Alkalosis: Difference between revisions
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* [[Renal]] [[potassium]] loss | * [[Renal]] [[potassium]] loss | ||
* [[Ddx:Nausea and Vomiting|Vomiting]] | * [[Ddx:Nausea and Vomiting|Vomiting]] | ||
===Pathophysiology=== | |||
====Metabolic Alkalosis==== | |||
It is thought that [metabolic alkalosis] is the result of the shift of hydrogen ions intracellularly, reduced blood volume, loss of gastric acid, and extracellular volume expansion. | |||
=====Shift of hydrogen ions intracellularly===== | |||
* Electrolyte imbalance like hypokalemia causes a shift of hydrogen ions intracellular caused defect of protons and an increase in bicarbonate ion concentration. <ref name="pmid7936014">{{cite journal| author=Halperin ML, Scheich A| title=Should we continue to recommend that a deficit of KCl be treated with NaCl? A fresh look at chloride-depletion metabolic alkalosis. | journal=Nephron | year= 1994 | volume= 67 | issue= 3 | pages= 263-9 | pmid=7936014 | doi=10.1159/000187977 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7936014 }} </ref> | |||
=====Reduced Blood volume===== | |||
* Volume depletion results in reduced glomerular filtration rate. This stimulates the production of Angiotensin II, sympathetic nervous system activation, and aldosterone secretion. The sympathetic nervous system and angiotensin II causes increased absorption of sodium in proximal convoluted tubules via sodium hydrogen exchange. Aldosterone acts primarily on the principal cells of the late distal convoluted tubule and collecting ducts. It causes sodium and water retention in exchange for potassium and hydrogen ions secretion. The loop and thiazide diuretics also act by similar mechanisms of action.<ref name="pmid26597304">{{cite journal| author=Hamm LL, Nakhoul N, Hering-Smith KS| title=Acid-Base Homeostasis. | journal=Clin J Am Soc Nephrol | year= 2015 | volume= 10 | issue= 12 | pages= 2232-42 | pmid=26597304 | doi=10.2215/CJN.07400715 | pmc=4670772 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26597304 }} </ref> | |||
=====Loss of Gastric acid===== | |||
The hydrogen ions are primarily secreted in large amounts in the gastric juice. The hydrogen ions are secreted via active transport mediated by hydrogen potassium ATPase pump. Excessive vomiting causes loss of a large amount of gastric juice with depletion of hydrogen and chloride from the body. | |||
=====Extracellular volume expansion===== | |||
Primary hyperaldosteronism (Conn’s syndrome) causes increased sodium reabsorption with the resultant increase in extracellular volume. The patient may be hypertensive or normotensive. The hypokalemia caused by the action of aldosterone causes increased reabsorption of sodium bicarbonate in the proximal convoluted tubule with a worsening of metabolic alkalosis. | |||
== References == | == References == | ||
Revision as of 11:27, 8 October 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Alkalosis refers to a condition reducing hydrogen ion concentration of arterial blood plasma (alkalemia) through the loss of acids or retention of bicarbonate. Generally alkalosis is said to occur when pH of the blood exceeds 7.45. The opposite condition is acidosis.
Classification
More specifically, alkalosis can refer to:
Causes
Common Causes
The main cause of respiratory alkalosis is hyperventilation, resulting in a loss of carbon dioxide. Compensatory mechanisms for this would include increased dissociation of the carbonic acid buffering intermediate into hydrogen ions, and the related consumption of bicarbonate, both of which would lower blood pH.
Metabolic alkalosis can be caused by prolonged vomitting, resulting in a loss of hydrochloric acid with the stomach content. Severe dehydration, and the consumption of alkali are other causes. Compensatory mechanism for metabolic alkalosis involve slowed breathing by the lungs to increase serum carbon dioxide, a condition leaning toward respiratory acidosis. As respiratory acidosis often accompanies the compensation for metabolic alkalosis, and visa versa, a delicate balance is created between these two conditions.
Causes in Alphabetical Order
Metabolic Alkalosis
- Administration of citrates
- After respiratory acidosis
- Alkali therapy for stomach problems
- Bartter's Syndrome
- Conn syndrome
- Cushing's Syndrome
- Cystic Fibrosis
- Diarrhea
- Gastric juice drainage
- Hepatic coma
- Hyperemesis gravidarum
- Milk Alkali Syndrome
- Mineralcorticoid therapy
- Overcorrection of acidosis with bicarbonates
- Renal potassium loss
- Vomiting
Pathophysiology
Metabolic Alkalosis
It is thought that [metabolic alkalosis] is the result of the shift of hydrogen ions intracellularly, reduced blood volume, loss of gastric acid, and extracellular volume expansion.
Shift of hydrogen ions intracellularly
- Electrolyte imbalance like hypokalemia causes a shift of hydrogen ions intracellular caused defect of protons and an increase in bicarbonate ion concentration. [1]
Reduced Blood volume
- Volume depletion results in reduced glomerular filtration rate. This stimulates the production of Angiotensin II, sympathetic nervous system activation, and aldosterone secretion. The sympathetic nervous system and angiotensin II causes increased absorption of sodium in proximal convoluted tubules via sodium hydrogen exchange. Aldosterone acts primarily on the principal cells of the late distal convoluted tubule and collecting ducts. It causes sodium and water retention in exchange for potassium and hydrogen ions secretion. The loop and thiazide diuretics also act by similar mechanisms of action.[2]
Loss of Gastric acid
The hydrogen ions are primarily secreted in large amounts in the gastric juice. The hydrogen ions are secreted via active transport mediated by hydrogen potassium ATPase pump. Excessive vomiting causes loss of a large amount of gastric juice with depletion of hydrogen and chloride from the body.
Extracellular volume expansion
Primary hyperaldosteronism (Conn’s syndrome) causes increased sodium reabsorption with the resultant increase in extracellular volume. The patient may be hypertensive or normotensive. The hypokalemia caused by the action of aldosterone causes increased reabsorption of sodium bicarbonate in the proximal convoluted tubule with a worsening of metabolic alkalosis.
References
- ↑ Halperin ML, Scheich A (1994). "Should we continue to recommend that a deficit of KCl be treated with NaCl? A fresh look at chloride-depletion metabolic alkalosis". Nephron. 67 (3): 263–9. doi:10.1159/000187977. PMID 7936014.
- ↑ Hamm LL, Nakhoul N, Hering-Smith KS (2015). "Acid-Base Homeostasis". Clin J Am Soc Nephrol. 10 (12): 2232–42. doi:10.2215/CJN.07400715. PMC 4670772. PMID 26597304.