Monday, November 7, 2016

Respiratory Symptoms and ST Elevation with Hyperacute T-waves

An elderly woman was brought to the ED for hypoxia.  She had a history of chronic respiratory failure with a tracheostomy and had had multiple episodes over the past few days of increased respiratory effort and hypoxia (down to an SpO2 in the 70s on supplemental O2 via nasal). Associated with this has been increased secretions requiring aggressive suctioning.

On exam in the ED, the patient did not appear nearly so ill and was not hypoxic.

A routine ECG was obtained:
There is inferior and lateral ST elevation with hyperacute T-waves, and reciprocal ST depression and T-wave inversion in aVL.
This is all but diagnostic of STEMI and should be considered to be so until proven otherwise. 


The cath lab was activated.

She was given a full dose of aspirin and a heparin bolus of 4000 units. A repeat ECG demonstrated no dynamic changes.  Bedside cardiac ultrasound had grossly normal systolic function with no apparent wall motion abnormality.

Because the patient had no symptoms specific to STEMI and an ECG that was not evolving, and while waiting for the cath lab to be ready, the very astute providers sought out a previous ECG and were able to get one faxed from another hospital.

It looked exactly the same!

So they waited for the first troponin and it was below the level of detection.

They decided against an angiogram.

The patient ruled out for MI by serial troponins.

This turned out to be the patient's baseline ECG!

Learning Point

Rarely, a patient's baseline ECG looks just like a STEMI.  It never hurts to find a previous one unless it delays care.

9 comments:

  1. What's the patients diagnosis? Hyperkalemia and Acidosis?

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    1. The diagnosis was excessive respiratory secretions, but there was no resp acidosis and on arrival to the ED the patient was not hypoxic. The ECG is simple the patient's very abnormal baseline. And very unusual.

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  2. Unbelievable and very concerning tracing. I would have activated cath lab me too.
    What have surprised me was that troponin was below the URL; in my experience with ultra-sensitive troponin almost all patients have positive troponin.
    Thanks for teaching once again!

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  3. Dr. Smith, thank you for sharing the case!
    As a medical student volunteering for the local ambulance team, I have seen a similar case and I was really confused since there was an older ECG recording and they were identical, just like the ones in your post. I could swear there was an evolving inferior STEMI on his ECG, but how could it be in that case?
    The patient was a white male in his mid-fifties, with a history of atrial flutter and high blood pressure, but in no acute distress. At the time he had no specific cardiac complaints. His chief complaint was a headache lasting for a couple of days. Unfortunately, I cannot remember his vitals or other details, but I can tell his systolic BP was roughly 180mmHg when in a supine position, on both hands and 150 when standing, on both hands, and his pulse roughly 90bpm. He was transported to the hospital and even if I couldn’t follow him up, I am quite sure they ruled out an AMI.
    Is there any “chronic” condition that could give this “acute” aspect on the ECG? Are there any electrocardiographic criteria to rule out an AMI in this case?
    Best regards,
    C.

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    Replies
    1. Sometimes people simply have false positive EKGs and you might need to do an angiogram to find out that it is not an MI.

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    2. Could it be a case of benign(-ish) early repolarization?

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    3. It doesn't look anything like early repol. It is its own STEMI look-alike!

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  4. I didnt measure any intervals, but the qtc seems abnormally short for stemi. Was there a previous inferior wall MI? Or was this baseline without previous coronary disease?

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    Replies
    1. Good observation! We published data on this: 8% of inferior STEMI have a QTc less than 390 ms. The QTc here is indeed short at about 370 ms, with a QTc-B of 389 ms.

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