5-10 years ago, a male in his 70's presented with weakness. There was no chest pain. Here is his initial ECG:
The cath lab was activated for STEMI. The patient had very poor IV access and bloods were only obtained just before leaving the ED for the cath lab. A second ECG was recorded 35 minutes later, just before transfer to the cath lab:
The potassium returned at 8.4 mEq/L. Unfortunately, the patient had a cardiac arrest on arrival to the cath lab, before return of the potassium. In spite of therapy for hyperkalemia, he was not resuscitated. He never underwent an angiogram.
A closer look at the ECGs reveals the hyperkalemia: In the first ECG, the T-waves are tented and the QRS is prolonged (the computer read it as 133 ms, which is also how I read it).
Here is another one: see full post here. There was no MI. Hyperkalemia alone can cause inferior-posterior pseudo-STEMI:
Notice that in both cases, the ST elevation is downsloping and the T-wave is inverted. After doing a literature search, I have found no formal studies of hyperkalemia causing pseudoSTEMI, though it is a well known phenomenon. So I can't say if this morphology is typical, or universal, or is just anecdotal.
So, in retrospect, the first patient probably did not have STEMI at all. A close reading of the ECG would have revealed that it is diagnostic of hyperkalemia.
History obtained later from the wife indicated that the patient had felt ill and thought that he was low on potassium (I don't know why he thought this). He took potassium pills and overdosed.
Lessons:
1. Always consider hyperkalemia. It is the great imitator. Especially when the patient comlains of weakness.
2. Hyperkalemia can result in ST elevation that imitates STEMI
3. A patient who does not present with chest pain should be particularly scrutinized for other causes of the ECG abnormalities.
 |
| There is sinus rhythm with first degree AV block. There is ST elevation in II, III, and aVF and reciprocal ST depression in aVL. The computer read inferior MI. As for precordial leads: this is from my files and I don't have all the information, but it is clearly a right sided ECG (QRS in V5, V6 is inverted from QRS in I, aVL) What else do you see? |
The cath lab was activated for STEMI. The patient had very poor IV access and bloods were only obtained just before leaving the ED for the cath lab. A second ECG was recorded 35 minutes later, just before transfer to the cath lab:
 |
| This one is left sided. There is still 1st degree AVB. There is much more ST elevation and depression. |
The potassium returned at 8.4 mEq/L. Unfortunately, the patient had a cardiac arrest on arrival to the cath lab, before return of the potassium. In spite of therapy for hyperkalemia, he was not resuscitated. He never underwent an angiogram.
A closer look at the ECGs reveals the hyperkalemia: In the first ECG, the T-waves are tented and the QRS is prolonged (the computer read it as 133 ms, which is also how I read it).
Here is another one: see full post here. There was no MI. Hyperkalemia alone can cause inferior-posterior pseudo-STEMI:
Notice that in both cases, the ST elevation is downsloping and the T-wave is inverted. After doing a literature search, I have found no formal studies of hyperkalemia causing pseudoSTEMI, though it is a well known phenomenon. So I can't say if this morphology is typical, or universal, or is just anecdotal.
So, in retrospect, the first patient probably did not have STEMI at all. A close reading of the ECG would have revealed that it is diagnostic of hyperkalemia.
History obtained later from the wife indicated that the patient had felt ill and thought that he was low on potassium (I don't know why he thought this). He took potassium pills and overdosed.
Lessons:
1. Always consider hyperkalemia. It is the great imitator. Especially when the patient comlains of weakness.
2. Hyperkalemia can result in ST elevation that imitates STEMI
3. A patient who does not present with chest pain should be particularly scrutinized for other causes of the ECG abnormalities.
Dr. Smith,
ReplyDeleteIn this situation would the pseudo-STEMI always appear in the inferior/lateral leads or could it present anteriorly or septal?
I have seen it most commonly in the septal and anterior leads. The last post makes that point.
DeleteSteve Smith
In the first EKG there's also a short QT, hypercalcemia ? can other electrolytes disturbances than hyperkaliemia mimic STEMI ?
ReplyDeletethanks
Dr Lotfi Djilali Bensekrane.
I don't have the computerized QTc, but I measure about 390 ms, so not so short. Hmmm.....
DeletePosted an ECG on the GMEP Global Medical Education Project site back in March from the pre-hospital Thrombolysis days. Luckily I said no (helped by warfarin for once) and patient had a potassium of 10.3 on arrival with a 'sine wave' trace. Can be difficult to do no harm in these situations.
ReplyDeleteTom