Thursday, April 25, 2013

Widespread ST Elevation. Activate the Cath Lab?

A 40 year old male with several chronic illnesses presented to the ED with decreased level of consciousness and hypotension.  He had an ECG recorded quite early and it was alarming:

When I was shown this ECG a day later, it took me about 1 second to say, "Cool case of Early Repol!"  A cardiologist who had been consulted had the same reaction.  How do we know that this is early repol in all 3 regions (inferior, anterior, lateral)?  That is hard to explain, but you can always use the early repol equation for anterior ST elevation (see sidebar, or the iPhone App "subtleSTEMI").  QRS duration 85 ms and Computerized QTc is 394 ms, STE at 60 ms after the J-point is 4mm, and R-wave amplitude in V4 is at least 22 mm.  Result = 20.85 (less than 23.4 is very unlikely to be an anterior STEMI).

But what about inferior and lateral STEMI?  Is it one or all of the above?   There appears to be ST depression in aVL, but, if you look closely, that is due to wandering baseline.  Without reciprocal ST depression in aVL, it is highly unlikely to be an inferior STEMI.

Certainly a widespread STEMI (anterior, inferior, lateral, from a large wraparound LAD) is consistent with hypotension, so we should not be quick to dismiss this possibility.

How about looking for a previous ECG?  There was an ECG available for comparison from 6 weeks earlier:

Computerized QTc = 359 ms.  This is quite different, and may make you more worried that the findings today are new, especially those that are inferior and lateral.
And another ECG from 4 months earlier was available, which I'm not sure that they saw:

Computerized QTc = 373 ms.  QRS 85 ms.  In this one, the anterior leads have some STE, but not as much as there is today.  And there is none in the inferior or lateral leads.

Not inappropriately, they activated the cath lab.  Then they did a bedside echocardiogram (this is a parasternal short axis view:

 (Right Ventricle is on the left, next to the septum, anterior wall is on the top of the image, inferior/posterior wall is at the bottom, and lateral on the right side of the image):
This shows a hyperdynamic heart with all walls functioning perfectly, and is not consistent with infarct.

Many of you are probably thinking "Widespread ST elevation! It must be pericarditis!"  And that is certainly high on the differential.  In my opinion, due to much researching for true pericarditis cases (with objective evidence such as effusion or rub or typical evolution of the ECG), I believe that pericarditis is a very unusual cause of ST elevation, and that benign (normal variant) ST elevation is much more common.

In any case, there is no PR depression anywhere on this ECG.  There was no rub or effusion.

The patient had sepsis and hypovolemia.

1) I do not think hyperkalemia was the etiology of the change.  I might be wrong.  It looks like early repolarization to me
2) Contrary to widespread belief, early repol may come and go; it is not always present in any given individual.  See article by Kambara below.
3) Tachycardia, or stress testing, may diminish the ST elevation of early repol.

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation. Elevations in inferior leads were less than 0.5mm in 18 of 20 cases. Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.


  1. The septum looks a little bit flattened, what about pulmonary embolism?

  2. Of course one should always consider PE when there is tachycardia and hypotension. The ultrasound does not suggest it, in my opinion: the RV should be larger. But it was a possibility, but in the end was not.

    Steve Smith

  3. regarding early repolarization, do you mean the rule is to involve only one area.. inferior or anterior..? rarely to involve both areas. ?!

    1. I mean that the early repolarization equation is only for differentiating anterior STEMI from normal variant ST elevation in precordial leads. The equation does not apply to normal variant STE in inferior or lateral leads.

  4. Dr. Smith,

    Do you have any references discussing the specificity of PR depression for pericarditis? I have recently seen a case of early repol with a small amount of PR depression in a few leads, and it has come to my attention during this case that most people are under the impression that even slight PR depression in just a couple leads (with obligate slight PR elevation in aVR) is highly specific, nearly pathognomonic, for pericarditis.

    Is this really true? Do you believe that some early repol can have slight PR depression? And isn't atrial repolarization a normal cause of PR depression? Finally, do you qualify or quantify PR depression in any way when considering pericarditis?

    1. Pendell,

      You have my book, right? See the chapter and annotated bibliography on pericarditis (chapter 24).

      They are wrong.

      Up to .5 mm of PR depression is very common. See these posts on the atrial repolarization wave:

      Charles et al. (Charles Arch Int Med 131(5):657, May 1973) reviewed old literature and called 0.8 mm very specific, but his data is slightly suspect because there was no angiography or even biomarker ruling out of MI.

      Other references:

      Ratio of ST elevation to T-wave height important because early repol has large T-waves.

      Most importantly: who cares?

      If the patient does not have a rub or effusion (do an ED bedside echo), then does it matter if the patient’s chest pain is chest wall pain or pericarditis?

      Both are treated with NSAIDs.

      The only ddx that matters is STEMI vs. either early repol or pericarditis.;jsessionid=A0289B051D0E9F4A7B5F6F3CB1A284A3.d03t04?deniedAccessCustomisedMessage=&userIsAuthenticated=false

      How would you like to write a blog post on this?



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