Thursday, January 3, 2019

What is the diagnosis?

I was reading a stack of ECGs when I came across this one:
What do you think?

I immediately saw that this ECG is DIAGNOSTIC of hyperkalemia.  There are very flat ST segments with a sharp upturn to the T-wave.  The base of the T-wave is very abnormally narrow, which is what creates the peaked T-wave.  This is best seen in lead V3, and is usually best seen in V3 or V4.

The computer read: "Normal ECG"
The physician overread: "Normal ECG, no change from previous"

When I saw these erroneous interpretations, I went to the chart:

Here is the previous.  This was recorded one day earlier:
This is normal.

I looked through the chart.  The patient was a dialysis patient who had presented for a fall and had that first ECG recorded.  The K measured simultaneously was 5.6 mEq/L.  The ECG abnormality was not noticed and the patient was discharged home.

She had presented the day prior for a vascular access problem which had limited her dialysis run.

The K at this one day prior visit was 4.7 mEq/L.

Notice the change in the ECG with an increase of K from only 4.6 to 5.6.

Even though the K is only minimally elevated, if it alters the ECG, then there is a risk for ventricular fibrillation.

See Case 3 in this very instructive post:

HyperKalemia with Cardiac Arrest. Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia

One further caution, illustrated in the above case:

If you see an ECG like this and it is unchanged from previous, you must be certain that the previous ECG was recorded under Non-pathologic conditions.  That is to say, in the presence of a normal potassium.

Comment by KEN GRAUER, MD (1/3/2019):
I call this a, “Who done it?” — because it’s the type of tracing that you look at, and hopefully (as per Dr. Smithinstantly recognize Hyperkalemia. Dr. Smith highlights a number of interesting points about this dialysis patient:
  • The initial ECG shown in this case ( = ECG #in Figure-1) — was not recognized by the treating clinician as abnormal — and as a result, the patient was discharged home. Perhaps the reason for the missed diagnosis was that the computer interpretation (which said, “Normal ECG” ) was trusted. Regardless of the reason — the diagnosis was missed ...
  • Despite the marked change in ECG appearance between the 2 ECGs in Figure-1 — the increase in serum K+ corresponding to these tracings was modest (from only 4.6 to 5.6 mEq/L). KEY Point — it sometimes doesn’t take that much of an increase in serum K+ to significantly affect the ECG (and the resultant risk for VFib).
Figure-1: The 2 ECGs discussed in this case (See text).
To these points, I’d add the following:
  • The treating clinician said, “No change in ECG #1 from the prior ECG”. This prior ECG = ECG #2, which was recorded just 1 day earlier. From this written statement in the chart ( = “No change from previous” ) — it is implied that comparison between ECG #1 and ECG #2 was made — though if true lead-to-lead comparison had been done, it is difficult to conceive that the change in ECG appearance could have been missed. Comparison between 2 tracings can be EASY — if one simply takes a moment to go lead-to-lead to note potential differences.
  • The 1st difference between ECG #1 and ECG #2 is in frontal plane axis. Note that the net QRS deflection in lead III of ECG #1 was isoelectric — whereas there is a small-but-definitely positive net QRS deflection in lead III of ECG #2. While this minor amount of axis deviation is not clinically important in this case — by training yourself to religiously pick up any change in axis, you will then recognize larger axis shifts that are clinically important.
  • Did YOU notice that there probably was malposition of leads V1, V2 in ECG #2 — because there is a deeply negative P wave in these 2 leads — and — an rSr’ complex that closely resembles the QRST appearance in lead aVR. (For more on how to quickly recognize lead V1,V2 misplacement — Please see My Comment at the bottom of Dr. Smith’s 11/4/2018 Blog).
  • The main difference between ECG #1 and ECG #2 (which was done a day earlier) — is that T waves are not only very tall and peaked (pointedin leads V2,V3,V4 in ECG #1 — but the base of these T waves has become much more narrow. This symmetric, very steep ascent and descent of peaked T waves is highly characteristic of HyperKalemia — and especially in a patient with a “reason” to be hyperkalemic (this is a dialysis patient) — hyperkalemia must be presumed!
  • In addition — I suspect HypoCalcemia in ECG #1. Corrected for heart rate, I estimate the QTc in ECG #1 at ~440-450msec ( = upper normal). Characteristic ECG changes of hypocalcemia typically include QT lengthening, with an unexpectedly long isoelectric ST segment, at the end of which the T wave appears. Given common clinical occurrence in renal patients of hyperkalemia with hypocalcemia — I’d be very curious to learn the serum Ca++ level at the time ECG #1 was obtained.



  1. Great ECG example of hyperK+. I agree with your comments 100%, but what disturbs me is that I have seen recent articles (I believe written by some residents elsewhere) promoting the idea that there is no danger from dysrhythmia until the potassium concentration reaches a rather high level (I think somewhere just below 7.0!). Like you, my experience has been that once changes start appearing on the 12-lead ECG, problems could develop at any time. The ECG reflects physiology and any changes represent physiological changes. Even a bundle branch block reflects the changes in the cells of one of the bundle branches. These T waves are not as huge as some and they don't have sharp peaks. But they are definitely not normal and they are definitely not hyperacute T's. I also agree with Ken that the isoelectric ST segment tends to hang around a bit too long. There is still a place in medicine for skill and experience although I'm afraid that it's sadly disappearing and being replaced by "rules" that don't require much thinking.

    1. Thanks, Jerry. In fact, in every case I've seen in which the physicians claimed that there was a complicatio from hyperK without any ECG changes, there were in fact ECG changes. They just are bad at seeing them. My belief, which seems to make a lot of sense, is that if the K is affecting the baseline 12-lead, it is dangerous. If it truly is not, it is NOT dangerous.

  2. this is very educative. thanks.


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