Authors: Andrew Parfitt, Emma Townsend / Editors: Steve Fordham / Reviewer: Chris Gray, William Gibbs / Codes: CC3, NepC2, NepC3, NepC5, NepP1, RP3, SLO1 / Published: 24/07/2023

Abnormal potassium levels are the most common electrolyte abnormalities encountered in the emergency department, and can be life threatening if not recognised and managed correctly. This is made all the more difficult as patients with hyper or hypokalaemia may be asymptomatic.

Disorders of potassium balance occur due to:

  • Abnormal intake
  • Abnormal distribution
  • Abnormal excretion

Laboratory reference ranges for normal serum potassium vary slightly, but are typically 3.5 – 5 mmol/L.


Table 1 Causes of Hyperkalaemia and Hypokalaemia

  Hyperkalaemia Hypokalaemia

Potassium supplements

Massive transfusion


Tumour lysis syndrome


Suxamethonium use

Insulin deficiency

Insulin use


ACE Inhibitors

Angiotensin Receptor Blockers




Type 4 Renal Tubular Acidosis

Acute Kidney Injury

Chronic Kidney Disease





Loop Diuretics

Thiazide Diuretics





Types 1 and 2 Renal Tubular Acidosis

Barter’s Syndrome

Liddle’s Syndrome

Gittleman’s Syndrome




Diarrhoea or vomiting



Villous adenoma



Cushing’s Syndrome

Conn’s Syndrome

A full history and examination, together with review of regular and other recent medications must be undertaken. Symptoms and signs of potassium disorders can be absent, subtle, or highly non-specific, such as lethargy and weakness, and therefore a serum potassium level is needed. Together with a serum potassium level, it is important to check:

  • Renal function as patients may have acute or chronic renal failure
  • Blood gases as potassium and hydrogen ion status are closely linked
  • ECG as high or low potassium levels can be associated with conduction defects or life-threatening arrhythmias

It’s important to note that ECG changes only occur in around 50% of patients with hyperkalaemia, so do not rely on the ECG for diagnosis.

In patients with hypokalaemia, it is also important to check serum magnesium levels, as low magnesium will need to be corrected first.


Traditional teaching of the ECG changes in hyperkalaemia lists the following in chronological order [4]:

  • Peaking of T waves (repolarisation abnormalities – Fig.1)
  • Shortening of the PR interval (progressive atrial paralysis)
  • Prolongation of the QRS complex (conduction abnormalities – Fig.2)
  • Flattening of the P wave
  • Bradycardia
  • “Sine wave” rhythm (a pre-terminal rhythm – Fig.3)
  • Asystole




Reference: Life in the Fast Lane ECG Library

It is important to note, however, that ECG changes only occur in around 50% of patients with hyperkalaemia [5], and that the ECG alone is not an adequate predictor of the severity of hyperkalaemia.


The causes of hyperkalaemia can be placed into the five categories shown below:


  • Angiotensin converting enzyme inhibitors (ACEI)
  • Angiotensin receptor blockers
  • Non-steroidal anti inflammatories (NSAIDs)
  • Beta blockers
  • Suxamethonium
  • K+ supplementation
  • K+ sparing diuretics

Renal and metabolic diseases

  • Acute and chronic renal failure
  • type 4 renal tubular acidosis (resulting from aldosterone insufficiency or insensitivity)
  • Metabolic acidosis


  • Fasting – caused by a relative lack of insulin

Endocrine disorders

  • Addison’s disease
  • Hyporeninaemia
  • Insulin deficiency


  • Tumour lysis
  • Rhabdomyolysis
  • Massive transfusion
  • Massive haemolysis

Learning bite

Spurious hyperkalaemia can occur, particularly due to haemolysis from difficult venepuncture. If the potassium result doesn’t fit the clinical picture, it is important to repeat this, performing a blood gas if possible to get a rapid result. However, don’t wait for a repeat lab result to start managing the patient if the clinical picture fits.

Symptoms and Arrhythmias

Patients with hyperkalaemia frequently appear well. In severe cases they can have these non-specific symptoms:

  • Lethargy, confusion, weakness
  • Palpitations
  • Flaccid paralysis
  • Paraesthesia

The whole spectrum of arrhythmias can occur, including ventricular tachycardia and ventricular fibrillation.

Hyperkalaemic cardiac arrest is almost always fatal unless potassium levels are reduced during resuscitation.




The aims of management are to:

  • Stabilise the myocardium
  • Drive potassium into the cells
  • Eliminate excess potassium from the body

Whilst doing all of this, we need to try to identify the underlying cause and treat this as well.

Fluid Resuscitation

In hyperkalaemic patients who require fluid resuscitation, there is often a debate about the best fluid to use. Clinicians are sometimes reluctant to use balanced crystalloids such as Hartmann’s solution (Ringer’s lactate) as these contain potassium.

However, a balanced crystalloid is preferable to 0.9% sodium chloride in these patients. Balanced crystalloids are more alkalinising and therefore would be expected to lead to a greater shift of potassium into cells. They have been shown to produce lower potassium levels in vivo compared with sodium chloride [6,7], and as they have less potassium per litre than the patient’s serum, they will actually lower the potassium level.

Medication Doses Caveat!

In the next few pages, doses given are acceptable standards with reference to evidence-based literature and the national formulary, however please ensure you consult your local guidelines when treating patients with hyperkalaemia.


Myocardial Stabilisation

In patients with cardiac arrhythmias or conduction abnormalities, the first step is to stabilise the myocardium.

Calcium does not lower the serum potassium level, but should be used when the ECG shows a widened QRS, sine wave pattern, arrhythmias, or in hyperkalaemic cardiac arrest, in order to stabilise the myocardium.

Either calcium chloride or calcium gluconate can be used and are widely available. Due to the greater potency of calcium chloride, larger doses of calcium gluconate can be needed if this is used in preference. Calcium gluconate is less irritating to veins and therefore a preferable choice if given peripherally.

Calcium chloride 10%

Dose: 5-10ml over 10 minutes

Complications: Thrombophlebitis

Calcium gluconate 10%

Dose: 10-20ml over 5-10 minutes

Further doses can be given until the ECG normalises, and calcium levels should be monitored on blood gases.

Hypertonic (3%) saline has been shown to reverse ECG changes in patients with hyperkalaemia and concurrent hyponatraemia. There is no evidence that its administration benefits eunatraemic patients, and so use of hypertonic saline should be restricted to hyponatraemic hyperkalaemic patients with an awareness of the potential volume overload it may cause. The dose is a 50ml push [8].


Potassium Shift

The next step is effectively to hide the potassium intracellularly, bringing the serum potassium level down, and reducing the serious complications that serum hyperkalaemia can lead to.

A recent Cochrane review found that salbutamol and IV insulin-dextrose appear to be the most effective at reducing serum potassium [9]. Sodium bicarbonate can be effective in metabolic acidosis but is not necessary if the bicarbonate is normal.


Dose: 10 units of short acting insulin (such as Actrapid) in 50ml 50% dextrose over 15-30 minutes

If the blood glucose levels are already high, insulin can be given intravenously without the dextrose carrier however close glucose monitoring should be undertaken.

Complications: hypoglycaemia

Blood glucose levels should be monitored every 15 minutes for 1 hour then hourly over the next 5 hours following insulin administration to ensure any resulting hypoglycaemia is identified and treated.


Dose: 10-20mg nebulised

Complications: tachycardia, inconsistent response

As many as 40% of patients seem to be resistant to the hypokalaemic effect of salbutamol, and therefore it should never be used as a single agent for the urgent treatment of hypokalaemia [8].

Sodium Bicarbonate

Dose: 100-150ml of 8.4% sodium bicarbonate over 3-4 hours

Complications: metabolic alkalosis

There isn’t a great deal of evidence surrounding the use of sodium bicarbonate in the management of hyperkalaemia. It can be used to drive potassium intracellularly in the context of metabolic acidosis, and there may be some role in potassium excretion also. Intensive care or nephrology advice should be sought before using bicarbonate, particularly in dialysis-dependent patients.


Potassium Elimination

There are three main routes of elimination available to us. We can use diuretics to increase urinary potassium excretion. Exchange resins can bind and excrete potassium in the GI tract. We can also filter the blood to remove potassium.


Dose: 40-80mg IV as a bolus

Can be very useful in patients with fluid overload

Calcium Resonium

Dose: 15g TDS orally, or 30g rectally retained for 9 hours followed by irrigation

Complications: constipation, gastrointestinal necrosis

There is little to no evidence that calcium resonium effectively reduces serum potassium levels, and multiple case reports of severe gastrointestinal complications. Consideration of this should be undertaken before prescription.


This is the definitive treatment for hyperkalaemia, particularly if this is refractory to medical management, the patient is acidotic, oligo/anuric, or already on dialysis. Such patients should be discussed early with the intensivists and nephrologists.

As well as trying to eliminate excess potassium, we also need to make sure we don’t contribute too much to the potassium load. It’s important to check the drug chart, and consider stopping potassium-sparing/containing drugs, and to put the patient on a low potassium diet.


In mild hypokalaemia there are usually no ECG changes.

Moderate to severe hypokalaemia may cause increased P wave amplitude, PR prolongation, U waves, T wave flattening and ST segment depression. Due to myocardial hyperexcitability, ectopics may occur. With worsening hypokalaemia, arrhythmias including atrial fibrillation, atrial flutter, ventricular tachycardia or ventricular fibrillation may result.

This ECG shows hypokalaemia with U waves.



The most common cause of hypokalaemia is potassium depletion. In critically ill patients the most common cause is abnormal losses which occur in stool and urine (from metabolic alkalosis and chloride depletion).

Other causes of hypokalaemia are:

  • Increased potassium loss
  • Transcellular shift
  • Decreased intake
  • Magnesium depletion

The following pages outline these causes in more detail.

Other causes of hypokalaemia include:

Transcellular shift

  • Glucose insulin therapy
  • Theophylline, caffeine
  • Hyperthyroidism
  • β2 adrenergic stimulation, e.g. salbutamol nebulisers
  • Alkalosis
  • Hypokalemic periodic paralysis

Decreased intake

  • Iatrogenic, e.g. inadequate intravenous supplementation
  • Poor dietary intake

Magnesium depletion

  • Poor dietary intake
  • Increased magnesium loss


Increased Potassium Loss

Examples of increased potassium loss are shown in the table:

Example Specifics
  • Diuretics (loop and thiazide)
  • Laxative abuse
  • Liquorice, steroids
GI losses
  • Vomiting
  • Diarrhoea
  • Ileostomy
  • Intestinal fistula
  • Villous adenoma
Renal disorders
  • Barters syndrome
  • Liddle’s syndrome
  • Gitelman’s syndrome
  • Nephrogenic diabetes insipidus
  • type 1 (distal) and type 2 (proximal) renal tubular acidosis
  • Hyperaldosteronism
  • Cushing’s and Conn’s syndromes
Osmotic diuresis As occurs in diabetic ketoacidosis

Further information about drugs and GI losses

Diuretics deliver increased loads of sodium and chloride to the distal tubules and thus increase potassium secretion. These drugs also deplete magnesium which leads to further increased potassium loss.

Upper GI losses usually involve small amounts of potassium but the coexistent chloride loss leads to secretion of potassium in the kidney. Potassium is secreted in the distal colon and thus, in ileostomy patients, effluent is not rich in potassium.

Metabolic alkalosis usually develops as a consequence of chloride loss (e.g. by diuretics or vomiting) and in this situation increased delivery of sodium occurs to the distal tubules and this results in increased secretion of potassium into urine.

Symptoms and Arrhythmias

Even severe hypokalaemia may be totally asymptomatic. Symptoms, when they occur, are due to decreased excitability of neuromuscular cardiac function. Muscular weakness, constipation and ileus are common [10].

In patients with pre-existing ischaemic myocardial damage there is an increased incidence of arrhythmias. Severe hypokalaemia, K(s) < 2.5 mmol/l can cause rhabdomyolysis and when K(s) < 2.0 mmol/l this can cause ascending paralysis with eventual respiratory arrest.

Patients may present with polyuria and polydipsia due to an impaired ability to concentrate urine.

Learning bite

In patients taking digoxin, hypokalaemia increases the incidence of arrhythmias.


Hypokalaemia, especially after acute myocardial infarction (MI), can predispose to VF and VT. Correction of the potassium may be required in such cases for antiarrhythmic drugs to be effective.

Sotalol is more likely to induce arrhythmias, such as torsades, in patients with hypokalaemia.

Learning bite

Arrhythmias are far more likely in patients with heart failure, ventricular hypertrophy and ischaemic heart disease who have abnormal potassium levels.


The decision of when to treat and how to treat patients with hypokalaemia must be based on the clinical state of the patient

State of Patient Possible Management
Mild hypokalaemia Dietary supplementation and monitoring
Potassium administration
Magnesium supplementation
Moderate hypokalaemia Potassium administration
Magnesium supplementation
Severe hypokalaemia Intravenous potassium replacement
Magnesium administration
Cardiac arrest Potassium chloride administration
Further investigation Determine cause

Mild/moderate hypokalaemia

Most patients who are asymptomatic with mild hypokalaemia do not require urgent correction (unless cardiac disease is present). Dietary supplementation and monitoring may suffice.

The treatment of hypokalaemia involves potassium administration. The deficit, calculated from serum potasssium, crudely approximates at 0.3 mmol/l for every 100 mmol reduction in body potassium. Thus the deficit is considerable despite small reductions in serum levels. Replacement must be gradual. Magnesium deficiency is associated with potassium depletion and magnesium supplementation facilitates more rapid correction of hypokalaemia. Magnesium levels should be obtained to determine coexistent hypomagnesaemia.

Severe hypokalaemia

In severe hypokalaemia intravenous replacement must be used. This must be rigorously controlled using infusion pumps according to local protocols.

The maximal rate of correction is 20 mmol/h K+. Some authorities recommend that the unstable patient suffering from rhythm disturbances may receive a rapid initial infusion of 2 mmol/min over 10 minutes if cardiac arrest is imminent.

Magnesium administration (5 ml of 50% over 30 minutes) should commence soon after. Never bolus inject potassium and always ensure adequate mixing of the solution occurs before the infusion is started.

Learning bite

  • Potassium replacement requires cardiac monitoring.
  • Take special care in patients with low serum potassium due to transcellular potassium shifts. Rebound hyperkalaemia can occur quickly.

Cardiac arrest

Cardiac arrest due to hypokalaemia may require 20 mmol potassium chloride IV over 2-3 minutes, repeated until potassium is > 4.0 mmol/l. Prompt correction increases the chances of successful defibrillation and may decrease the incidence of post arrest arrhythmias.

Further investigation

Longer term further investigation is directed towards the cause. It may involve measurement of renin, aldosterone and computerised tomography (CT) of adrenal glands.

Learning bite

Mortality in patients with hypokalaemia in hospital is ten fold higher than the general hospitalised population. It is important to detect, monitor and treat the condition correctly.

You should keep the following points in mind when treating patients in the Emergency Department:

Patient statistics

  • The majority of patients with disturbances of potassium balance are asymptomatic
  • The majority of patients with hyperkalaemia have some underlying renal dysfunction
  • Mortality as an inpatient is tenfold higher in hypokalemic patients. Careful monitoring and correction +/- supplementation must be achieved prior to discharge

Serum levels

  • Serum levels can be raised, normal or low in excess or deficiency of total body potassium
  • If a serum potassium level is raised in a well patient with normal renal function, take a repeat sample to check the first result was not spuriously elevated
  • Rapidly rising levels of serum potassium are more serious than slower rising levels


  • Remember medications are common causes of potassium disturbance
  • Potassium balance is intimately related to sodium, water, acid base balance and cannot be interpreted in isolation
  • ECG findings in hyperkalaemia are non-specific and the ECG is not a predictor of the presence or severity of hyperkalaemia
  • Remember to monitor glucose levels and administer glucose during treatment with insulin
  • Renal replacement therapy with haemofiltration or haemodialysis is the treatment of choice for life threatening hyperkalaemia refractory to medical management.
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