Saturday, August 1, 2015

"Early Repolarization" followed by ventricular fibrillation.

This is a repost of part of one of the most viewed posts ever.

This patient with little past medical history presented feeling moderately ill.  He had an ECG recorded:   
QRS duration = 102 ms.  What do you think?

Due to the peaked T-waves, the residents were immediately concerned for hyperkalemia and sought an old ECG, which they immediately found in the medical record.  It was recorded with a K of 4.5 mEq/L: 
QRS 82 ms.  

The residents interpretation was that these were identical.  After viewing this previous ECG, and knowing that the K was 4.5 at the time it was recorded, the residents believed that the peaked T waves in ECG #1 were this patient's baseline.  

Are they identical?  

Inspect lead V4 more closely, here for a side by side comparison:
On the left, the ST segment is nearly flat and rises abruptly.  On the right, it is not flat (though nearly so) and rises slightly less abruptly

It is true that early repolarization has tall and relatively peaked T waves, but not to the extent seen in ECG #1. Without seeing them side by side, it is hard to appreciate the difference. 

This patient, then, did not get immediate treatment for hyperK. 

I saw these ECGs at a slightly later time than the resident, recognized the difference and, worried about the patient, started toward his bedside.  As I was approaching the patient, he had a v fib arrest.  He was immediately resuscitated, then his K returned at 7.0 mEq/L.   This was a presumed hyperkalemic arrest.  

Some say you don't need to treat hyperK unless there is QRS widening.  They claim that peaked T-waves are not enough.  This is only one case, and anecdotal, but we found no other etiology of arrest in this patient.  I always treat immediately if the ECG is affected by hyperK

There is a definite difference, with EKG 1 pathognomonic for hyperkalemia.


  1. Are they epsilon waves in inferior leads?

  2. Dr Smith,

    Instinctively my eyes were drawn to the more significant differences in t wave amplitude in V2/3 rather than the more subtle V4 change. Would I be wrong?



    1. Richard,
      No. that is an excellent observation.
      I think the ST segment is V4 is a more specific change though.
      Steve Smith

  3. Great case report! Thanks.
    As I look in V3 and especially V4, the tall and peaked T waves confuse me, as I could wrongly think of a grade I ischemia. And in V4V5 I see a ST depression that strengthens this... What do you think?
    Thank you all

  4. Excellent tracing and a great lesson for all. Like "Bauldy," my eyes were also immediately drawn to the changes in V2-3. And I couldn't agree with you more about testing for and treating hyper K+ as soon as you are able to detect it on the 12-lead ECG. During my residency in internal medicine, it was always pounded into us that once there are changes indicating hyper K+ on a tracing, arrest can occur AT ANY TIME - one doesn't wait for an ECG to show a progression to QRS widening and sinoventricular conduction. Your case - though anecdotal - certainly supports that concept (and no one has ever been harmed by running a serum K+). Regarding "darren early's" question - by the time one sees epsilon waves in ARVD, there are usually wide, inverted T waves - just the opposite of the situation here.

  5. I think the apparent ST depression is a wandering baseline.
    Thanks for the feedback!
    Steve Smith


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