Define Hyperkalaemia. Describe its causes and management.

Potassium Physiology — WHY the Level Matters

About 98% of the body's potassium is intracellular, and this steep gradient sets the resting membrane potential of excitable tissues. Hyperkalaemia (serum K⁺ > ~5.5 mmol/L) is dangerous because a high extracellular potassium partially depolarises cardiac cells, destabilising the myocardium and risking fatal arrhythmias or arrest — often with little warning. It is therefore treated on the level and the ECG, not on symptoms.

Causes — Three Mechanisms

• Reduced excretion — acute/chronic kidney disease (commonest), Addison's, drugs (ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs).
• Transcellular shift out of cells — metabolic acidosis, insulin deficiency, and tissue breakdown (crush injury, burns, rhabdomyolysis, tumour lysis, haemolysis).
• Increased load — potassium supplements and stored-blood transfusion.

Before treating, exclude pseudohyperkalaemia — a falsely high result from potassium leaking out of cells in the sample tube (haemolysed/delayed sample) — suspected when the level is unexpectedly high in a well patient with a normal ECG.

Clinical & ECG

It is often silent until the arrhythmia, though muscle weakness may occur. The ECG evolves in order: tall 'tented' T waves → flattened P waves and PR prolongation → widening QRS → sine wave → VF/asystole.

Management — Stabilise, Shift, Remove

Three logical steps, used together in a severe case:

• stabilise the myocardium with IV calcium gluconate (protects the heart but does not lower potassium)
• shift potassium into cells temporarily with insulin plus dextrose (± nebulised salbutamol, and correcting acidosis)
• remove it with potassium binders or, definitively, dialysis. Stop contributing drugs, treat the cause, and monitor the ECG and glucose.

How the Common Drugs Cause It

ACE inhibitors and ARBs reduce aldosterone, the hormone that drives renal potassium excretion — so blocking it retains potassium. Potassium-sparing diuretics (spironolactone, amiloride) act on the distal tubule to retain potassium, and NSAIDs reduce renal blood flow and aldosterone. These are especially dangerous in combination or in renal impairment, and are the first drugs to review in a hyperkalaemic patient.

The Emergency Algorithm

Confirm the level + attach ECG/monitor (exclude pseudohyperkalaemia) → Calcium gluconate IV — protect the myocardium → Insulin-dextrose ± nebulised salbutamol — shift K⁺ into cells → Potassium binders / dialysis — remove K⁺ from the body → Stop culprit drugs, treat the cause, recheck K⁺ and glucose

Contrast with Hypokalaemia & Chronic Care

It helps to hold the two disorders side by side: hyperkalaemia gives tall tented T waves, a widening QRS and asystole, whereas hypokalaemia hyperpolarises cells and gives the opposite — flat T waves, ST depression, prominent U waves and tachyarrhythmias. Beyond the acute emergency, chronic hyperkalaemia (usually renal) is managed by dietary potassium restriction, stopping or adjusting offending drugs, treating acidosis, potassium binders, and dialysis for established renal failure. In surgical patients, cautious potassium prescribing and awareness of the load from stored blood prevent it.

• Calcium gluconate 10% — 10 mL IV over 5–10 min (cardioprotection); repeat if ECG changes persist.
• Insulin-dextrose — ~10 units soluble insulin in 50 mL of 50% dextrose IV.
• Salbutamol 10–20 mg nebulised; dialysis for definitive removal.

Calcium gluconate stabilises the myocardium first, before shifting potassium.

• 98% of K⁺ is intracellular and sets the membrane potential — high K⁺ destabilises the myocardium → arrhythmia/arrest.
• Causes: reduced excretion (renal failure, drugs), transcellular shift (acidosis, tissue breakdown), increased load (supplements, stored blood).
• Exclude pseudohyperkalaemia (haemolysed sample) if the patient is well with a normal ECG.
• ECG: tented T → flat P/long PR → wide QRS → sine wave.
• Stabilise (calcium gluconate) → shift (insulin-dextrose/salbutamol) → remove (binders/dialysis).