Thursday, June 1, 2017

ST Elevation in I and aVL, with reciprocal ST depression in lead III

This ECG was texted to me with no clinical information:
What do you think?

Here is my response:

"This EKG looks a bit worrisome.  The only reason I hesitate to say that the STE in aVL with reciprocal STD in III is NOT due to MI is that there are very well formed J-waves in aVL.   But not in I.  aVL does not usually have normal variant ST elevation.  aVF is very abnormal too, with a down up T-wave.  If you have suspicion of MI, I would be very worried.  Not diagnostic, but needs an echo."

After going to the chart and reading the history, this is what I texted back:

"I just read the HPI. With a chief complaint of weakness, I would not be very concerned.  Pretest probability is low."

Here is the history.

An approximately 50 year old woman with no cardiac history, but on multiple medications for diabetes, hypertension, and psychiatric disorders complained of weakness.  Since weakness is certainly potentially a symptom of ACS, an ECG was immediately ordered.

Here is the first ECG again:
What do you think?

Here is an old ECG for comparison:

So the ST Elevation is new, but the STE of normal variant (often called "early repolarization") can change.  Is this a strange kind of normal variant in aVL?  Or is there a subtle STEMI?  Or something else?

And that wave in aVF is distinctly abnormal.

What is going on??

Any time you don't know what is going on, it might be hyperkalemia, especially if the chief complaint is weakness.

The K was 7.0 mEq/L

And the Na was 99 mEq/L !!!!!

Now look at aVF again, and you'll see in retrospect that the T-wave is peaked.  In fact, all of the T-waves are subtly peaked.

(There are case reports, but I have not been able to find any actual literature to support any specific findings on the ECG for hyponatremia, or even hypernatremia.  This is contrary to intuition.  I would think that hyponatremia might show similar findings to sodium channel blockers (just as hypokalemia and K channel blockers often show U-waves).

If you know of any literature, please let me know.

The hyperK was treated.

Here is the post-treatment ECG:
The STE is gone and the T-waves are far less peaked.

The patient was admitted and treated.  Her K went down to normal.

Some time later, her K rose again to 6.4 mEq/L (and Na of 108) and another ECG was recorded:
There is some recurrent STE in I and aVL, with, again, reciprocal STD in III.
And even a biphasic (down-up) T-wave, which usually indicates ischemia.

The etiology of the electrolyte abnormalities was uncertain. The patient was quite dehydrated.  Renal function was ok.  There was probably some polydispsia.  Adrenal function was normal.  Kidneys were excreting appropriately dilute urine.

Learning Points:

1. Hyperkalemia is the syphilis of ECG findings: it can present as anything.
2. Hyperkalemia is a common source of pseudoSTEMI.

See these cases:

Hyperkalemia and ST Segment Elevation, Post 1

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