Monday, July 6, 2015

Diffuse ST Elevation and Chest Pain, What is it?

A male in his 40s presented by EMS with 24 hours of chest pain.  The pain was central, anterior, dull and squeezing, and 5/10, not worsened with activity but associated with mild shortness of breath.

No prehospital 12-lead could be found.

Here is the initial ECG at time zero:
QTc is 386 ms.  There is scary ST elevation especially in V2 and aVL, with some reciprocal ST depression in III.
However, the ST elevation in V2 has a saddleback appearance.  I have seen Anterior saddleback ST elevation as a finding in anterior MI only once ever, in all the ECGs and MIs I have reviewed.
If you apply the early repol vs. LAD occlusion formula, it comes out positive.

This is a one of the recognizable patterns of early repolarization.
But of course diffuse ST elevation can also be due to pericarditis.


The emergency physicians were appropriately worried about STEMI, but recognized that this could be a false positive.  They obtained a second ECG at 11 minutes:
No change

Still not convinced, they called for a formal Definity contrast echo.

This was done and was completely normal during the pain and during the ECG findings.  No wall motion abnormality.  The patient ruled out for MI.  All trops were undetectable.  There was no effusion.

Was this early repolarization or pericarditis?

The final diagnosis was pericarditis, but I am not entirely convinced.

Some comments on the ECG were that there was PR segment depression.  This is true, but it was consistent with a normal amount of PR depression. PR segment depression is a normal finding, and only if greater than 0.8 mm is it specific for pericarditis (Charles MA et al.  Arch Int Med 1973;131:657).

One later history said there might be some pleuritic component.  Another history stated that is was worse lying back, but these were late notes, written only after some diagnostic anchoring may have taken place, and written without conviction. 

There is a Spodick's sign, which is a downsloping TP segment.  This is widely claimed to be specific for pericarditis, but I cannot find any original study that shows this.  It seems to me that this is also commonly seen in early repol.  Amal Mattu has done an as yet unpublished study in which he found it unreliable (personal communication).  Does anyone know of original literature on Spodick's sign (not just case reports) that convincingly shows that Spodick's sign is specific for pericarditis?  

There is also ST depression in lead III, which really should very much heighten suspicion for high lateral STEMI.  However, Spodick did find ST depression in lead III in 14% of pericarditis, and I have cases of early repolarization which also have this finding. (This image is from this interesting post.)

One small study (n = 20 in each group) from 1982 showed good sensitivity and specificity of ST/T ratio in lead V6, greater than 0.25 for pericarditis and less than 0.25 for early repol. This is because early repol has large T-waves.  We see a ratio of 0.4 in this case, and it is the most convincing evidence that this case does indeed represent pericarditis.

Spodick himself compared early repol to pericarditis (NEJM 1976; 295:523), and found:
1. PR depression always occurred in both limb and precordial leads in pericarditis, but only in one or the other in early repol.  This finding was 100% sensitive and specific.  Here there is minimal PR depression in limb leads.
2. ST vector in pericarditis is leftward and to the left of the T Vector.  ST vector in early repol is vertical and the right of the T vector.  In this case they are the same.
3. ST depression in V1 was almost never present in early repol, but was present in about 1/3 of pericarditis.  There is STE in V1 here.
4. Also, of less value: STE occurred in both limb leads and precordial leads in all pericarditis, and only 2/3 of early repol.

He says nothing about "Spodick's sign" in this paper.  I have found Spodick's sign to be unreliable.

There are a few ways to definitively diagnose pericarditis, as I see it:

1. Presence of definite pericardial friction rub
2. Presence of PR depression greater than 0.8 mm, with PR depression in limb and precordial leads
3. Presence of typical widespread ST elevation in which both a) MI is ruled out and b) the morphology is clearly not right for early repolarization
4. Presence of effusion (be certain it is not hemopericardium due to MI or dissection) 
5. Typical evolution of ECG findings, in stages: 1) ST elevation 2) resolution of ST elevation 3) Evolution of T-wave inversion 4) Resolution of T-wave inversion.  Not all cases of pericarditis manifest all 4 stages, and one must also time the ECGs correctly to see it.
6. Is the ST/T ratio in V6 reliable? Maybe.
7.  MRI???

There are many cases of pericarditis which are not diagnosed because they don't fulfill any of these criteria.

But two mistakes are often made:

1. The MI patient is diagnosed with pericarditis, or myopericarditis.  See this case.  And this case.   There seems to be a certain joy that clinicians take in diagnosing pericarditis and it leads to anchoring prematurely on the diagnosis.  That is why I say: "You diagnose pericarditis at your peril."
2. The patient has early repol but is falsely diagnosed with pericarditis. Usually this is of no consequence, as the pericarditis is not serious and is treated similarly to chest wall pain (NSAIDs), although one would give colchicine too for true pericarditis.

Here is a case in which this confusing early repol with pericarditis led to diagnostic anchoring and possible catastrophic outcome:
http://hqmeded-ecg.blogspot.com/2013/12/31-year-old-male-with-ruq-pain-and.html

The next posts will be cases of definite pericarditis.

4 comments:

  1. Hi Smith
    Is there any progression of ECG if this male is dignosed as pericarditis?

    ReplyDelete
  2. Greetings,
    That P wave in II is huge! Was this judged to be a finding of no significance?

    ReplyDelete
    Replies
    1. Yes, it is large, and could represent right atrial enlargement and possibly pulmonary hypertension, but is not terribly specific for that and does not contribute to the diagnosis of the acute symptoms.
      thanks,
      Steve Smith

      Delete

Recommended Resources