SSmith Blog- that he duplicated-HyperK-Low Ca (1-7-2019)

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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. 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).

PUT FIGURE-1 HERE

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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 (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.