What is the pathophysiology of hypokalemia?

Answer 1

Hypokalemia can occur due to 1 of 3 pathogenetic mechanisms.

The first is deficient intake. Poor potassium intake alone is an uncommon cause of hypokalemia but occasionally can be seen in very elderly individuals unable to cook for themselves or unable to chew or swallow well. Over time, such individuals can accumulate a significant potassium deficit. Another clinical situation where hypokalemia may occur due to poor intake is in patients receiving total parenteral nutrition (TPN), where potassium supplementation may be inadequate for a prolonged period of time.

The second is increased excretion. Increased excretion of potassium, especially coupled with poor intake, is the most common cause of hypokalemia. The most common mechanisms leading to increased renal potassium losses include enhanced sodium delivery to the collecting duct, as with diuretics; mineralocorticoid excess, as with primary or secondary hyperaldosteronism; or increased urine flow, as with an osmotic diuresis.

Gastrointestinal losses, most commonly from diarrhea, also are common causes of hypokalemia. Vomiting is a common cause of hypokalemia, but the pathogenesis of the hypokalemia is complex. Gastric fluid itself contains little potassium, approximately 10 mEq/L. However, vomiting produces volume depletion and metabolic alkalosis. These 2 processes are accompanied by increased renal potassium excretion. Volume depletion leads to secondary hyperaldosteronism, which, in turn, leads to enhanced cortical collecting tubule secretion of potassium in response to enhanced sodium reabsorption. Metabolic alkalosis also increases collecting tubule potassium secretion due to the decreased availability of hydrogen ions for secretion in response to sodium reabsorption.

The third is due to a shift from extracellular to intracellular space. This pathogenetic mechanism also often accompanies increased excretion, leading to a potentiation of the hypokalemic effect of excessive loss. Intracellular shifts of potassium often are episodic and frequently are self-limited, for example, with acute insulin therapy for hyperglycemia.