39 year old male CC: "Sick" – Discussion (Pericarditis)

Here’s the conclusion to 39 year old male CC: “Sick”

Let’s take another look at the 12-lead ECG.

Several findings in this case point toward pericarditis.

In the first place, the patient is feeling unwell and has a temperature of 100.2 F, the chest pain is “sharp” in quality and is reproducible with deep inspiration so it’s atypical for coronary ischemia.

Secondly, the constellation of ST-elevation (or at least J-point elevation) is unusual. For example, you can see J-point elevation in lead I and also leads II and aVF which are reciprocal leads.

It’s not impossible for a STEMI to have ST-elevation in leads I and II (see this case from Dr. Smith’s ECG Blog) but you will notice that the computer incorrectly reads the ECG as pericarditis!


Here are the last few tips to help you identify pericarditis. In the above image which shows a single cardiac cycle in lead II, you can see (A.) PR-segment depression, (B.) a “notched” J-point, and (C.) upwardly concave ST-segment elevation (if in fact the ST-segment is really elevated in comparison to the TP segment).

An easy way to remember the difference between “upwardly concave” and “upwardly convex” (or non-concave in the case of a straight ST-segment which is also bad) is that and “upwardly concave” ST-segment looks like a smiley face (good) and “upwardly convex” looks like a frowny face (bad).

It’s important to remember that acute STEMI can, and often does, present with upwardly concave ST-segments, so the mere fact that the ST-segments are upwardly concave does not mean it’s not a STEMI.

It’s one piece of the puzzle.

So what happened to the patient? Here’s what Matt from Mass had to say.

“Follow-up with the ER nurse a week later revealed a diagnosis of pericarditis with an unremarkable clinical course after intravenous antibiotics. Etiology of the infection was not determined.

In addition, patient was referred for outpatient cardiologist evaluation for possible Wolff-Parkinson-White syndrome.”

One of the really cool things about Web 2.0 and social media is “peer sourcing”. Since I too thought that lead V3 looked very suspicious (meaning that it looks like a delta wave is present even though the PR interval is not short) I forwarded the ECG to Mark P. from the Electrophysiology Fellow blog.

He sometimes leaves comments on my case studies which I always appreciate very much!

Here’s what he had to say.

“It is very unlikely to be WPW:

  • the ‘deltas’ in in the mid praecordial leads, in the absence of deltas elsewhere, do not fit the usual patterns of preexcitation
  • the septal q waves in V5 and V6 suggest that conduction to the septum is first i.e. the normal pattern, rather than preexcitation of the ventricle elsewhere (see reference here)
  • it is not unusual to see a little slurring in some leads as appears in V3

On the other hand he has a number of interesting features:

  • ST depression in aVR, the most specific ECG marker for pericarditis
  • ‘early repolarisation’ in an infero-lateral pattern; once considered a normal finding, now known to be associated with SCD (although this is weak marker for sudden cardiac death; useful in populations, practically useless for predicting an individual’s risk)

This case did make we wonder about the differential diagnosis for a slurred beginning to the QRS in precordial leads. Obviously WPW and the other preexcitation syndromes, HCM (read recently about one lab’s experience with patients referred with HCM for suspected preexcitation and not a single patient had an accessory pathway), presumably LVH, and intramyocardial conduction delay of whatever cause, and electrolyte abnormalities.”

Pretty cool, huh? Thanks, Mark!

By the way, you can follow Mark the EP Fellow on Twitter here: @epfellow


  • Christopher says:

    I thought it was PR-elevation rather than depression in aVR that was the most specific?

  • Christopher says:

    Scratch that, I read the note from Mark wrong (thought I saw PR-depression). So, sidenote: you can have PR-elevation in aVR in pericarditis.

  • Tom B says:

    I misread it too, Christopher! I’m glad you corrected your correction because I thought it was a misprint and changed elevation to depression (and now back to elevation). See how much I trust you? HAHAHA! 🙂

  • Ches R says:

    Look at the comments I made in the original post. I mentioned all this as the criteria for pericarditis, just stated it sooner 🙂

  • Christopher says:

    Tom, Brandon O can chime in about the importance of reliability when you trust someone 🙂

    The other interesting thing about this case, for me, was the normocardic rate coupled with the clinical presentation and ECG changes. My mind says I’d be more likely to see tachycardia with the fever, sharp chest pain, and then the ECG changes.

  • Tom B says:

    Well done, Ches R!

  • Brandon O says:

    Ha, thanks Christopher.

    The back and forth is a little befuddling — in my reading the current version (“ST depression in aVR, the most specific ECG marker for pericarditis”) is correct, although I wasn’t aware of the “most specific” part. In my understanding, these general findings coupled with ST ELEVATION in aVR would make me scared about LCA occlusion, not pericarditis, although how specific THAT is depends on who you ask.

    But high fives all around to the Greek chorus who nailed this one pretty well. I like how we even caught that odd delta wave (and NYCMedic could still be right about the LVH!).

    If Mark’s reading, or anyone else has wisdom, I’m curious about two of his remarks:

    — early repol as risk factor for sudden death. Any references on this?
    — delta waves caused by “intramyocardial conduction delay” — what sort of thing does this refer to?

  • Ches R says:

    Definitely recommend 12-lead ECG: the Art of Interpretation by Garcia. I’d recommend Dr. Steve Smith’s ECG book but it is our of print, crossing my fingers that it will come back to print though.

  • Tom B says:

    You and me both, Ches R! Either way I’m getting myself a copy. I’m also a fan of Garcia and Holtz (and Chou).

  • VinceD says:

    Here’s the article on cardiac arrest associated with early repolarization. http://www.nejm.org/doi/full/10.1056/NEJMoa071968

    At this point there’s nowhere near strong enough evidence to warrant further workup in everyone with evidence of early-repole, but it’s an interesting finding and perhaps sometimes in the future someone will work out a criteria for high-risk features.

  • VinceD says:

    Here’s the article on cardiac arrest associated with early repolarization. hxxp://www.nejm.org/doi/full/10.1056/NEJMoa071968
    (switch out http for hxxp in the address, comments won’t post with links in them)

    At this point there’s nowhere near strong enough evidence to warrant further workup in everyone with evidence of early-repole, but it’s an interesting finding and perhaps sometimes in the future someone will work out a criteria for high-risk features.

  • Brandon O says:

    Thanks Vince! I think I bumped into that once but never got around to reading it. Interesting stuff for sure, although I’m not sure I’d characterize those patterns as typical “BER” per se.

  • Tracy says:


  • Tracy says:


  • NICE POST Tom! – with LOTS of neat teaching points.

    The history is highly suggestive of acute pericarditis. Given this history – to me the ECG is virtually diagnostic. Clearly one can’t rule out some underlying component of ERP (Early Repolarization Pattern) – esp. without benefit of a baseline ECG … and given J-point notching in multiple leads . – but I see upward concavity ST elevation in virtually all leads except the 3 “right-sided” ones (ie, leads III, aVR and V1) – and that is highly typical for Stage I acute pericarditis.

    Supporting the diagnosis of acute pericarditis are: i) Lead I ST segment looking like lead II (vs leads II and III looking similar as is usual for acute inf. MI); ii) PR depression in a number of leads (subtle but real); iii) PR elevation in lead aVR (hard to say how much of what we see in aVR is ST depression vs PR elevation vs some combination thereof); iv) no more than small q waves (which are common as a baseline); and v) lack of any reciprocal ST depression.

    The concept of “smiley-shaped” ST elevation (which I popularized in my textbooks several decades ago) is worthy of mention. It’s a GREAT visual aid – but you may want to describe upward concavity or ST coving (downward convexity) to your consulting cardiologist (rather than “smiley” or “frowny”) so as to enhance your credibility. But “smiley” vs “frowny” ST segments works as a great descriptor among colleagues.

    Great teaching points about WPW! – and how the normal septal q waves makes this unlikely despite lead V3’s appearance. In general – one should see delta waves in more than just a single lead. That said – I’ll add 2 points: i) You CAN have WPW with a normal PR (ie, you have baseline 1st degree before you hook into the AP [accessory pathway] connection); and ii) The ECG of a patient with accessory pathways is not always “fixed” – but instead you may have all AP conduction (yielding consistent delta waves) – all normal conducted (‘concealed AP’) – or conduction down normal and/or AP alternating with varying relative degree of conduction down one pathway or the other.

    Finally – Why the IV antibiotics for an “unknown infection”? Acute pericarditis is most often viral – as the patient would be a whole LOT sicker if this was acute bacterial pericarditis … I understand the treating physicians may have wanted to “cover things” – and we may not know the full story – but I’m skeptical about the indication for antibiotics that may cloud the issue given presumptive acute viral pericarditis …

    BOTTOM LINE: Great case Tom! Thanks for posting – : )

3 Trackbacks

Leave a Reply

Your email address will not be published. Required fields are marked *