You Diagnose Pericarditis at your Peril (at the Patient’s Peril!)

The source of this case is anonymous.

A 40 something woman with a history of hyperlipidemia and additional risk factors including a smoking history presented with substernal chest pain radiating to "both axilla" as well as the upper back.  She was reportedly "pacing in her room while holding her chest".

The initial tracing (EKG 1) was obtained.
Clinician and EKG machine read of acute pericarditis.
What do you think?

There is sinus rhythm.  There is diffuse ST elevation in II, III, aVF and V3-V6.  One might agree with the computer and the clinician because there is inferolateral ST elevation without any reciprocal ST depression.  While it is true that inferior MI has ST depression in aVL 99% of the time (Bischof and Smith), and that inferolateral ST elevation is the most common distribution for pericarditis, the ST elevation in V3 has "terminal QRS distortion (TQRSD)," (diagnostic of LAD occlusion)

Paper published: Terminal QRS distortion not found in any ECG of Early Repolarization

TQRSD is defined as the absence of BOTH an S-wave and a J-wave in leads V2 or V3.  While I have shown that early repolarization never has this feature which is common to LAD occlusion, no one has ever studied it in pericarditis.  I strongly suspect that pericarditis does not have this feature, and would never assume that it might.  When I see this feature, the ECG represents LAD occlusion until proven otherwise.

First, this is so clearly an LAD occlusion that I would simply activate the cath lab.  However, if you were prevented from doing that, then an emergent contrast echo is indicated.  If there is no wall motion abnormality, then you can be confident that it is not an LAD occlusion.

Why is there diffuse ST elevation (also in inferior leads?).  This is almost certainly due to a type 3 ("wraparound") LAD that supplies the inferior wall.

How about the use of the LAD occlusion formula?  

This formula was developed comparing early repol to LAD occlusion, so it may not apply when the DDx is pericarditis vs. LAD occlusion.    

1. Forget about diagnosing pericarditis here; it is too rare and it is too dangerous to diagnose it in lieu of MI.  

2.  Much of what is called pericarditis is really early repolarization.  
See this case, written by Pendell Meyers when he was a student: 

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

3.  TQRSD is a sign of obvious LAD occlusion.  These cases were excluded from the study that derived and validated the formulas, and so you should not rely on the formula when there is TQRSD.  Just diagnose LAD occlusion!

Nevertheless, here are the values if you use the formula:

QTc = 431, STE60V3 = 2 mm, RAV4 = 5 mm, QRSV2 = 5 mm
3-variable: 26.2 (greater than 23.4 is LAD occlusion)
4-variable: 22.4 (greater than 18.2 is LAD occlusion)

Clinical course 

Later, the first troponin I returned at 2.67 ng/mL (quite elevated).  

Comment: If you are still somehow convinced that this ECG represents pericarditis, then you must at least change your diagnosis to myo- pericarditis (because the elevated troponin shows myocyte necrosis).  But in patients with ST elevation due to myocarditis, there will be a wall motion abnormality and elevated troponin, so it usually can't be differentiated from MI without an angiogram.  

Another ECG was recorded:
Is it true that there is "no significant change"?

In the intervening 3 hours, new Q-waves have developed in leads V3 and V4, and deepened in V5 and V6.

The patient was admitted to medicine service for pericarditis where she had intermittent pain throughout the rest of the night.  The medicine note documents that the patient had worsening pain with lying flat and relief with leaning forward.  There was no history of preceding viral symptoms.

Another ECG was recorded at t = 6 hours:
The Q-waves are more pronounced and now the computer sees it.
Also, the ST elevation has diminished as myocardium infarcts

Outcome and comments by the source of the case:

"The following morning the cardio consult service saw the patient.  The repeat TnI at that time was 19.20 ng/mL and an official echo showed: 'Severe hypokinesis to akinesis of the apical 1/3 anteroseptal wall with partial wall thinning c/w apical anterospetal MI.'"

"Cath showed a 100% mid LAD lesion which was successfully intervened upon."

"TnI peaked at 67.10 ng/mL post PCI."

"I know from reading your blog that you "diagnose pericarditis at your own peril", but are there any signs on that initial ECG that would make you think ischemia?  No PR depression, no Spodicks sign, but concave segments which are diffusely elevated... no reciprocal depressions (aVL looks isoelectric to me, maybe make an argument for slight depression?)."

"In the clinical context I would have performed a bedside echo and had I seen the RWMA the diagnosis would have been made, but in the absence of this I thought that initial ECG looked like pericarditis."


1. 40-50% of acute LAD occlusion have upwardly concave ST segments in all of V2-V5.   
--Smith SW.  Upwardly Concave ST Segment Morphology Is Common in Acute Left Anterior Descending Coronary Artery Occlusion.  Journal of Emergency Medicine 2006; 31(1):67-77. 

2. 40-50% of LAD occlusion have zero reciprocal ST depression.
--> --Walsh B.  Grauer K.  Smith SW.  Proximal RCA occlusion producing anterior ST segment elevation, Q-waves, and T-wave inversion.  Journal of Electrocardiology 2018.

Did absence of reciprocal ST depression in aVL lead to this erroneous diagnosis?

That may be the case.  The absence of STD in aVL should only be reassuring when you are trying to differeniate the inferior ST elevation of MI from that of pericarditis.  If that were the differential diagnosis, then pericarditis would be a reasonable thought, and one should look for PR depression (not present), STE in II greater than III (which is present), Spodick's sign (downsloping TP segment - to my knowledge this has never been verified as a true sign of pericarditis), as well as clinical factors such as a rub or effusion.  However, in almost every case, one should confirm absence of OMI (Occlusion MI) at least by contrast ultrasound.

But absence of ST depression in aVL is not meant to rule out anterior MI!  

Positive troponin: this transformed the differential Dx from MI vs. pericarditis to MI vs. myocarditis.  Myocarditis is virtually indistinguishable in the ED from MI.  These patients may have ECGs, troponin profiles, and echo exams that are identical to acute OMI.  If there is ST elevation, they almost always need an angiogram to rule out OMI.

Learning Points:

It is very dangerous to diagnose pericarditis unless there is overwhelming evidence to support it.  This ECG was diagnostic of OMI (not pericarditis).  Even if it was a more ambiguous ECG, a more detailed investigation would be warranted because OMI is far more common and it cannot be missed!

Final thought:

In my experience, I have noticed that clinicians love to make the diagnosis of pericarditis, and will use any evidence, no matter how weak, to support that diagnosis if they think of it. I am not sure why this bias exists, and don't even know what kind of bias it is. Confirmation bias? But confirming what?  And why do they want it confirmed?

See this case:

Pericarditis, or Anterior STEMI? The QRS proves it.

Pendell Meyers comment: when teaching interns, I tell them to think about pericarditis (but not myocarditis or pericarditis with pericardial effusion) as a wastebasket diagnosis, almost on the same level as "costochondritis," as if that were a thing. It appears to me that the only reason pericarditis exists is to trick emergency physicians into missing OMIs (and less commonly PEs, dissections, etc). Like costochondritis or GERD, it is a diagnosis from which nothing good can come. Pericarditis (without myocarditis or pericardial effusion) simply does not matter in the grand scheme of things. The treatment for pericarditis (which probably doesn't relieve the pain of pericarditis any more than placebo or tylenol or anything else) is simply NSAIDs (which can have complications) or colchicine (which some toxicologists believe should simply never be used given the astounding mortality of its overdose). Nothing good comes from diagnosing pericarditis, and there are huge risks of doing so, as illustrated by this case and so many others on this blog. If you correctly diagnose 99 patients with pericarditis and misdiagnose 1 OMI as pericarditis, you have failed, because the harm of missing OMI far outweighs the nearly nonexistent harms of missing pericarditis. Just say no to diagnosing pericarditis, and the problem is solved. Dr. Smith appropriately wonders what type of bias this is that makes clinicians so obsessed with diagnosing pericarditis. I'm not sure if this bias has been described before, but it seems to me to be related to the fun of making a relatively rare, "interesting" diagnosis. So maybe it should be called the "shiny distracting zebra bias." That seems to be what's happening - the shiny fun diagnosis of pericarditis is distracting us from the actual emergencies.

Comment by KEN GRAUER, MD (6/20/2018):
Great case & supporting comments by Drs. Smith & Meyers. I’d add the following:
  • Dr. Smith’s concept of terminal QRS distortion is worth repeat emphasis (link to his paper given above in the text). A picture is worth 1,000 words — and lead V3 illustrates this concept to perfection. Like visual recognition of what a Brugada-1 ECG pattern looks like — the picture of terminal QRS distortion in a patient with new chest pain (as seen in lead V3 of this 1st ECG) is a pattern to be memorized by all emergency care providers.
  • I love Dr. Smith’s quote, “You Diagnose Pericarditis at Your Peril (and at the Patient’s Peril!)”. I use this quote often when questions regarding this diagnosis arise. But not only is acute pericarditis a diagnosis of exclusion — the clinician should also be knowledgeable about how acute pericarditis (on those occasions when it does occur) presents. The most common form of acute pericarditis is associated with recent viral infection — and, the nature of the chest pain is typically positional (worse in supine position) and pleuritic (aggravated by deep inspiration). Although a pericardial friction rub is not always present — it should always be carefully listened for, because if you do hear a rub in the right clinical setting — then you have made the diagnosis. Why then in the literally hundreds of suspected cases that I’ve seen ECGs posted on the internet in recent years with a query about pericarditis — is it so very rare for anyone to ever describe the nature of the patient’s chest pain? — and rarer still to even mention having thought about listening with a stethoscope to see if a rub might be present? 


Lessons Learned in Academic Scholarship

During my PGY-4 year, I had the opportunity to pursue a specialization in Academic Scholarship.1 My year had two primary components: (1) I was the inaugural Editorial Intern at the Canadian Journal of Emergency Medicine,2 and; (2) I was the Digital Scholars Fellow at CanadiEM.3 Over the course of the year, I learned many lessons about publishing in academics. I wanted to share three of the most pertinent lessons with our community to ...

The post Lessons Learned in Academic Scholarship appeared first on CanadiEM and was written by Daniel Ting.

EM in 5: Transient Global Amnesia

Author: Anna Pickens, MD (@AnnaEMin5, Creator of EM in 5) // Edited by: Alex Koyfman, MD (@EMHighAK), Brit Long, MD (@long_brit), and Manpreet Singh, MD (@MprizzleER)

Welcome to another edition of EMin5 with Dr. Anna Pickens. Today we cover transient global amnesia (TGA). Enjoy the video!


Transient global amnesia: typically anterograde, with normal short recall


Plus Normal Neurologic Exam!

What should you consider?



Suggested/Further Reading:


The post EM in 5: Transient Global Amnesia appeared first on - Emergency Medicine Education.