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Hyperkalaemia is defined as plasma potassium β‰₯ 5.5 mmol/L.1,2

Hyperkalaemia is further classified by the European Resuscitation Guidelines as follows:

  • Mild: 5.5-5.9 mmol/L
  • Moderate: 6.0-6.4 mmol/L
  • Severe: >6.5 mmol/L

The incidence of complications rises with increasing severity of hyperkalemia. The rate at which serum potassium rises is also an important factor influencing the likelihood of complications.

Severe hyperkalaemia is aΒ medical emergency due to the risk of life-threatening arrhythmias. Hyperkalaemia is one of the reversible causes of cardiac arrest. Prompt treatment is vital, especially in patients who have ECG changes. This article will cover the causes, investigation and emergency management of hyperkalaemia.Β 

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Renal causes of hyperkalaemia

The kidneys are responsible for 90% of potassium excretion in healthy individuals, with the remainder excreted via the gastrointestinal tract. As a result, renal impairment is one of the commonest causes of hyperkalaemia.

Iatrogenic causes of hyperkalaemia

Many medications can cause or contribute to hyperkalemia directly or indirectly:

  • ACE inhibitors
  • Angiotensin receptor blockers
  • Potassium-sparing diuretics
  • NSAIDs/COX 2 inhibitors
  • Digoxin (in toxicity)
  • Trimethoprim
  • Beta-blockers – selective and non-selective can cause it
  • Nicorandil
  • Heparin –Β unfractionatedΒ and LMWH
  • Ciclosporin
  • Tacrolimus
  • Renin-inhibitors (e.g. aliskiren)
  • Potassium supplements

Intravenous fluids containing potassium also have the potential to cause hyperkalaemia when prescribed inappropriately.

Blood transfusion is another potential cause of hyperkalaemia.

Trauma and burns

Tissue damage sustained secondary to trauma or burns results in the release of significant volumes of potassium from damaged cells.

Diabetic ketoacidosis

In diabetic ketoacidosis (DKA), potassium shifts from the intracellular to the extracellular space due to a lack of insulin, resulting in hyperkalaemia.

Addison’s disease

Aldosterone promotes the excretion of potassium by the kidneys.

In Addison’s disease, the adrenal glands cannot produce adequate aldosterone levels, which results in reduced renal excretion of potassium.


Pseudohyperkalaemia can occur for a wide variety of reasons, including:

  • Haemolysis (e.g. prolonged tourniquet time, prolonged sample transport time, use of incorrect blood bottles)
  • Blood sample being taken from a limb receiving IV fluids containing potassium
  • Leukocytosis and thrombocytosis

If there are concerns about pseudohyperkalaemia, a sample should be urgently repeated to check the validity of the result.

Clinical features


Symptoms of hyperkalaemia are typically vague and include general weakness and fatigue. Patients may sometimes experience palpitations, chest pain or shortness of breath.

Clinical examination

In most cases, there are no obvious clinical signs of hyperkalaemia.

Potential clinical signs include:

  • Bradycardia secondary to hyperkalaemia-induced atrioventricular block
  • Depressed or absent tendon reflexes


Serum potassium is reported as part ofΒ urea & electrolytesΒ (U&Es). The first consideration is whether this could beΒ pseudohyperkalaemia (e.g. a spurious sample). AΒ repeat U&EΒ should be sent. A venous blood gas can be used to rapidly confirm hyperkalaemia.Β Β 

Bedside investigations

Relevant bedsideΒ investigations include:

  • 12-lead ECG: to identify ECG changes which suggest cardiotoxicity
  • Blood gas (venous or arterial): to exclude metabolic acidosis (e.g. hyperkalaemic renal tubular acidosis or DKA) and rapidly check serum potassium
  • Capillary blood glucose: to exclude hyperglycaemia (e.g. DKA)

ECG changes in hyperkalaemia

An ECG is an essential investigation in the context of hyperkalaemia. Abnormalities can include:

  • Tall tented T waves (early sign)
  • Prolonged PR interval
  • Flattened P waves
  • Wide QRS complexes
  • Sine wave pattern (late sign)
  • Arrhythmias
    ECG changes in hyperkalaemia
    Progression of ECG changes in hyperkalaemia

Laboratory investigations

Relevant laboratory investigations include:

  • U&E: a repeat U&E sample should be sent
  • Full blood count: to exclude haemolysis (e.g. normocytic normochromic anaemia) and leukocytosis or thrombocytosis
  • Serum cortisol: to exclude Addison’s disease (low serum cortisol is found in Addison’s)
  • Digoxin level: to exclude toxicity (if relevant)


The potassium level and the presence/absence of associated ECG changes determine the urgency by which hyperkalemia needs to be treated.

A potassium level of β‰₯6.5 mmol/L and/or a hyperkalaemia-associated ECG changes requires urgent treatmentΒ (a medical emergency).Β 

All patients with hyperkalaemia will ultimately require further monitoring and management.

Prevent further accumulation of potassium

Further accumulation of potassium can be prevented by:

  • Stopping any intravenous fluids containing potassium
  • Suspending any medications that have the potential to increase serum potassium
  • Suspending any supplements containing potassium

Stabilise the cardiac membrane (protect the heart)

If ECG changes are present, then administer intravenousΒ calcium:

  • 10mls 10% calcium chloride
  • 30mls 10% calcium gluconate

This stabilises the myocardium temporarily for 30-60 minutes and reduces the risk of fatal arrhythmia.

Further doses may be required if ECG changes persist. Usually, ECG changes begin to improve within 1-3 minutes of administering calcium. The administration of calcium without hyperkalaemia-associated ECG changes is not recommended.

The role of intravenous calcium

Intravenous calcium stabilises the myocardium and reduces the risk of life-threatening arrhythmias. CalciumΒ does notΒ reduce serum potassium levels. The role of intravenous calcium is to buy time until potassium-lowering treatments can be initiated.

Shift potassium intracellularly (reduce serum potassium)

Treatments which can shift potassium into cells and out of the serum include:

  • Insulin-glucose infusion: insulin shifts potassium from the extracellular to the intracellular compartment, while glucose helps maintain capillary blood glucose levels
  • Salbutamol: often used as adjuvant therapy for hyperkalaemia as it promotes the movement of potassium into cells and out of the serum

Patients receiving an insulin-glucose infusion should undergo regular monitoring of blood glucose levels and serum potassium levels.Β 

Remove potassium from the body

Methods to remove potassium from the body include:

  • Calcium polystyrene sulfonate resin (Calcium resonium) can remove potassium via the gastrointestinal tract.
  • Correction of the underlying cause: the kidneys should then resume their normal function of excreting adequate volumes of potassium via the urine.
  • Haemodialysis is an invasive treatment reserved as a last resort for resistant hyperkalaemia that has failed to respond to all other therapies.

Key points

  • Hyperkalaemia is defined as plasma potassium β‰₯ 5.5 mmol/L.1,2
  • There is a wide range of causes of hyperkalaemia, including renal, iatrogenic, trauma/burns, DKA and Addison’s disease.
  • Symptoms of hyperkalaemia are typically vague and include general weakness and fatigue.
  • In most cases, there are no obvious clinical signs of hyperkalaemia.
  • Key investigations in hyperkalaemia include U&Es, ECG, serum cortisol, FBC and capillary blood glucose.
  • Typical ECG findings in hyperkalaemia include tall tented T waves, broad QRS complexes, prolonged PR intervals and flattened P waves.
  • Management of hyperkalaemia involves preventing further accumulation of potassium, stabilising the cardiac membrane (if ECG changes present), shifting potassium intracellularly and removing potassium from the body.


  1. Soar J, Perkins GD, Abbas G et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Resuscitation 2010; 81:Β 1400-1433.
  2. Nyirenda MJ, Tang JI, Padfield PL, et al. Hyperkalaemia. BMJ 2009; 339: 1019-1024. Β Mahoney BA, Smith WAD, Lo DS, Tsoi K, Tonelli M and Clase CM. Emergency interventions for hyperkalaemia (Review). Cochrane Review, Cochrane Library Issue 2, 2008
  3. Emerg Med Clin N Am 23 (2005) 723–747. Disorders of Potassium.Β Timothy J. Schaefer, MDa,b,*, Robert W. Wolford, MD, MMMc,d
  4. Clinical Practical Guidelines. Treatment of acute hyperkalaemia in adults.Β UK Renal Association.Β 2012


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