I recently admitted a woman overnight with prerenal AKI and serum K+ of 7 mmol/L. A passing ED physician mumbled to me not to worry as their ECG didn’t require calcium gluconate, and besides, they had an ICD inserted recently.
As I looked over the ECG, I realised I had no idea what effect hyperkalaemia would have on a pacemaker. Furthermore I always suspected that ECG changes were not a sensitive method of alerting physicians to danger and just delayed treatment. So firstly, what effect does hyperkalaemia have on those pacing/ICD leads?
A recent review from europace describes 3 key changes:
1. The QRS complex can widen due to intraventricular conduction delay
2. The increased ventricular pacing thresholds can cause failure to capture
3. It can lead to over-sensing of spontaneous T waves and inappropriate shocks if the device is an ICD
An hour later this lady had multiple long runs of ventricular tachycardia and lost consciousness .The overdrive pacing spikes could be seen on the monitor but there was no electrical capture and after 20 seconds the device ultimately defibrillated the patient each time. Could this have been avoided with quicker initial treatment and administration of calcium?
Given the potentially disastrous consequences of hyperkalaemia in a patient with a pacemaker, just fix it, and don’t rely on the ECG to reassure you!
So what about my suspicion that ECG changes are not particularly sensitive?
It would seem that physicians cannot predict clinical severity based on ECG changes alone. A blinded reading of 200 ECGs gave a best positive predictive value for the presence of hyperkalaemia of 0.65. In addition to this, another study in CJASN could find no correlation between T waves changes and serum K+. The problem worsens in dialysis patients who appear even less likely to ever manifest ECG changes. This is associated with having a higher serum calcium. Furthermore there are multiple case reports of profound hyperkalaemia both in patients with and without CKD who do not manifest any ECG changes. It is hypothesised that perhaps it if the rate of change that produces the ECG abnormalities, which makes some sense as to why the RRT cohort do not manifest these.
Furthermore it has been shown worsening stages of CKD tolerate any given level of hyperkalaemia better, again perhaps due to the rate of change. I could find no good study showing that ECG changes, except for sinusoidal waves, predicted death or morbidity. The long described progression of t wave changes through to QRS widening and then sinusoidal waves is a physiologically pleasing one, it feels right and is very logical. The ECG itself however, would seem not to be particularly useful in treating real patients, and I am going to force myself to ignore normal ECGs. I think my assessment of the urgency will centre around how the patient looks and the rate of flux, background CKD, serum K+, likelihood of rapid improvement, medications and cardiac history.A final point I stumbled across which I found interesting was the interaction between verapamil and hyperkalaemia. Both dogs and humans on verapamil have profoundly lower cardiac indexes when hyperkalaemic. I’m not sure is it the Ca2+ blocking effect worsening the hyperkalaemic effect on myocardium or the cumulative negative inotropy, but I can see a logical argument for empirical calcium therapy in those on verapamil and perhaps other calcium channel blockers.