This patient presented from dialysis because his shunt was malfunctioning. He had no definite indication for dialysis unless his K was high.
But every time we drew the K level, it was “hemolyzed.”
So we looked closely at his ECG for evidence of hyperkalemia.
|Is there evidence of hyperkalemia?
Here is his previous ECG when K is normal and all his medications were the same at that time.
|Are they different?
The objective evidence of hyperkalemia on that top ECG is the prolonged PR interval. It is over 300 ms! (The PR in the previous is 218 ms) This prolonged AV conduction puts the patient at risk if his K were to rise further.
Further, one might be tempted to blame a prolonged PR interval on vagal tone, especially at a slow heart rate of 60 beats per minute. But since the sinus rate in the old ECG is the same as the new ECG, there is no difference in vagal tone.
So we ordered an admission bed and he underwent dialysis. A bit later, we obtained non-hemolyzed blood and the K was 5.5 mEq/L, which is elevated but not extremely so. Nevertheless, the patient is on carvedilol (as he was at the time of the ECG with a PR of 218 ms), and the combination could lead to significant AV conduction delay.
I am a believer that if the ECG truly shows no evidence of hyperkalemia, that there will be no short term adverse events from that hyperkalemia.
The caveat is that one must be able to see all those possible abnormalities. Some are exceedingly subtle, but real.
Case 3 on this post illustrates this problem very well:
There was an article on this published a year ago in Western J Emerg Med:
Severe Hyperkalemia: can the ECG risk stratify for short-term adverse events?
Pendell Meyers wrote a fine FOAM article on this topic on EmCrit: