Hypokalaemia
Low potassium — causes, symptoms and safe replacement
Hypokalaemia (serum potassium <3.5 mmol/L) is one of the most common electrolyte disorders in clinical practice, particularly in patients on diuretics, with gastrointestinal losses, or with poor nutritional intake. It affects cardiac and neuromuscular function and can precipitate life-threatening arrhythmias — particularly dangerous in patients taking digoxin.
What is Hypokalaemia?
Hypokalaemia is classified as mild (3.0–3.5 mmol/L), moderate (2.5–3.0 mmol/L), or severe (<2.5 mmol/L). Potassium is critical for maintaining the resting membrane potential of muscle and nerve cells. When serum potassium falls, the membrane potential becomes more negative (hyperpolarisation), making cells harder to excite — resulting in muscle weakness, reduced intestinal motility, and cardiac conduction abnormalities. The ECG hallmark of hypokalaemia is the U wave (a positive deflection after the T wave, most visible in leads V4–V6) and flattened/inverted T waves. Hypokalaemia also predisposes to digoxin toxicity by reducing competition at the Na+/K+ ATPase pump.
Causes & Risk Factors
Hypokalaemia results from inadequate intake, increased renal losses, or gastrointestinal losses. The most common cause in hospital is diuretic therapy — loop diuretics (furosemide, bumetanide) and thiazide diuretics (indapamide, bendroflumethiazide) all cause renal potassium wasting. Other renal causes include primary hyperaldosteronism (Conn's syndrome — hypertension + hypokalaemia + suppressed renin), Cushing's syndrome, renal tubular acidosis, and hypomagnesaemia (magnesium deficiency causes refractory hypokalaemia by impairing renal K+ conservation — must be corrected concurrently). Gastrointestinal causes: vomiting, diarrhoea, ileostomy, laxative misuse. Medications: corticosteroids, amphotericin B, insulin (drives K+ into cells), salbutamol (nebulised in large doses). Eating disorders (particularly bulimia with purging) are an important and often underdiagnosed cause.
Signs & Symptoms
Mild hypokalaemia is often asymptomatic. As levels fall, symptoms include muscle weakness (legs first, then arms), fatigue, cramps, constipation and reduced bowel sounds (paralytic ileus in severe cases), palpitations, and polyuria (nephrogenic diabetes insipidus). Severe hypokalaemia (<2.5) can cause ascending paralysis resembling Guillain-Barré syndrome, respiratory muscle weakness (hypoventilation), and rhabdomyolysis. On ECG: flattened T waves, prominent U waves, prolonged QU interval, ST depression. Ventricular arrhythmias (VT, VF) are the primary cardiac risk — particularly when hypokalaemia coexists with digoxin, other QT-prolonging drugs, or cardiac disease.
Treatment & Safe Replacement
A careful evaluation of the underlying cause guides the approach to potassium replacement and prevention of recurrence. Oral replacement is always preferred when safe and tolerated — it is safer and better absorbed than IV. Sando-K tablets (12 mmol K+ per tablet) given 2–4 tablets TDS are first-line for mild-moderate hypokalaemia. IV potassium must NEVER be given as a bolus — this is fatal. IV replacement is reserved for severe hypokalaemia (<2.5 mmol/L) or when oral intake is not possible. Hypomagnesaemia must always be checked and corrected — if magnesium is low, potassium replacement will fail. Review and modify the diuretic regimen where possible: switching to a potassium-sparing diuretic, reducing dose, or adding spironolactone.