There is no universal definition of hyperkalaemia, but a serum K+ ≥ 5.5 mmol/L is widely used.¹,² The incidence of complications rise with increasing severity of hyperkalaemia. The rate of rise of serum potassium is also an important factor which influences the likelihood of complications occurring.
Causes of hyperkalaemia
Many drugs can cause hyperkalaemia. Some of them are listed below:³
Beta blockers – selective and non-selective can cause it
Heparin – unfractionated and LMWH
Ciclosporin / Tacrolimus
Renin inhibitors (e.g. aliskiren)
Renal impairment can occur for a wide range of reasons (e.g. dehydration / nephrotoxic drugs / intrinsic renal disease) and can be acute or chronic.
The kidneys are responsible for controlling the excretion of potassium and therefore deranged renal function results in altered potassium excretion.
This is a very common cause, usually due to:
Drugs as shown above
Over-replacement of K+ with intravenous fluids
Errors in sampling
This is another common cause of apparent hyperkalaemia:
Haemolysis of sample – red blood cells lyse and spill out potassium
Delay in performing sample – potassium leaks out of red blood cells
It’s referred to as pseudohyperkalemia because the actually plasma K+ level is normal.
When you see a very high potassium, it’s always worth sending off another sample (however you should assume the result is accurate and treat accordingly until proven otherwise).
Excessive release from cells
Tissue necrosis – burns / rhabdomyolysis / trauma (K+ spills out of cells into plasma) Massive haemolysis – RBCs lyse and spill intracellular K+ into the plasma(e.g. ABO incompatibility) Low insulin levels – low insulin levels allow K+ to move out of cells into plasma (e.g. diabetic ketoacidosis)
Acidosis can occur for a number of reasons including sepsis and type 2 respiratory failure.
When the plasma becomes acidotic the body attempts to correct this by promoting muscle cells to absorb hydrogen ions out of the plasma.
This exchange mechanism involves the transfer of potassium ions into the serum, resulting in plasma K+ levels rising.
The long term solution is to treat the underlying cause(e.g. antibiotics in sepsis).
The adrenal glands are normally responsible for producing aldosterone
Aldosterone promotes excretion of potassium by the kidneys
In Addison’s disease the adrenal glands do not function correctly, resulting in lack of aldosterone
As a result K+ excretion by the kidneys is reduced and plasma levels rise
This is a rare cause, but still worth keeping in your differential
Symptoms and signs
Patients are asymptomatic in the majority of cases.
Sometimes they can experience weakness and fatigue.
In rare cases individuals with a very raised potassium can experience:
Chest pain – often with associated ECG changes
The biggest risk of hyperkalaemia is the development of life threatening arrhythmias (e.g. ventricular fibrillation)
The risk of arrhythmias increases with values above 6.5mmol/L
Often other ECG changes are observed prior to the development of arrhythmias (e.g. tall tented T-waves).
This is discussed more in the investigations section
Regular U&Es are useful to monitor the trend of the serum K+ level. ↑ creatinine and urea would suggest a diagnosis of hyperkalaemia secondary to acute kidney injury.
A sudden drop in haemoglobin levels would be noted in acute haemolysis.
The following ECG changes are associated with hyperkalaemia:
Tall tented T-waves
Flattening of P-waves
Broad QRS complexes
The presence of any of these changes indicates the need for rapid management hyperkalaemia.
↓ in Addison’s disease
Arterial blood gas
This is a useful investigation if you suspect acidosis to be the underlying cause or contributing factor.
STEP 1 – Protect the heart
Intravenous calcium chloride or calcium gluconate, at an equivalent dose is given to patients with hyperkalaemia in the presence of ECG evidence of hyperkalaemia.
This stabilises the myocardium – reducing the risk of arrhythmia
Onset of action is 1-3 minutes – effects last for 30-60 minutes
STEP 2 – Shift potassium into cells
Insulin + glucose infusion
Rapidly acting insulin combined with glucose as an infusion helps drive potassium into the cells and out of the serum. The glucose is used to prevent hypoglycaemia whilst the potassium is being shifted intracellularly.
Onset of action – 10-20 minutes – duration 2-6 hours
Monitor blood glucose closely
Salbutamol is often used as an adjuvant therapy for hyperkalaemia. It also promotes movement of potassium into cells and therefore out of the serum.
Onset of action 15-30mins
Duration of effect – 4-6 hours
CHECK SERUM POTASSIUM AT1 / 2 / 6 / 12 hours after treatment (give further treatment if indicated)
If hyperkalaemia is resistant to medical treatment you should seek specialist advice from the renal team.
Long-term correction of hyperkalaemia
Once acute management is complete you need to consider the underlying cause.
Think about the common causes and consider if any could apply in the context of your patient:
Are they, or have they recently had IV fluids or blood transfusions?
Are they receiving any causative drugs?
Do they have renal impairment?
Are they acidotic? – arterial blood gas
The correction of the underlying cause is incredibly important, because acute management provides only temporary reduction of K+ levels via shifting K+ out of the plasma and into cells, meaning total body K+ levels remain unchanged. As a result, the patient will likely become hyperkalemic once again if the underlying cause is not treated.
Calcium resonium can be useful in certain circumstances:
However it is not a first line therapy
It provides a slow method of reducing K+ levels – onset of 2-12 hours
It works by binding K+ in the bowel, preventing its reabsorption
It is used in patients with resistant hyperkalaemia who require long term management
Most commonly it is used in those with chronic renal failure
As mentioned above, senior input should be sought before using this drug
As with all drugs that lower K+, there is the risk of causing hypokalaemia
1. Soar J, Perkins GD, Abbas G et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Resuscitation 2010; 81: 1400-1433.
2. Nyirenda MJ, Tang JI, Padfield PL, et al. Hyperkalaemia. BMJ 2009; 339: 1019-1024. 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. Timothy J. Schaefer, MDa,b,*, Robert W. Wolford, MD, MMMc,d
4. Clinical Practical Guidelines. Treatment of acute hyperkalaemia in adults. UK Renal Association. 2012