While I had a few moments, I was reading a series of consecutive ECGs recorded in the ED.
I came across this one:
|The computer read was:
The cardiologist formal overread was
“No significant change”
However, it is diagnostic. Of what?
In V2-V6, the flat ST segments, sharp upturn of the T-waves, narrow base of the T-waves, and peaked T-waves are diagnostic of hyperkalemia.
So I looked to see the patient chart.
The patient was a dialysis patient who was there for a clotted dialysis shunt. The K was 5.6 and the ECG hyperkalemia was noticed by the ED physicians.
She had been in the ED the day before with the same problem, and had this ECG recorded:
|The T-waves are normal
The K was 4.6 mEq/L
This one is close to normal.
Do you see the change?
Here I put them side-by-side:
|There is clearly a change from 4.6 mEq/L (day before) to 5.6 mEq/L (next day).
1. The computer interpretation of “normal” cannot be trusted. It often reads “normal” when the ECG is anything but normal.
2. The formal read in the system is often inaccurate. These may be read in a long queue without any clinical information and are therefore much less reliable.
3. It is all too easy to just “confirm” the computer interpretation.
4. A potassium as low as 5.6 mEq/L, even in a dialysis patient (they often have such high K that they are less sensitive to it)*.
*it is a truism that I do not believe is proven, and would be a good topic for study.
5. Even if the ECG was truly “unchanged”, one could not say it is normal. One must find an ECG recorded under normal conditions (i.e., normal K, or no chest pain, etc.) in order for “absence of change” to be safe.
6. A K that is minimally elevated can result in ECG alterations. Any time it does so, there is a danger of ventricular dysrhythmias. Even just subtly changed T-waves may portend ventricular fibrillation. See case 3 in this illustrative post:
Comment by KEN GRAUER, MD (1/7/2019):
I call this a, “Who done it?” — because it’s the type of tracing that you look at, and hopefully (as per Dr. Smith) instantly recognize Hyperkalemia. Dr. Smith highlights a number of interesting points about this dialysis patient:
- The initial ECG shown in this case ( = ECG #1 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 (pointed) in 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.