Monday, October 26, 2015

This ECG is pathognomonic and you must recognize it.

This patient was found with a bottle of alcohol and altered mental status.  His breath alcohol was 0.259.  Due to bradycardia, a 12-lead ECG was obtained:
There is atrial fibrillation at a rate of 54.  The QRS is 166 ms.
Why is it slow?  What is the diagnosis?

This is pathognomonic and you must recognize this!  There is a wide QRS and peaked T-waves.   In particular, notice how flat the ST segment is before it abruptly rises into the T-wave! 

HyperKalemia was immediately recognized and the patient was given Calcium.

A followup ECG was obtained after Calcium:
The QRS is now 129 ms.

The potassium returned at 7.8 mEq/L.  His pH was 6.97.  It was caused by new onset of acute renal failure.

This patient could easily have been just assumed to be intoxicated.  He might have been brought to detox, or might have just been observed in the ED.

But because of bradycardia, a 12-lead was obtained, which gave the critical diagnosis.

Learning Points:
1.  When a patient is bradycardic, especially if irregular, one must always think of hyperK and one must get a 12-lead ECG.
2. One must recognize this pattern as hyperK
3. Calcium's effect is almost miraculous
4. Slow atrial fibrillation implies an sick AV node, or one affected by electrolytes, ischemia, or medications/drugs.  Otherwise, the ventricular response should be fast.


  1. Steve...

    Great case and kudos to the very astute physicians who recognized this for what it was! The T waves in V4 - V6 are "peaked" but they aren't needle sharp like the classic hyperkalemic T's. I think too much emphasis is put on the classic morphology and it's anyone's guess how many cases like this are overlooked.

    Also, a very telling feature is the width of the tiny r waves in V1 - V3. There's just too much daylight between the ascending and descending limbs of those r waves. And I want to point out that the widening of the r waves is still present post Ca++ infusion. Ca++ can rapidly stabilize the cell membranes and move the threshold potential further away from the resting potential - but it doesn't get rid of the hyperkalemia. It's important to realize that once you give the Ca++, the patient still isn't "out of the woods," so to speak. (Obviously, in this case, potassium-lowering measures were most likely undertaken at the same time the Ca++ was given.)

    I especially appreciate your comment about the slow ventricular rate in atrial fibrillation. I think too many people looking at this ECG would have stopped at the diagnosis of atrial fibrillation - as though there can't be more than one diagnosis per ECG.


    Jerry W. Jones, MD FACEP FAAEM

    P.S. - I notice you're turning out a lot of cases lately. Keep'em coming!

  2. awsome ecgs, awsome posts! is there any chance to subscribe your blog via email?

    best wishes

    1. Alex,
      I can put you on a list of people that I tell of new posts.
      email me at:
      sometimes I forget to send notification out.
      But I always tweet them, so follow me on Twitter (@smithECGBlog)
      Also, there is a box down the right hand side "Followers". I think you can sign up there to be notified, but I am not sure whether that is true or, if so, how it works.
      If you find out, let me know!
      Steve Smith


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