Friday, November 22, 2013

You MUST recognize this pattern, even if it is not common

Disclaimer: I never state from where I get a case.  They come from all over the world.   Any case may or may not be from my own institution.  Do not make any assumptions.


A non-English speaking woman in her 60's with h/o HTN, type II DM, hyperlipidemia, CAD s/p CABG 16 years prior, and end stage renal disease on dialysis  presented to the ED at time 0.  She had awoken 7 hours prior with severe headache followed by upper chest heaviness and vomited x 2.   EMS placed an 18 gauge IV, gave 2 NTG, and aspirin.  She stated the pain was not similar to a previous MI.  BP was 200 systolic.   The patient stated that her chest pain was more of an issue than her headache.

Here is her initial ECG:

There is sinus rhythm, left axis deviation (probable LAFB), and new ST elevation in V1-V3.  What do you think?  See more discussion below.

What was not seen is that there is QRS widening (120 ms) and peaked T-waves diagnostic of hyperkalemia and a pathognomonic, though unusual, pseudoSTEMI pattern.  Cardiology was called and the cardiologist activated the cath lab.

The angiogram showed no acute disease.  However, following the procedure, during the sheath pull, she experienced VT arrest and was administered multiple shocks for wide complex tachycardia.  3 "amps" of lidocaine, 300 mg amiodarone, Sodium Bicarbonate x 2 "amps", D50 x 1 "amp", and calcium gluconate x 1 "amp" were all given.  She had return to sinus rhythm with narrow complex.   After resuscitation, she was comatose and was intubated.

It is uncertain when the K returned, but it was 7.5 mEq/L when it did.

Here is the post-resus ECG:
Now there is sinus bradycardia with an accelerated junctional rhythm and AV dissociation (no evidence of AV block on this ECG).  There is diffuse T-wave inversion, with massive T-waves, all but diagnostic of stress cardiomyopathy.

 The stress cardiomyopathy gets even more pronounced here (20 minutes after the previous):
Sinus brady with nodal escape and AV dissociation persists.  T-waves are massive and bizarre, with precordial T-waves inverted.

Echo confirmed tako-tsubo like apical ballooning of stress cardiomyopathy.  The stress was doubtless her cardiac arrest.

She was dialyzed, cooled (therapeutic hypothermia for comatose survivor of cardiac arrest).  One of my blog followers (an EM G2) was on the neurology service and recognized the initial ECG pattern as diagnostic of hyperkalemia.  He could do so because of these previous posts (and because he is very smart, hard-working, and attentive):

Hyperkalemia PseudoSTEMIs

HyperK pseudoSTEMI Post 1
HyperK pseudoSTEMI Post 2
HyperK pseudoSTEMI Post 3

Patient course

The patient awoke and went to rehab.  She was discharged with some minor neurologic deficits. 


1. Remember this pattern of ST elevation in hyperkalemia.  It is an unusual but pathognomonic pseudoSTEMI pattern
2. Potassium will hurt you and your patients if you are not always thinking about it!



  1. hi dear professor
    Very intresting and stressing case :D, i think it may be there in V2 a saddle back morphology of STE in the first ECG, is it right ? i'm talking about because you've said that it's very unlikely to be a STEMI when such morphology is present .
    can IV calcium gluconate hurt in setting of MI ? can we, when in doubt, use it as a therapeutic test ?

    merci beaucoup, from your biggest fan in Algeria

    1. Good point: saddleback should always make you doubt STEMI. Calcium will not harm a patient with STEMI. It may help as a test. Best is just to give it therapeutically while you are waiting for the K. If K comes back normal, no harm done.
      Steve Smith

  2. Is there any way you could elaborate on the deep T wave inversions in I and aVL? Is this a reflection of t wave amplitude in the inferior leads, or is there any significance at all?

    1. I can't say with certainty, but the combination of LAFB and severe hyperkalemia may be the etiology. Also, we don't know the cause of the headache; was it SAH? This can of course lead to widespread ischemia and T-wave abnormalities.
      Steve Smith

  3. In second ecg about rhythm u said that it's not a complete AV block
    Pz elaborate in details sir

  4. It is possible there is AV block, but no evidence here. there is no P-wave that should have been conducted but did NOT conduct. all p-waves that did not conduct came at times when, if they did conduct, the QRS would be refractory.

  5. Hello Dr Smith. Another excellent case. Can we assume that hyperkalemia can lead to blockade in sodium channel and that will produce pseudo brugada pattern on the ECG?

    1. Koste,
      Good observation, but I must say I don't know the exact molecular physiology, but the principle is correct: Na Channel blockade and hyperK lead to very similar morphologies which are very similar to Brugada pattern.

    2. Amal mattu has said that TCA overdose can also cause a brugada type pattern in V1. So my differential for a brugada type pattern in V1 is TCA overdose, hyperkalemia, and Brugada.

      Do you agree with this?

    3. Definitely. Here is a case on my blog:

  6. In my hospital, before activate cath, we see basal laboratory... Normally, levels of K takes 20 minutes... In end stage renal disease... I'd think in hyperkalemia...


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