Hyperkalaemia

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Overview

Hyperkalaemia describes an elevated blood potassium ion concentration. Hyperkalaemia must be diagnosed and managed appropriately due to the risk of cardiac arrhythmia.

Potassium is regulated using:

  • Aldosterone:
    • Leads to sodium retention and potassium excretion
  • Acid-base homeostasis:
    • Acidosis (increased H+ ions) displace potassium in cells leading to potassium leaving cells and entering the bloodstream
  • Insulin:
    • Insulin increases the uptake of potassium into cells

Classification

The European Resuscitation Guidelines have produced a classification system for hyperkalaemia:

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

Effect on the cardiac action potential

Increased potassium leads to faster repolarisation of the cardiac action potential, which can lead to tented T waves on an ECG. They also lead to the inactivation of sodium ion channels (which are involved in depolarisation of the cardiac action potential), leading to smaller P waves, an increased PR interval, a shortened QT interval, and a wider QRS complex, until eventually the p-waves are absent and the ECG becomes sinusoidal. In severe cases, asystole may result.

Causes

Increased intake

In patients with normal renal function, an increased intake of potassium is unlikely to cause hyperkalaemia, however, in patients with renal failure, this is possible. As well as this, a normal intake of potassium can lead to hyperkalaemia in individuals with renal failure.

Decreased excretion

Causes may be:

  • Renal diseases:
  • Adrenal disorders (reduced aldosterone):
  • Drugs:
    • Potassium-sparing diuretics:
      • Aldosterone antagonists (spironolactone, eplerenone)
      • Epithelial sodium channel blockers (triamterene and amiloride)
    • ACE inhibitors (ACEi) or angiotensin-receptor blockers (ARBs):
      • They reduce the release of aldosterone
    • NSAIDs:
      • They reduce the release of renin and hence, aldosterone
    • Trimethoprim:
      • Can behave as a potassium-sparing diuretic
    • Heparin – both unfractionated and low molecular weight:
      • Can lead to reduced aldosterone secretion
    • Calcineurin inhibitors (e.g. ciclosporin and tacrolimus)
      • They are both nephrotoxic and can cause hyperkalaemia directly

Shifting from intracellular to the extracellular space

  • Causes of metabolic acidosis:
    • H+ ions displace potassium ions in cells leading to their release into the blood
  • Digoxin toxicity
    • Due to the inhibition of Na-K-ATPase
  • Beta-blockers
    • Beta-agonists facilitate the entry of potassium ions, therefore blockade can lead to shifts into the extracellular space
  • Suxamethonium:
    • Normally causes a transient increase in serum potassium, but this is more profound in those with neuromuscular disease or prolonged disuse

Other causes

  • Increased cell turnover:
  • Pseudohyperkalaemia:
    • Test tube haemolysis (e.g. the tube has been shaken)

Presentation

Features can be non-specific:

Investigations

  • Consider repeat blood test – if the result is unexpected
  • ECG – is essential as hyperkalaemia can cause arrhythmia. May show:
    • Peaked or ‘tented’ T waves
    • PR prolongation
    • QRS widening
    • Reduced/absent P waves
    • Sinusoidal pattern
    • Asystole

Management

Any patient with severe hyperkalaemia or with ECG changes needs emergency treatment:

  • 1st-line: stabilise cardiac membrane with IV calcium gluconate
    • This does not reduce serum potassium levels
  • Shift potassium into cells: combined insulin + dextrose infusion or nebulised salbutamol
    • This leads to a short-term shift in potassium from the extracellular fluid into the intracellular fluid
  • Remove potassium from the body: oral/rectal calcium resonium
    • The rectal formulation is more effective as some potassium is excreted by the rectum
    • Loop diuretics
    • Consider dialysis in patients with an AKI or persisting hyperkalaemia
  • Stop exacerbating factors + treat the underlying cause

Complications

  • Cardiac arrhythmia and asystole
  • Muscle weakness
  • Paralysis

Prognosis

  • Most cases that result in death are complicated by AKI

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