Clinical meaning
Hyperkalemia (serum potassium >5.0 mEq/L) is a life-threatening electrolyte emergency due to its effects on cardiac conduction. Potassium is the major intracellular cation (98% intracellular, 2% extracellular), and the ratio of intracellular to extracellular potassium determines the resting membrane potential of excitable cells (cardiac myocytes, skeletal muscle, neurons). Even small changes in extracellular K+ dramatically alter membrane excitability. Hyperkalemia depolarizes the resting membrane potential, making cells more excitable initially (peaked T waves) but ultimately impairing depolarization and conduction as sodium channels become inactivated (prolonged PR, widened QRS, loss of P waves, sine wave pattern → cardiac arrest). ECG changes follow a predictable progression with rising K+ levels: 5.5-6.0 = peaked T waves (narrow, tall); 6.0-7.0 = prolonged PR interval, flattened P waves; 7.0-8.0 = widened QRS, loss of P waves; >8.0 = sine wave pattern → VF/asystole. However, ECG changes do not always correlate perfectly with K+ levels. Causes include: decreased renal excretion (AKI, CKD, hypoaldosteronism, K-sparing diuretics, ACEi/ARB), transcellular shift (acidosis drives K+ out of cells in exchange for H+, insulin deficiency/DKA, beta-blockers, cell lysis — rhabdomyolysis, tumor lysis syndrome, massive hemolysis), increased intake (K+ supplements, salt substitutes), and pseudohyperkalemia (hemolyzed specimen, extreme thrombocytosis/leukocytosis). Treatment follows three principles in order: (1) Stabilize cardiac membrane (IV calcium — does NOT lower K+ but protects the heart), (2) Shift K+ intracellularly (insulin + dextrose, beta-2 agonists, sodium bicarbonate if acidotic), (3) Remove K+ from body (loop diuretics, sodium polystyrene sulfonate/patiromer/SZC, hemodialysis).