Potassium Homeostasis

Aka: Potassium Homeostasis, Potassium, Potassium Ion

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II. Physiology: Potassium Function

  1. Cellular Function
    1. Cellular volume and fluid osmolality
    2. Metabolic process Cofactor (e.g. Protein synthesis, Glycogen synthesis)
  2. Neuromuscular transmission
    1. Resting Membrane Potential (large gradient between intracellular and extracellular Potassium concentration)

III. Images

  1. potassiumHomeostasis.png

IV. Physiology: Potassium Distribution

  1. Background
    1. Potassium is primary intracellular cation and critical for normal cellular function
    2. Intracellular Potassium concentration of 130-140 mEq/L accounts for 98% of total body Potassium
    3. Extracellular Potassium (~4 mEq/L) is only 2% of total body Potassium (56 mEq total for entire ECF in 70 kg male)
  2. Maintenance of intracellular Potassium
    1. Sodium-Potassium ATPase pump (cellular membrane)
      1. sodiumPotassiumATPase.jpg
      2. Pumps 2 Potassium into cells in exchange for every 3 Sodium out
  3. Transcellular Potassium Shifts
    1. Mediators that promote Potassium movement INTO cells
      1. See Hypokalemia due to Transcellular Potassium Shift
      2. See Hyperkalemia Management
      3. Insulin
      4. Alkalosis (Potassium influx exchanged for Hydrogen Ion out of cells)
      5. Beta 2 Adrenergic Receptor stimulation (e.g. Epinephrine, Albuterol)
    2. Mediators that promote Potassium movement OUT of cells
      1. See Hyperkalemia due to Redistribution
      2. Acidosis (Potassium exchanged for Hydrogen Ion into cells)
        1. Inorganic acids have a much greater effect on Potassium shifts than organic acids (e.g. lactate)
      3. Increased Serum Osmolality
        1. Water flow out of cells concentrates intracellular Potassium
        2. Potassium gradient favors movement of Potassium out of cells

V. Physiology: Potassium Sources

  1. Dietary Potassium
    1. See Dietary Potassium
    2. Daily intake of 1 mEq/kg typically balances renal (90%) and hepatic (10%) excretion
  2. Excess Potassium sources
    1. See Hyperkalemia
    2. Tissue breakdown
      1. Rhabdomyolysis
      2. Hemolysis
      3. Tumor lysis with Chemotherapy (e.g. Lymphoma)
    3. Gastrointestinal Hemorrhage
      1. Potassium is absorbed from the intestinal tract
    4. Potassium administration
      1. Blood Transfusion
      2. Potassium containing medications
      3. Potassium in Intravenous Fluids
      4. Tube Feedings with Potassium

VI. Physiology: Renal Potassium Losses (primary excretion)

  1. See Hypokalemia due to Renal Potassium Loss
  2. Normal renal Potassium excretion (primary mechanism for Potassium excretion)
    1. Daily Potassium Excretion range: 10 mEq (in Hypokalemia) to 10 mEq/kg (in Hyperkalemia)
    2. Relies on intact Glomerular Filtration Rate (GFR), at a minimum >20% of normal
  3. Potassium at collecting tubule
    1. Potassium moves freely across the glomerulus, but 90% is reabsorbed in the loop of henle
    2. Potassium that reaches the collecting tubule (10%) may be adjusted by mechanisms below
  4. Potassium excretion by Sodium-Potassium ATPase pump (Sodium exchange)
    1. Potassium is pumped from the capillary into the cells lining the collecting duct
      1. Sodium-Potassium ATPase pumps Sodium into the interstitium and capillaries
      2. Sodium-Potassium ATPase pumps Potassium into the collecting duct lining cells
    2. Potassium may then flow freely via cell channels into collecting duct lumen toward excretion
      1. Flows out of the cell's high Potassium concentration
      2. Flows into the collecting duct lumen, where the Potassium concentration is lower
    3. Contrast with Sodium which is reabsorbed in exactly opposite fashion
      1. Sodium flows from the collecting duct lumen into the lining cells down its concentration gradient
      2. Sodium is then actively pumped into the interstitium and capillaries via the Sodium-Potassium ATPase
  5. Factors increasing renal Potassium excretion
    1. Hyperkalemia
    2. Aldosterone increase (see below)
    3. Increased Sodium concentration in the collecting tubule
      1. Occurs with Diuretics or osmotic diuresis (e.g. Diabetic Ketoacidosis)
      2. Results in greater Sodium influx into tubule cells with greater ATPase pump activity
    4. Metabolic Alkalosis
      1. Bicarbonate is increased anion in the collecting tubule, and is poorly reabsorbed alone
      2. Bicarbonate is reabsorbed with Sodium, resulting in greater ATPase activity (see above)
  6. Aldosterone mediates Potassium excretion (and Sodium reabsorption)
    1. Aldosterone mediates Sodium-Potassium ATPase pump
      1. Increasing pump activity results in greater Potassium influx from capillary into the collecting duct cell
    2. Aldosterone mediates the number of Sodium and Potassium channels on the collecting duct cells
      1. Increasing the channels allows for greater Potassium outflux into the collecting duct (excretion)
    3. Factors increasing Aldosterone (and decreasing Serum Potassium)
      1. Renin-Angiotensin System stimulation (e.g. Hypovolemia)
      2. Hyperkalemia
    4. Factors decreasing Aldosterone (and increasing Serum Potassium)
      1. Aldosterone Antagonist (e.g. Spironolactone, Eplerenone)
  7. Images: Nephron
    1. nephron.png

VII. Physiology: Extrarenal Potassium Losses

  1. See Hypokalemia due to Extrarenal Potassium Loss
  2. Sweat-related Potassium losses
    1. Sweat contains 9 mEq/L and losses are minimal with typical sweating (200 ml)
    2. Sweat related Potassium daily loss varies from 2 mEq (normal) to 90 mEq with severe sweating (10 L)
  3. Gastrointestinal Potassium losses
    1. Stool losses are typically 10% of Dietary Potassium (7-9 mEq/day)
    2. Osmotic Diarrhea typically contains 20 mEq/L
    3. Secretory Diarrhea may contain up to 130-170 mEq/L
      1. Results in up to >250 mEq Potassium loss daily
      2. van Dinter (2005) Gastroenterology 129(4):1268-73 +PMID:16230079 [PubMed]

VIII. References

  1. Marino (2014) ICU Book, p. 653-72
  2. Preston (2011) Acid-Base Fluids and Electrolytes, p. 3-30
  3. Rose (1989) Clinical Physiology of Acid-Base and Electrolyte Disorders, p. 3-27

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