37 Year Old Male–CC: Chest Pain, Part II

This is part II to “37 year old male–CC: Chest Pain“. You may wish to review the case.

So, while many of our cases are straightforward, this one is not.

But hey, our patients don’t read the textbooks!

First, let’s review the chief complaint:

Our 37 year old male had “chest tightness”, but complained of lethargy and “chills” for at least a couple of days. While we must take the complaint of chest pain seriously, many of you pointed out that the history did not seem like typical ACS. We can’t blow off chest tightness, but the history is no slam dunk.

Here again is the 12 lead ECG:

casestudy9:13-1

There is sinus rhythm at a rate of about 83 bpm. Axis is normal. QRS is slightly widened. PRI is normal, and we can debate whether or not there is slight PR segment depression. There is some artifact present. Using the TP segment, there is slight (<1mm) STE in leads II, III, aVF, V5 and V6. If you use the PR segment, which may have some slight depression, you will see a bit more ST elevation. All ST segments are upsloping. Regarding V2-V4, is there any ST elevation? Some will say yes, but there is some wandering of the baseline, and I am not convinced. If there is any, it is a small amount. All ST segments seem to be concave up. There is no reciprocal ST depression. We do not have the computer interpretation/measurements for this ECG.

What do we make of this ECG? Again, as in the history, no slam dunk. I think we can realistically consider three possiblities:

  • ACS
  • Pericarditis
  • Early repol

ACS: Was it reasonable for the crew to run this as ACS? I think so. Even if the story sounds a little odd, we can’t rule out ACS based on anything here. Does the ECG show STEMI? The constellation of changes we have is not really consistent with the ST elevation of STEMI. Some may point out the inferior ST elevations, but where is the ST depression in aVL? We don’t have it, and if it were inferior STEMI we should see it. In fact, there does not seem to be any reciprocal depressions anywhere.

In his most recent post, Dr. Smith writes: “Does inferolateral STEMI also have reciprocal depression in aVL? In my experience, yes. I have yet to see an inferolateral STEMI without some reciprocal depression in aVL, in spite of the lateral ST elevation in V5 and V6″.

We can treat for ACS, but I don’t think anyone is activating the cath lab based on this ECG.

Pericarditis: The favorite choice in the comments section was pericarditis. The history, especially feeling “sick” with “chills” for a few days opened up the possibility of infection. On the ECG, we have some widespread ST elevations, although not a large amount. There seems to be some slight PR depression, which is why I used the TP segment to measure the STE. The axis is towards lead II but slightly away from aVL, so I think the axis is somewhere between 70-80 degrees. This could be consistent with pericarditis, which is usually towards 60 degrees.

Early Repol: Could this be early repol? With slight concave up ST elevation, it could also be early repol and his normal baseline ECG.

Playing the odds, we can recall that pericarditis is in fact a relatively rare diagnosis.

In his most recent post, Dr. Smith writes that “baseline inferior ST elevation (early repol of the inferior leads) is more common than pericarditis, and if a patient complains of chest pain, and happens to have baseline inferior early repol, they are likely to get a diagnosis of pericarditis if they rule out for ACS”.

How do we manage our patient? I don’t think we can tell from this one ECG what the issue is. The ECG is non-diagnostic. As I said earlier, I think it is reasonable to treat for ACS. While this case may not scream ACS, we can’t rule it out either. It doesn’t appear to be STEMI, so I don’t think we need to activate the cath lab.

Supportive care is in order, but what I really think would be helpful are serial ECGs. We may see evolutionary changes of ACS or of pericarditis, or we may see no dynamic changes at all. But it would probably give us more insight into his condition.

In the ED, echo and troponins would likely give us the diagnosis.

So how did the crew handle our patient? They opted to activate the cath lab and treat with ASA and NTG. Upon arrival at the cath lab, the cardiology team is split as to what to do before finally deciding on angiogram to rule out any blockages. The cath was clean.

The final diagnosis was “reaction to medication”. Apparently he had not been compliant with how to take his regimen of pain meds.

This case was not straightforward, but sometimes these types of cases can be the most interesting. They inspire a lot of great comments and discussions as well. Thanks to all who participated!

2 Comments

  • JBuckle says:

    With the final part of the case posted I feel I can finally acknowledge how great it has been to read the discussion around this case. It was a really odd case and really split us as a crew so it was interesting to see what other people would conclude.

  • David Baumrind says:

    Thank you again for the excellent case Jack!

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