Hyperkalaemia

Hyperkalaemia is defined as a serum potassium concentration >5.5 mmol/L. It is classified as mild (5.5–5.9), moderate (6.0–6.4), or severe (≥6.5 mmol/L or any level with ECG changes). In the UK hospital setting, common causes include Acute Kidney Injury, Chronic Kidney Disease, and medications (ACE inhibitors, ARBs, Spironolactone, NSAIDs). Other causes include metabolic acidosis, rhabdomyolysis (cell lysis releasing K+), and Addison’s disease (mineralocorticoid deficiency). The main clinical risk is cardiac arrhythmia; as potassium increases, the resting membrane potential of the myocardium is depolarized, leading to venticular fibrillation or asystole. In any patient with K+ ≥6.0 mmol/L, an urgent 12-lead ECG is mandatory. Management is an emergency if changes are present or K+ is ≥6.5. This involves three phases: 1. Protecing the heart (Calcium Gluconate). 2. Shifting K+ into cells (Insulin/Dextrose, Salbutamol). 3. Removing K+ from the body (Diuretics, Calcium Resonium, or Dialysis).

Potassium is primarily an intracellular cation (98% of total body K+). The concentration gradient across the cell membrane, maintained by the Na+/K+ ATPase pump, determines the resting membrane potential (RMP). Hyperkalaemia raises the RMP (making it less negative), bringing it closer to the threshold for depolarization. Ironically, while this initially makes cells more excitable, it eventually leads to less excitability because sodium channels remain in an inactivated state, slowing conduction. This slow conduction manifests as widening of the QRS complex. The kidney is the primary regulator of potassium balance, primarily via the action of Aldosterone in the distal convoluted tubule and collecting duct, which promotes K+ secretion. Failure of renal excretion (AKI/CKD) or lack of aldosterone (hypoadrenalism) are the primary drivers of clinical hyperkalaemia.

Hyperkalaemia is often asymptomatic until a catastrophic cardiac event occurs. Some patients may report non-specific muscle weakness, palpitations, or lightheadedness. Clinical signs are generally absent unless the patient has an underlying cause (e.g., signs of AKI or Addison's). The 12-lead ECG is the most sensitive bedside monitor for the physiological effect of hyperkalaemia. Progression of ECG changes: 1. Tall 'tented' T waves (global). 2. Prolonged PR interval. 3. Flattened/absent P waves. 4. Widening of the QRS. 5. 'Sine-wave' pattern (pre-terminal). Complications include VF, asystole, and sudden cardiac death. Medical residents must always check for haemolysis (pseudohyperkalaemia) if the patient is well and the ECG is normal, but they should never delay treatment of a high result in an unwell patient.

Bedside: Urgent 12-lead ECG (repeat frequently during treatment). Lab: U&Es (Creatinine, Urea, K+), Bone profile (Calcium), FBC (check for thrombocytosis/leukocytosis which can cause pseudo-high K+). Blood gas (VBG/ABG): Fast assessment of K+ and pH (acidosis shifts K+ out of cells). Digoxin level (if the patient takes Digoxin, as hyperkalaemia worsens toxicity).

1. Myocardial Stabilization: IV Calcium Gluconate (10ml of 10%) over 5-10 mins if K+ ≥6.5 or ECG changes. 2. Intracellular Shift: IV Actrapid Insulin (10 units) in 50ml 50% Dextrose over 15-30 mins. Salbutamol nebulisers (10-20mg) can also be used as an adjunct. 3. Excretion: Stop all K+-sparing drugs/supplements. Loop diuretics (e.g., Furosemide) if the patient is producing urine. Potassium-binding resins (e.g., Patiromer or Sodium Zirconium Cyclosilicate). 4. Definitive: Haemodialysis if K+ is refractory to medical management or if AKI is severe. 5. Follow-up: Re-check K+ within 1-2 hours and then every 4-6 hours until stable.