Wednesday, June 3, 2020

A man in his sixties with chest pain

Written by Pendell Meyers


A man in his sixties with no prior history of CAD presented with fluctuating central chest pain that started the night before presentation, then went away, then woke him up from sleep the morning of presentation. The pain was 10/10 on arrival, with SOB. Although he also had some nasal drip and sore throat, he had no cough or fevers (this occurred during peak COVID).

Here is his triage ECG:
What do you think?










Normal P-waves would have upright morphology in the inferior leads (especially lead II) and usually biphasic (up-down) morphology in V1. These p-waves are negative in almost all leads except for aVR and aVL, so the axis of the P-wave is almost directly upward. In addition, the P-wave is very close to the QRS, signifying that the atrial rhythm originates close to the AV node and creates a retrograde P-wave by going from the bottom of the atrium to the top.

Therefore this is likely an ectopic rhythm, originating from the low atrium or the junction.

There is apparent STE in II, III, aVF, and reciprocal STD in aVL.




I texted this ECG with no clinical information to Dr. Smith, and he said: 

"High junctional rhythm with retrograde P wave before QRS. This often causes false positive ST elevation in inferior leads, so I think pseudoSTEMI."

I asked for more explanation, and Dr. Smith said: "Because the atrial repolarization wave, which usually causes PR depression, will cause PR elevation when the atrium is depolarized in the opposite direction. Then because the P-wave is so close to the QRS, that PR elevation extends beyond the QRS and looks like ST elevation."


The patient went for emergent cardiac catheterization and was found to have no obstructive CAD.

Here are two repeat ECGs soon after cath:





These ECGs show resolution of the ectopic atrial rhythm, now with sinus rhythm. There is no longer any ST elevation in the inferior leads.

His chest pain subsided without further therapy.

He had a negative CXR, completely normal echocardiogram without any pericardial effusion.

Four serial troponins were undetectable.

CT pulmonary angiogram was negative for pulmonary embolism.

Covid swab was negative.

A right upper quadrant ultrasound showed mild extrahepatic biliary ductal dilatation (post cholecystecomy), and a subsequent MRCP showed mild dilation of the common bile duct and cystic duct to the level of the ampulla, favoring sphincter of Oddi dysfunction.

The patient was discharged with primary care and GI follow up.



Learning Points: 

Low atrial or junctional ectopic pacemaker presents with negative (retrograde) P-waves in the inferior leads and usually fully upright P-waves in V1.

With normal P-waves (usually upright P-waves in most leads) the atrial repolarization wave causes PR depression when it is noticeable at all (many times it is not noticeable at all, as there is low relative amount of atrial myocardium). When the atrium is depolarized in the opposite direction, as in a low atrial ectopic pacemaker, then the atrial repolarization wave would cause PR elevation. However, because the inverted ectopic P-wave is so close to the QRS, the PR elevation extends beyond the QRS and looks like ST elevation instead.


See more posts on the atrial repolarization wave: 


K. Wang Video lecture: the Atrial Repolarization Wave (Ta Wave)


Look at this ST Depression


Here is another case (Case 6-1 on p. 32 of Smith's book, The ECG in Acute MI)--link to free full text pdf.




===================================
MY Comment by KEN GRAUER, MD (6/2/2020):
===================================
This is a case that almost everyone gets fooled on the 1st time they see it. So, if you hadn’t previously encountered the Emery Phenomenon — you’ll be READY for it the next time you see a patient with this.

To illustrate this phenomenon that is explained above by Dr. Meyers — I’ve adapted Figure-1, which I’ve taken from a 2015 post on the ECG Rhythms website.
  • As suggested in Figure-1 (and explained by Dr. Meyers) — the atrial repolarization wave (ie, the T of the P wave) is always present — but with sinus rhythm, the timing of the Tp will largely coincide with the timing of the QRS complex, and therefore not be noticed on the ECG (dotted RED half circle, seen to the left in Figure-1).
  • As shown in Figure-1 — the Tp will be oppositely directed to the P wave. Therefore, with normal sinus rhythm (in which by definition, the P wave will be upright in lead II) — the TP will be negative.
  • IF the P wave in lead II is negative (as may occur with either a low atrial or junctional rhythm) — then the Tp will be upright (dotted RED half circle, seen to the right in Figure-1). If the Tp wave is large in size and upright — it may distort the end of the QRS complex, and produce the false impression of ST elevation.

KEY Points:
  • The size of the Tp wave will be proportional to the size of its P wave. A small P wave will produce a correspondingly small Tp wave. A large P wave will produce a much bigger Tp wave.
  • I preserved the same relative proportions in Figure-1 as were seen in the original version of this Figure taken from the ECG Rhythms website. Note that the PR interval for the negative P wave in Figure-1 is almost as long as the PR interval for normal sinus rhythm. But IF the PR interval for the negative P wave in lead II is much shorter (as occurs in today’s case) — then the upright Tp wave that will be seen with a low atrial rhythm will be further displaced to the right, which will produce a much greater degree of pseudo- ST-elevation!

Figure-1: Illustration of the Emery Phenomenon. (I have adapted this Figure from the 2015 post by Dr. Bojana Uzelac on Armel Carmona’s ECG Rhythms website).



For clarity — I’ve reproduced in Figure-2 the initial ECG in today’s case — and have placed the 1st post-cath tracing below it. Note the following:
  • The P wave in each of the inferior leads of ECG #1 is negative — fairly large in size — and manifests a very short PR interval. As a result — the Tp wave will be positive, and of fairly large size, and the Tp wave will be displaced to the right. As I schematically show in RED in the magnified view of lead II — this results in significant pseudo- ST elevation.
  • The P wave in lead aVL of ECG #1 is positive — surprisingly large in size (for a P wave in lead aVL) — and manifests a very short PR interval. As a result — the Tp wave in lead aVL will be negative, and of fairly large size, and it will produce reciprocal ST depression that mirrors the pseudo-ST elevation we saw in the inferior leads.
  • That the T wave in lead aVL of ECG #1 is negative is not at all unexpected — because T wave negativity is commonly seen in lead aVL when the QRS complex in this lead is predominantly negative. Confirmation that this negative T wave in lead aVL of ECG #1 was not abnormal — is forthcoming from the post-cath ECG ( = ECG #2) — which still shows T wave inversion in lead aVL, even after resolution of the pseudo- ST depression.
  • PEARL — An additional reason to suspect that ECG #1 does not reflect true inferior lead ST elevation (with reciprocal ST depression in lead aVL) — is the complete lack of any suggestion of posterior wall involvement (ie, there is no anterior lead ST depression, as is almost always present to at least some degree with true acute inferior STEMI).
  • Finally — ECG #2 (that was performed after the negative cardiac cath) — shows no abnormalities. The persistently negative T wave in lead aVL is not abnormal (as mentioned above) — since the QRS complex is predominantly negative in this lead. As I schematically show in light BLUE in the magnified view of lead II — the Tp wave is now opposite (negative) to the upright P wave in this lead. Because the PR interval is normal — this negative Tp wave will for the most part occur within the confines of the QRS complex, and therefore not be visible on the ECG.

BOTTOM Line: This 60-something man needed to be cathed — since he presented to the ED with 10/10 chest pain that awakened him from sleep, in association with the ECG findings seen in the TOP tracing of Figure-1.
  • That said, even though a patient like this may merit prompt cath for diagnostic purposes — my hope is that the next time you see an ECG like this, you’ll immediately recognize it as most likely the result of a pseudo-infarct pattern produced by the large, negative P waves with very short PR interval in each of the inferior leads.

Our THANKS to Dr. Meyers for presenting this important case!

Figure-2: The initial ECG in the ED — with the 1st post-cath tracing below it (See text).





12 comments:

  1. Great learning case on Emery phenomenon that seems to be responsible of junctional and ascendeing ST depression during exercise test when the PR interval shortens due to the fast rate and the Tp reveals itself outside the QRS complex therefore causing the STD.
    Very, very interesting case!

    Mario Parrinello

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    1. Grazie Mario. Yes, would make sense for the Emery phenomenon to contribute to rapid-upslope ST depression, that is a normal phenomenon with exercise — as opposed to flat or downsloping ST depression which is abnormal when it occurs during exercise — :)

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  2. Replies
    1. Thank you for your comment Alessandro. The ECG pattern in ECG #1 of my Figure-2 is one you WILL encounter again. While I agree that the explanation for the Emery Phenomenon IS complex — just like with a Brugada-1 ECG pattern — this is a "visual picture" that you train your eye to remember — and the NEXT time you see it, you'll remember that a big negative P wave in lead II with a short PR interval may produce a pseudo-MI pattern by making it look like there is ST elevation when in fact there isn't — :)

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  3. Another great case, a helpful explanation of the Emery phenomenon, and a reminder to begin with P waves before analyzing ST segment and T waves. If it's unclear whether the inverted P waves are responsible for the apparent ST elevation, could you discuss a couple of discrepancies in the ECG:
    1) PQ vs TP: there's debate about where to measure ST elevation from, and you teach to measure from the PQ junction instead of the TP segment. In cases like this one, where there is apparent ST elevation from the PQ junction but no ST elevation relative to the TP segment, is this discrepancy useful in highlighting the potential of a pseudo-STEMI?
    2) ST vs T wave: there seems to be straightening of inferior the ST segments, and this non-concave morphology can be seen in acute coronary occlusion, but there are no hyperacute T waves. Is the lack of hyperacute T waves helpful in cautioning against assuming that straight ST segments are ischemic?
    Thanks again for such a great blog.

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    1. THANKS so much Jesse for your kind words and your excellent questions. I’ll answer the question about whether to use the PQ (or PR) segment vs the TP segment by giving my opinion. I researched this area thoroughly before I wrote my ECG books. My impression was that the literature was not definitive — and that different experts voiced different opinions. What I have always recommended is, “It depends … “. By this I mean — that sometimes, one or the other (PR or TP segment) may be better for the tracing at hand. For example — with faster rates, the PR shortens — so the TP might be better for that tracing. Sometimes there is “baseline wander” — in which case either the PR or TP might be better. Then there is pericarditis; the Emery phenomenon; PR segment depression that may occur from either pericarditis, acute MI or as a normal variant; ST elevation from acute stemi, and so on. As a result — although I personally prefer to use the PR segment baseline when it is well defined (in such cases, I favor the PR as more accurate) — I think EITHER segment might be appropriately used — and at times, when for a given tracing the TP seems better — then I use that. And sometimes (ie, when there is artifact or baseline wander) — I may use a combination of both to help me get a better “feel” for what the true baseline is likely to be.

      As to the ST segments — I agree that the inferior ST segments ARE straightened in ECG #1 — but in the context of the Emery phenomenon, I don’t know what to make of this finding! I suspect it is a “false straightening”, also caused by the Tp from the large negative P in lead II — but I can’t be sure. Resolution of this straightening in ECG #2 supports my theory. But it is precisely because we can’t be certain about the ST-T wave in ECG #1 that I said in the Bottom Line of My Comment that cath was clearly justified in 60s man with very worrisome new-onset symptoms. The “Learning Point” — is simply to recognize that although cath IS needed in this case — I would have suspect because of the Emery phenomenon that the cath was going to be normal. THANKS again for your questions — :)

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  4. Well... this post has just made a few hundred of ECG enthusiasts yet another notch wiser,,, thank you

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    1. Thanks for the kind words. So far (in ~1 day) — over 4,000 views of this post — :)

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  5. i have again learned a lot from this case, Thank you so much!
    2 short Questions
    What do you think was the reason for der junctional rhythm in this patient. the Case record describes possible shincter oddi dysfunction. Can GI disorders like gallstones cause this disorder
    Secondly there is also STD in avL, is this also Emmery (pos p wave in avL) and how can one differentiate this from real reciprocal STD due to ischemia
    Thank you again for your great cases and comments

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    1. THANK YOU for your questions Christian. I believe I touched on your questions in detail in My Comment above. As to the rhythm — when the P wave in lead II is negative — assuming there is no lead misplacement, you are generally dealing with either a low atrial rhythm or a junctional rhythm (especially when the P wave is upright in lead aVL).

      Although many assume that if the PR interval of a negative P in lead II is short, that the rhythm is junctional — but that if it is longer that the rhythm is low atrial — that is NOT necessarily the case. Rather than “distance” of the initiating impulse from the AV node — it is SPEED of conduction that has a great effect on whether the PR interval for a neg P in lead II rhythm will have a shorter or more normal PR interval. That said — clinically, this does NOT matter that much — because if new, then an ectopic low atrial rhythm would have similar clinical implications as a slightly accelerated junctional rhythm. Neither is overly common as a new rhythm — but “sick patient” (ie, a patient in pain from an acute GI problem) could conceivably contribute (cause) such a rhythm. AND, it is of interest that normal sinus rhythm was restored on ECG #2 (in my Figure-2) after the normal cardiac catheterization — which supports your theory that “acute illness” may have caused the ectopic (low atrial or junctional) rhythm.

      Otherwise — I address your 2nd question about the ST dep in aVL in detail in my explanation to my Figure-2 above. As I state in my “Bottom Line” — although I strongly suspected that the appearance of lead aVL was not indicative of true reciprocal ST dep from acute stemi — given the case presentation (ie, 10/10 new chest pain!) in association with the limb lead appearance that we see in ECG #1 — cardiac cath WAS clearly indicated, because it was impossible to be 100% certain without cath that all ECG findings would be explained by the Emery Phenomenon + T negativity in aVL due to predominant negativity of the QRS in that lead.

      THANKS again for your interest! — :)

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