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{{Hypokalemia}}
{{Hypokalemia}}
{{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]]
{{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}''',''' {{AIDA}}'''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]], {{ABehjat}}


==Overview==
==Overview==
Potassium is the most abundant intracellular cation. Any derangement of potassium serum levels can disturb the transmembrane potential and renders excitable cells (nerve and muscle) hyperpolarized and less excitable. However, cardiac cells don't obey this rule and become hyperexcitable. Potassium regulation is essential to maintain a normal activity of excitable cells. Failure to regulate potassium serum levels can have severe consequences on several organs especially the heart and the nervous system. Normally, total potassium excretion in stool is low and most ingested potassium is absorbed. The kidney is the main regulator of potassium balance through excretion (the kidney excretes 90-95% of dietary potassium); the gut excretes a minimal amount of dietary potassium (approximately 10%).
 
*[[Potassium]] is the most common [[intracellular cation]]. Approximately 98% of total [[potassium]] exists in the [[intracellular fluid]] (ICF), which has a normal range of  140–150 mEq/l. Merely 2% of this cation is placed in the [[extracellular fluids]] (ECF), where it ranges from 3.5 to 5 mEq/l. [[Potassium]] is essential during numerous body functions, particularly for [[excitable cells]] such as [[muscle]] and [[nerve cells]]. Any disorder of [[potassium]] serum levels can disturb the transmembrane [[potential]] and renders excitable cells ([[nerve]] and [[muscle]]) [[Hyperpolarization (biology)|hyperpolariz]]<nowiki/>ed and less sensitive. However, [[Cardiac|cardiac cells]] don't obey this rule and become [[hyperexcitable]]. [[Potassium]] regulation is essential to maintain a normal activity in cells. Any impairment in potassium serum levels will have severe consequences on several organs especially the [[heart]] and the [[nervous system]]. Typically, total [[potassium]] [[excretion]] in the [[stool]] is low and most [[ingested]] [[potassium]] is absorbed. The [[Kidney|kidne]]<nowiki/>y is the primary regulator of potassium balance through excretion (the [[kidney]] excretes 90-95% of dietary potassium); the [[gut]] excretes a minimal amount of dietary [[potassium]] (approximately 10%).


== Pathophysiology ==
== Pathophysiology ==
Hypokalemia can result from several conditions:
Hypokalemia can result from several conditions:
* Trans-cellular shifts of potassium inside the cells (most common)
* Trans-cellular shifts of potassium inside the cells (most common)
* Increased renal loss of potassium
* [[Renal]] loss of [[potassium]]
* Increased hematopoiesis (increased cellular use of potassium)
** Increased distal Na delivery
** Increased urine flow
** [[Metabolic alkalosis]]
** Increased [[aldosterone]] level
* Gastrointestinal (GI) loss of potassium
* Increased [[hematopoiesis]] (increased cellular use of potassium)
* Decreased intake of potassium (least common)
* Decreased intake of potassium (least common)


Shown below is a table summarizing the different pathophysiological processes that can lead to hypokalemia.
Shown below is a table summarizing the different pathophysiological processes that can lead to hypokalemia. <ref name="pmid24139581">{{cite journal |vauthors=Daly K, Farrington E |title=Hypokalemia and hyperkalemia in infants and children: pathophysiology and treatment |journal=J Pediatr Health Care |volume=27 |issue=6 |pages=486–96; quiz 497–8 |date=2013 |pmid=24139581 |doi=10.1016/j.pedhc.2013.08.003 |url=}}</ref> <ref name="pmid21278718">{{cite journal |vauthors=Unwin RJ, Luft FC, Shirley DG |title=Pathophysiology and management of hypokalemia: a clinical perspective |journal=Nat Rev Nephrol |volume=7 |issue=2 |pages=75–84 |date=February 2011 |pmid=21278718 |doi=10.1038/nrneph.2010.175 |url=}}</ref> <ref name="pmid22169581">{{cite journal |vauthors=Cheungpasitporn W, Suksaranjit P, Chanprasert S |title=Pathophysiology of vomiting-induced hypokalemia and diagnostic approach |journal=Am J Emerg Med |volume=30 |issue=2 |pages=384 |date=February 2012 |pmid=22169581 |doi=10.1016/j.ajem.2011.10.005 |url=}}</ref> <ref name="pmid24053336">{{cite journal |vauthors=Bisogni V, Rossi GP, Calò LA |title=Apparent mineralcorticoid excess syndrome, an often forgotten or unrecognized cause of hypokalemia and hypertension: case report and appraisal of the pathophysiology |journal=Blood Press. |volume=23 |issue=3 |pages=189–92 |date=June 2014 |pmid=24053336 |doi=10.3109/08037051.2013.832967 |url=}}</ref>


{| '''Trans-cellular shifts of potassium inside the cells''' || '''Increased renal loss of potassium''' || '''Increased hematopoiesis''' ||'''Decreased intake of potassium'''
{| style="cellpadding=0; cellspacing= 0; width: 900px;"
|-
|-
|
| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''Trans-cellular shifts''' || colspan="2" style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''Renal loss''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''GI loss'''|| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''Increased hematopoiesis''' || style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align="center" |'''Decreased intake of potassium'''
* Metabolic alkalosis (K+/H+ exchanger)
|-
* Insulin (activates Na+/K+ ATPase)
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
* Catecholamine
* [[Metabolic alkalosis]] (K+/H+ exchanger)
|
* [[Insulin]] (activates Na+/K+ ATPase)
* Increased distal Na delivery
* [[Catecholamine]] (activates Na+/K+ ATPase)
* Increased urine flow
* [[Hypokalemic thyrotoxic periodic paralysis]]
* Metabolic alkalosis
* [[Hypothermia]]
* Increased aldosterone
* [[Chloroquine]]
|
* [[Barium]] intoxication
* Megaloblastic anemia
* [[Cesium]] intoxication
* Treatment of anemia
* [[Antipsychotic]] overdose
* Crisis of AML
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
|
'''''Subject is normo or hypotensive'''''<br>
''Associated with acidosis''
* [[Diabetic ketoacidosis]]
* [[Renal tubular acidosis type 1]]
* [[Renal tubular acidosis type 2]]
''Associated with alkalosis''
* [[Diuretics]]
* [[Vomiting]] (increase in [[aldosterone]])
* [[Bartter's syndrome]] (dysfunction of in loop of Henle)
* [[Gitelman's syndrome]] (dysfunction in distal convoluted tubules)
''Variable acid/base status''
* [[Hypomagnesemia]]
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
'''''Subject is hypertensive'''''<br>
''Primary hyperaldosteronism''
* Conn's syndrome
''Secondary hyperaldosteronism''
* Renovascular disease
* Renin secreting tumor
''Non aldosterone increase in mineralcorticoid''
* [[Cushing's disease]]
* [[Congenital adrenal hyperplasia]]
* Increased [[mineralcorticoid]]s
* Licorice ingestion
* [[Liddle's syndrome]]
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
''Associated with metabolic acidosis''
* [[Diarrhea]]
* [[Laxative abuse]]
* [[Villous adenoma]]
''Associated with metabolic alkalosis''
* [[Vomiting]]
* [[Nasogastric tube]] drainage
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
* [[Megaloblastic anemia]]
* Treatment of [[anemia]]
* Crisis of [[AML]]
| style="font-size: 100; padding: 0 5px; background: #B8B8B8" align="left" |
* Tea and toast diet
* Tea and toast diet
* Anorexia nervosa
* [[Anorexia nervosa]]
* Alcoholism
* [[Alcoholism]]
|}
|}


=== The Role of the Kidney ===
=== The Role of the Kidney ===
At the [[glomerulus]], potassium is freely filtered and then largely reabsorbed in the proximal tubule and thick ascending [[loop of Henle]] (>60 % of filtered potassium). The cortical collecting duct receives 10–15% of filtered potassium and constitutes the kidney’s major site of potassium excretion. Potassium excretion at the cortical collecting duct depends on the amount of sodium delivered there and the activity of [[aldosterone]]. The absorption of sodium by the principal cells of the cortical collecting ducts is mediated by the apical epithelial sodium channels (ENaC); when the amount of sodium delivered to the cortical collecting duct is very high, the absorption of sodium increases without concomitant absorption of the accompanying anions (eg, bicarbonates and chloride ions) which are not easy to absorb. This physiologic process causes the formation of a negative charge within the cortical collecting duct lumen causing potassium and proton secretion. Aldosterone increases sodium absorption at the cortical collecting duct by means of enhancing the activity of Na-K-ATPase pumps, and augmenting the number of the ENaC channels.
* The [[Kidneys]] play a vital role in keeping the balance of [[potassium]].
* At the [[glomerulus]], [[potassium]] is freely filtered and reabsorbed mainly in the [[proximal tubule]] and [[thick ascending limb of loop of Henle]] (>60 % of [[filtered potassium]]).  
* The [[cortical collecting duct]] receives 10–15% of [[filtered potassium]] and constitutes the kidney’s primary site of [[potassium excretion]].  
* Potassium excretion at the cortical collecting duct depends on the amount of [[sodium]] delivered there and the activity of [[aldosterone]].  
* The absorption of [[sodium]] by the [[principal cells]] of the [[cortical collecting ducts]] is mediated by the apical epithelial [[sodium channels]] (ENaC); when the amount of [[sodium]] delivered to the cortical [[collecting duct]] is very high, the absorption of sodium increases without concomitant absorption of the accompanying anions (e.g., [[Bicarbonates|bicarbonate]]<nowiki/>s and chloride ions) which are not easy to absorb. This physiologic process causes the formation of a negative charge within the [[cortical collecting duct]] lumen, causing [[potassium]] and proton secretion.  
* [[Aldosterone]] increases sodium [[absorption]] at the [[cortical collecting duct]] by means of enhancing the activity of Na-K-ATPase pumps and augmenting the number of the [[ENaC]] channels.
 
 
 
{{#ev:youtube|https:watch?v=DlrEQg_68r0&t=69s}}


=== Factors Increasing Kidney Potassium Excretion ===
=== Factors Increasing Kidney Potassium Excretion ===
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*High distal sodium delivery
*High distal sodium delivery
*[[Metabolic alkalosis]]
*[[Metabolic alkalosis]]
*High extracellular fluid K+ concentration <ref>{{cite book | last = Hall | first = John | title = Guyton and Hall textbook of medical physiology | publisher = Elsevier | location = Philadelphia, PA | year = 2016 | isbn = 978-1-4557-7005-2 }} </ref>


=== Some Factors Affecting Potassium Distribution Between the Cells and the Extracellular Fluid ===
=== Some Factors Affecting Potassium Distribution Between the Cells and the Extracellular Fluid ===
Line 51: Line 110:
*Plasma potassium concentration
*Plasma potassium concentration
*Extracellular pH
*Extracellular pH
*[[Hyperosmolarity]]
*[[Hyperosmolarity]] <ref>{{cite book | last = Hall | first = John | title = Guyton and Hall textbook of medical physiology | publisher = Elsevier | location = Philadelphia, PA | year = 2016 | isbn = 978-1-4557-7005-2 }} </ref>


=== The Physiologic Role of Potassium ===
=== The Physiologic Role of Potassium ===
*Potassium is the most common intracellular cation. Approximately 98% of total potassium exists in the intracellular fluid (ICF), which has a normal range of  140–150 mEq/l. Merely 2% of this cation is placed in the extracellular fluids (ECF), where it ranges from 3.5 to 5 mEq/l.
* Potassium is essential during numerous body functions, particularly for excitable cells such as muscle and nerve cells. 
* Diet, mostly fruits and vegetables, is the major source of potassium for the body.<ref name="pmid23674806">{{cite journal| author=Weaver CM| title=Potassium and health. | journal=Adv Nutr | year= 2013 | volume= 4 | issue= 3 | pages= 368S-77S | pmid=23674806 | doi=10.3945/an.112.003533 | pmc=3650509 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23674806  }} </ref> <ref>{{cite journal|doi=10.1159/000446268 Received:}}</ref>


Potassium is essential for many body functions, especially excitable cells such as [[muscle]] and [[nerve]] cells. Diet, mostly meats and fruits, is the major source of potassium for the body. Potassium is the principal [[intracellular]] [[cation]], with a concentration of about 145 mEq/L, as compared with a normal value of 3.5 - 5.0 mEq/L in [[extracellular]] fluid, including blood. More than 98% of the body's potassium is intracellular; measuring it from a blood sample is relatively insensitive, with small fluctuations in the blood corresponding to very large changes in the total bodily reservoir of potassium.
=== The Cellular Effect of Hypokalemia ===
The normal ratio of [[intracellular]] to [[extracellular]] potassium in the body is vital for the generation of [[action potential]] and results in appropriate cardiac and [[neuromuscular]] cells performance. By decreasing the potassium concentration in [[extracellular]] space, the amount of the potassium gradient across the [[cell membrane]] is risen and results in [[hyperpolarization]]. This alteration moves the resting membrane potential from the threshold to a higher level; hence, a bigger than standard stimulus is necessary to generate an [[action potential]]. Consequently, reduced excitability in the [[neuron]]s and [[muscle cell]]s would appear and cause flaccid muscle paralysis, [[rhabdomyolysis]] (in severe hypokalemia), and [[paralytic ileus]].<ref name="PalmerClegg2016">{{cite journal|last1=Palmer|first1=Biff F.|last2=Clegg|first2=Deborah J.|title=Physiology and pathophysiology of potassium homeostasis|journal=Advances in Physiology Education|volume=40|issue=4|year=2016|pages=480–490|issn=1043-4046|doi=10.1152/advan.00121.2016}}</ref>


=== The Cellular Effect of Hypokalemia ===


The electrochemical gradient of potassium between intracellular and extracellular space is essential for nerve function; in particular, potassium is needed to repolarize the [[cell membrane]] to a resting state after an [[action potential]] has passed. Decreased potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential ie, it becomes more negative. This [[hyperpolarization (biology)|hyperpolarization]] is caused by the effect of the altered potassium gradient on [[resting membrane potential]] as defined by the [[Goldman equation]].  As a result, the cell becomes less sensitive to excitation and a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential. Clinically, this membrane hyperpolarization results in muscle flaccid paralysis, [[rhabdomyolysis]] (in severe hypokalemia) and paralytic ileus. At the renal level, hypokalemia can cause metabolic alkalosis due to potassium/proton exchange across the cells and nephrogenic diabetes insipidus.
[[Image:Hypokalemia .png|right|400px]]


=== Pathophysiology of Hypokalemic Heart Arrhythmias ===
=== Pathophysiology of Hypokalemic Heart Arrhythmias ===
Potassium is essential to the normal muscular function, in both voluntary (i.e skeletal muscle, e.g. the arms and hands) and involuntary muscle (i.e. smooth muscle in the intestines or cardiac muscle in the heart). Severe abnormalities in potassium levels can seriously disrupt [[heart|cardiac function]], even to the point of causing [[cardiac arrest]] and [[death]]. As explained above, hypokalemia makes the resting potential of potassium [E(K)] more negative.  In certain conditions, this will make cells less excitable. However, in the heart, it causes [[myocytes]] to become hyperexcitable.   This is due to two independent effects that may lead to aberrant cardiac conduction and subsequent arrhythmia:  
* Hypokalemia in [[neurons]] and [[muscle cells]] reduces the [[membrane]] responsiveness and causes [[hyperpolarization]]. But in cardiac cells, specifically in the conducting system, [[depolarization]] is observed. The main reason is the alteration of ion selectivity of TWIK-1 K+ channels, which in standard situation leak potassium. During pathological hypokalemia, these channels transport sodium inward the cells, leading to paradoxical depolarization and may result in [[cardiac arrhythmia]]s.
#There are more inactivated sodium (Na) channels available to fire.
 
#The overall potassium permeability of the ventricle is reduced (perhaps by the loss of a direct effect of extracellular potassium on some of the potassium channels), which can delay ventricular repolarization.
* Decreased [[extracellular]] potassium also suppresses the activity of some potassium channels conductance, and in turn, it delays ventricular [[repolarization]]. Prolonged [[repolarization]] could also predispose [[re-entrant arrhythmia]]s.
 
* Moreover, Hypokalemia can inhibit Na+-K+ ATPase activity, leading to [[intracellular]] Na+ And Ca2+ increase. The accumulation of [[intracellular]] ca2+ activates calmodulin kinase and, in turn, induces late Na+ and Ca2+ currents and causes a further reduction in [[repolarization]] reserve. This would result in early after-depolarization (EAD)–mediated arrhythmias.<ref name="MaZhang2011">{{cite journal|last1=Ma|first1=L.|last2=Zhang|first2=X.|last3=Chen|first3=H.|title=TWIK-1 Two-Pore Domain Potassium Channels Change Ion Selectivity and Conduct Inward Leak Sodium Currents in Hypokalemia|journal=Science Signaling|volume=4|issue=176|year=2011|pages=ra37–ra37|issn=1945-0877|doi=10.1126/scisignal.2001726}}</ref> <ref name="WeissQu2017">{{cite journal|last1=Weiss|first1=James N.|last2=Qu|first2=Zhilin|last3=Shivkumar|first3=Kalyanam|title=Electrophysiology of Hypokalemia and Hyperkalemia|journal=Circulation: Arrhythmia and Electrophysiology|volume=10|issue=3|year=2017|issn=1941-3149|doi=10.1161/CIRCEP.116.004667}}</ref>
 
=== Pathophysiology of Hypokalemic in GI system: ===
* A low level of potassium [[Category:Electrophysiology]] [[Category:Cardiology]] [[Category:Endocrinology]] [[Category:Emergency medicine]] [[Category:Nephrology]] [[Category:Electrolyte disturbance]] [[Category:Blood tests]] [[Category:Intensive care medicine]]  causes dysfunctional gastrointestinal [[smooth muscle]] performance, the slow movement of the [[GI]] system, [[constipation]], and  [[paralytic ileus]]. The primary rationale behind them is the impairment of normal [[action potential]] in the [[muscle cell]] membrane, which disturbs favorable [[contraction]] and cellular [[depolarization]]. <ref name="StreetenWilliams1952">{{cite journal|last1=Streeten|first1=D. H. P.|last2=Williams|first2=E. M. Vaughan|title=Loss of cellular potassium as a cause of intestinal paralysis in dogs|journal=The Journal of Physiology|volume=118|issue=2|year=1952|pages=149–170|issn=00223751|doi=10.1113/jphysiol.1952.sp004782}}</ref> <ref name="PalmerClegg2016">{{cite journal|last1=Palmer|first1=Biff F.|last2=Clegg|first2=Deborah J.|title=Physiology and pathophysiology of potassium homeostasis|journal=Advances in Physiology Education|volume=40|issue=4|year=2016|pages=480–490|issn=1043-4046|doi=10.1152/advan.00121.2016}}</ref>


==References==
==References==
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Aida Javanbakht, M.D.Assistant Editor(s)-In-Chief: Jack Khouri, Alieh Behjat, M.D.[3]

Overview

Pathophysiology

Hypokalemia can result from several conditions:

  • Trans-cellular shifts of potassium inside the cells (most common)
  • Renal loss of potassium
  • Gastrointestinal (GI) loss of potassium
  • Increased hematopoiesis (increased cellular use of potassium)
  • Decreased intake of potassium (least common)

Shown below is a table summarizing the different pathophysiological processes that can lead to hypokalemia. [1] [2] [3] [4]

Trans-cellular shifts Renal loss GI loss Increased hematopoiesis Decreased intake of potassium

Subject is normo or hypotensive
Associated with acidosis

Associated with alkalosis

Variable acid/base status

Subject is hypertensive
Primary hyperaldosteronism

  • Conn's syndrome

Secondary hyperaldosteronism

  • Renovascular disease
  • Renin secreting tumor

Non aldosterone increase in mineralcorticoid

Associated with metabolic acidosis

Associated with metabolic alkalosis

The Role of the Kidney


{{#ev:youtube|https:watch?v=DlrEQg_68r0&t=69s}}

Factors Increasing Kidney Potassium Excretion

Some Factors Affecting Potassium Distribution Between the Cells and the Extracellular Fluid

The Physiologic Role of Potassium

  • Potassium is the most common intracellular cation. Approximately 98% of total potassium exists in the intracellular fluid (ICF), which has a normal range of 140–150 mEq/l. Merely 2% of this cation is placed in the extracellular fluids (ECF), where it ranges from 3.5 to 5 mEq/l.
  • Potassium is essential during numerous body functions, particularly for excitable cells such as muscle and nerve cells.
  • Diet, mostly fruits and vegetables, is the major source of potassium for the body.[7] [8]

The Cellular Effect of Hypokalemia

The normal ratio of intracellular to extracellular potassium in the body is vital for the generation of action potential and results in appropriate cardiac and neuromuscular cells performance. By decreasing the potassium concentration in extracellular space, the amount of the potassium gradient across the cell membrane is risen and results in hyperpolarization. This alteration moves the resting membrane potential from the threshold to a higher level; hence, a bigger than standard stimulus is necessary to generate an action potential. Consequently, reduced excitability in the neurons and muscle cells would appear and cause flaccid muscle paralysis, rhabdomyolysis (in severe hypokalemia), and paralytic ileus.[9]


Pathophysiology of Hypokalemic Heart Arrhythmias

  • Hypokalemia in neurons and muscle cells reduces the membrane responsiveness and causes hyperpolarization. But in cardiac cells, specifically in the conducting system, depolarization is observed. The main reason is the alteration of ion selectivity of TWIK-1 K+ channels, which in standard situation leak potassium. During pathological hypokalemia, these channels transport sodium inward the cells, leading to paradoxical depolarization and may result in cardiac arrhythmias.
  • Moreover, Hypokalemia can inhibit Na+-K+ ATPase activity, leading to intracellular Na+ And Ca2+ increase. The accumulation of intracellular ca2+ activates calmodulin kinase and, in turn, induces late Na+ and Ca2+ currents and causes a further reduction in repolarization reserve. This would result in early after-depolarization (EAD)–mediated arrhythmias.[10] [11]

Pathophysiology of Hypokalemic in GI system:

References

  1. ↑ Daly K, Farrington E (2013). "Hypokalemia and hyperkalemia in infants and children: pathophysiology and treatment". J Pediatr Health Care. 27 (6): 486–96, quiz 497–8. doi:10.1016/j.pedhc.2013.08.003. PMID 24139581.
  2. ↑ Unwin RJ, Luft FC, Shirley DG (February 2011). "Pathophysiology and management of hypokalemia: a clinical perspective". Nat Rev Nephrol. 7 (2): 75–84. doi:10.1038/nrneph.2010.175. PMID 21278718.
  3. ↑ Cheungpasitporn W, Suksaranjit P, Chanprasert S (February 2012). "Pathophysiology of vomiting-induced hypokalemia and diagnostic approach". Am J Emerg Med. 30 (2): 384. doi:10.1016/j.ajem.2011.10.005. PMID 22169581.
  4. ↑ Bisogni V, Rossi GP, Calò LA (June 2014). "Apparent mineralcorticoid excess syndrome, an often forgotten or unrecognized cause of hypokalemia and hypertension: case report and appraisal of the pathophysiology". Blood Press. 23 (3): 189–92. doi:10.3109/08037051.2013.832967. PMID 24053336.
  5. ↑ Hall, John (2016). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Elsevier. ISBN 978-1-4557-7005-2.
  6. ↑ Hall, John (2016). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Elsevier. ISBN 978-1-4557-7005-2.
  7. ↑ Weaver CM (2013). "Potassium and health". Adv Nutr. 4 (3): 368S–77S. doi:10.3945/an.112.003533. PMC 3650509. PMID 23674806.
  8. ↑ . doi:10.1159/000446268 Received: Check |doi= value (help). Missing or empty |title= (help)
  9. ↑ 9.0 9.1 Palmer, Biff F.; Clegg, Deborah J. (2016). "Physiology and pathophysiology of potassium homeostasis". Advances in Physiology Education. 40 (4): 480–490. doi:10.1152/advan.00121.2016. ISSN 1043-4046.
  10. ↑ Ma, L.; Zhang, X.; Chen, H. (2011). "TWIK-1 Two-Pore Domain Potassium Channels Change Ion Selectivity and Conduct Inward Leak Sodium Currents in Hypokalemia". Science Signaling. 4 (176): ra37–ra37. doi:10.1126/scisignal.2001726. ISSN 1945-0877.
  11. ↑ Weiss, James N.; Qu, Zhilin; Shivkumar, Kalyanam (2017). "Electrophysiology of Hypokalemia and Hyperkalemia". Circulation: Arrhythmia and Electrophysiology. 10 (3). doi:10.1161/CIRCEP.116.004667. ISSN 1941-3149.
  12. ↑ Streeten, D. H. P.; Williams, E. M. Vaughan (1952). "Loss of cellular potassium as a cause of intestinal paralysis in dogs". The Journal of Physiology. 118 (2): 149–170. doi:10.1113/jphysiol.1952.sp004782. ISSN 0022-3751.


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