Potassium (K+) is the primary intracellular cation (normal serum 3.5-5.0 mEq/L), with 98% residing inside cells. This steep concentration gradient across cell membranes is maintained by the Na+/K+-ATPase pump and is essential for maintaining resting membrane potential, which governs cardiac conduction, skeletal muscle contraction, and nerve impulse transmission. Hypokalemia (<3.5 mEq/L) causes hyperpolarization of cells, making them harder to depolarize. In the heart, this manifests as flattened T waves, prominent U waves, ST depression, and risk of ventricular arrhythmias (PVCs, V-tach, torsades de pointes). Skeletal muscle effects include weakness, cramping, and paralytic ileus. Hypokalemia also impairs insulin release and concentrating ability of the kidneys. Hyperkalemia (>5.0 mEq/L) causes partial depolarization of cells, disrupting normal cardiac conduction. ECG changes progress with severity: peaked (tall, narrow) T waves (5.5-6.5), PR prolongation and P wave flattening (6.5-7.5), widened QRS (7.0-8.0), sine wave pattern (>8.0), ventricular fibrillation or asystole. The insulin-glucose mechanism is used therapeutically: insulin activates Na+/K+-ATPase, driving K+ from serum into cells, temporarily lowering serum K+. On the exam, writers often pair stable-sounding options with unstable data—notice the mismatch before you commit.