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Potassium metabolism
Hyperkalaemia
Hypokalaemia
Aetiology
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
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
Treatment
- 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
Hyperkalaemia
Aetiology
Spurious
- haemolysis
- failure to separate red cells from plasma
- thrombocythaemia
Iatrogenic
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
Redistribution
- 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
ECG
Treatment
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
© Charles Gomersall November 1999, August 2004
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