A pathognomonic ECG you should recognize instantly

Written by Pendell Meyers

Here's a pathognomonic ECG from a patient presenting with generalized weakness and malaise.

After so many examples of this on the blog, you should recognize it instantly with almost zero mental effort! What is it?

Hypokalemia. There is prolonged QT interval with characteristic ST depression followed by down-up T-waves in the precordial leads. The "up" portion of the T-wave is considered a U-wave. No signs of ischemia. Sinus rhythm.


Indeed, the potassium level was 2.3 mEq/L.

Serial troponins were negative. The patient was rehydrated and potassium was repleted.


To prove that these changes were new and associated with hypokalemia, here is the patient's baseline ECG on file from 1 year ago:

Normal ECG. All findings of hypokalemia absent at baseline.


Key Points:

You must be able to recognize such clear cases of hypokalemia instantly.

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Comment by KEN GRAUER, MD (7/22/2018):

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I agree completely with Dr. Meyers that on seeing this ECG and being told that the patient presented to the ED with “generalized weakness” — that your reflexive response (ie, that should be made in no more than 2-3 seconds) — should be, “What’s the serum K+?” That said — I’d add the following points:

• What is the serum Mg++ level? I was taught that hypomagnesemia may result in virtually identical physiologic and ECG effects as hypokalemia. These 2 conditions often coexist — and some patients with hypokalemia are relatively resistant to correction of K+ until low Mg++ is also corrected. Since serum Mg++ is not always included in routine “electrolyte panels” — it is worth checking. As is the case for K+, most body Mg++ is intracellular — so extracellular (ie, serum) levels do not necessarily reflect accurate body (and intracardiac) levels of cation. As a result, the serum levels we get back from the lab tell only part of the story — and a “low normal level” (ie, a serum Mg++ ~1.7 mEq/L) may still reflect low body stores of this cation if the patient’s baseline level was initially >2.0 mEq/L. Clinical context and serial values over time may be needed to accurately gauge optimal cation replacement.
• Could “something else” (ie, in addition to low K+) be going on in this patient? Other entities may contribute to nonspecific ST-T wave flattening with QT (or QU) prolongation. Could there have been ST elevation from “silent infarction” in this patient with new weakness — with the ST-T wave changes seen here being attenuated by coexistent hypokalemia? And while I fully acknowledge that this is NOT a likely scenario — if you see enough patients, a “1 in a 100 situation” will eventually occur on your watch if you fail to consider other possibilities. NOTE: U waves can be seen with bradycardia — and both medication use and CNS disorders may produce weakness, nonspecific ST-T wave abnormalities and QT prolongation. Clearly — Hypokalemia is the #1, #2 and #3 diagnosis in this case until proven otherwise. That said — other entities should still be considered until lab results return and careful clinical correlation is completed.
• I LOVE this case — because we are provided with a comparison tracing. Thus the Bottom ECG (BLUE border) in Figure-1 was obtained 1 year earlier on this patient. Note that there was some ST elevation in the prior ECG in the inferior leads. This most probably reflects the benign variant of early repolarization — but I suspect it accounts for the fact that although inferior lead ST-T waves are flattened in the ED ECG (RED border in Figure-1) — they are not as depressed as I might have expected with the exceedingly low serum K+ level of 2.3 mEq/L. I find it helpful to repeat the ECG of a patient with a new electrolyte disorder after treatment — in this case, just to be sure that the T wave inversion in leads V3, V4 and other nonspecific ST-T wave abnormalities on the initial tracing are improving.

Spend another moment reviewing the prior ECG (BLUE border in Figure-1):

• For educational purposes — I think it worthwhile to point out: i) That the T wave inversion in lead aVL of the prior tracing is not abnormal, given the relatively vertical frontal plane axis with resultant predominant negativity for the QRS in aVL (ie, the T wave axis often "follows" the QRS axis); and ii) That there is probably some misplacement of one or more chest leads — given P wave negativity with shallow T wave inversion in leads V1 and V2 (often suggests these leads have been positioned 1 or 2 interspaces too high) — with then rather abrupt transition from the tiny r wave in V2, to a much more positive R wave already by V3.

Figure-1: Comparison of the 2 ECGs in this case (See text).

Our THANKS to Dr. Meyers for this insightful case!