EKG - What do you think?

Sublime

Sublime

LP, RN
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Just saw this case through a facebook post.

Would like to hear opinions on interpretation, causes, and treatment.

http://captainchairconfessions.com/2012/09/10/sick-dude/

To me it looks like Hyperkalemia (Flat / non-existent P-Wave, bizarre/widened QRS morphology).
However I would suspect with all the vomiting, diarrhea, and lasix that his K+ would be low. I would also suspect him to be tachycardic in this situation, but then again he is on a beta blocker, and he had a pacemaker that has obviously failed.

So I am second guessing myself here. What do you guys think?
 
That man is having a rather spectacular anterior MI.
 
Aidey said:
That man is having a rather spectacular anterior MI.
Click to expand...

Agreed. Seems to me the crew caught it early on and serial 12-leads revealed the progression of the MI.

I looked at the first 12-lead and disagreed with you then realized there was another one :p
 
His potassium is also likely high, given the T wave morphology. Although it is possible that could also be because of the underlying heart disease and the acute injury.

Depending on how well the Pts medical conditions are controlled the dehydration from the GI issues could have tipped him into kidney failure.
 
*sigh*

I'm never going to understand all this stuff.
 
Aidey said:
His potassium is also likely high, given the T wave morphology. Although it is possible that could also be because of the underlying heart disease and the acute injury.

Depending on how well the Pts medical conditions are controlled the dehydration from the GI issues could have tipped him into kidney failure.
Click to expand...

ARF and a STEMI? Now that's just cruel!
 
Just because we assume horses before zebras doesn't mean you can't have a herd of horses :P
 
The next blog post has the labs

RBC 3.95
WBC 16.7
K+ 7.7 :blink:
Lactic acid 11.2
Hemoglobin 12.2
Hematocrit 37
Na 118
Creatinine 16.4
BUN >150

Bad kidneys + ACE Inhibitors + K+ replacement....
 
On the front page of the blog he explains it in detail. It was HyperK+.

He didn't mention in the first post that the patient was on Potassium pills, now I understand.

Aidey, you called the kidney failure. But from his follow up it looks like it was in fact not a STEMI.

My question now is, how would you guys of treated this? I don't even have a protocol for Hyperkalemia. I know the standard is Calcium, Bicarb, Glucose and Insulin.. but never heard of all those being done in the field.

What are you guys protocols on this?
 
Calcium with a quickness, then look at bicarbonate and albuterol. But only if there is hemodynamic instability.
 
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I would not completely rule out a STEMI but it looks like the change in QRS morphology / STE is a result of a bundle change. Also the STE in V2-4 on EKG #2 looks off, the concavity and how it slopes up off the QRS looks more like hyperK than a typical hyperacute T wave of a MI. **Not too much experience with 12 leads so I could be way off.
 
What is especially interesting about this (for me at least) is the "reciprocal" changes. I've seen hyper K mimicking ST elevation before, but never with reciprocal changes in the appropriate leads. It is possible the Pts low BP was causing ischemia which contributed to the changes.
 
For a great discussion of hyperkalemia that includes an ECG very similar to that on CCC, check out Smith's ECG Blog.

One of the points he makes is that a BBB is wide, but hyperkalemia is really wide. At 0.176 ms, I think that CCC's ECG is pretty wide. Combined with the T-waves, hyper-K should be the first thought, and calcium (chloride or gluconate) should be the second!
 
The post mention that the patient pacemaker wouldn't work under the hyperkalemic state. Is this true with transdermal pacing?
 
Anjel1030 said:
The post mention that the patient pacemaker wouldn't work under the hyperkalemic state. Is this true with transdermal pacing?
Click to expand...

Yes, absolutely. Some places suggest calcium in bradycardia cases that don't respond to atropine or pacing.
 
Oh okay. But why the albuterol? I get the other treatments. The calcium bicarbonate etc. But why albuterol?
 
Albuterol causes a temporary influx of potassium into the cells, decreasing potassium levels in the blood, which decreases the immediate risk of arrhythmia.
 
Aidey said:
Albuterol causes a temporary influx of potassium into the cells, decreasing potassium levels in the blood, which decreases the immediate risk of arrhythmia.
Click to expand...

Oh wow. I will have to read up on that some more.
 
Anjel1030 said:
Oh okay. But why the albuterol? I get the other treatments. The calcium bicarbonate etc. But why albuterol?
Click to expand...

Albuterol works by stimulating glucose, in turn increasing insulin production, which helps to reduce serum potassium levels by driving potassium back into the cells. I saw a study (that I can't cite now because I'm on my iPhone) that stated albuterol, in doses of 10 to 20 mg, was as effective in treating hyperK as insulin and glucose together.

That's why it's in most crush injury protocols.
 
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I just tried explaining this To a couple medics I work with.

They looked at me like I had 5 heads.

One said, and I quote,

"but what does this have to do with hyperkalemia. We don't have a lab in our truck. There is no way to tell if they are hyperkalemic or not."

I just walked away.
 
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