Monday, August 6, 2012

Hyperacute T-waves that one might attribute to hyperkalemia and acidosis

A 32 yo type I diabetic woman presented with chest pain, nausea, vomiting and diffuse abdominal pain.  She was in DKA with an anion gap of 35, a glucose of 1128, and a K of 5.5. 

pH = 7.17, pCO2 = 24, HCO3 =  8. 

Here is here ED EKG:
There is sinus tach.  The T-waves are somewhat peaked, suggesting hyperkalemia.  But what is atypical is that the T-wave in V3 towers over the R-wave, and there is terminal QRS distortion in lead V3 (meaning there is neither a J-wave nor an S-wave).  QTc is 462 ms.  These are suspicious findings for a hyperacute T-wave and anterior injury.  Her equation/formula score is 24.8, also consistent with anterior injury.

In any case, one would not expect profound T-wave changes from a K of only 5.5.  Some might argue that acidosis would exacerbate this, but I would not attribute peaked T-waves to a pH of 7.17.

The possibility of anterior STEMI was not noticed.  I noticed it much later on looking through a random stack of EKGs.

Troponin I were followed and rose to a peak of 12.4 ng/ml. 

Here is her ECG the next day (with a normal K):
T-waves are much more normal, less peaked, but also with better R-wave amplitude.  The ST segment is back to 0.  Equation value is 23.0.

Also the next AM, echocardiography (done for the positive troponins) showed a wall motion abnormality in the anterior, anterolateral, and apical walls, consistent with LAD myocardial infarction.  Therefore, she underwent angiography and had a 95% LAD culprit that fortunately had opened on its own (that's why the troponin was only 12).  It was stented.  Had it not opened on its own, it could have resulted in a very large anterior wall MI.

The possibility of anterior STEMI was not noticed during patient care.  I noticed it much later on looking through a random stack of EKGs.  I mention this only to point out that these findings can be noticed, and differentiated from more benign etiologies, prospectively.

Lesson: Hyperacute T-waves and hyperkalemia may be confused, and they may be simultaneous.  Here the potassium was barely high enough to result in a change in T-waves, so one should be especially suspicious in this case.


  1. Dr. Smith,

    This observation may seem retrospective, but at first glance of the ECG, the bases of the T waves seemed wider than I've seen for hyper-k T waves..

    Do you agree with that observation?

    Dave B

  2. Yes, t-waves of hyperK are usually preceded by a horizontal ST segment, such that there is an exaggeration of the upward concavity.

  3. Steve,
    If the artery spontaneously opened and there was re-perfusion, how do you explain the still uniformly upright T's on the 2nd ECG, as opposed to reperfusion T's or "Wellen's" waves?


    1. Sam,
      Reperfusion T-waves are not universal. Generally, it depends on the level of troponin, although in this case there was plenty of infarction (peak trop I = 12). Also, it sometimes take more time for the T-wave inversion to develop. I'm not sure if it did so on subsequent ECGs.
      I haven't looked at this case for a long time. It is pretty cool!

  4. Yes! I suspect the progression from Hyperacute T-waves (vessel closed), to "Reperfusion/Wellen's" Waves must sometimes involve an "intermediate phase" where the Hyperacute T's lessen in magnitude. How often? How transient? I have no idea! Super interesting.

    1. I have seen this many times: hyperacute T-waves become less hyperacute, then evolve over time to inverted T-waves.
      This one shows what happens after the T-wave normalizes:


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