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."

2 comments: 

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.

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A Wide Complex Rhythm in an Intoxicated Patient

This patient presented with altered mental status and was thought to be intoxicated.  He did not have any other apparent medical issues.

I'm not certain why an ECG was recorded, but it was:

The computer and the overreading physician diagnosed "Sinus rhythm with LVH."
What is it?

This is an accelerated idioventricular rhythm (AIVR).  There is also isorhythmic dissociation (P-waves and QRS co-incidentally going the same rate, but without the P-waves consistently conducting through the AV node because frequently the ventricular rhythm usurps it (comes too early for the P-wave to conduct).

I point out the salient features on the annotated image below:

There is a wide QRS that is at regular intervals at a rate of about 65.
They are either not preceded by a P-wave, or by a P-wave that is too close to be conducting.
Black arrows points to normal P-wave that conducts to a normal QRS.
Green Arrows point to upright sinus beats that are close to the QRS and create a "fusion" beat, in which the ventricular beat and the normal beat meet up (fuse) and create a hybrid QRS that is longer than a normal one, but shorter than the idioventricular ones.
Red Arrows point to retrograde P-waves.  The idioventricular rhythm conducts up the AV node to the atrium, creating an upside down P-wave after the QRS.
Blue arrows point to upright P-waves that are within or after the QRS; they occurred too late to affect the QRS (they did not fuse).

See below how this resembles WPW and why it is not WPW.


AIVR is an automatic ventricular rhythm that is:
1.  Faster than a normal ventricular escape rhythm (which is also automatic at rates as high as 50).  AIVR is caused by enhanced automaticity (faster than normal automaticity).
2.  Slower than ventricular tachycardia (less than 100-120).  VT is a re-entrant rhythm.

It is a benign rhythm but may be seen in dangerous pathologies, particularly in the reperfusion phase of acute STEMI, digoxin toxicity, and sympathetic overload.

Clinical course

Although the overreading physician did not see the AIVR, the resident did diagnose "Idiopathic Ventricular Rhythm without Tachycardia," which does pretty well (but not exactly) describe the ECG, but does not conform to the standard terminology.  "AIVR" is much more accurate and precise.

The patient had negative troponins in the ED.   He was not on digoxin.  He did not have other evidence of sympathetic overload.

He metabolized his toxin, whatever it was, and was discharged.

It is important to know that AIVR can occur any time and does not necessarily imply significant pathology.

Since there is a great and succinct article on AIVR at Life in the Fast Lane, I do not feel the need to explain in greater detail: https://lifeinthefastlane.com/ecg-library/aivr/


The QRSs do resemble those of WPW; is this intermittent WPW? 
  
However, here we do not see the typical slurred upstroke (delta wave) of WPW; the QRS is uniformly wide, whereas a delta wave has a slower initial upstroke that later. 

Moreover, an interpretation of WPW would require there to be P-waves prior to these abnormal QRSs.

So it is not WPW.

Here is an example of intermittent WPW:
http://hqmeded-ecg.blogspot.com/2016/06/it-is-easy-to-be-led-astray-by-computer.html

In this case, the computer also interpreted "Normal"
But complexes 3, 4, 5 have delta waves and a short PR interval.

Here is a case of WPW in which the QRSs do resemble those of AIVR:

Looks similar, right?  But here there are P-waves before every QRS and the first part of the QRS is more slurred.
You can read here why the PR interval is not short in this case of WPW:

A large R-wave in lead V1. And why is the PR interval not short?

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Comment by KEN GRAUER, MD (6/18/2018):

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Interesting case in which an ECG was probably not essential to management — but for which we are thankful, since it provides such an instructive teaching case! As per Dr. Smith — AIVR is generally a benign rhythm that will often be seen in dangerous pathologies (most commonly as a “reperfusion rhythm” in occlusion-related infarction). As Dr. Smith also emphasized — AIVR may on occasion be seen in otherwise healthy individuals who do not have underlying heart disease. So, as is the case with most cardiac rhythms — the clinical setting is KEY to determining the significance (or lack thereof) of the arrhythmia! I’ll offer a different viewpoint to one aspect of Dr. Smith’s interpretation:

• I suspect there are no retrograde P waves here (which if present, might then be expected to reset the sinus rate). Instead, I favor the hypothesis that all colored arrows in Figure-1 represent sinus-generated P waves — with the underlying rhythm being sinus arrhythmia.
• We see evidence of this variation in sinus rate at the beginning of the tracing. Thus the P-P interval between the 1st black and 1st green arrows measures 960 msec (corresponding to a rate of ~62/minute) — which is clearly longer than the P-P intervals once normal sinus conduction resumes for the last 2 beats on the tracing. Thus, the P-P intervals for these last few sinus beats = 740 and 720 msec (corresponding to a faster sinus rate of 81 and 83/minute, respectively).
• It is because of this sinus arrhythmia with bradycardia that AIVR is seen! With periods of sinus rate slowing (as occurs at the beginning of Figure-1) — once the sinus rate drops below the 65/minute threshold of the slightly accelerated ventricular escape focus — AIVR takes over — until, the sinus rate speeds back up toward the end of the tracing.

Figure-1: Perhaps all P waves are sinus-initiated — with an underlying sinus arrhythmia + bradycardia leading to intermittent AIVR? (Details in my Comment above).

P.S.— AIVR is not always completely benign. As a result of “takeover” by this ventricular rhythm — the “atrial kick” is lost. In some settings — this loss of atrial contribution to cardiac output may result in hypotension. In those rare instances in which excessive slowing of sinus P waves results AIVR with hemodynamic compromise — Atropine may be the drug of choice. That said, in the vast majority of cases — AIVR will not produce symptoms, and no specific treatment is needed.

Chest Pain and Inferior ST Elevation.

A middle-aged patient with lung cancer had presented to clinic complaining of generalized malaise, cough, and chest pain.   He had an ECG in clinic which worried the providers because of possible inferior MI, and they sent him to the ED.

Here is that ECG:

What do you think?

There is sinus tachycardia.
There is ST Elevation at the J-point, relative to the PQ junction (end of PR segment) in II, III, aVF.
There is some T-wave inversion in aVL (which is a soft sign of inferior MI, but no reciprocal ST depression).

Notice, however, that there is profound PR depression.  The apparent ST elevation is mostly just relative to the depressed PR segment.

He was sent to the ED and had this ECG at t = 1 hour:

Similar

There are several issues which mitigate against acute inferior MI, and these are the Learning Points:

1. Symptoms other than chest pain (malaise, cough in a cancer patient)

2. Sinus tachycardia, which exaggerates ST segments and implies that there is another pathology.  I have always said that tachycardia should argue against acute MI unless there is cardiogenic shock or 2 simultaneous pathologies.  We showed this in a recent analysis of UTROPIA data (see abstract below).

3. PR depression, which suggests pericarditis

4. Absence of large inferior T-waves, which are very common in OMI (acute occlusion MI).

5. Absence of any ST depression in aVL.  (We showed that absence of STD i aVL rules out inferior MI, even subtle inferior MI, with 99% accuracy.  We also showed that, of 47 cases of pericarditis with ST elevation, none had ST depression in aVL.)  T-wave inversion in aVL was also very sensitive, but not as good as ST depression.


The patient underwent an emergent formal echocardiogram to look for wall motion abnormality:

The estimated left ventricular ejection fraction is 63 %.

No wall motion abnormality .

Pericardial effusion very small

No evidence for pericardial tamponade.

Multiple fibrin strands in (lateral) pericardial space, c/w fibrinous pericarditis

FINDINGS C/W WITH FIBRINOUS PERICARDITIS AND SUSPICIOUS FOR

EFFUSIVE-CONSTRICTIVE PERICARDITIS

Here is a still image from a bedside cardiac ultrasound:

See small effusion in upper right of image

The patient turned out to be septic from pneumonia, received 3 liters of fluids and antibiotics, and had the following ECG recorded:

ECG (t = 7 hours)

Fluids have resolved the sinus tachycardia.
ST elevation persists, but there is less PR depression (interesting!)
Still no reciprocal ST depression in aVL 

TITLE:

The Negative Predictive Value of Tachycardia for Type I MI in Hemodynamically Stable Patients with Chest Pain

AUTHORS:

Daniel H. Lee, MD – Department of Emergency Medicine, Hennepin County Medical Center, Minneapolis, MN

Yader Sandoval, MD - Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN.

Fred S. Apple, Ph.D. - Department of Laboratory Medicine, Hennepin County Medical Center; Professor, University of Minnesota School of Medicine

Stephen W. Smith, MD – Department of Emergency Medicine, Hennepin County Medical Center, Professor, University of Minnesota School of Medicine, Minneapolis, MN

ABSTRACT:

Background:

Patients with type 1 myocardial infarction with normal left ventricular function that are hemodynamically stable do not usually manifest with sinus tachycardia. The goal of the present analysis was to examine whether the presence of tachycardia identified patients unlikely to have type 1 myocardial infarction.

Methods:

This was a secondary post-hoc analysis of a prospective, observational data study of 1927 consecutive ED patients over 4 months who had at least 1 contemporary troponin I (cTnI) resulted.  

Inclusion criteria were chest pain, ≥ 2 serial cTnI, sinus rhythm, and ≥ 1 ECG. 

Exclusion criteria included age <18 b="" years="">SBP <100 b="" echocardiogram="" ejection="" fraction="" mi="" mmhg="" st-elevation="" with="">, pregnancy, and trauma. 

All cases with at least one elevated cTnI were adjudicated into specific MI type (or no MI) by two clinicians who reviewed all medical records. Patients were stratified according to presence or absence of type I MI, and of heart rate (HR) > 99 bpm, and > 120 bpm on presenting ECG. All ECGs were coded by an expert clinician as having ST-elevation, ST-depression, T-wave inversion [ST/T abnormalities, (ST/T-A)], or none of the above.

Results:

877 patients were included, of whom 135 had HR > 99 bpm (742 ≤ 99 bpm) and 23 had HR > 120 bpm (854 ≤ 120 bpm).  Of the 877, 58 (6.6%) had type I MI and 819 did not; 4 of 58 (6.9%) with type I MI, and 131 of 819 (16.0%) without, had HR > 99 (P=0.02).  The negative predictive value (NPV) of HR > 99 for type I MI was 97.04% (95%CI 92.6-98.8) and the negative likelihood ratio [(-)LR] was 0.43 (95%CI 0.17-1.12).  23 had HR > 120 bpm (854 ≤ 120 bpm); 0/23 with HR > 120 bpm had type 1 MI.  The NPV of HR > 100 bpm for type I MI among those with ST/T-A was the same as in those without, at 92.0% (95%CI 74.7.6-97.8).  Of 23 patients with HR > 120 bpm, 4 had ST/T-A.  See Table for diagnostic utility.

Conclusion:

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In hemodynamically stable patients with chest pain, sinus tachycardia aids in the identification of patients unlikely to have type I MI, especially in those with HR > 120 bpm.

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Comment by KEN GRAUER, MD (6/17/2018):

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Excellent case with insightful learning points explaining why these serial tracings are not indicative of acute inferior infarction. I’ll add the following 2 comments:

• i) This patient presumably has effusive-constrictive pericarditis. ECG findings of constrictive pericarditis are generally not overly helpful clinically. Low voltage and nonspecific ST-T wave abnormalities are commonly seen but non-diagnostic. Electrical alternans is generally only seen with a large pericardial effusion. Other nonspecific findings may include P wave abnormalities, PR segment deviations, and atrial arrhythmias — though none of these findings are seen in a majority of patients. So while the ECG will often not be normal with constrictive pericarditis — nonspecificity of ECG findings offers little diagnostic assistance.
• ii) All 3 of the ECGs in this case manifest Schamroth’s Sign! This is the presence of an almost “null vector” in standard lead I (ie, P wave, QRS complex and T wave all under 2mm in size). While sensitivity of this sign is very low — its presence is highly suggestive of longstanding and severe pulmonary disease. A small percentage of patients with effusive-constrictive pericarditis are found to have RVH — with potential explanation for this finding as a sequela of fibrous band narrowing of the RV outflow tract (Mehta A et al: Constrictive Pericarditis. Clin Cardiol 22:334-344, 1999).

The ECG diagnosis of RVH is often challenging. On occasion, I have found awareness of Schamroth’s sign to be helpful in recognizing probable severe pulmonary disease with RVH when other ECG findings were inconclusive.