Management of acute hyperkalaemia: evidence, practice and pitfalls

SUMMARY

Acute hyperkalaemia is a medical emergency requiring rapid clinical evaluation. Point-of-care blood gas analysis may overestimate serum potassium concentration and should be confirmed with a laboratory sample unless urgent treatment is required.

When ECG (electrocardiogram) changes are present, immediate cardiac protection is a priority. Current guidelines recommend administering intravenous 10% calcium gluconate to restore cardiac conduction velocity.

Intravenous insulin rapidly shifts potassium into cells. It is given with intravenous dextrose to reduce the risk of hypoglycaemia. A reduced insulin dose can be considered in patients with significant kidney dysfunction.

Salbutamol shifts potassium into cells and has a synergistic effect with insulin. Nebulised salbutamol administration offers similar efficacy to intravenous delivery with fewer adverse effects.

The routine use of intravenous sodium bicarbonate or oral potassium binders is not recommended for immediate lowering of serum potassium in acute hyperkalaemia. Sodium bicarbonate should be reserved as an adjunctive treatment for patients with concurrent metabolic acidosis.

Post-acute care focuses on addressing reversible triggers and, once hyperkalaemia resolves, restarting important drugs that can increase potassium concentrations, if their benefit outweighs the risk (e.g. renin–angiotensin–aldosterone system inhibitors).

 

Introduction

Severe hyperkalaemia is potentially life threatening. Patients with severe hyperkalaemia in the community should be transferred to an emergency department for assessment and management.

High concentrations of extracellular potassium disrupt normal cellular excitation. Patients with hyperkalaemia are often asymptomatic, but symptoms can range from nausea and muscle weakness to cardiac arrhythmias and cardiac arrest. Morbidity is related to the absolute serum potassium concentration, how rapidly the potassium concentration increased and the underlying cause(s).¹

This article provides an overview of the acute management of moderate to severe hyperkalaemia, summarising current evidence and highlighting practical considerations for clinicians. The management of chronic hyperkalaemia is not addressed.

 

Risk factors for hyperkalaemia

Kidney impairment is the major risk factor for developing acute hyperkalaemia, especially a glomerular filtration rate below approximately 15 mL/min.¹ Additional risk factors include diabetes, adrenal disease and the use of drugs that may increase serum potassium concentrations (Box 1).^2,3

 

Assessment

Although there is no universally accepted definition of hyperkalaemia severity, the Kidney Disease: Improving Global Outcomes (KDIGO) group stratifies risk according to the absolute potassium concentration and the presence or absence of electrocardiogram (ECG) changes (Figure 1).⁴

Potassium sample types and pseudohyperkalaemia

Potassium concentrations can be measured via point-of-care blood gas analysis (BGA) or laboratory samples. The results from these are not directly interchangeable because BGA measures whole-blood concentrations whereas laboratory serum samples require clotting, which releases potassium from platelets and leucocytes. Consequently, laboratory serum potassium concentrations are typically 0.2 to 0.3 mmol/L higher than matched BGA results.⁵

BGA does not detect pseudohyperkalaemia (falsely raised potassium concentrations), which can be caused by haemolysis of the sample, severe thrombocytosis, or leucocytosis. Haemolysis affects up to one-third of all emergency department samples, and undetected haemolysis can prompt unnecessary treatment.⁵ Therefore, it is important to confirm hyperkalaemia detected on BGA with a formal laboratory sample and a full blood count before commencing treatment, unless the patient has haemodynamic instability, ECG changes, or extreme elevations in the setting of known risk factors for hyperkalaemia.

Electrocardiography

An ECG assists in assessment of hyperkalaemia and risk stratification. An urgent 12-lead ECG is recommended when the serum potassium concentration is 6.0 mmol/L or above. Continuous cardiac monitoring is advised when potassium concentrations are 6.5 mmol/L or above, or when ECG abnormalities are present.⁶

Peaked T waves are the most frequently observed abnormality but, alone, are poor predictors of adverse clinical outcomes. ECG features most strongly associated with clinical deterioration are QRS prolongation, bradycardia (heart rate below 50 beats per minute) and junctional rhythms.⁷

ECG abnormalities become more common with increasing potassium concentrations and may progress in severity (Figure 2);⁶ however, up to half of patients have a normal ECG despite severe hyperkalaemia.^7,8 Therefore, ECG findings should be integrated with the overall clinical context rather than used in isolation to guide management decisions.

 

Management of acute hyperkalaemia

In general, mild-to-moderate hyperkalaemia (e.g. serum potassium below 6 mmol/L) can be treated conservatively by addressing reversible causes, such as medications that increase potassium concentrations and oral potassium intake.⁹

Severe hyperkalaemia requires a stepwise approach that includes restoration of cardiac conduction with intravenous calcium, followed by the intracellular shifting of potassium using intravenous insulin (with dextrose), nebulised salbutamol and, if metabolic acidosis is present, intravenous sodium bicarbonate. Robust evidence for acute interventions is limited, but randomised controlled trials are underway to address some of the longstanding evidence gaps.^10-12

Restoring cardiac conduction with intravenous calcium

The priority in severe hyperkalaemia with associated ECG changes is rapid restoration of normal cardiac conduction. Intravenous calcium is the standard of care, based mostly on expert consensus and preclinical studies rather than clinical trials.^9,13 A 2024 systematic review found no robust evidence of clinical benefit.¹⁴ This lack of high-quality data is likely to persist due to the ethical dilemma of enrolling patients with life-threatening hyperkalaemia into a placebo-controlled study.

Recent research challenges the long-accepted mechanism of ‘cardiac membrane stabilisation’ with intravenous calcium. The evidence indicates calcium does not alter the resting membrane potential but restores conduction velocity via L-type calcium channels, bypassing hyperkalaemia-inactivated sodium channels.^13,15

Calcium gluconate 10% (0.22 mmol/mL elemental calcium), administered as a slow intravenous push over 5 to 10 minutes into a large vein, is usually preferred over calcium chloride due to the lower risk of tissue damage and necrosis following extravasation. Calcium chloride (0.68 mmol/mL elemental calcium) is useful when faster delivery (over 3 to 5 minutes) is required during cardiac arrest or imminent collapse.¹⁶

Traditionally, 10 mL of 10% calcium gluconate (2.2 mmol elemental calcium) has been recommended, but this is often insufficient to resolve ECG changes.⁷ Recent guidelines recommend 30 mL (6.6 mmol elemental calcium) to eliminate under-dosing risks.^6,17 The equivalent calcium chloride dose is 10 mL (6.8 mmol elemental calcium). The initially selected dose can be repeated once after 10 minutes if ECG changes persist or, in the context of a cardiac arrest, if a return to spontaneous circulation has not been achieved.¹⁷

This intervention provides a 30- to 60-minute window for potassium-lowering therapies to take effect.^9,17

Shifting potassium into cells

Shifting potassium into cells can rapidly lower the serum potassium concentration, but the shift is temporary and a rebound elevation of the potassium concentration often occurs. These treatments buy time while the underlying cause of hyperkalaemia is addressed or access to haemodialysis is arranged.

Insulin with dextrose

Insulin, administered intravenously, stimulates rapid cellular potassium uptake via the sodium–potassium pump (Na⁺/K⁺-ATPase). Insulin should be considered for patients with a serum potassium concentration of 6 mmol/L or above.^1,6 Intravenous dextrose is administered concurrently to reduce the risk of hypoglycaemia. Dextrose may be omitted if the pretreatment blood glucose concentration exceeds 14 mmol/L.¹⁸

The conventional regimen is 10 units of a short-acting insulin and 25 g of dextrose (e.g. 50 mL of 50% dextrose), administered intravenously as a bolus. This is largely based on small studies involving haemodialysis patients with acute hyperkalaemia.⁶ Serum potassium usually falls by 0.65 to 1.4 mmol/L.⁶

Systematic reviews have found that a lower insulin dose (e.g. 5 units of short-acting insulin with 25 g of dextrose) is associated with a lower risk of hypoglycaemia, without compromising potassium-lowering efficacy.^19,20 However, two recent studies observed a dose-dependent effect of insulin on potassium reduction and no significant decrease in hypoglycaemia risk with the lower dose, underscoring the need for prospective trials to determine the optimal dose.^21,22

Reduced-dose insulin (5 units) should be considered for patients with severe kidney dysfunction.

Iatrogenic hypoglycaemia is common, occurring in up to 30% of patients.^23-25 Iatrogenic hypoglycaemia typically occurs at a median of 2 hours after insulin, rarely appearing before 30 minutes or after 5 hours.^19,24,25 Risk factors for hypoglycaemia are outlined in Box 2; a pretreatment blood glucose concentration below 7 mmol/L is the strongest predictor.²⁴

If the pretreatment blood glucose concentration is less than 7 mmol/L, the initial dextrose 25 g bolus should be followed with a dextrose 25 g infusion (250 mL of 10% dextrose at 50 mL/hour over 5 hours); this gives a total dextrose dose of 50 g.⁶

Salbutamol

Salbutamol, a beta₂-adrenoceptor agonist, lowers serum potassium by stimulating Na⁺/K⁺-ATPase activity, which facilitates potassium uptake into skeletal muscle.²⁶ Nebulised salbutamol administration (10 to 20 mg) is the preferred route because it offers similar efficacy to intravenous delivery with fewer adverse effects such as tremor and palpitations.²⁷ The onset of action is typically under 30 minutes, peaking at 90 to 120 minutes, with a mean potassium reduction ranging from 0.53 to 0.98 mmol/L.³

Adding salbutamol to insulin and dextrose therapy provides a synergistic effect and may reduce the risk of insulin-induced hypoglycaemia by increasing beta₂-adrenoceptor mediated hepatic glycogenolysis and gluconeogenesis.^4,27,28

Up to 40% of patients on haemodialysis exhibit resistance to the potassium-lowering effect of salbutamol but the mechanism is not well understood.²⁹ Efficacy may also be reduced in patients taking nonselective beta blockers.³⁰

Sodium bicarbonate

Intravenous sodium bicarbonate is thought to promote a transcellular potassium shift via serum alkalinisation, triggering hydrogen–potassium exchange and increasing Na⁺/K⁺-ATPase activity.^31,32 A recent systematic review and meta-analysis found no robust evidence supporting a clinical effect of bicarbonate on potassium concentrations.¹⁴ Data on efficacy are marked by significant variability, particularly in patients receiving haemodialysis, in whom bicarbonate monotherapy does not provide a predictable potassium-lowering effect.^33-35 Consequently, international guidelines now recommend that sodium bicarbonate should not be used routinely for acute hyperkalaemia.⁶ However, some evidence suggests it may still be useful as an adjunctive therapy in patients with severe hyperkalaemia that is accompanied by metabolic acidosis but not lactic acidosis or ketoacidosis.^32,36

Enhancing potassium excretion with binding agents

Potassium binding agents are given orally to reduce absorption and increase faecal potassium elimination.³⁷

The onset of action for polystyrene sulfonate binders (e.g. Resonium A, Calcium Resonium) is hours to days, which limits their utility in acute hyperkalaemia.^27,38 Furthermore, serious risks, such as intestinal ischaemia and colonic necrosis, have been documented.^37,39

Patiromer and sodium zirconium cyclosilicate are newer agents that act more rapidly (4 to 7 hours and approximately 2 hours, respectively) and have not been associated with serious gastrointestinal adverse effects.⁴⁰ If used continuously, they are effective at preventing recurrence and facilitating continuation of important chronic therapies, such as renin–angiotensin–aldosterone system (RAAS) inhibitors.^37,41-43 However, evidence for these binding agents, as adjuncts to standard care in acute moderate-to-severe hyperkalaemia, is mixed. Adding patiromer to usual care in the emergency department yielded no significant difference in serum potassium reduction or the need for additional potassium-lowering interventions within 6 hours.⁴⁴ Sodium zirconium cyclosilicate resulted in small potassium reductions at 2 hours compared with standard care, but showed no significant benefit at 1, 4 or 6 hours.⁴⁵

The potential for potassium binders to bind other oral medications is an important practical consideration.

Monitoring potassium and glucose

The potassium-lowering effect of insulin and salbutamol should be assessed 1 to 2 hours after treatment is started. Repeat potassium measurement at 2 to 4 hours is also essential to identify rebound hyperkalaemia as the effects of shifting agents diminish. A follow-up measurement at 24 hours is recommended to confirm sustained normokalaemia.⁶

Following insulin administration, blood glucose should be monitored every 30 minutes for the first 2 hours, then hourly for at least 6 hours.⁶ This 6-hour monitoring window must be reset if subsequent insulin doses are administered. Insufficient monitoring is common, especially in patients without diabetes who are at highest risk of hypoglycaemia.²⁵

 

Preventing recurrence of hyperkalaemia

Strategies to prevent hyperkalaemia recurrence should focus on mitigating transient reversible factors (e.g. hypovolaemia, acute kidney injury, short-term use of potassium-elevating drugs) rather than permanent discontinuation of essential chronic therapies, specifically RAAS inhibitors. Although RAAS inhibitors may be withheld initially, they should be reintroduced sequentially once serum potassium is below 5.5 mmol/L because of their association with mortality reduction in heart failure or proteinuric kidney disease.^46,47 The use of sodium-glucose co-transporter 2 (SGLT2) inhibitors, loop diuretics or potassium binders can help maintain the potassium concentration within range while using RAAS inhibitors at target doses.⁶

Optimising the management of comorbidities and physiological factors is central to maintaining normokalaemia. This includes improving glycaemic control, correcting metabolic acidosis and managing constipation. Gastrointestinal excretion of potassium becomes increasingly important as glomerular filtration declines; potassium-containing aperients such as macrogol should be avoided.⁶

Blanket dietary potassium restriction is not recommended due to a paucity of evidence for benefit and increased risk of malnutrition and cardiovascular disease.^6,46 Referral to a renal dietitian should be considered for patients with severe kidney dysfunction who have persistent hyperkalaemia.^4,6

‘Sick day’ instructions to withhold drugs that increase the risk of hyperkalaemia during acute dehydrating illnesses should be provided.⁴⁸

Key practice points for the management of acute hyperkalaemia are summarised in Box 3.

 

Conclusion

Recent changes to guidance for acute hyperkalaemia management, based on emerging evidence, favour higher doses of calcium gluconate for cardiac protection. Insulin and salbutamol are effective for temporarily lowering serum potassium concentrations while underlying causes of hyperkalaemia are addressed. Proactive dextrose administration and blood glucose monitoring mitigates the risk of insulin-induced hypoglycaemia. Intravenous sodium bicarbonate has limited effect on potassium concentrations and is only indicated in patients with metabolic acidosis. Potassium binders have limited effectiveness for acute hyperkalaemia.

This article was finalised on 24 August 2026.

Acknowledgements: The authors thank Associate Professor Adam La Caze for his valuable supervision and critical review during the development of this manuscript.

Conflicts of interest: Samuel Ford has received funding from the Emergency Medicine Foundation (Leading Edge grant) to support a clinical trial related to hyperkalaemia management. He has received scholarships to support his PhD studies from The University of Queensland and the Dr Jian Zhou Memorial Scholarship fund.

Anna Zipf and Julian Williams reported no conflicts of interest.

This article is peer reviewed.

 

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