Saturday, December 23, 2017

Serial ECG recordings are essential: paramedic makes a great call!

This case was sent by Andrew, an Intensive Care Paramedic from Melbourne, Australia.


Case

We were dispatched to a female in her 50's who had been experiencing L) sided, intermittent chest heaviness, radiating to her L) arm for the past ~24 hours. 

She had a past Hx of IDDM, hypertension, high cholesterol and was an ex-smoker. She had called the ambulance today as the pain was more severe and persistent than it had been previously. She had never experienced symptoms like this in the past.

When we arrived, she was c/o 8/10 pain and was mildly diaphoretic, but not looking overly unwell. I recorded this ECG.

I read this as normal


The pt was given 300 mg aspirin and 300 mcg sublingual GTN, with the pain reducing to 5/10.

A few minutes later, her pain then increased to 7/10 and she appeared a bit more diaphoretic. I took the following ECG.
Now there is new ST elevation in V2-V4, with tiny new Q-waves


was concerned with the 1mm STE she developed in V2 and 0.5mm in V3-V4 as well as the presence of small Q waves. The T waves also looked bigger and fatter to me when compared to the initial ECG. Unsurprisingly, the computer interpretation failed to recognize these changes.


Her pain then reduced to 3/10, which prompted me to record another ECG. 

All the segments have returned to isoelectric, the Q waves and T waves also appear smaller and are consistent with the initial ECG.


Based on the presence of dynamic ST segments and T waves, I chose to bypass two smaller hospitals and transport her to a PCI centre with a STEMI notification. 

Throughout the transport to hospital, there was no change in the ECG from #3, but upon arrival at ED, she was pale and profusely diaphoretic, and still complained of 1/10 pain post IV analgesia.

The ED consultants were skeptical of my read.

About an hour after our arrival, she became agitated and hypotensive and the final ECG was taken.
Obvious Anterior STEMI



The pt was taken to Cath Lab where her LAD was stented. There was minimal rise in her troponin and CK and she was doing well the following day.



1 comment:

  1. GREAT case, with tremendous credit to the Intensive Care Paramedic Andrew whose close clinical follow-up was key to optimal management of this patient! I would be VERY curious to know specifics of the cath report, as well as about this patient’s prior cardiac history and baseline ECG. I’d add the following thoughts. ECG #1 is NOT “normal”. In a patient with new chest pain — the ST segment flattening and more-prominent-than-should-be rounded T wave in lead III is clearly suspicious (though not diagnostic). The flattened ST segment in lead aVL is also nonspecific (and not really a “mirror-image” of what we see in lead III) — but one wonders WHY this ST segment is so FLAT (this is usually not seen in a patient with chest pain when the ST-T wave in lead I is so normal … ). Finally, there is early transition (R wave already taller than the S wave by lead V2!) — and there is hint of a small q in at least 2 (if not 3) of the 4 complexes we see in lead V2 (which is not “normal”). The meaning of these findings is admittedly uncertain — but certainly merits the close follow-up with serial tracings, as was done. ECG #2 — now shows small q waves in leads II and aVF, in addition to the more prominent initial q waves in leads V2-thru-V6. Not only is there now subtle-but-real ST elevation in leads V1-thru-V4, but also in lead aVF. This made me wonder about whether the “culprit artery” was the RCA, LAD, or perhaps an LAD with “wraparound”? In ECG #3 (at which time the patient’s chest pain had lessened) — anterior ST segment elevation had come down, as was mentioned. BUT, in addition — there IS now clear ST elevation in each of the inferior leads that was NOT present initially … ECG #4 obviously removes all doubt about an acute evolving STEMI — and localizes the “culprit” to the proximal LAD (in addition to marked chest lead ST elevation that is maximal in V2 — there is now clear ST elevation in lead aVL + marked reciprocal inferior ST depression). It now makes sense why q waves developed in leads V2,V3. My QUESTIONS — are why did we see the dynamic inferior lead QRST changes that we did? My Theory — I suspect the reason for modest initial ECG changes was a “cancellation effect” between inferior wall ST elevation + reciprocal ST depression in lead aVL + anterior ST depression from posterior wall involvement — AND — impending proximal LAD occlusion in process of producing opposing changes (ie, inferior ST depression; ST elevation in aVL; marked ST elevation in anterior chest leads). How else can you explain the uncharacteristically FLAT ST segment in lead aVL initially — that eventually evolves to clear ST elevation when ECG effects of the anterior STEMI predominate? Is this from multi-vessel disease? From an LAD with “wraparound”? Unusual collateral circulation effect? Obviously there is the large anterior STEMI to deal with — but I thought the above observations fascinating from an academic standpoint. P.S. Without access to prior ECGs on this patient — we don’t know if the very early transition (marked tall R wave already by lead V2 as soon as the 1st ECG) is an acute effect — or reflective of prior posterior infarction … Enticing issues for discussion! THANKS for presenting — and GREAT job by Andrew on this case!

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