potassium physiology

see also:

• hypokalaemia
  • Western Health procedure: Potassium chloride infusion
• hyperkalaemia
• sodium physiology

• total body potassium
  • = 45 meq/kg (young adult males as mainly prop.to muscle mass);
  • = 20 meq/kg (malnourished, wasted person);
• non-exchangeable = 10% - bone 7.6%;
• exchangeable = 41 meq/kg (90%) - intracellular (89.6%), plasma (0.4%);
• ie. for average adult, total body K = 250g with 1g in plasma & average daily intake of 10g which is normally excreted renally within the limits of 1-40g/day but in pts with renal disease or on K-sparing diuretics, the renal excretion may be restricted to 5g/day, hence potentially allowing for build up in total body potassium and thus hyperkalaemia.

• end-point for homeostatic control of [K] is:
  • ratio [K]i : [K]e to maintain transmembrane potential;
  • constant [K]i important for many i/cellular functions;

• K is present at ~constant levels in animal and vegetable tissues av. 300mg/100g, but processed foods vary 10-4000mg/100g;
• No regulation;
• normal intake 1-2mEq/kg/d but varies

• reasonably complete in upper GIT but body K exchanged for lumenal Na in lower GIT;

• 90% filtered K is reabsorbed in prox. tubule along with water & thus little is presented to thick ascending limb with the final urine [K] dependent on K secretion in distal tubule & water reabsorption:
  • increased distal tubule secretion due to:
    • increased Na distal tubule reabsorption ( increased by increased serum [K])
    • alkalosis
    • aldosterone (partly due to pre-existing K intake levels)
    • increased tubular fluid flow rate (eg. diuretics) → incr. [] gradient
• daily excretion of potassium:
  • normally 50-100mmol;
  • stressed 10-500mmol;
  • renal disease or K-sparing diuretics 10-60mmol;

• important way of dealing with acute K load is to translocate into cells, esp. liver, muscle, which is increased by:
  • insulin
  • beta 2 adrenergic receptor activation (eg. salbutamol)
  • aldosterone - lowers slope of linear relationship of [K]serum vs total body K
  • amino acids (eg. TPN or administered amino acids)
  • periodic hyperkalaemic paralysis & periodic hypokalaemic paralysis
  • direct Na-K ATPase inhibition: digoxin toxicity, suxamethonium
  • alkalosis → incr. cell uptake and vice versa for acidosis
• ⇒ need to correct serum [K] for pH & exclude other causes of redistribution to ascertain total body K, as “corrected [K]” of 1mM is approx. 6-10% total body K
  • for each decrease in pH by 0.1 ⇒ se [K] increases by ~0.7 (artificially high)
  • for each increase in pH by 0.1 ⇒ se [K] decreases by ~0.6 (artificially low)
  • thus, if serum [HCO3] abnormal, then pH likely to be abnormal → need to calculate adjusted [K] to allow for redistribution before deciding to treat the [K] level.