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Potassium balance in acid-base disorders

Author
David B Mount, MD
Section Editor
Richard H Sterns, MD
Deputy Editor
John P Forman, MD, MSc

INTRODUCTION

There are important interactions between potassium and acid-base balance that involve both transcellular cation exchanges and alterations in renal function [1]. These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid-base disorders.

INTERNAL POTASSIUM BALANCE

Acid-base disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" [2]. An often-quoted study found that the plasma potassium concentration will rise by 0.6 meq/L for every 0.1 unit reduction of the extracellular pH [3]. However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 meq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4].

Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid (figure 1). Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores. The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [5,6]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected.

A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis or ketoacidosis [3,7]. The hyperkalemia that is commonly seen in diabetic ketoacidosis, for example, is more closely related to the insulin deficiency and hyperosmolality than to the degree of acidemia. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".)

Why this occurs is not well understood. Two factors that may contribute are the ability of the organic anion to accompany the hydrogen ion into the cell, perhaps as the lipid-soluble, intact acid [8], and differential effects on insulin and glucagon secretion [4,9].

      

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Literature review current through: Nov 2016. | This topic last updated: Fri Oct 30 00:00:00 GMT 2015.
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References
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