This is a repost of part of one of the most viewed posts ever.
This patient with little past medical history presented feeling moderately ill. He had an ECG recorded:
Due to the peaked T-waves, the residents were immediately concerned for hyperkalemia and sought an old ECG, which they immediately found in the medical record. It was recorded with a K of 4.5 mEq/L:
The residents interpretation was that these were identical. After viewing this previous ECG, and knowing that the K was 4.5 at the time it was recorded, the residents believed that the peaked T waves in ECG #1 were this patient's baseline.
Are they identical?
Inspect lead V4 more closely, here for a side by side comparison:
It is true that early repolarization has tall and relatively peaked T waves, but not to the extent seen in ECG #1. Without seeing them side by side, it is hard to appreciate the difference.
This patient, then, did not get immediate treatment for hyperK.
I saw these ECGs at a slightly later time than the resident, recognized the difference and, worried about the patient, started toward his bedside. As I was approaching the patient, he had a v fib arrest. He was immediately resuscitated, then his K returned at 7.0 mEq/L. This was a presumed hyperkalemic arrest.
Some say you don't need to treat hyperK unless there is QRS widening. They claim that peaked T-waves are not enough. This is only one case, and anecdotal, but we found no other etiology of arrest in this patient. I always treat immediately if the ECG is affected by hyperK.
There is a definite difference, with EKG 1 pathognomonic for hyperkalemia.
This patient with little past medical history presented feeling moderately ill. He had an ECG recorded:
QRS duration = 102 ms. What do you think? |
QRS 82 ms. |
The residents interpretation was that these were identical. After viewing this previous ECG, and knowing that the K was 4.5 at the time it was recorded, the residents believed that the peaked T waves in ECG #1 were this patient's baseline.
Are they identical?
Inspect lead V4 more closely, here for a side by side comparison:
On the left, the ST segment is nearly flat and rises abruptly. On the right, it is not flat (though nearly so) and rises slightly less abruptly |
It is true that early repolarization has tall and relatively peaked T waves, but not to the extent seen in ECG #1. Without seeing them side by side, it is hard to appreciate the difference.
This patient, then, did not get immediate treatment for hyperK.
I saw these ECGs at a slightly later time than the resident, recognized the difference and, worried about the patient, started toward his bedside. As I was approaching the patient, he had a v fib arrest. He was immediately resuscitated, then his K returned at 7.0 mEq/L. This was a presumed hyperkalemic arrest.
Some say you don't need to treat hyperK unless there is QRS widening. They claim that peaked T-waves are not enough. This is only one case, and anecdotal, but we found no other etiology of arrest in this patient. I always treat immediately if the ECG is affected by hyperK.
There is a definite difference, with EKG 1 pathognomonic for hyperkalemia.
Are they epsilon waves in inferior leads?
ReplyDeleteNo, those are J-waves of early repol.
DeleteDr Smith,
ReplyDeleteInstinctively my eyes were drawn to the more significant differences in t wave amplitude in V2/3 rather than the more subtle V4 change. Would I be wrong?
Regards,
Richard
Richard,
DeleteNo. that is an excellent observation.
I think the ST segment is V4 is a more specific change though.
Steve Smith
Great case report! Thanks.
ReplyDeleteAs I look in V3 and especially V4, the tall and peaked T waves confuse me, as I could wrongly think of a grade I ischemia. And in V4V5 I see a ST depression that strengthens this... What do you think?
Thank you all
Excellent tracing and a great lesson for all. Like "Bauldy," my eyes were also immediately drawn to the changes in V2-3. And I couldn't agree with you more about testing for and treating hyper K+ as soon as you are able to detect it on the 12-lead ECG. During my residency in internal medicine, it was always pounded into us that once there are changes indicating hyper K+ on a tracing, arrest can occur AT ANY TIME - one doesn't wait for an ECG to show a progression to QRS widening and sinoventricular conduction. Your case - though anecdotal - certainly supports that concept (and no one has ever been harmed by running a serum K+). Regarding "darren early's" question - by the time one sees epsilon waves in ARVD, there are usually wide, inverted T waves - just the opposite of the situation here.
ReplyDeleteThanks, Jerry!
DeleteI think the apparent ST depression is a wandering baseline.
ReplyDeleteThanks for the feedback!
Steve Smith