AKT · Renal & urology/Fluid, electrolyte & acid-base

Potassium disorders

Hyperkalaemia (retention/shift/release) / hypokalaemia (loss/shift) — both arrhythmogenic

Overview

Disorders of plasma potassium, both potentially fatal through cardiac arrhythmia. Hyperkalaemia (AKI/CKD, ACEi/ARB/spironolactone, Addison's, rhabdomyolysis, acidosis) is the classic medical emergency with a defined ECG progression and a fixed treatment sequence. Hypokalaemia (GI/renal loss, diuretics, alkalosis, hyperaldosteronism) prolongs the QT and causes U waves.

Recognise

Hyperkalaemia: often asymptomatic until arrhythmia; ECG progression — tall TENTED T waves → small/flat P waves → broad QRS → sine wave → VF/asystole
Hypokalaemia: weakness, cramps, palpitations, constipation; ECG — flattened T waves, U waves, ST depression, long QT
Causes — hyperK: AKI/CKD, K-sparing drugs (ACEi/ARB/spironolactone), Addison's, acidosis, rhabdomyolysis, haemolysed sample (pseudo); hypoK: D&V, diuretics, alkalosis, Conn's, Cushing's

Red flags

Hyperkalaemia with ECG changes (or K ≥6.5) → EMERGENCY: IV calcium gluconate first (cardioprotection) then insulin-dextrose
Severe hypokalaemia (<2.5 / arrhythmia) → cardiac-monitored IV replacement; replace magnesium too (won't correct otherwise)

Differentials & how to tell them apart

Pseudohyperkalaemiahaemolysed sample, delayed processing, very high WCC/platelets — repeat properly, no ECG changes

Addison's diseasehyperkalaemia + hyponatraemia + hypotension/pigmentation — cross-ref endocrine

Hyperaldosteronism (Conn's)hypokalaemia + hypertension + metabolic alkalosis — cross-ref endocrine

Bartter / Gitelman syndromeinherited renal tubular salt-wasting → hypokalaemic metabolic alkalosis with NORMAL/low BP (mimics loop/thiazide diuretics); Gitelman also low magnesium/calcium

Hyperkalaemia — peaked (tented) T waves on the ECG
M. Rosengarten, CardioNetworks ECGpedia / CC BY-SA 3.0 — Wikimedia Commons

Investigations

U&Es (confirm — exclude a haemolysed/pseudohyperkalaemia sample), ECG (the key bedside test), VBG (acid-base), glucose; cause work-up — renal function, drugs, cortisol (Addison's), aldosterone/renin (Conn's), magnesium (with hypokalaemia).

Management

HyperK → calcium gluconate then insulin-dextrose; hypoK → KCl (+ magnesium)

1Get an ECG immediately. Hyperkalaemia with ECG changes (or K ≥6.5) → IV calcium gluconate FIRST (cardioprotection), then insulin + dextrose to shift potassium in (± salbutamol).Gate: Calcium gluconate protects the heart but does NOT lower potassium — you still need insulin-dextrose to shift it and treatment of the cause/binders/dialysis to remove it. Always exclude a haemolysed (pseudo) sample.
2Remove potassium from the body (treat cause, stop K-sparing drugs, binders, dialysis if refractory). Hypokalaemia → replace KCl at a safe rate AND replace magnesium (potassium won't correct without it).

Hyperkalaemia: IV calcium gluconate (cardioprotection) → insulin + dextrose (shifts K in) ± salbutamol nebs — calcium protects the myocardium but does NOT lower K; insulin-dextrose shifts it; recheck glucose

Hyperkalaemia: remove K from the body — treat the cause, stop K-sparing drugs, potassium binders; dialysis if refractory

Hypokalaemia: replace potassium (oral or cardiac-monitored IV) + replace magnesium — IV KCl no faster than 10 mmol/h peripherally; magnesium is needed for potassium to correct

Treat the underlying cause — diuretic/drug review, treat Addison's/Conn's, correct acid-base

Key points

Hyperkalaemia ECG: tall TENTED T waves → flat P → broad QRS → sine wave. Treatment ORDER: calcium gluconate (protects heart, doesn't lower K) → insulin-dextrose (shifts) → remove (binders/dialysis). Hypokalaemia: U waves, long QT — replace K AND magnesium. Exclude a haemolysed sample.

Monitor & prognosis

Serial K + ECG, glucose after insulin-dextrose, magnesium; renal function and the cause.

Excellent with prompt treatment; untreated extremes cause fatal arrhythmia.

Source: UK Kidney Association hyperkalaemia; Resus Council UK; cross-ref endocrine (Addison's/Conn's)