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Up Acid-base Hyponatraemia Lactate Magnesium Phosphate Potassium

Potassium metabolism




Inadequate intake

Excessive GI loss

  • prolonged vomiting
  • diarrhoea
  • loss through intestinal fistulae or via recent ileostomy
  • villous adenoma of intestine
  • purgative abuse

Renal loss

  • Hyperaldosteronism: Conn’s, Bartter’s, secondary
  • Cushing’s syndrome: adrenal tumour, pituitary adenoma, ectopic ACTH
  • Renal tubular acidosis type I and II (latter causes hyperaldosteronism and hence ¯ K+)
  • Drugs eg diuretics, amphotericin, acetazolamide, carbenoxolone, liquorice
  • Magnesium deficiency
  • reduced proximal tubular K+ reabsorption: renal tubular failure eg polyuric phase acute renal failure, Fanconi syndrome

Shift into ICF

  • insulin
  • hypokalaemic periodic paralysis

Renal loss plus shift into ICF

  • alkalosis

Renal & GI loss plus shift into ICF

Clinical features

  • weakness, hypotonicity, depression
  • ileus, constipation
  • ventricular arrhythmias (classically torsades), atrial arrhythmias
  • ventilatory failure
  • coma
  • rhabdomyolysis in severe and prolonged cases 
  • nephrogenic DI (chronic hypokalaemia)
  • ECG changes: prolonged PR, inverted T waves and U waves


  • decrease in serum concentration from 4 to 3 mmol/L corresponds to about a 10% reduction in total body potassium (approx 300 mmol). Decline to 2 suggests a deficit of about 600 mmol. Below 2 mmol/L difficult to estimate absolute deficit because relationship between serum concentration and total body potassium becomes less linear
  • 0.75 mmol/kg of potassium infused over 1-2 h will increase plasma K from 3 to 4-4.5mmol/L and while this might lead to ECG changes it is unlikely to produce life-threatening arrhythmias. When there is profound hypokalaemia (<2-2.5 mmol/L) a greater percentage of the administered potassium will enter cells and therefore the rise in plasma concentration will be less than 1-1.5 mmol/L
  • in presence of cardiac arrhythmias and severe (£ 2 mmol/L) hypokalaemia up to 80 mmol may need to be infused in first hour




  • haemolysis
  • failure to separate red cells from plasma
  • thrombocythaemia


Failure of renal secretion of potassium

  • decreased Na:K exchange in distal tubule
    • hypoaldosteronism
    • diuretics
  • too little Na available for exchange in distal tubule
    • renal glomerular failure
    • Na depletion


  • severe tissue damage
  • severe acute starvation (eg anorexia): due to cell damage
  • suxamethonium
  • fluoride poisoning
  • hyperkalaemic periodic paralysis

More than one mechanism

  • reduced renal excretion in spite of ECF gain from cells
    • acidosis
    • global hypoxia (failure of Na pump in all cells)
    • digoxin overdose
  • diabetic ketoacidosis. Early stages K leaves cells due to partial failure of Na pump as result of impaired glucose metabolism. (Urinary loss high but hyperkalaemia usual). As condition progresses dehydration with low GFR and acidosis also contribute.

Clinical features

  • tingling, parasthesia, weakness, flaccid paralysis
  • hypotension, bradycardia


  • peaked T waves
  • p wave flattened
  • PR prolonged
  • sinus arrest and nodal rhythm
  • widened QRS
  • deep S
  • sine wave
  • asystole



Shift of potassium into cells

  • glucose and insulin
    • 20U insulin bolus plus 100g glucose
  • ± sodium bicarbonate
    • only likely to be effective in the presence of acidosis because Na/H antiport only active when there is intracellular acidosis
  • ± ß2 agonists
    • 25-40% of patients do not respond

Cation exchange resins

  • ineffective

© Charles Gomersall November 1999, August 2004

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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