HYPERKALAEMIA

Alice Winch
Hyperkalaemia:
◦ DEFINTION: A serum potassium concentration higher than the normal range of 3.5 – 5.0 mmol/L.
◦ Mild = 5.5-6.5mmol/L Moderate = 6.5-8mmol/L High = >8mmol/L
◦ Potassium is 98% intracellular and 2% extracellular but plasma potassium is important in maintaining
membrane potentials.
 Causes of Hyperkalaemia
SPLIT INTO RENAL CAUSES (kidney problems) AND EXTRA-RENAL CAUSES (anything else outside the kidneys):

RENAL Causes: EXTRA-RENAL Causes:

• Renal Failure (most common) • Pseudohyperkalaemia
- Acute Kidney Injury - Haemolysis
- End stage Chronic Kidney Disease - Leukocytosis
• Drugs - Thrombocytosis
- Potassium sparing diuretics, such as • Increased Intracellular Output
Spironolactone - Exogenous e.g. catecholamines
- ACE Inhibitors, such as Enalapril - Endogenous; tissue necrosis, haemolysis,
- Alpha-2 Adrenergic receptor antagonists, malignancy, chemotherapy
such as Clonidine • Intracellular to Extracellular shift
• Mineralocorticoid Deficiency - Acidosis
- Addison’s Disease - Insulin Deficiency
- Hyporenaemic hypoaldosteronism
 Causes of Hyperkalaemia RENAL

• Renal Failure
- Acute Kidney Injury
- End stage Chronic Kidney Disease

Potassium is filtered in the glomerulus,

then the bulk is reabsorbed in the
proximal tubule and loop of Henle. Only
the last 10% of filtered potassium reaches
the distal nephron.
 Mechanism of Spironolactone:

Causes of Hyperkalaemia It competitively binds at receptors

at the aldosterone-dependent
sodium-potassium exchange site
RENAL in the distal convolutes tubule,
which helps potassium to be
• Drugs reabsorbed.
- Potassium sparing diuretics, such as Spironolactone
- ACE Inhibitors, such as Enalapril
- Alpha-2 Adrenergic receptor antagonists, such as Clonidine

A2 blockers act in the brain to reduce the sympathetic

outflow from the central nervous system and decrease
peripheral and renal vascular resistance and heart rate.
This leads to less activation of the RAAS.

Aldosterone directly affects potassium secretion

at the collecting duct. ACE Inhibitors reduces
the amount of aldosterone produced and so less
potassium is excreted in exchange for sodium.
Causes of Hyperkalaemia RENAL

• Mineralocorticoid Deficiency
- Addison’s Disease
- Hyporenaemic hypoaldosteronism (low renin levels
which then lead to low aldosterone levels – associated
with mild or moderate renal insufficiency)

Addison’s disease and HH both

cause a deficiency in aldosterone so
as explained by the mechanism
before, low aldosterone leads to
hyperkalaemia.
Causes of Hyperkalaemia EXTRA- RENAL

PSEUDOHYPERKALAEMIA – a false reading of potassium due to activity intracellularly which alters the
serum or plasma potassium concentration.
◦ Haemolysis – rupture of red blood cells in the blood sample leads to leaked potassium into the sample.
◦ Leukocytosis – large increase in levels of leukocytes (common in patients with CLL) leads to fragility of
leukemic lymphocytes.
◦ Thrombocytosis – potassium is released by activated platelets during clotting.

Avoiding Hyperkalaemia:
- Avoid using vacuum tubes
- Avoid prolonged incubation of the blood sample.
Causes of Hyperkalaemia EXTRA- RENAL

• Increased Intracellular Output

- Exogenous e.g. catecholamines – adrenaline and nor-adrenaline
- Endogenous; tissue necrosis, haemolysis, malignancy, chemotherapy
With rapid cellular
destruction all of the cell
Adrenaline and noradrenaline components move outside
cause an initial short transient the cell. So potassium leaves
hyperkalaemia (alpha 1 and 2 the cell and into the
receptors) and then a maintained
hyperkalaemia (beta 1 and 2
receptors).
 Causes of Hyperkalaemia EXTRA- RENAL

• Intracellular to Extracellular shift

Acidosis causes potassium to move
- Acidosis
from the cells into the extracellular
- Insulin Deficiency fluid in exchange for hydrogen ions (as
there are raised H+ ions in the blood.

A low insulin can cause ketones to be released

into the blood leading to ketoacidosis. This
combined with high glucose in the blood can
cause fluid and potassium to leave the cells
and enter the blood.
Symptoms of
Hyperkalaemia
 N.B: Patients with chronic

Investigations and Diagnosis renal failure may be able to

tolerate a slightly raised
potassium, but if levels
>6.5mmol/L it needs urgent
◦ Use FBC value as diagnosis. Always repeat the blood test if >6mmol/L attention. Use the difference
Mild = 5.5-6.5mmol/L Moderate = 6.5-8mmol/L High = >8mmol/L in levels as an indicator
◦ Every person with potassium >6mmol/L should have an ECG
instead: A change
>0.5mmol/L in 6-12 hours
◦ Check any previous blood results for potassium rise >0.5mmol/L requires treatment.
◦ Organise appropriate tests:
•Look for evidence of renal impairment (U&E)
•Look for evidence of acidosis (venous bicarbonate)
•Look for possible diabetes (Fasting glucose)
•If relevant consider DKA (urine ketones)
•Consider Addison’s if hyponatraemia and hyperkalaemia (9am Cortisol)
•Look for underlying condition that may increase cell fragility (FBC)
• Prolonged PR interval.
• Broad, bizarre QRS
complexes — merging
of P wave and T wave.
• Peaked T waves

Potassium level –
9.3mmol/L
• Tall Peaked T
waves

Potassium level
7mmol/L
Management of Hyperkalaemia:
Mild Hyperkalaemia 5.5-5.9 mmol/L If eGFR hasn’t increased by >10% or no acute
increase in potassium repeat in 1-2 weeks.
Review medications and diet for cause of
hyperkalaemia.
Moderate 6.0-6.4mmol/L Recheck ASAP
Hyperkalaemia If there are ECG changes admit
Stop medications that may elevate potassium
Severe ≥6.5mmol/L Urgent repeat
Hyperkalaemia Or if ECG changes Admit patient
present
Treatment of Hyperkalaemia
◦ Acute severe hyperkalaemia (>6.5mmol/L) requires urgent treatment with calcium gluconate 10%
by slow intravenous injection. This antagonises the hyperkalaemia to give temporary protection
against myocardial excitability.
◦ Insulin injections (5-10 units IV) over 5-15 minutes will reduce serum potassium concentration by
shifting it into the cells. This can be repeated if necessary.
◦ Nebulised salbutamol, 20mg over 4-6 hours can reduce plasma potassium but should be used
with caution in patients with CVD.
◦ If it presents with acidosis, sodium bicarbonate infusion can correct the blood pH level.
◦ In order to remove excess potassium, administer 15-30mg Calcium Resonium (ion-exchange resin)
PO/PR.
◦ Occasional heamodialysis may be needed.
Case Study
◦ A 46 year old male collapsed at work in his office. On a GP check up two weeks ago he had appeared well and
his blood results were normal. His past medical history consists of Cushing’s Disease which they have had a
bilateral adrenalectomy for 10 years previously.
What is Cushing’s Disease?
◦ U&Es Results:

Serum Result Units Reference Range

Sodium 116 Mmol/L 133-146
Potassium 5.9 Mmol/L 3.5-5.3
Urea 17.3 Mmol/L 2.5-7.8
Creatinine 120 µmol/L 45-84
Bicarbonate 15 Mmol/L 22-29

What is wrong with these results?

Serum Result Units Reference Range
Sodium 116 Mmol/L 133-146
Low sodium
Potassium 5.9 Mmol/L 3.5-5.3 High Potassium
Urea 17.3 Mmol/L 2.5-7.8 High Urea and Creatinine –
intravascular volume depletion
Creatinine 120 µmol/L 45-84
Bicarbonate – metabolic
Bicarbonate 15 Mmol/L 22-29 acidosis

What Endocrine disorder does this pattern of results resemble?

Addison’s Disease
- The patient has had a bilateral adrenalectomy (both adrenal glands removed) so the patient
will have been on cortisol and aldosterone replacement.
- What could have happened to cause the collapse?

The patient could have potentially misunderstood his GP and thought that because his blood
tests were normal he could stop taking his medications, leading to an Addisonian crisis.
MCQ 1:
Which of these is not an ECG change in
Hyperkalaemia?
◦ A – Tented T waves
◦ B – Prolonged PR
◦ C – Narrow QRS
◦ D – Absent P waves

Answer – C
Widened QRS complex is seen in severe hyperkalaemia.
MCQ 2:
How can you avoid Pseudohyperkalaemia?
◦ A – Avoid prolonged incubation of the blood sample
◦ B – Add water to the sample

◦ C – Take 4 samples of blood from the patient

◦ D – Ask patient to be NBM 6 hours before the test

Answer – A
The shorter amount of time the blood is in the tube the less likely it is to haemolyse.
MCQ 3:
Where in the nephron is the bulk of
potassium reabsorbed?
◦ A – Collecting Duct
◦ B – Bowman’s Capsule
◦ C – Distal Convoluted tubule
◦ D – Proximal Convoluted tubule

Answer – D
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