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UP-PGH Division of
Cardiovascular Medicine


Abstract
Severe hyperkalemia can present with ECG changes that mimic anteroseptal STEMI—including ST elevation in anteroseptal walls and aVR with reciprocal changes in lateral walls, peaked T waves, QRS widening, and a prolonged QTc. Recognizing the “STEMI-mimic” pattern is critical because the immediate, lifesaving treatment is potassium-lowering therapy rather than cath lab activation.
Case presentation:
A 62/M arrived for behavioral change beginning with a 3-day history of loose diarrhea and 2-day history of epigastric pain associated with generalized body weakness and hallucinations. Initial ECG showed:
• STE in V1-V5 and aVR with reciprocal changes in lateral leads » raised suspicion for LM/proximal LAD occlusion.
• Tall, symmetric (“tented”) T waves, widened QRS, and prolonged QTc.
Serum potassium returned at 8.4 mmol/L. After hyperkalemia therapy, the ECG abnormalities improved—supporting a hyperkalemia STEMI-mimic rather than true transmural infarction.
ECG diagnosis:
Severe hyperkalemia with “pseudoinfarction” pattern (STEMI-mimic) featuring:
1. V1-V5 and aVR STE + reciprocal changes in V6, I to aVL and I
2. Peaked T waves
3. Progressive QRS widening
4. QTc prolongation
Explanation:
This aVR STE pattern is classically associated with left main or proximal LAD disease, but it is not specific and can occur with non-occlusive causes—including severe hyperkalemia.
Hyperkalemia’s ECG progression: rising K⁺ shortens action potential duration » tall, symmetric T; then PR prolongation, P-wave flattening/loss, QRS widening, and, at extremes, a sine-wave pattern and arrest.
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