Lucan · Conditions

Hyperkalaemia management

Australian guidance: eTG Cardiovascular — Hyperkalaemia + CARI

1. Definition and epidemiology

Hyperkalaemia is defined as a serum potassium concentration above 5.0 mmol/L, with severe hyperkalaemia conventionally exceeding 6.0 mmol/L and life-threatening hyperkalaemia exceeding 6.5 mmol/L or any level with ECG changes. It occurs in approximately 2 to 3% of hospitalised patients in Australia, rising to 15 to 40% in those with chronic kidney disease (CKD) stages 4 and 5, particularly when renin-angiotensin-aldosterone system (RAAS) inhibitors are co-prescribed. The condition is a leading cause of preventable cardiac arrhythmia and arrest in hospital settings.

2. Pathophysiology

Potassium homeostasis depends on two mechanisms: cellular buffering (which shifts potassium rapidly between intracellular and extracellular compartments) and renal excretion (which eliminates the daily dietary load over hours). Ninety-eight percent of total body potassium is intracellular, maintained by the sodium-potassium ATPase pump. Hyperkalaemia results from (a) reduced renal excretion as seen in CKD, acute kidney injury (AKI), hypoaldosteronism, or type 4 renal tubular acidosis; (b) transcellular shift from the intracellular compartment due to acidosis (each 0.1 unit fall in pH raises serum potassium by approximately 0.4 to 0.6 mmol/L), insulin deficiency, beta-blockade, or cell lysis; or (c) excessive exogenous or endogenous load from dietary excess, haemolysis, rhabdomyolysis, or massive tissue necrosis. RAAS inhibition with ACE inhibitors (ACEi) or angiotensin receptor blockers (ARB) reduces aldosterone-driven urinary potassium excretion and is a major iatrogenic contributor, particularly in patients who already have impaired renal function. Potassium-sparing diuretics such as spironolactone and amiloride amplify this risk and should not be initiated when serum potassium is 5.0 mmol/L or above.

3. Clinical presentation and diagnostic criteria

Most patients with mild to moderate hyperkalaemia (5.0 to 6.0 mmol/L) are asymptomatic and the diagnosis is made incidentally on routine biochemistry. Symptomatic hyperkalaemia most commonly presents with neuromuscular features: skeletal muscle weakness, cramps, and in severe cases ascending flaccid paralysis. Cardiac manifestations are the most dangerous and include palpitations, bradycardia, and syncope preceding cardiac arrest. A thorough history should elicit medication use (ACEi, ARB, spironolactone, amiloride, NSAIDs, trimethoprim), known CKD, adrenal insufficiency, recent dietary changes, and symptoms of uraemia. Examination may reveal proximal weakness and reduced deep tendon reflexes in severe cases.

4. Investigations and AU-specific cutoffs

Initial investigations should proceed in the following order:

1. Repeat serum potassium on a fresh, non-haemolysed sample to exclude pseudohyperkalaemia from in-vitro red cell lysis (a common laboratory artefact, particularly in patients with thrombocytosis or leucocytosis).
2. Twelve-lead ECG immediately for any potassium above 6.0 mmol/L or when clinical concern exists at lower levels. ECG changes progress sequentially: peaked (tent-shaped) T waves are the earliest finding, followed by PR interval prolongation, flattening and disappearance of P waves, widening of the QRS complex, a sine-wave pattern, and finally ventricular fibrillation or asystole.
3. Urea, creatinine, and eGFR to assess renal function.
4. Venous blood gas to quantify any coexisting metabolic acidosis and to obtain a simultaneous pH for interpreting transcellular shifts.
5. Urinary potassium-to-creatinine ratio or transtubular potassium gradient (TTKG) to distinguish renal from non-renal aetiology when the cause is unclear.
6. Cortisol and renin-aldosterone axis if adrenal insufficiency is suspected.

AU-specific cutoff: eTG and most AU hospital protocols use a threshold of 5.0 mmol/L for initiating monitoring and medication adjustment. For patients with CKD on RAAS inhibitors, checking renal function and serum potassium 1 to 2 weeks after any dose change is mandated.

5. Management

Management is stratified by severity and the presence of ECG changes. The three priorities are cardiac membrane stabilisation, rapid intracellular potassium shift, and total body potassium elimination.

Emergency management (ECG changes or potassium above 6.5 mmol/L):

Intravenous calcium gluconate 10% (10 mL over 2 to 3 minutes) or calcium chloride (preferred if central access is available) is the immediate first step. Calcium does not lower serum potassium but stabilises the cardiac membrane within 1 to 3 minutes. The effect lasts 30 to 60 minutes and can be repeated if ECG changes persist.

Simultaneous shift therapy using intravenous insulin-dextrose (10 units of soluble insulin with 50 mL of 50% dextrose, or 10 units insulin with 250 mL of 10% dextrose over 15 to 30 minutes) moves potassium into cells within 15 to 30 minutes, reducing serum potassium by approximately 0.5 to 1.5 mmol/L for 4 to 6 hours. Nebulised salbutamol 10 to 20 mg provides an additive shift effect via beta-2 adrenoceptor stimulation of sodium-potassium ATPase and is particularly useful when IV access is being established.

Sodium bicarbonate (100 to 150 mmol IV) is adjunctive when a metabolic acidosis is documented; it has minimal effect in the absence of acidosis.

Elimination:

Resonium (calcium or sodium polystyrene sulphonate) 15 to 30 g orally or rectally is an ion-exchange resin that binds potassium in the gut. Onset is slow (2 to 4 hours) and it should not be used alone in emergency settings. Patiromer and sodium zirconium cyclosilicate (SZC) are newer potassium binders with faster onset, better tolerability, and no risk of intestinal necrosis; SZC 10 g orally three times daily for 48 hours is approved in Australia and can reduce potassium within 1 hour. Frusemide (furosemide) 40 to 80 mg IV promotes kaliuresis in patients with residual renal function. Haemodialysis is the most effective and reliable elimination method and is indicated in refractory severe hyperkalaemia, particularly in AKI or end-stage kidney disease.

Medication review:

All contributing medications (ACEi, ARB, NSAID, spironolactone, amiloride, trimethoprim) should be reviewed urgently. In patients with CKD and albuminuria who require ongoing RAAS inhibition for reno-protection and cardiovascular benefit, the lowest effective dose should be maintained with close monitoring rather than blanket cessation, in accordance with CARI recommendations that ACEi or ARB remain preferred agents in this population.

6. Pharmacology and AU PBS notes

Calcium gluconate 10%: IV formulation, not PBS listed as a community prescription item; supplied as a ward stock medication in all Australian hospitals.

Insulin-dextrose: Standard ward stock. Soluble insulin (Actrapid or Humulin R) used in AU. Monitor blood glucose at 30, 60, and 120 minutes to detect hypoglycaemia.

Salbutamol (Ventolin, GSK): Nebulised 10 to 20 mg is approximately 4 to 8 times the usual bronchodilator dose. Available as PBS item for asthma; off-label for hyperkalaemia. AU brand: Ventolin nebules 2.5 mg/2.5 mL (4 to 8 nebules).

Sodium zirconium cyclosilicate (Lokelma, AstraZeneca): PBS listed (Streamlined Authority required) for chronic hyperkalaemia in CKD patients on RAAS inhibitors. PBS Restriction: patient must have serum potassium above 5.0 mmol/L confirmed on two occasions. Dose: 10 g three times daily for 48 hours (acute), then 5 to 10 g once daily (maintenance).

Patiromer (Veltassa): Not yet PBS listed in Australia as of mid-2026; available via private prescription.

Calcium polystyrene sulphonate (Resonium Calcium): PBS General Schedule; 15 g sachet. Avoid in patients with reduced bowel motility due to risk of intestinal necrosis.

Frusemide (Lasix, many generics): PBS listed; standard kaliuretic dose 40 to 80 mg IV or oral. AU spelling is frusemide.

7. Complications and monitoring

Immediate complications include ventricular arrhythmia, cardiac arrest, and respiratory failure from respiratory muscle paralysis. Hypoglycaemia from insulin-dextrose treatment is common and mandates glucose monitoring for at least 2 hours after administration.

Chronic monitoring is required in all patients with CKD, heart failure, or who are prescribed RAAS inhibitors or potassium-sparing diuretics. The eTG recommends checking renal function and serum potassium 1 to 2 weeks after any dose initiation or escalation of these agents. Ongoing surveillance frequency depends on CKD stage: at least 3 monthly in eGFR below 30, and 6 monthly in eGFR 30 to 60. Dietary potassium restriction (less than 60 to 70 mmol per day) is advised for patients with recurrent hyperkalaemia, with referral to a renal dietitian recommended in patients with CKD on dialysis or predialysis.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.