Hyperkalaemia
High potassium — cardiac risk, causes and emergency management
Hyperkalaemia (serum potassium >5.0 mmol/L, clinically significant >5.5 mmol/L) is a potentially life-threatening electrolyte emergency. It disrupts cardiac conduction and can cause fatal ventricular arrhythmias with little warning. It is particularly common in patients with CKD, diabetes, and heart failure on ACE inhibitors or ARBs.
What is Hyperkalaemia?
Potassium (K+) is the principal intracellular cation, with only ~2% of total body potassium in the extracellular fluid. The resting membrane potential of cardiac and muscle cells depends critically on the ratio of intracellular to extracellular potassium. When extracellular potassium rises, this ratio decreases, causing partial depolarisation — cells become more excitable initially, then fail to repolarise properly. On ECG, hyperkalaemia causes a progressive sequence: peaked (tall, narrow, symmetrical) T waves → prolonged PR interval → widened QRS → loss of P waves → sine wave pattern → ventricular fibrillation. Hyperkalaemia is classified as mild (5.0–5.9 mmol/L), moderate (6.0–6.4 mmol/L), or severe (≥6.5 mmol/L).
Causes & Risk Factors
The most common causes of hyperkalaemia are renal impairment (reduced potassium excretion), medications, and cellular release of potassium. Medication causes: ACE inhibitors (ramipril, lisinopril), ARBs (losartan, candesartan), potassium-sparing diuretics (spironolactone, amiloride, eplerenone), NSAIDs, and beta-blockers (interfere with K+ uptake). The dangerous 'triple whammy' combination of ACEi + ARB + diuretic in CKD is a common preventable cause. Other causes include diabetic ketoacidosis (acidosis shifts K+ out of cells), rhabdomyolysis (massive cell breakdown), excessive potassium supplementation, Addison's disease (lack of aldosterone — the hormone responsible for urinary K+ excretion), and haemolysis in blood samples (pseudohyperkalaemia — repeat sample before treating if no symptoms or ECG changes).
Signs & ECG Changes
Mild hyperkalaemia is usually asymptomatic. At higher levels, patients may experience muscle weakness, fatigue, palpitations, and paraesthesia. The most dangerous manifestation is cardiac — ECG changes are the key monitoring tool. Peaked T waves appear first (K+ ~5.5–6.5), then P wave flattening/prolongation of PR (>6.0), then QRS widening (>6.5), then sine wave pattern — at this point ventricular fibrillation is imminent. Any ECG change with hyperkalaemia is a medical emergency regardless of the absolute potassium level. Pseudohyperkalaemia should always be excluded in the absence of symptoms or ECG changes — haemolysis in the sample tube is common and causes falsely elevated readings.
Emergency Management & Prevention
A rapid evaluation of ECG changes, potassium level, and likely cause guides the urgency and sequence of treatment. The approach follows three sequential steps: stabilise the heart, shift potassium into cells, then remove potassium from the body. Stabilise: calcium gluconate IV — does NOT lower potassium but protects the heart immediately. Shift: insulin/dextrose and nebulised salbutamol drive potassium into cells temporarily. Remove: potassium binders (patiromer, sodium zirconium cyclosilicate) or dialysis for refractory cases. Long-term prevention involves reviewing and stopping unnecessary ACEi/ARBs/K+-sparing diuretics, dietary potassium restriction in CKD, and regular electrolyte monitoring in at-risk patients.