Early Repolarization vs LAD Occlusion
First ECG in Video 2nd ECG in Video
Critical Hyperkalemia Cases
Associate Editors:
— Pendell Meyers & Ken Grauer (2018)
— Jesse McLaren & Emre Aslanger (2022)
— Willy Frick (2024)
The hyperkalemia V2 morphology you present in your second case reminds me a bit of Brugada variants; it seems you can even get a “saddle back” STEMI mimic from some of these presentations—as evidenced here:
http://int-prop.lf2.cuni.cz/heart_sounds/ekg4/ekg16.jpg .
What your case illustrates is obviously much more dramatic, however, and I appreciate your instruction in calling attention to this hyperkalemia signature.
In considering this, I wonder how well these relatively subtle morphological issues translate into an algorithmic approach. I am unaware, for example, of any portable ECG system presently capable of suggesting hyperkalemia as a potential interpretation.
Thank you again for these superior case presentations.
Type II and III Brugada have not turned out to be more dangerous than early repol, which also has a slightly increased long term arrhythmia risk over those without it. In fact, you can see ECGs of patients who meet type II and III criteria almost every day. So is it early repol, or is it type II or III Brugada? I don't think it matters. See this article:
http://eurheartj.oxfordjournals.org/content/25/10/874.abstract
I have a treatment question.
You mentioned in the cardiac arrest patient, that the treating paramedics didn't consider hyperkalemia, instead assuming the patient had a ventricular escape rhythm. Given the presentation and rhythm morphology, I doubt I would have thought any different.
My question is, in the absence of pathognomonic signs of hyperkalemia in the post-arrest patient, are there contraindications to giving calcium in the field?
3 amps of calcium gluconate is harmless, except in the relatively rare case of hypercalemia. Compared to the potential benefit, as in a patient wwith a wide complex that is possbly hyperK, the risk is tiny.
Dr. Smith, in your other post about hyperkalemia, you cite a paper : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/ which states that calcium gluconate's duration of action is 60 minutes tops. If a hyperkalemic patient is unable to have dialysis, should he be administered calcium gluconate hourly until serum potassium level returns to normal ?
Dialysis patients need dialysis though Kayexelate may have some (though minimal) positive effect. Patients who put out urine can be given loop diuretics. If there is no way to actually lower total body potassium, one must lower the serum potassium with insulin/glucose and beta 2 adrenergic agonists, and use calcium for persistent ECG abnormalities.
I see , many thanks for the explanation !