Tuesday, July 5, 2011

Missed STEMI, spontaneously reperfused

Click here for other very instructive cases of missed STEMI.

This is a 48 yo female with no risk factors for CAD had sudden onset of arm numbness radiating to bilateral arms, followed by substernal chest heaviness that radiated to both sides of chest.  She had some associated SOB.  In previous weeks she had been having SOB when climbing 2 flights of stairs.  She called 911.  Medics arrived and recorded the following ECG at 1756:
There is sinus rhythm and a wandering baseline.  There is no ST elevation nor hyperacute T-waves, nor ST depression anywhere.   The ST segments are upwardly concave.  R-wave progression is normal.  It is a normal ECG.

The medics gave her sublingual NTG with some decrease in symptoms. They gave her an aspirin.



She presented to the ED at 1832 is some distress; the nurse's note mentions "grunting, mottled." 

This is the patient's first ED ECG, recorded at 1845:
There is now 1 mm of ST elevation in V2 and minimal STE in V3.  The ST segments are straight.  There is poor R-wave progression.  The T-waves are larger.  This description makes it sound like MI, but really, at a glance, it is not terribly remarkable on its own -- until you compare it with the previous.



The physicians caring for the patient were unaware of the prehospital ECG, and did not go look for it.  The patient remained in some discomfort, but no serial ECGs were obtained.  The first troponin was negative.  At 2016 the patient had no more grunting respirations.

With the ECG read as normal, a negative troponin, and a low risk patient, the providers did not have a high suspicion for ACS, so admitted her to observation with no further antiplatelet or antithrombotic therapy.  By the time of admission to observation, she had no more chest pain.  No more ECGs had been done.

Troponins

First trop at 1932 "normal" (negative)


Drawn at 2335: 34.8 (this returned at 0100, prompting the following ECG at 0111, 6.5 hours after the last one)
There are now Wellens' T-waves in V1-V5 and poor R-wave progression.


What happened?

One needs to view the prehospital ECG and the ED ECG side by side:
ED ECG is on the right.  Notice the T-waves are taller and fatter, the ST segments straight, and the R-waves have less voltage.  This is almost certainly a developing anterior STEMI.



Had this side by side comparison been done, the index of suspicion would have been much higher.  Perhaps a second, or third, ED ECG would have been recorded.  It almost certainly would have revealed more ST elevation and had indication for immediate reperfusion.

That her pain eventually spontaneously subsided indicates probable spontaneous reperfusion.

Subsequent troponins
0250: 41.7
0455: 35.6

An echocardiogram the next day showed an EF 55% and a regional wall motion abnormality in the distal septum, anterior and apex.

An angiogram later that day showed the culprit lesion at a 60% LAD stenosis (the patient did indeed have spontaneous reperfusion, but not before losing a significant amount of myocardium).

Learning points
1.  This is labelled a NonSTEMI, and shows one of the many ways in which a damaging coronary occlusion is called a NonSTEMI rather than a STEMI: the fewer ECGs you record, the less chance your STEMI is called a STEMI.
2. Always do serial ECGs in patients with ongoing unexplained substernal chest pain.
3. Always compare the ED ECG with the prehospital ECG
4. Beware of straight ST segments, and any ST elevation that is not accompanied by well-formed R-waves.  Early repolarization always has well formed R-waves.  This is the main reason why my early repol vs. MI equation works (although, in the study, I excluded any patients with straight ST segments).

2 comments:

  1. Wow... same MI as mine, minus the R-wave progression. This must be missed all the time. Thank you so much for educating people about this.

    Just curious thouogh..., why did you not classify this as Wellens? Not enough EKGs to show a progression?

    ReplyDelete
  2. Wellens', strictly speaking, refers to T-wave inversions in the anterior precordial leads, with persistently present R-waves, and in the absence of chest pain (pain resolved). Other T-wave inversions may be analogous, depending on the situation.

    ReplyDelete

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