Hypokalemia

Hypokalemia is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

  • Hypokalemia is defined as a plasma [K+] <3.5 mEq/L.
  • Spurious hypokalemia may be seen in situations in which high numbers of metabolically active cells present in the blood sample absorb the ECF potassium.
  • True hypokalemia may result from one or more of the following: (1) decreased net intake, (2) shift into cells, or (3) increased net loss.
    • Diminished intake is seldom the sole cause of K+ depletion because urinary excretion can be effectively decreased to <15 mEq/d. However, dietary K+ restriction may exacerbate the hypokalemia from GI or renal loss.
    • Transcellular shift. Movement of K+ into cells may transiently decrease the plasma [K+] without altering total body K+ content. These shifts can result from alkalemia, insulin, and catecholamine release. Hypokalemic periodic paralysis is a rare disorder that predisposes patients to transcellular K+ shifts that result in episodic muscle weakness. The hypokalemic form can be triggered after a carbohydrate-rich meal.
    • Nonrenal K+ loss. Hypokalemia may result from the loss of potassium-rich fluids from the lower GI tract. Hypokalemia from the loss of upper GI contents is typically more attributable to renal K+ secretion from secondary hyperaldosteronism. Rarely, in excessive sweating, loss of K+ through the integument can provoke hypokalemia.
    • Renal K+ loss accounts for most cases of chronic hypokalemia. This may be caused by any of the following factors:
      • Augmented distal urine flow occurs commonly with diuretic use and osmotic diuresis (e.g., glycosuria). Bartter and Gitelman syndromes mimic diuretic use and promote renal K+ loss by the same mechanism.
      • Hyperaldosteronism can result in increased renal K+ loss because aldosterone plays a central role in coupling the reabsorption of sodium with the excretion of potassium.
        • Primary mineralocorticoid excess can be the result of an adrenal adenoma or adrenocortical hyperplasia.
        • Cortisol also has an affinity for mineralocorticoid receptors but is typically converted quickly to cortisone, which has markedly less mineralocorticoid activity. Still, if cortisol is present in abundance (Cushing syndrome) or fails to be converted to cortisone (syndrome of mineralocorticoid excess), it may mimic hyperaldosteronism.
        • Secondary hyperaldosteronism can be seen in any situation with a decreased effective circulating volume.
        • Constitutive activation of the distal renal epithelial Na+ channel can mimic hyperaldosteronism. This occurs in a number of monogenic disorders, including Liddle syndrome, and leads to hypertension and hypokalemia. Unlike primary or secondary hyperaldosteronism, aldosterone levels are often suppressed in disorders of the epithelial Na+ channel.
      • Increased distal delivery of a non-reabsorbable anion such as bicarbonate, ketones, and hippurate (from toluene intoxication or glue sniffing) can also potentiate the lumen-negative gradient that drives K+ secretion.

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