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".
|Clinician and EKG machine read of acute pericarditis.|
What do you think?
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.
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
4-variable: 22.4 (greater than 18.2 is LAD occlusion)
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.
|Is it true that there is "no significant change"?|
|The Q-waves are more pronounced and now the computer sees it.|
Also, the ST elevation has diminished as myocardium infarcts
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.
But absence of ST depression in aVL is not meant to rule out anterior MI!
See this case:
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.
- 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?