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Potassium is for the most part an intracellular element. 98% resides within the cell and 2% outside (just 0.5% in the plasma). This means that measurement of serum plasma can sometimes mislead as a representation of total body potassium.

The daily requirements for potassium are 70 mmol per day. It is excreted mainly by the kidneys but also the skin and faeces (a common cause of hypokalaemia is diarrhoea). In the kidneys potassium is excreted actively via a sodium-potassium pump. Aldosterone promotes its excretion (and hence the absorption of sodium). Additionally the pump can also excrete hydrogen ions and in situations of acidosis this ion has preference, and hyperkalaemia can result.

Movement of potassium in the renal distal convoluted tubule

In cells there is active pumping of potassium inside the cell whilst simultaneously countertransporting sodium. This pump is promoted by insulin and catecholamines.

Movement of potassium in the cell

The risk of both hyper and hypokalaemia is arrhythmias and eventually arrest, but hyperkalamia is generally the more dangerous of the two.



  1. Renal
    1. Alkalosis
    2. Loop and thiazide diuretics: these block sodium reabsorption and hence there is more sodium in the DCT, which favours potassium excretion.
    3. Mineralocorticoid excess: this includes primary hyperaldosteronsim (Conn's), secondary hyperaldosteronism, and Cushings. Hypokalaemia and hypernatraemia is observed.
    4. Renal Disease: renal tubular acidosis, interstitial nephritis
    5. Miscellaneous: hypomagnasaemia (magnesium is required for the ATPase pump), hypercalcaemia (interferes with reabsorption)
  2. Extra-renal
    1. GI loss: mainly diarrhoea
    2. ECF to ICF shift: insulin and catecholamines
    3. Inadequate intake


Muscle weakness, paralytic ileus, polyuria.

ECG: flat T waves, ST depression, U waves, wide QT


Oral potassium (sando-K): unpleasant. IV potassium: only if oral impossible.



  1. Renal
    1. Renal failure: acute or chronic
    2. Drugs: potassium sparing diuretics such as amiloride or spironolactone, ACE inhbitors
    3. Mineralocorticoid deficiency: Addisons
  2. Extra-renal
    1. Increased intake: exogenous, endogenous (tissue necrosis, haemolysis
    2. ICF to ECF shift: acidosis, hypoxia (dysfunction of ATPase), insulin deficiency (DKA)


Cardiac arrhythmias and risk of arrest.

ECG: Tall T waves, absent P waves, broad QRS complex, sine wave ECG, asystole


See the Renal failure emergency section. Outlines of management are:
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