Friday, March 3, 2017

Another 40-something with intermittent chest pain

I was sent this ECG by a resident from elsewhere, with the following information:



"Young previously healthy man with several 10-20 minute episodes of chest pain over the past few hours, asymptomatic on presentation and during this ECG."

"What do you think?"

There are Q-waves in V2 and aVL.  The T-wave in V2 is too large for this Q to be due to old MI.  There is minimal STE in aVL and a proportionally large T-wave, with a reciprocally large T-wave in lead III and a biphasic down-up T-wave in aVF.
There is some STE in V2 and V3, but this cannot be called normal variant because there is a Q-wave in V2 and poor R-wave progression.
All of these are very worrisome for LAD or D1 ischemia.


Here is my response:

"Old MI with superimposed LAD or First Diagonal acute ischemia.  Q-wave in V2, aVL suggest old MI, but T-wave is too large in both to be old.  Alternative is subacute MI of these vessels."

"Please send info."


Case:

This is a 40-something who complained of several 10-20 minute episodes of chest pain over the previous few hours.  He had no prior medical history, but is a smoker with a positive family history of CAD.  He arrived at 7:30 pain free and had this ECG recorded at 7:32.  I will repost it here:
See above description


The first troponin was undetectable (cTnT, < 0.01 ng/mL) and he was sent to the observation unit for serial troponins without recording any more ECGs.


Smith comment: this is not acceptable.  One should at least perform many serial ECGs to look for either resolution or evolution of these T-waves.  Since his pain had resolved and was still gone, one would expect resolution of the large T-waves and minimal ST elevation and this would be diagnostic.

Case continued:

At 8:30 he complained that his pain was returning and another ECG was recorded at 8:42:
This is slightly BETTER than the previous  There are smaller T-waves, and less STE in aVL, and the reciprocally inverted T-wave in III is not as deep.  The down-up T-wave in aVF is now all up.
This ECG represents dynamic ACS

--Proving that serial ECGs recorded in the ED would have shown resolution of the T-waves.  
--Now they are growing larger from what would have been seen on an intervening ECG 


The ECG was interpreted as No Change.


Case continued:

At 8:50 he had "seizure like activity" that resolved (probably an episode of pulseless VT) and was moved to the ICU, where he had this ECG:
Obvious proximal LAD occlusion (STEMI)



Here is his next 12-lead:
Ventricular Fibrillation is not supposed to be captured on a 12-lead ECG!


This is after defibrillation and the patient had a pulse and was awake:
Slow and sick!  Take me to the cath lab!!


This was recorded just before he was taken to the cath lab:


Here is the angiogram:
Proximal LAD occlusion


Here annotated with arrows:




Learning Points:

1. Real ECG findings of coronary occlusion can be extremely subtle!
2. Learn to recognize hyperacute T-waves.
3. Learn to recognize down-up T-waves
4. Learn to recognize the reciprocity between aVL and III
5. Troponins are not reliable for diagnosis of early ischemia/occlusion
6. There is still a role for observation!

6 comments:

  1. Very interesting case and many learning points, as always; thank you! I noticed in the last ECG, recorded before cath lab, ST elevation in lead II (instead of ST depression seen in the ECG showing clear STEMI) and ST-T anomalies resembling DeWinter. Did angio results show a wraparound LAD?

    ReplyDelete
    Replies
    1. Mario,
      I don't believe it was wraparound. I do think that on the 8:50 ECG, lead II looks like a de Winter's T-wave. Which is pretty interesting because that has only been described in precordial leads.
      Steve

      Delete
  2. Indeed very helpful case, and I probably would have missed this finding too. Great to learn from you!
    For your initial response ("Old MI with superimposed LAD or First Diagonal acute ischemia. Q-wave in V2, aVL suggest old MI, but T-wave is too large in both to be old."), is there a single finding you'd consider significant for acute ischemia, or is it the combination of hyperacute T and down-up T-waves? For those of us not seeing hyperacute T-waves on a daily basis, is there any guide you can give to e.g. differentiate from early repol in left vent. hypertrophy? And for the Q-Wave in aVL: I learned that Q-waves need to be in two contiguous leads to be considered "pathologic" (what aVL and V2 are not, as far as I know), but you consider this pathologic and are obviously right in the context of the angiogram. When do you start to consider a Q wave as pathologic?

    ReplyDelete
    Replies
    1. Not just a combination of hyperacute T and down-up T-waves. There is ST elevation in V2 and V3. Of course that amount of STE can be normal. But when it is normal, there are always well formed R-waves. In this case, there are not. In fact, V2 has a Q-wave. so it cannot be normal variant ST elevation!

      Read my paper here: http://www.annemergmed.com/article/S0196-0644(12)00160-6/pdf

      Delete
  3. Steve,
    Great ECGs. I too wondered about a wraparound LAD. Any other plausible explanation for the HyperAcute almost "DeWinter" Inferior T's on the last ECG? Co-culprits? It is interesting.
    Sam

    ReplyDelete
    Replies
    1. Sam,
      sometimes the low flow state of cardiac arrest can lead to type II STEMI. Especially if there are flow limiting fixed lesions in the involved artery (in this case, the RCA).
      I don't know if that is the case here, but I suspect so.
      Steve

      Delete

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