Hypokalemia pathophysiology: Difference between revisions
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=== The Cellular Effect of Hypokalemia === | === 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.<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> | |||
[[Image:Hypokalemia .png|right|400px]] | |||
=== Pathophysiology of Hypokalemic Heart Arrhythmias === | === Pathophysiology of Hypokalemic Heart Arrhythmias === | ||
Revision as of 14:36, 19 June 2020
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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
Overview
- 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) hyperpolarized and less sensitive. However, 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 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
Hypokalemia can result from several conditions:
- Trans-cellular shifts of potassium inside the cells (most common)
- Renal loss 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)
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 | |
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Subject is normo or hypotensive Associated with alkalosis
Variable acid/base status |
Subject is hypertensive
Secondary hyperaldosteronism
Non aldosterone increase in mineralcorticoid
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Associated with metabolic acidosis Associated with metabolic alkalosis
|
|
|
The Role of the Kidney
- 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 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.
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Factors Increasing Kidney Potassium Excretion
- Aldosterone
- High urine flow rate
- High distal sodium delivery
- Metabolic alkalosis
- High extracellular fluid K+ concentration
Some Factors Affecting Potassium Distribution Between the Cells and the Extracellular Fluid
- Na/K ATPase
- Insulin
- Catecholamines
- Plasma potassium concentration
- Extracellular pH
- Hyperosmolarity [5]
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.[6] [7]
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.[8]
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 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:
- 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.
Pathophysiology of Hypokalemic in GI system:
- Low level of potassium cause slow movement of GI system and illeus.
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Hall, John (2016). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Elsevier. ISBN 978-1-4557-7005-2.
- ↑ Weaver CM (2013). "Potassium and health". Adv Nutr. 4 (3): 368S–77S. doi:10.3945/an.112.003533. PMC 3650509. PMID 23674806.
- ↑ . doi:10.1159/000446268 Received: Check
|doi=value (help). Missing or empty|title=(help) - ↑ 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.