Wednesday, March 1, 2017

A 40-something with chest pain in the middle of the night

This was sent by one of our former residents.

Case

"A 40-something year old man awoke with chest pain in the middle of the night.  He had a h/o HTN and positive family history of CAD.   He had no other risk factors.  His pain was very typical sounding, with nausea, diaphoresis, and SOB."

"He was given 4 aspirin given by EMS, and was given 3 NTG and his pain went from 8/10 to 3/10.  He looked a bit sick.  His prehospital ECG was pretty identical to this initial ED ECG as #1.   There was no prior for comparison."  

Initial ED ECG, time zero:
What do you think?













Thoughts from the doc who sent it:

"I had a ton of concern about his T waves being too big in the lateral precordial leads."

Smith comment: Agree!  The T-waves are not large at all, but relative to the small QRS, they are indeed huge!  The T-waves in I and aVL are also far too large, and have a reciprocally inverted and large T-wave in lead III.  The T-wave in V2 is far too large for that small QRS.


Case continued:

"We did a repeat ECG at about 30 minutes:"
No significant evolution, but some small resolution of T-wave size.





"I thought it showed no significant evolution.  My own bedside echo looked to have some septal WMA (but our machines are suboptimal and he was a little technically difficult)."

"So we did another repeat ECG:"
About the same




"The ECG was still the same.  The chest pain waxed and waned.  I gave another 3 rounds of NTG with improvement, but the pain was still there."

"I called cardiology and told them the story.  I told them very clearly of my concern for hyperacute T-waves, and the cardiologist said that this was an "overcall" and that they were normal.  Honestly, this was what I expected to hear them say."

The initial troponin then returned at 0.080 (99% = 0.045.  This slightly elevated troponin should clinch the diagnosis.  However, it apparently did not change management.

It is important know that it would be very common for the initial troponin to be entirely negative, as it is in about 50% of full blown STEMI.

But the ED doc did the right thing!

"Still concerned I called in the Echo tech in the middle of the night."

"I sent him to the ICU on Heparin and NTG drips.  About 20-30 min after admission, I heard the cath lab announcement overhead.  I look and he did in fact have a wall motion abnormality."  

"He went to the cath lab and there was a 100% mid-LAD occlusion with thrombus and also thrombus in the posterior descending artery but this artery was open (dual culprits!).  He got two stents: one in the mid LAD, restoring TIMI-3 flow, and also one in the distal Left Posterior Descending Artery.  All in all, he went to the cath lab in about 3-4 hours from arrival."

Here is the post-cath ECG:
These are normal T-waves.
Note the difference!!
Note that they are proportional to the small QRS!!


Learning Points:

1. Acute LAD occlusion can be very subtle on the ECG.  In a study by Marti et al., who took all patient with any suspicion of coronary occlusion to the cath lab, 13% of acute LAD occlusion had less than 1 mm of ST elevation in V2 and V3.
2.  Beware hyperacute T-waves!!
3.  When you are concerned about acute coronary occlusion, but the ECG is not definitely diagnostic, there is a middle way between cath lab activation and no activation: pursue agressively with diagnostic adjuncts: compare with old ECG, do serial ECGs, do high quality echo.
4. You are not held to the same Door to Balloon Time standard in these occlusions that to not meet STEMI criteria.  They will be called NonSTEMIs!  But these NonSTEMI patients have better outcomes with early reperfusion, compared to next day angiogram and PCI.
5.  If you are concerned about subtle coronary occlusion, pursue it with formal echocardiogram
6.  It is not the size of the T-wave, or the height of the ST segment, that makes the diagnosis, it is there size in proportion to the QRS!

14 comments:

  1. Thanks for a nice case! a small query. Although both LAD and LPDA were acutely occuluded, this LPDA would be the primary culprit as hyperacute T WAVES were prominent in high lateral leads and V2. your thoughts sir?

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    Replies
    1. It is a good question! I think the primary culprit was the LAD, but it's not certain, and may have been both.

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  2. I have learned about proportionality in this blog. Thank you, Dr. Smith!

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  3. What are your criteria for "oversized" T-waves? >25% of QRS?

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    Replies
    1. Good question, but I do not have a good answer. There is more to it than just height. Also "bulkiness" and width.

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    2. For Pierre Taboulet (Paris - Dr Smith knows him) from Minnesota-Code 1960:

      < l'onde T a une amplitude maximum < 2/3 du QRS >

      merci

      Al

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    3. But based on what angiographic research? Show me the study.

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    4. We did study this: we found that the T/R wave amplitude ratio in early repolarization had a mean of 0.7. The mean in acute left anterior descending artery occlusion was 3.1. We did not look for a cut off value. Here's the study: http://www.annemergmed.com/article/S0196-0644(12)00160-6/pdf. See the main big table.

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  4. Repeat troponin value?

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    Replies
    1. A later troponin returned at 51 ng/mL. Very high.

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  5. What to mention about poor R Wave Progression in the Precordial Leads !

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  6. GREAT case! My initial impression looking at the initial ECG was that the leads (especially leads III and aVF) just “looked funny” — almost as if there was some type of lead misplacement. That is, the amount of T wave inversion (especially in lead III) looked extreme — albeit both QRS and ST-T wave appearance in lead III was indeed the precise “mirror-image” of the QRST & ST-T wave in lead aVL …But there is no lead misplacement — as the P wave in lead II is upright, and there is global negativity in lead aVR as there is expected to be. Looking next at the chest leads — not only R wave progression, but also R wave amplitude looks uncharacteristically reduced — which if not due to large body habitus (I don’t think this patient’s body habitus was described … ?) should raise the question if loss of R wave on this initial ECG is the result of an acute ongoing event. Regardless of questions raised by these findings — there is little doubt (as recognized by the treating ED physician) that T wave amplitude in lead V2 in a patient with new chest pain is clearly abnormal given morphology and amplitude of the QRS complex in this lead. The fascinating part of this case to me is lack of evolution in serial tracings — with credit to the treating ED physician who pursued his instincts until they were finally confirmed by the abnormal Echo findings. Final comparison with the post-stent ECG is enlightening. Lack of R wave progression persists (still wondering if that was due to large body habitus?) — but the “funny” (ie, abnormal) ST-T wave appearance in all leads has resolved — confirming that distinctly unusual ST-T wave appearance on an initial ECG from a patient with new-onset chest pain, even if the ECG fails to evolve over serial tracings — should prompt consideration of an acute ongoing event until proven otherwise. THANKS for presenting this case!

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  7. Great case. With reading this blog and your book, I am much more confident interpreting ekgs and formulating plans for chest pain patients, and was able to get a 30 year old with nondiagnostic EKG to the cath lab (99% LCX). I'm 5 months from graduating residency and cannot imagine heading out without that self-study. Thanks!

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