Wolff-Parkinson-White (WPW) – STEMI Mimic

A really interesting 12-Lead ECG was posted to the Cardiology & Electrocardiography (ECG, EKG) Experts group on Facebook the other day.

If you’re not familiar, this is one of the groups / fan pages on Facebook I help moderate with Jason Winter who also started the Cardiology & Electrocardiography Experts blog.

What’s so interesting about this ECG is that it shows a relatively infrequent STEMI mimic. In addition, it helps demonstrate a point I’ve been pondering about several of the STEMI mimics in general.

Let’s take a look.



The patient was a 29 year old male with no complaints. The ECG was captured during a routine workup according to the contributor Chris de Beer (thanks again for the interesting ECG, Chris).

The ECG shows a WPW pattern as evidenced by a short PR interval and delta waves. The delta waves create a pseudo-infarct pattern (Q-waves) in the septal leads.

You might recall from my previous post about left ventricular hypertrophy (LVH) that I think recognizing the so-called “strain pattern” is actually more important than knowing the “voltage criteria” for LVH.

I’m sure some of you are waiting for “Part II” of the left ventricular hypertrophy series, but I’m still waiting for inspiration! :)

What does this ECG have in common with a strain pattern from left ventricular hypertrophy (LVH)? What does it have in common with left bundle branch block (LBBB)? What does it have in common with ventricular rhythms? Including paced rhythms?

The answer is, it has a widened QRS-T angle! To put it another way, the T-waves and ST-segments are deflected opposite the main deflection of the QRS complex, and (this point is the most critical) the degree of the ST-T abnormality is proportional to the size of the QRS complex.

Think of this as a supplement to Sgarbossa’s criteria and the “rule of appropriate T-wave (and ST-segment) discordance”.

Here’s a graphic to help illustrate the point.



When you see a pattern like this, regardless of cause, it should set off alarm bells that you are dealing with a STE-mimic and not acute STEMI!

Note that the S-wave in lead V3 is cut off by the bottom of the ECG paper. This is a common problem with prehospital 12-lead ECGs! We must presume that the S-wave would be the deepest in lead V3 if we were able to view the entire QRS complex.

That doesn’t mean the patient isn’t experiencing acute myocardial infarction (although this patient is asymptomatic so let’s pretend he was over the age of 30 and complaining of chest discomfort).

It just means you should wait before pulling the trigger on the cardiac cath lab.

Look for changes on serially obtained ECGs instead!

2 Comments

  • Jesse says:

    So not to blog jump my questions on you, but..Youve stated elsewhere that an accessory pathway (such as WPW) can be indicated by polymorphic QRS complexes, (which Im guessing is a by product of the different conduction locations of the pathway and AV node?)and an R-R interval of 240 ms.If you dont mind answering.. How specific of a finding is this? And while I can speculate the reasons these criteria exist, Im curious of the actual etiologies behind them.Thank you!

  • Tom B says:

    Jesse – Keep in mind that there's a difference between the WPW pattern on the 12-lead ECG (like this one, a short PR-interval and delta waves) and the WPW Syndrome, which involves various tachycardias that are enabled by the presence of an accessory pathway.Atrial fibrillation in the presence of an accessory pathway can be quite dangerous. That's the polymorphic rhythm where the shortest R-R interval of 240 ms or less indicates an increased danger of VF.The other tachycardias you might hear about are the orthodromic reciprocating tachycardia (down the AV-node and up the accessory pathway) which is generally a narrow complex rhythm, and the antidromic reciprocating tachycarida (down the accessory pathway and up the AV-node) which is generally a wide complex tachycardia.These tachycardias are sometimes referred to as AVRT (AV-reentrant tachycardias) as opposed to AVNRT (AV-nodal reentrant tachycardias) which do not involve an accessory pathway.At least, that's my limited understanding! You can learn more by Googling these terms.Thanks for commenting!Tom

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EMS 12-Lead

Cardiac Rhythm Analysis, 12-Lead ECG Interpretation, Resuscitation

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Comments
Kevin
44 year old male CC: Palpitations
Why on earth would you risk VF, by giving Adenosine to rule out rhythms.. This is dangerous, and foolish. There might be a slight chance that this is WPW.. You might as well just give him Cardizem, they are both AV nodal blockers... I don't know why the AHA even added this stupid idea..
2014-10-22 13:31:06
Vince DiGiulio
The 360 Degree Heart – Part II
It is standard practice in electrocardiography to label the first 90 degrees counter-clockwise from "zero" that way. When you see a patient with "left axis deviation" you'll see that their measured QRS axis is somewhere between -30 and -90 degrees. Imagine if you saw someone with a mean QRS axis at 5 degrees. Now imagine…
2014-10-21 14:00:37
Bryan
The 360 Degree Heart – Part II
I don't understand why (-)III and aVL are be labeled -60 and -30 degrees instead of 300 and 330 degrees?
2014-10-21 13:43:29
The 360 Degree Heart – Part II | EMS 12 Lead
The 360 Degree Heart – Part I
[…] first post in our “360 Degree Heart” series attempted to visualize how the different frontal plane […]
2014-10-21 12:50:56
Eric Strong
Axis Determination – Part VI
This is a great discussion of axis determination. One minor suggestion: I think it's potentially misleading to refer to an axis between 0 and -30 as "physiologic left axis deviation", since "axis devitation" implies deviation from normal, and axes between 0 and -30 are perfectly normal, (depending on age and body habitus). It may be…
2014-10-05 17:09:00

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