Electrolytes Explained: Sodium, Potassium, Chloride, and Bicarbonate

Electrolytes are electrically charged minerals that regulate fluid balance, nerve conduction, and acid-base homeostasis. The four main serum electrolytes — sodium, potassium, chloride, and bicarbonate — are measured as part of a standard urea and electrolytes (U&E) panel and are among the most frequently ordered laboratory tests in clinical medicine.

Sodium (Na+)

Reference range: 135–145 mmol/L. Sodium is the dominant extracellular cation and controls plasma osmolality and water distribution. Hyponatraemia (<135 mmol/L) is the commonest electrolyte abnormality in hospitalised patients. Causes include SIADH (syndrome of inappropriate ADH secretion), heart failure, liver cirrhosis, hypothyroidism, and excessive water intake. Hypernatraemia (>145 mmol/L) reflects a relative water deficit — caused by dehydration, diabetes insipidus, or excessive sodium intake. Symptoms of both depend on the rate of change as much as the magnitude; acute shifts are more dangerous than chronic ones.

Potassium (K+)

Reference range: 3.5–5.0 mmol/L. Potassium is predominantly intracellular (98% intracellular vs. 2% extracellular). Hypokalaemia (<3.5 mmol/L) causes muscle weakness, cramps, ileus, and cardiac arrhythmias (U waves on ECG). Causes include diuretic use, vomiting, diarrhoea, alkalosis, and hypomagnesaemia. Hyperkalaemia (>5.0 mmol/L) can cause peaked T waves, widened QRS, and ventricular fibrillation. Causes include renal failure, ACE inhibitor/potassium-sparing diuretic use, Addison’s disease, acidosis, and haemolysis (which releases intracellular K+, causing spuriously high results).

Chloride (Cl-)

Reference range: 98–106 mmol/L. Chloride is the principal extracellular anion and generally follows sodium. Hyperchloraemia occurs in hypernatraemia, normal saline infusion (dilutional), and metabolic acidosis with normal anion gap (e.g. diarrhoea, renal tubular acidosis). Hypochloraemia occurs in vomiting (loss of HCl), diuretic use, and metabolic alkalosis. Chloride is essential for calculating the anion gap: Anion Gap = Na+ − (Cl− + HCO3−); normal is 8–12 mmol/L (or up to 16 mmol/L if albumin not corrected).

Bicarbonate (HCO3-)

Reference range: 22–29 mmol/L. Bicarbonate is the principal blood buffer and the metabolic component of acid-base balance. Low HCO3− indicates metabolic acidosis (DKA, lactic acidosis, renal failure, diarrhoea). High HCO3− indicates metabolic alkalosis (vomiting, diuretic use, hypokalaemia). HCO3− on a standard biochemistry panel is measured as total CO2 and is slightly higher than true HCO3−. Full acid-base interpretation requires arterial blood gas (ABG) analysis, providing pH, pCO2, and HCO3− together.

Interpreting the U&E Panel Together

Electrolytes are always interpreted as a panel. A low sodium with low potassium in a patient on diuretics tells a different story to the same values in someone with renal failure. The anion gap, osmolar gap, and acid-base status all add context. Urea and creatinine from the same panel assess renal function — see Kidney Function Test Explained for more detail. Clinical assessment of fluid status — hydration, blood pressure, oedema — is essential to interpret electrolyte abnormalities correctly. As with all biochemistry panels, results should be interpreted by a qualified healthcare professional in the context of symptoms, history, medicines, and other findings.

References

1. MedlinePlus. Electrolytes. medlineplus.gov
2. NHS. Blood tests: urea and electrolytes. nhs.uk
3. Kasper DL, et al. Harrison’s Principles of Internal Medicine. 20th ed. McGraw-Hill; 2018. Ch. 49: Fluid and Electrolyte Disturbances.