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.


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Comment by KEN GRAUER, MD (1/3/2019):
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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).
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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.


3 comments:

  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.

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    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.

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  2. this is very educative. thanks.

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