Wednesday, January 17, 2018

I was texted this ECG: "Middle-aged male with Prehospital Cath Lab Activation"

A physician caring for his new arrival, a 50-something with acute chest pain and dyspnea and syncope, texted me this initial ED ED ECG.

The computer read was "Marked ST Elevation, ***Acute MI***" 

No previous ECG was available.
What do you think?
Computerized QTc = 399 ms
















My response was: "Normal variant"

Question: "De-activate cath lab?"

Answer: "It does not look like myocardial infarction".

He sent the prehospital ECG.  This also was read by the computer as "***Acute MI*** and was the basis for the prehospital activation.

Here it is:
My response: "Normal Variant"







I added: "One must always remember that there can be a coronary occlusion in the presence of a normal ECG.  So I cannot tell you that this patient does not have a coronary occlusion, but I can say that it does not show on the ECG."

He de-activated the cath lab.

The patient ruled out for MI by 4 serial troponins below the level of detection.



Let's look at the ED ECG more closely:
Sinus rhythm
There is ST Elevation in anterior leads: V2-V6
There is ST elevation in I, II, aVL

Why is this not STEMI?

First, I prefer to use my formulas and expertise to recognize coronary occlusion when it was not previously diagnosed or suspected.  I am reluctant to reverse a diagnosis of ***STEMI*** because I would rather there be a false positive cath lab activation than a false negative.

However, with some practice and expertise, this can be done with very high accuracy.

First, let's address the precordial STE:
1. The T-waves are not tall: the T/ST ratio is low (T-wave not much taller than ST segment)
2. High R-wave voltage (the single best predictor of whether subtle precordial STE is due to LAD occlusion or not!)
3. Very well-formed J-waves in V4-V6

You could consider using the formulas for differentiation of subtle LAD occlusion from normal variant STE.

One problem with this: there is a non-concave ST Segment in lead V2.  This is rarely seen in early repolarization (normal variant), and such cases were excluded from our study.  However, in this case, I happen to know from simple expert recognition that this ECG is an exception to the rule.

Using QTc = 399
RAV4        = 19
QRSV2     = 23
STE60V3  = 2.5

3 variable = 20.34 (very low, most accurate cutoff is 23.4)
4 variable = 14.84 (very low, most accurate cutoff is 18.2)

Second, let's address the limb lead STE

Inferior MI?  No
1. The inferior STE is limited to lead II, and has significant PR depression
2. There is no reciprocal ST depression in aVL, which is present in 99% of inferior MI.

High lateral MI?  No
1. The STE in I and aVL are associated with flat T-waves
2. There are well formed J-waves
3. There is no reciprocal ST depression in lead III.


ECG Diagnosis:

Normal variant ST Elevation vs. Pericarditis.  No evidence of MI (which is different than saying that the patient does not have MI)

Final Diagnosis:

No MI.  Uncertain whether there is pericarditis or normal variant.

I favor normal variant for several reasons
1. No active chest pain
2. No objective signs of pericarditis (no rub, no effusion, no positional pain)
3. Normal variant is far more common
4. It simply looks to me like normal variant
5.  I believe that in this age of highly sensitive troponins that any ST elevation caused by pericarditis should be associated with some release of troponin.  Here all were below the level of detection.

7 comments:

  1. Insightful example of when ST elevation is not the result of acute stemi. Nice discussion by Dr. Smith covering both the negative formula values, as well as qualitative reasons for why the ST elevation here was not suggestive of an acute event. To simplify, the ST elevation here is diffuse in virtually all leads except leads III, aVF and aVR — whereas ST elevation with acute stemi is most often localized to one or more lead areas — but not everywhere. ST elevation with acute stemi typically shows a unified picture in the 3 inferior leads (either elevation or reciprocal ST depression) — and not ST elevation in lead II, but flat ST segments in leads III and aVF as we see here. As a final thought — there ARE definite Q waves in leads II, III and aVF, with fragmentation of the QRS complex in the latter 2 inferior leads. As the patient is “50-something” — this does raise the question of whether there may have been previous inferior infarction. And possibly the early transition (between V1-to-V2) with abnormally shaped ST segment in lead V2 could reflect prior posterior involvement. Additional history and availability of a prior ECG for comparison would be extremely helpful. In the absence of such a prior tracing — it seems unlikely that this tracing represents an acute syndrome for the reasons detailed by Dr. Smith.

    ReplyDelete
  2. Dear Professor!
    It is really not STEMI and not MI, but in my humble opinion possible CAD.
    The QRS visibly changed in lead III and aVL. (reversible WMA?)
    Made cardioecho from the patient?
    Did not more ecg recordings be made on ED?
    Best regards:
    Laszlo Farkas

    ReplyDelete
    Replies
    1. Laszlo, I'm not sure what you're trying to say.
      Steve

      Delete
  3. Sir, is there fish hook pattern in V3-V6?

    ReplyDelete
    Replies
    1. Yes, that is what is meant by "J-waves"

      Delete

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