (done 15 minutes after ECG #1) below the initial tracing (See text).




Ken Grauer Assessment of ECG #1: As noted above — the rhythm in ECG #1 is sinus, here with a rate of ~75-80/minute. The PR, QRS and QTc intervals are normal. The frontal plane axis is normal at about +40 degrees. There is no chamber enlargement. Regarding Q-R-S-T Changes:

  • Other than a small and narrow Q wave in lead aVL — no Q waves are seen. That said — there is a surprising amount of notching ( = fragmentation) in the QRS complex in each of the inferior leads, especially considering the young age of this patient.
  • R wave progression — is remarkable for an R=S in lead V1, with correspondingly tall R waves beginning as early as lead V2. The R wave attains 24 mm in lead V3 — which is unusual.


Regarding ST-T Wave Changes:

  • As noted — there appears to be ST elevation in each of the inferior leads. There is no reciprocal ST depression in either lead aVL or lead I.
  • In the chest leads — T waves appear somewhat peaked in leads V2-thru-V5, though they do not appear to be disproportionately tall given substantial R wave amplitude in corresponding leads. The ST-T wave in lead V1 is flat. Small U waves are seen in leads V2-thru-V6. Finally — S waves persist across the precordium.

Assessment of ECG #2 and Our Overall Impression: 

The repeat ECG that Dr. Smith ordered is the bottom tracing in Figure-2. The ST elevation that raised concern in ECG #1 is now gone. Other than resolution of the inferior lead artifact waveform — there is no significant change between ECG #1 and ECG #2.

  • When Dr. Smith first saw ECG #1 — he thought, “This looks weird. I don’t know what is causing the ST elevation in the inferior leads — but this has to be artifact."
  • I agreed. I sent both of the above tracings to 2 expert colleagues of ours who have special expertise regarding technical aspects of ECG interpretation. (I suspect both David Richley and Christopher Watford are familiar names to regular readers of Dr. Smith’s ECG Blog, and to readers of other internet ECG forums).


David Richley said the Following:

I find this tracing fascinating but ultimately, I’m afraid, unfathomable. The artifact appears to affect only leads II, III and aVF — in other words it seems to involve the Left Leg connection. The problem, whatever it is — seems to manifest mainly as an upsloping TP segment, slight ST elevation, and a descending limb of the T wave that dips below baseline level, producing a biphasic T wave.

  • Dave continued — I don’t think this is a problem with the level of high-pass filtering — because that particular problem is usually caused by a manually activated rhythm strip where real time recording prevents the operation of the 2-way filtering system that is designed to prevent low frequency distortion. This appears to be a fully automatic 12-lead recording, so this kind of distortion should not occur. If, however, the recording was obtained by manually switching between the lead sets every 2.5 seconds, and the lower frequency limit was set at 0.5 Hz — then this could explain it.
  • Alternatively, there is the potential problem of electromechanical association, in which a limb electrode is placed over a pulsatile artery. Usually, the ECG looks much more bizarre than what we see here — but I wonder if this could be a mild example of that phenomenon. A final possibility could be a technical malfunction with the ECG machine. Sorry Ken that I can’t be of more help ...


Christopher Watford said the Following:

Fascinating ECG! This looks to me like an instance of isolated artifact. I'd agree the Left Leg electrode is the source — and it even looks like this plays into the monitor's calculation of Wilson's Central Terminal for the V-leads when I layered the 2 strips on top of one another.

  • As far as cardiac pulsations — this ECG definitely manifests the regular undulations we see associated with a pulse point moving an electrode — but which artery? It isn’t often that I see a bounding pulse in a leg or ankle. If this was due to contact with a pulsating artery — I would expect the undulations to be a bit closer to the T-wave than the P-wave. Perhaps given the right body habitus and placement — it could be possible to see this sort of movement. But it is not one that I've seen before. Then again, it’s possible the patient may have had an arm lying on the cable itself, and perhaps the radial pulsations were bumping the LL cable ...
  • Christopher continued — Given the filter settings, some noise could cause a 'ringing' artifact — but I don't recall having seen this on an ECG. This is rather something that may be seen with certain types of filters (e.g. notch filters). That said — I’m not sure a 60Hz notch filter would introduce such low frequency artifact. All-in-all, a fun find! If the patient was tachycardic in the first tracing — you'd almost wonder if someone would call this atrial flutter?


SUMMARY: Between the 4 of us — we all recognized that the appearance of ST elevation in ECG #1 was a “pseudo-infarction” pattern due to some sort of artifact — though none of us had a satisfactory explanation for the cause of this artifact.



Some Additional Thoughts I Had ...

The BEST way to confirm artifact — is to identify essential components of the underlying tracing that are unaffected by what you suspect is the overlying artifact.

  • Equally helpful is to LOOK at the patient while the ECG with suspected artifact is being recorded. Observing the patient with a tremor, shaking from chills, scratching, coughing, or performing some other unanticipated activity will often be diagnostic (especially if repeat ECG after cessation of that activity yields a normal tracing).
  • Unfortunately — the patient in today's case was not observed while ECG #1 was recorded. 
  • So, I decided to STEP BACK — and take another LOOK at the initial tracing. I've labeled my thoughts from this 2nd look at ECG #1 in Figure-3:


Figure-3: I’ve labeled my thoughts regarding the artifact in ECG #1 (See text).



MY Thoughts regarding the Artifact in Figure-3: 

As noted above by David Richley — the artifact appears to affect only leads II, III and aVF. This localizes the “culprit extremity” to the Left Leg connection.

  • In My Comment, at the bottom of the page in the September 27, 2019 post in Dr. Smith’s ECG Blog — I attached the 3-page article by Rowlands & Moore, which is the BEST description I’ve seen for how to quickly determine WHICH extremity is the source of artifact. Full discussion for my rationale employed in the next 2 bullets below appears in this article by Rowlands & Moore.
  • The quick way to identify the “culprit” extremity — is to see IF the artifact is maximal in 2 of the 3 limb leads, and absent in the remaining limb lead. In ECG #1 — we see an equal amplitude of artifact in limb leads II and III — and virtually nothing in lead I. This suggests the Left Leg as the “culprit” extremity — because by Einthoven’s Triangle, this LL electrode is equally involved in electrical derivation of leads II and III. The reason lead I shows no artifact — is that the LL electrode is not used in electrical derivation of that lead.
  • That the Left Leg is the “culprit” extremity — is confirmed by recognizing that the artifactual deflection in the 3 augmented leads is most noticeable in lead aVF (on which the LL electrode is placed).


Stepping BACK to look at ECG #1 in Figure-3 from a short distance away:

  • I thought there were actually 2 similar-looking, small rounded negative “dips” that were equally spaced within each R-R interval in each of the 3 inferior leads (slanted RED lines in ECG #1). These “negative dips” are not seen elsewhere. To again borrow the words used by Dr. Smith — this just looks weird. Biphasic T waves do not have this wide of a terminal negative component — and PR interval depression is generally not expected to produce the type of rounded, negative component that we see in each of the inferior leads.
  • In rhythm strip — I’ve traced out in light BLUE the ECG waveform for several beats in the long lead II. The upward-sloping linear light BLUE line extending from the negative “dip” of the T wave until the peak of the next P wave just does not look real. As per Christopher Watford (who thought some observers might mistakenly consider a slow atrial flutter) — the initial linear upward-sloping of the ST segment (which I’ve traced out in light BLUE for a few beats) — is almost equally spaced and parallel to the linear upsloping line from the negative “dip” of the T to the peak of the next P wave.
  • BOTTOM LINE: Stepping back a little bit — the ECG appearance in the 3 inferior leads of ECG #1 does not look real. In support of this conclusion (ie, that the inferior lead ST elevation in ECG #1 is not real) are the following: i) The lack of any reciprocal ST depression in lead aVL (which virtually always shows reciprocal changes when there is inferior OMI); andii) Complete resolution of all artifact 15 minutes later when ECG #2 was obtained.


Final THOUGHTS: We need to go back to the original presenting complaint — in which this young man presented in agony to the ED (holding his chest) because of suspected esophageal reflux.

  • ECG #2 confirmed that there was no inferior lead ST elevation. T wave peaking in the chest leads looks like a repolarization variant. So, there are no acute ECG changes on either of these tracings!
  • That said — ECG #2 is still unusual for a presumably healthy young man because: i) There is a surprising amount of notching (fragmentation) in each of the inferior leads; ii) The finding of an R wave = S wave in lead V1 is not normal; andiii) There is a surprising amount of R wave amplitude in early anterior leads. Therefore — I’d consider an Echo on this young man to rule out underlying structural heart disease (that perhaps might have a role in his presenting symptoms).


LEARNING Point: If certain repetitive waveforms on an ECG look like artifact — there is a good chance that these unusual-looking repetitive waveforms are artifact. Repeating the ECG (as ordered by Dr. Smith) — resolved all doubt in this case.


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  • NOTE #1: My sincere THANKS to Christopher Watford & David Richley for their input into this case.
  • NOTE #2: For additional practice in detecting artifact — Please SEE our October 17, 2020 post in Dr. Smith’s ECG Blog.

  • NOTE To Our Readers: If anyone has further insight into the likely cause of the artifact in this case — Please WRITE US!

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4 comments:

  1. Ken and Steve and everyone...

    When I was an internal medicine resident many years ago I had a male patient who was about 40 years old present with acute, severe epigastric pain. A work up was done including a panel of abdominal labs and a 12-lead ECG. Remember: back then we only had LDH, SGOT and CPK (no MB bands) so an abdominal panel covered just about everything that pertained to the heart as well. The ECG surprised us because it really looked like he was having an acute inferior MI. However, his serum amylase was about 6,000 and alk phos was very elevated also. It turned out that he had severe gallbladder disease and no heart disease.

    Could this young man have passed a gallstone for instance and produced a similar ECG which could have resolved after the stone passed? If he had been given any NTG, that could also relieve the pain of passing a gallstone (and probably facilitate its passing). I googled several articles on gall bladder disease with ECG changes. The most common changes appeared to be STE in the inferior and sometimes inferolateral leads and there were NO reciprocal changes. All ECGs normalized as soon as the gall bladder disease was addressed or the episode ended.

    I also recall treating several patients with acute pancreatitis that had similar ECG changes (one of them I treated in the ICU because it was thought he was having an acute MI).

    I think this could be an example of a non-cardiac condition resulting to ECG changes.


    Jerry W. Jones, MD FACEP

    ReplyDelete
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    1. THANK YOU for your thoughts Jerry! (I was hoping you would comment on this tracing.) Like many (most of us) — I also remember that acute cholecystitis patient I saw in the ED, and was certain was having an acute MI … only to be totally fooled. I thought artifact distortion was the cause of the ECG changes in today’s case because of those equally spaced double negative “dips” and that unusual T-P upsloping which just looked “strange” — but this was clearly a challenging case!

      Delete
  2. i fear that i would have called the cath team. out of ignorance, i would have been concerned about the ST elevation inferiorly, the "fat " T waves there, (compared to the respective QRS complexes), and would have convinced myself that the flat T in aVL was enough to represent reciprocity.
    also, we know that "reflux" is often confused with cardiac ischemia/occlusion, especially inferiorly, i think.
    and i would have been wrong.
    thank all four of you.
    excellent blog.
    tom

    ReplyDelete
    Replies
    1. Thanks Tom! As per my reply just now to Jerry Jones — this was clearly a challenging case! Live & learn — :)

      Delete

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