Mastering Hyperkalemia: A Case Based Physiology Deep Dive

Hyperkalemia is not one diagnosis. In this Nephrology Notebook lecture, we use case based physiology to build a practical bedside framework for evaluating and treating hyperkalemia. We cover pseudohyperkalemia, transcellular shift, rhabdomyolysis, type four renal tubular acidosis, trimethoprim associated hyperkalemia, ECG limitations, acute stabilization, potassium shifting, definitive removal, dialysis indications, chronic RAAS inhibitor preservation, and modern potassium binders. This lecture is designed for interns, residents, fellows, hospitalists, nephrology trainees, and attendings who want a clinically useful approach to hyperkalemia beyond memorized algorithms. Key Points 1. Always ask whether hyperkalemia is real, dangerous, shifting, accumulating, or failing excretion. 2. Insulin and albuterol shift potassium temporarily. They do not remove potassium from the body. 3. A normal ECG does not rule out dangerous hyperkalemia. 4. Intravenous calcium stabilizes the myocardium when ECG toxicity is present. 5. Definitive potassium removal occurs through urine, stool, or dialysis. 6. Chronic hyperkalemia should prompt correction of reversible drivers before reflexively abandoning outcome improving RAAS inhibitor therapy.