Potassium (K) — Normal Range & Interpretation

Clinical Context

Potassium is the primary intracellular cation and drives resting membrane potential in cardiac, skeletal, and smooth muscle. Tight regulation by the kidneys, aldosterone, and acid-base status keeps serum levels in a narrow range, and small deviations produce large effects on cardiac conduction and neuromuscular function.

Hypokalemia develops from loop and thiazide diuretics, vomiting, diarrhea, nasogastric suction, hyperaldosteronism, insulin administration, and beta-agonist use. Patients present with muscle weakness, cramps, constipation, U waves, and ventricular arrhythmias. Hyperkalemia results from acute kidney injury, chronic kidney disease, ACE inhibitors, ARBs, potassium-sparing diuretics, tissue breakdown, and Addison disease. It produces peaked T waves, widened QRS, and cardiac arrest if untreated.

Board-style questions on potassium pair classic ECG patterns tied to each derangement with drug classes that raise or lower potassium, and the link between potassium and digoxin toxicity. Expect questions pairing a medication regimen with a predicted potassium shift, identifying which antihypertensives require monitoring, and selecting the next step when a patient on an ACE inhibitor plus spironolactone presents with weakness. Know that hypokalemia potentiates digoxin toxicity and that calcium gluconate stabilizes the myocardium in hyperkalemia before insulin, dextrose, or kayexalate shift or remove potassium.

Practice Questions

Related Labs

• Sodium (Na) — mEq/L
• Chloride (Cl) — mEq/L
• CO2 (Bicarbonate) — mEq/L
• BUN — mg/dL
• Creatinine — mg/dL

Sources

• MedlinePlus