Saturday, June 8, 2019

A 40-something woman with no medical history presented with 2 days of chest pain

A 40-something called 911 for 2 days of CP.  It was difficult to get a history because of language, but of course a prehospital ECG was recorded.  It is not available but looked just like the first ED ECG.

(click on the image to enlarge)

Here is the computer interpretation:


What do you think?

The medics noticed the inferior STE with reciprocal STD and were worried about inferior MI.  My partner saw this and thought "No, I think it is LVH, not MI."

They did a couple negative troponins and another (identical) ECG.

I came on to relieve my partner and he asked me to look at the ECG.

I looked at it briefly and said: "WPW"

There is a short PR interval, and all the abnormal QRS is due to accessory pathway activation.  The beginning of the QRS in every lead is slurred.  It looks somewhat like a left bundle branch block because the accessory pathway is on the right and results in right to left activation, just like LBBB.

The abnormal depolarization leads to abnormal repolarization and mimics acute MI and also, with apparent QR- and QS-waves, old MI.

I went back to talk to her through an interpreter and was able to elicit several episodes of syncope in recent months.

I consulted our Electrophysiologist.

He came down and was worried enough that he schedule her for ablation within 4 days.

At EP study:

1.  SVT was easily induced under isuprel infusion
2.  Pacing maneuvers suggestive of SVT to be AVRT
3.  The accessory pathway was mapped in antegrade fashion using CARTO system
4.  RF ablation was performed and conduction via accessory pathway ceased with ablation. 

5.  SVT could not be re-induced post ablation. No pre-excitation post ablation.

Here is the ECG post ablation:
It is still abnormal, but improved.
There still appear to be (smaller) delta waves.
But SVT could no longer be induced.

Learning Point:
Whenever there are ST-T abnormalities (repolarization abnormalities), FIRST look at the QRS (intervals, voltage, axis, etc.) to see if these are not a result of depolarization abnormalities.  Common depolarization abnormalities that cause false positive ischemia (ST-T) are:


Any of these can result in both ST elevation and reciprocal ST depression.

When I showed this to several of my residents and colleagues, none of them recognized it.  I have recently been studying all the patients with WPW in our institution and finding that the ECGs were consistently missed by both the computer and the physician.

Here are a number of similar cases:

WPW mimicking and obscuring acute MI

Comment by KEN GRAUER, MD (6/8/2019):
Great case for educational purposes — with the KEY teaching point being, “How can I prevent the embarrassing mistake of not recognizing WPW?” In my experience from teaching ECG interpretation over many decades — the answer is simple = Use a Systematic Approach each and every time you interpret any ECG!
  • Using a system does not slow you down. With a little practice — it speeds you up with great advantage that you’ll be far less likely to miss findings that should be detected ...
  • I’ve previously suggested the System that I favor (CLICK HERE). Many systems exist — and whichever YOU favor is fine, as long as you always use your systematic approach before you jump to conclusions about what an ECG shows.
In the hope of illustrating how not to miss the diagnosis of WPW in this case — I’ve added some time-lines to the ECG (Figure-1).
  • NOTE: WPW is easiest to pick up when there is complete preexcitation — and, when delta waves are seen in most leads. But — impulses may not always conduct uniformly down the AP (Accessory Pathway). Instead, impulses may partially or totally be conducted down the normal AV nodal pathway. This explains why despite WPW, the QRS complex will not always be widened — and why you may not always see delta waves in all leads. Another reason why delta waves may not always be evident on ECG, is that the delta wave may be isoelectric to the ECG baseline.
Figure-1: The ECG in this case — with timelines added to show the onset of the delta wave in each of the 12 leads (See text).

MApproach to this Tracing: Regardless of the system you use — it’s best to begin the interpretation of any 12-lead tracing by assessing the Rate and Rhythm. I always look to see if there is a long lead II — since it literally takes me no more than 2-3 seconds to scan a long lead II to determine if there is normal sinus rhythm with upright P waves + fixed PR interval preceding each QRS complex.
  • The problems in this tracing are: iThat there is a LOT of artifact in lead II (and also in leads I and aVR — most probably from movement/tremor in the right arm extremity)andiiThe rhythm looks like a normal sinus mechanism in lead II, because the PR interval does not really look abnormal !!! (Technically — the slight R-R interval irregularity qualifies as sinus arrhythmia here).
  • TAKE HOME — Most of the time you’ll be able to recognize WPW on ECG because the PR interval in lead II (which is the best lead for rhythm determination) will be shortened. BUT — this wasn’t at all obvious in this case, and I admit that I did not recognize WPW from my initial inspection of lead II in Figure-1.
After assessment of Rate & Rhythm — I favor looking next at intervals. My reason for assessing Intervals (ie, the PR/QRS & QTcearly in my interpretation — is that IF the QRS complex is widened, you need to figure out WHY before proceeding further.
  • When the rhythm is sinus — the 3 common causes of QRS widening are LBBBRBBB — or IVCD (intraventricular conduction defect). The ECG in Figure-1 is definitely not RBBB. While this tracing superficially looks like LBBB in the limb leads — it lacks the monophasic (all upright) QRS complex in lead V6 — and — the initial R wave in anterior leads V1 and V2 looked to be clearly much wider than usual for LBBB (CLICK HERE — for “My Take” on ECG diagnosis of Bundle Branch Block).
  • TAKE HOME — It was at this point in this case that I noticed the PR interval in leads I and aVL was clearly shortened. Looking closer at leads V1 and V2 now made sense — in that those wider-than-they-should-be initial R waves were actually delta waves in these anterior leads.
  • For clarity — I’ve drawn in time-lines in Figure-1 that start from the onset of the delta wave in each of the 12 leads. From these time-lines — it becomes much easier to see the long, negative delta wave in lead III — as well as the reason why the isoelectric PR segment in lead II was not initially recognized by me as a delta wave. It’s now evident that delta waves are present in leads V1,V2,V3 — but the initial part of the QRS in V4,V5,V6 does not look at all like what we typically expect a delta wave to look like.
  • BOTTOM LINE: Much of the time when the diagnosis of WPW has not been immediately forthcoming to me — I’ve picked up WPW by finding a couple of leads (like leads I and aVL in this tracing) in which I knew there was PR shortening + a delta wave. I’ve found that identifying a few leads that definitely show a short PR + delta wave greatly facilitates my ability to recognize delta waves in other leads by mentally imagining those simultaneous time-lines that I’ve drawn in Figure-1.
SUGGESTION: Check out THIS TRACING — in which the way this subtle example of WPW was picked up by recognizing the unusual ECG finding of a Tall wave in Lead V1.
  • At the bottom of the page at the above link — I review How to Advise the asymptomatic patient with WPW!
How to Localize the AP on ECG: While our task as clinicians who are not EP cardiologists is simply to recognize WPW, and not to “localize” the AP — it is interesting to be able to predict the probable location of the AP. Having reviewed numerous algorithms in the literature — I’ve adapted a few of them to come up with an easy-to-use and rapid way to predict the probable location of the AP based on its ECG presentation.
  • CLICK HERE — for my method. Read on for how I apply this method for predicting AP localization for the ECG in Figure-1.
  • The initial STEP in my approach is based on where Transition occurs in the chest leads (ie, where the R wave becomes taller than the S wave is deep). Since the QRS complex in lead V1 is not predominantly positive — we can skip STEP A-1 in my algorithm. In fact, since transition does not occur in this ECG until between V4-to-V5 (a predominant R wave is finally seen in V5) — we begin with STEP B-5.
  • STEP B-5 tells that we have a right-sided AP that is probably located in the RV free wall. To measure the delta wave frontal plane axis — we can look at the time-lines in Figure-1. The delta wave in lead I (ie,the first ~40 msec of the QRSis positive (upright). The delta wave in lead aVF is negative. This yields a negative delta wave frontal plane axis.
  • According to STEP B-5 — We look next at the R wave in lead III. The QRS complex in lead III is all negative (ie, there is no R wave) — which according to my algorithm suggests there is a Postero-Lateral RV Free Wall AP.
FINAL TAKE HOME — I bet you’ll miss WPW much less often (if ever again) IF you regularly use a systematic approach to ECG interpretation. THIS case is humbling because of how many capable providers overlooked the diagnosis. WPW should not have been missed in this case ...

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