A normal serum potassium level of 3.5 to 5.0 mEq/L is maintained via potassium ingestion, excretion, and distribution between intra- and extracellular fluid. Potassium balance is essential for maintenance of normal resting cell membrane potential in excitatory tissues. Abnormalities in serum potassium, whether low or high, can cause life-threatening complications due to cardiac, respiratory, or neurologic compromise. Hypokalemia results from renal or gastrointestinal losses, or transcellular shifts. In the absence of an identified cause, evaluation of urinary potassium excretion and acid-base status can help determine the etiology. Patients with severe (ie, serum potassium less than 2.5 mEq/L) or symptomatic hypokalemia should be admitted to the hospital for intravenous potassium replacement and cardiac monitoring. Patients with mild to moderate hypokalemia are often asymptomatic and can be treated with oral potassium while the underlying cause is addressed. Hyperkalemia is usually due to low urinary excretion, and less often to cellular release and transcellular shifts. Patients with acute hyperkalemia with associated electrocardiography findings and those with potassium levels 6.5 mEq/L or greater require inpatient treatment with calcium gluconate and other measures. Asymptomatic patients with chronic mild to moderate hyperkalemia can be managed as outpatients with dietary modification, diuretics, and medication adjustments.
Beekhuizen J. Acid-Base and Electrolyte Disorders: Potassium Disorders. FP Essent. 2026;565:14-22.
Case 2. CP is a 45-year-old patient with hypertension who is taking amlodipine 10 mg daily. His home blood pressure measurements have been higher than 150/90 mm Hg, so your colleague prescribed lisinopril 20 mg daily in addition to his current regimen. One month after starting lisinopril, CP returns to your clinic with a blood pressure of 126/84 mm Hg. Routine laboratory tests show an elevated serum potassium of 6.2 mEq/L (6.2 mmol/L).
Physiology
A normal serum potassium level of 3.5 to 5.0 mEq/L (3.5-5.0 mmol/L) is maintained via potassium ingestion, excretion, and distribution between intra- and extracellular fluid.1 Approximately 2% of potassium in the body is extracellular, whereas 98% is intracellular. This gradient is maintained by the sodium-potassium pumps that move three sodium ions out of the cell and two potassium ions into the cell.2
In excitatory tissues, the potassium concentration gradient across the cell membrane sets the resting membrane potential and allows for generation of the action potential required for normal neural and musculoskeletal function. Abnormalities in serum potassium, whether low or high, can cause devastating clinical manifestations.
Aldosterone and kidney function play key roles in potassium homeostasis. Approximately 90% of potassium intake is excreted in the urine and 10% by the gastrointestinal tract.1,3
After ingestion of potassium, cellular uptake is stimulated via insulin and beta-2 adrenergic receptors in the muscle and liver. A mild increase in serum potassium stimulates aldosterone release, which increases potassium excretion in the principal cells of the distal nephron by stimulating sodium channels.
This increases sodium uptake into the principal cells, creating a negative charge in the lumen, which then draws in potassium to be excreted. Thus, sodium and water delivery are required for adequate sodium uptake into the principal cells of the distal nephron, and for potassium excretion. Increased serum potassium also stimulates apical potassium secretory channels in the principal cells, causing more potassium to flow into the lumen for excretion.1–3
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