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HYPOKALEMIA is a topic covered in the Harrison's Manual of Medicine.

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Major causes of hypokalemia are outlined in Table 1-3. Atrial and ventricular arrhythmias are the most serious health consequences of hypokalemia. Pts with concurrent Mg deficit and/or digoxin therapy are at a particularly increased risk of arrhythmias. Hypokalemia can directly prolong the QT interval and is a significant cofactor in arrhythmias due to other causes of a prolonged QT interval. Other clinical manifestations include muscle weakness, which may be profound at serum [K+] <2.5 mmol/L, and, if hypokalemia is sustained, hypertension, ileus, polyuria, renal cysts, and even renal failure.


I. Decreased intake

  1. Starvation
  2. Clay ingestion

II. Redistribution into cells

  1. Acid-base
    1. Metabolic alkalosis
  2. Hormonal
    1. Insulin
    2. Increased β2-adrenergic sympathetic activity: post–myocardial infarction, head injury, theophylline
    3. β2-Adrenergic agonists: bronchodilators, tocolytics
    4. α-Adrenergic antagonists
    5. Thyrotoxic periodic paralysis
    6. Downstream stimulation of Na+/K+-ATPase: theophylline, caffeine
  3. Anabolic state
    1. Vitamin B12 or folic acid administration (red blood cell production)
    2. Granulocyte-macrophage colony-stimulating factor (white blood cell production)
    3. Total parenteral nutrition
  4. Other
    1. Pseudohypokalemia
    2. Hypothermia
    3. Familial hypokalemic periodic paralysis
    4. Barium toxicity: systemic inhibition of “leak” K+ channels

III. Increased loss

  1. Nonrenal
    1. Gastrointestinal loss (diarrhea)
    2. Integumentary loss (sweat)
  2. Renal
    1. Increased distal flow and distal Na+ delivery: diuretics, osmotic diuresis, salt-wasting nephropathies
    2. Increased secretion of potassium
      1. Mineralocorticoid excess: primary hyperaldosteronism (APAs), PAH or UAH, IHA due to bilateral adrenal hyperplasia and adrenal carcinoma, familial hyperaldosteronism (FH-I, FH-II, congenital adrenal hyperplasias), secondary hyperaldosteronism (malignant hypertension, renin-secreting tumors, renal artery stenosis, hypovolemia), Cushing’s syndrome, Bartter’s syndrome, Gitelman’s syndrome
      2. Apparent mineralocorticoid excess: genetic deficiency of 11β-dehydrogenase-2 (syndrome of apparent mineralocorticoid excess), inhibition of 11β-dehydrogenase-2 (glycyrrhetinic/glycyrrhizinic acid and/or carbenoxolone; licorice, food products, drugs), Liddle’s syndrome (genetic activation of ENaC)
      3. Distal delivery of nonreabsorbed anions: vomiting, nasogastric suction, proximal renal tubular acidosis, diabetic ketoacidosis, glue sniffing (toluene abuse), penicillin derivatives (penicillin, nafcillin, dicloxacillin, ticarcillin, oxacillin, and carbenicillin)
    3. Magnesium deficiency, amphotericin B, Liddle’s syndrome

Abbreviations: APA, aldosterone-producing adenoma; ENaC, epithelial Na+ channels; IHA, idiopathic hyperaldosteronism; PAH, primary adrenal hyperplasia; UAH, unilateral adrenal hyperplasia.

The cause of hypokalemia is usually obvious from history, physical examination, and/or basic laboratory tests. However, persistent hypokalemia may require a more thorough, systematic evaluation (Fig. 1-2). Initial laboratory evaluation should include electrolytes, BUN, creatinine, serum osmolality, Mg2+, and Ca2+, a complete blood count, and urinary pH, osmolality, creatinine, and electrolytes. Serum and urine osmolality are required for calculation of the transtubular K+ gradient (TTKG), which should be <3 in the presence of hypokalemia (See Also Hyperkalemia). Alternatively, a urinary K+-to-creatinine ratio of >13-mmol/g creatinine (>1.5-mmol/mmol creatinine) is compatible with excessive K+ excretion. Further tests such as urinary Mg2+ and Ca2+ and/or plasma renin and aldosterone levels may be necessary in specific cases.


The diagnostic approach to hypokalemia. See text for details. bp, blood pressure; DKA, diabetic ketoacidosis; FH-I, familial hyperaldosteronism type I; FHPP, familial hypokalemic periodic paralysis; HTN, hypertension; PA, primary aldosteronism; RAS, renal artery stenosis; RST, renin-secreting tumor; RTA, renal tubular acidosis; SAME, syndrome of apparent mineralocorticoid excess; TTKG, transtubular potassium gradient. (From Mount DB, Zandi-Nejad K: Disorders of potassium balance, in The Kidney, 8th ed, BM Brenner [ed]. Philadelphia, Saunders, 2008; with permission.)

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Loscalzo, Joseph, et al., editors. "HYPOKALEMIA." Harrison's Manual of Medicine, 19th ed., McGraw Hill Inc., 2017. harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623468/all/HYPOKALEMIA.
HYPOKALEMIA. In: Loscalzo J, Jameson JL, Longo DL, et al, eds. Harrison's Manual of Medicine. 19th ed. McGraw Hill Inc.; 2017. https://harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623468/all/HYPOKALEMIA. Accessed April 23, 2019.
HYPOKALEMIA. (2017). In Loscalzo, J., Jameson, J. L., Longo, D. L., Hauser, S. L., Fauci, A. S., & Kasper, D. L. (Eds.), Harrison's Manual of Medicine. Available from https://harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623468/all/HYPOKALEMIA
HYPOKALEMIA [Internet]. In: Loscalzo J, Jameson JL, Longo DL, Hauser SL, Fauci AS, Kasper DL, editors. Harrison's Manual of Medicine. McGraw Hill Inc.; 2017. [cited 2019 April 23]. Available from: https://harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623468/all/HYPOKALEMIA.
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TY - ELEC T1 - HYPOKALEMIA ID - 623468 ED - Loscalzo,Joseph, ED - Jameson,J Larry, ED - Longo,Dan L, ED - Hauser,Stephen L, ED - Fauci,Anthony S, ED - Kasper,Dennis L, BT - Harrison's Manual of Medicine UR - https://harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623468/all/HYPOKALEMIA PB - McGraw Hill Inc. ET - 19 DB - Harrison's Manual of Medicine DP - Unbound Medicine ER -