Electrolytes
SODIUM
Disturbances of sodium concentration [Na+] result in most cases from abnormalities of H2O homeostasis, which change the relative ratio of Na+ to H2O. Disorders of Na+ balance per se are, in contrast, associated with changes in extracellular fluid volume, either hypo- or hypervolemia. Maintenance of “arterial circulatory integrity” is achieved in large part by changes in urinary sodium excretion and vascular tone, whereas H2O balance is achieved by changes in both H2O intake and urinary H2O excretion (Table 1-1). Confusion can result from the coexistence of defects in both H2O and Na+ balance. For example, a hypovolemic pt may have an appropriately low urinary Na+ due to increased renal tubular reabsorption of filtered NaCl; a concomitant increase in circulating arginine vasopressin (AVP)—part of the defense of effective circulating volume (Table 1-1)—will cause the renal retention of ingested H2O and the development of hyponatremia.
OSMOREGULATION | VOLUME REGULATION | |
---|---|---|
What is sensed | Plasma osmolality | Arterial filling |
Sensors | Hypothalamic osmoreceptors | Carotid sinus Afferent arteriole Atria |
Effectors | AVP | Sympathetic nervous system |
Thirst | Renin-angiotensin-aldosterone system | |
ANP/BNP | ||
AVP | ||
What is affected | Urine osmolality | Urinary sodium excretion |
H2O intake | Vascular tone |
Note: See text for details.
Abbreviations: ANP, atrial natriuretic peptide; AVP, arginine vasopressin; BNP, brain natriuretic peptide.
Source: Adapted from Rose BD, Black RM (eds): Manual of Clinical Problems in Nephrology. Boston, Little Brown, 1988.
Sections
POTASSIUM
Because potassium (K+) is the major intracellular cation, discussion of disorders of K+ balance must take into consideration changes in the exchange of intra- and extracellular K+ stores. (Extracellular K+ constitutes <2% of total-body K+ content.) Insulin, β2-adrenergic agonists, and alkalosis tend to promote K+ uptake by cells; acidosis, insulinopenia, or acute hyperosmolality (e.g., after treatment with mannitol or D50W) promotes the efflux or reduced uptake of K+. A corollary is that tissue necrosis and the attendant release of K+ can cause severe hyperkalemia, particularly in the setting of acute kidney injury. Hyperkalemia due to rhabdomyolysis is thus particularly common, due to the enormous store of K+ in muscle; hyperkalemia may also be prominent in tumor lysis syndrome.
The kidney plays a dominant role in K+ excretion. Although K+ is transported along the entire nephron, it is the principal cells of the connecting segment and cortical collecting duct that play a dominant role in K+ excretion. Apical Na+ entry into principal cells via the amiloride-sensitive ENaC generates a lumen-negative potential difference, which drives passive K+ exit through apical K+ channels. This relationship is key to the bedside understanding of potassium disorders. For example, decreased distal delivery of Na+ tends to blunt the ability to excrete K+, leading to hyperkalemia. Abnormalities in the renin-angiotensin-aldosterone system (RAAS) can cause both hypo- and hyperkalemia; aldosterone has a major influence on potassium excretion, increasing the activity of ENaC channels and the basolateral Na+/K+-ATPase, thus amplifying the driving force for K+ secretion across the luminal membrane of principal cells.
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Citation
Kasper, Dennis L., et al., editors. "Electrolytes." Harrison's Manual of Medicine, 20th ed., McGraw Hill Inc., 2020. harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623742/all/Electrolytes.
Electrolytes. In: Kasper DLD, Fauci ASA, Hauser SLS, et al, eds. Harrison's Manual of Medicine. McGraw Hill Inc.; 2020. https://harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623742/all/Electrolytes. Accessed December 2, 2024.
Electrolytes. (2020). In Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L., Jameson, J. L., & Loscalzo, J. (Eds.), Harrison's Manual of Medicine (20th ed.). McGraw Hill Inc.. https://harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623742/all/Electrolytes
Electrolytes [Internet]. In: Kasper DLD, Fauci ASA, Hauser SLS, Longo DLD, Jameson JLJ, Loscalzo JJ, editors. Harrison's Manual of Medicine. McGraw Hill Inc.; 2020. [cited 2024 December 02]. Available from: https://harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623742/all/Electrolytes.
* Article titles in AMA citation format should be in sentence-case
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ED - Fauci,Anthony S,
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ED - Longo,Dan L,
BT - Harrison's Manual of Medicine
UR - https://harrisons.unboundmedicine.com/harrisons/view/Harrisons-Manual-of-Medicine/623742/all/Electrolytes
PB - McGraw Hill Inc.
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DB - Harrison's Manual of Medicine
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