PE15.2 | Sodium Potassium Imbalance — Summary & Reflection

KEY TAKEAWAYS

Sodium disorders reflect the ratio of total body sodium to water: hyponatraemia (Na < 135) results from excess free water or sodium loss, classified by volume status (hypovolaemic, euvolaemic/SIADH, hypervolaemic); hypernatraemia (Na > 145) from water deficit relative to sodium. Safe sodium correction: acute symptomatic hyponatraemia → hypertonic 3% NaCl 2-3 mL/kg to abort seizures, then ≤ 10-12 mmol/L rise per 24 hours; hypernatraemia → ≤ 10-12 mmol/L fall per 24 hours. Potassium disorders alter cardiac membrane potential: hypokalaemia (K < 3.5) → hyperpolarisation → flattened T + U waves; hyperkalaemia (K > 5.5) → depolarisation → peaked T → wide QRS → sine wave. Hyperkalaemia with ECG changes requires immediate calcium gluconate (membrane stabilisation) before K-lowering measures (insulin + dextrose, nebulised salbutamol). Always interpret electrolytes with clinical context — volume status, urine sodium, medications, and acid-base status together reveal the mechanism.

REFLECT

Return to the opening scenario — the 7-year-old with nephrotic syndrome on furosemide: Na 128, K 2.8, ECG flattened T waves. Now, with your new framework: identify the mechanism linking the two electrolyte abnormalities, write the initial management steps in order, and specify what monitoring you would perform over the next 6 hours. Then reflect: what change in management would you make if her serum K was 2.6 but she was also vomiting and unable to take anything orally? Writing out this decision tree — orally vs IV, which fluid, which rate — consolidates the key clinical reasoning this module is designed to build.