Plasma potassium levels are determined by the balance between absorption and excretion and by internal shifts between the extracellular fluid and cells. Normal daily intake is 50 to 150 mmol, of which 5 to 15 mmol appears in the stools and sweat. Potassium excesses are usually excreted rapidly; however, if this is impossible, plasma potassium rises sharply, with each increase of 1 mmol/l above 4 mmol/l corresponding to an increase in total body potassium of 50 to 100 mmol. Plasma potassium reflects total body potassium only in stable states at normal pH. In acutely ill patients, particularly those with acid-base disturbances, plasma and total body potassium may vary in opposite directions, with plasma potassium rising in response to acidosis. These changes are more marked with metabolic than with respiratory disturbances.
There is no control of gastrointestinal absorption of potassium; 85 to 90 per cent is absorbed and 10 to 15 per cent is excreted in the feces. Short-term control of potassium balance is exerted by changes in renal excretion and by shifts of potassium into and out of cells. Beta-blockers and a-adrenergic agonists impair cellular potassium uptake. Long-term control is effected mainly by the rate of renal excretion, controlled by intrinsic renal mechanisms and aldosterone. The range of renal excretion is normally 3 to 300 mmol/day. In subjects with a chronically high potassium intake, renal adaptation allows the excretory capacity to reach 500 mmol/day. Renal responses to excessive intake are relatively rapid; approximately half an acute load appears in the urine within 12 h.
Hyperkalemia is defined as a plasma potassium level greater than 5.0 mmol/l. This may be associated with low, normal, or high total body potassium. True hyperkalemia should be distinguished from pseudohyperkalemia, which may follow in vitro hemolysis and lysis of white blood cells (usually only at levels above 200 * 109/1) or platelets (usually only when the platelet count is above 750 * 10 9/1).
A more detailed discussion of hyperkalemia is given by TanneD.(19,9,2). Adaptations to a raised potassium intake
A chronically high intake of potassium produces an increase in the distal tubular excretory capacity for potassium; this capacity may increase by a factor of 10 to 20. The main mechanisms are an increase in the surface area and the Na+, K+-ATPase concentration of the basolateral membranes in the cortical collecting ducts. Similar increases in Na+, K+-ATPase are seen in the colon. Raised potassium concentrations stimulate aldosterone release; this not only stimulates Na +, K+-ATPase but also increases potassium conductance in the luminal membrane of the principal cells in the collecting ducts.
Other mechanisms that may be relevant include the following: a reduction in potassium absorption in the thick ascending limb contributes to kaliuresis, and a high medullary potassium concentration inhibits sodium reabsorption in the thick ascending limb, thereby increasing sodium delivery to the distal tubule where it is exchanged for potassium. In the distal tubule, potassium moves into the urine down electrical and chemical gradients determined by the luminal concentration of sodium and its accompanying anion. In the cortical collecting ducts, active transport of potassium into the urine takes place. This is further stimulated by ADH.
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