A middle-aged patient presented feeling moderately ill. He had an ECG recorded.
By history, the patient had no reason to have hyperK on history. A recent previous ECG, done at a K of 4.5 mEq/L, was sought by the residents:
No! Notice the ST segments in the ECG at presentation are much more flat, and they then rise much more quickly to a peaked T-wave, especially in lead V4.
Case Conclusion
Residents had already made the comparison and decided that it was not different. Several minutes later, I saw these two ECGs and immediately saw the difference. I could see that the new ECG was diagnostic of hyperkalemia, and told the residents that they must immediately start treatment. As we were walking to his room, and before Calcium could be given, the patient had a v fib arrest while in his room, before his K returned from the lab. This was a presumed hyperkalemic arrest. He was immediately defibrillated and given Calcium. His K returned at 7.0 mEq/L.
Some say you don't need to treat hyperK unless there is QRS widening, claiming that merely having peaked T-waves is not enough. This is only one case, and anecdotal, but we found no other etiology of arrest in this patient. The patient had new renal failure as the etiology of hyperK.
By history, the patient had no reason to have hyperK on history. A recent previous ECG, done at a K of 4.5 mEq/L, was sought by the residents:
The old ECG also shows very peaked T-waves. The residents concluded that these were his baseline T-waves. Were they correct? |
No! Notice the ST segments in the ECG at presentation are much more flat, and they then rise much more quickly to a peaked T-wave, especially in lead V4.
Case Conclusion
Residents had already made the comparison and decided that it was not different. Several minutes later, I saw these two ECGs and immediately saw the difference. I could see that the new ECG was diagnostic of hyperkalemia, and told the residents that they must immediately start treatment. As we were walking to his room, and before Calcium could be given, the patient had a v fib arrest while in his room, before his K returned from the lab. This was a presumed hyperkalemic arrest. He was immediately defibrillated and given Calcium. His K returned at 7.0 mEq/L.
Some say you don't need to treat hyperK unless there is QRS widening, claiming that merely having peaked T-waves is not enough. This is only one case, and anecdotal, but we found no other etiology of arrest in this patient. The patient had new renal failure as the etiology of hyperK.
1. Peaking of T-waves occurs in other conditions than hyperkalemia, such as early repolarization. Comparison with the previous ECG must be done very carefully
2. I always treat immediately if I think the ECG is affected by hyperK. I do not wait for the laboratory results
Hi Steve
ReplyDeleteYou scared us as always!
I found a long JT segment on the first ECG; that is not consitent with hyperkalemia but hypocalcemia (frequent in renal failure).
How was his calcemia (I know he has received IV calcium after his defibrillation)? could it be responsible for the VF too ?
Pierre,
Deletevery good point. Unfortunately I don't have that data. K. Wang says that the long QT (due to a long ST segment) does not lead to dysrhythmias. I have never been able to substantiate his claim. True or not true?
Steve
Dear doctor,I think there is inferior leads early repolaposition and peaked t waves are the result of vagal over drive as inferior leads ERP can cause afib,other than the cause the residents explain
ReplyDeleteDr. Gupta, I'm not quite sure what you mean. Mostly, this post refers to the precordial T-waves.
DeleteSteve Smith
DeR doctors vagal overdrive produces tall t wave in chest leads and erp according to study. And ERP ate not benign in inferior leads and in middle aged person.according to your residents these is hyper kelmia and in jk systole can occur but not afib. Erp is the nuisance. Take patients history of mental stress over a few weeks before he feel ill
Delete