Metabolic alkalosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Marufa Marium, M.B.B.S[2]
Overview
The normal physiological pH of blood is 7.35 to 7.45. An increase above this range is known to be Alkalosis. Metabolic Alkalosis is defined as a disease state where blood pH is more than 7.45 due to secondary metabolic processes. The primary pH buffers in maintaining chemical equilibrium of physiological Blood pH are alkaline Bicarbonate ions(HCO3) and acidic carbon dioxide(CO2). When there is increase amount of Bicarbonate(HCO3) in body or decrease amount of carbon dioxide or loss of hydrogen ions it causes alkalosis. Metabolic alkalosis occurs due to trapping of Bicarbonate ions (HCO3) or loss of hydrogen ions in body due to some metabolic causes for example- gastrointestinal loss of hydrogen ions, intracellular shifting of hydrogen ions, renal hydrogen loss, increased bicarbonate ions in extracellular compartment, diuretic induced alkalosis or contraction alkalosis. Patient with normal renal physiology will compensate this increase amount of bicarbonate through excretion. But impaired renal function secondary to chloride depletion, hypokalemia, hyperaldosteronism, reduced glomerular function rate, reduced effective arterial blood volume (EABV)) in heart failure or cirrhosis will lead to metabolic alkalosis. When the physiologic blood pH is above 7.45, it triggers respiratory center to cause hypoventilation, thus decreased PCO2 leading to compensatory respiratory acidosis. The PCO2 elavates from 0.5 to 0.7 mmHg per 1.0 millimole elevation in plasma bicarbonate concentration. In severe Metabolic alkalosis PCO2 can reach 60 mmHg. The mortality rate with metabolic alkalosis is 45% with arterial blood pH 7.55 to 80% with arterial blood pH of 7.65. Supportive Treatment is usually given according to cause of the disease.
Pathophysiology
Loss of hydrogen ions
GI loss
- Vomiting (most commonly seen in pyloric stenosis), NG suction , Zollinger-ellison syndrome, Bulimia.[1]
- Diuretics: Loop and thiazide diuretics.
- Diarrhea: Villous adenoma[2], congenital chloride diarrhea[3]
- Cystic fibrosis.[4]
- Chloride deficient infant formula.
- Gastrocystoplasty [5]
- Post hypercapneic metabolic alkalosis.
Renal
- Dietary potassium depletion.[6]
- Primary hyperaldosteronism: Conn syndrome or adenoma, hyperplasia, carcinoma, renin or glucocorticoid responsive.
- Secondary hyperaldosteronism: Reno vascular hypertension, edema (cirrhosis, heart failure, nephrotic syndrome), juxtaglomerular cell(renin producing) tumor, renal cell carcinoma, hemangiopericytoma, nephroblastoma
- Mineralocorticoid excess due to primary decorticosterone excess (11 beta, 17 alpha hydroxylase deficiency), licorice(glycyrrhetinic acid), liddle syndrome.[7] [8]
- Bartter and Gitelman syndrome. [9]
Increase in the serum bicarbonate
- Ingestion of sodium bicarbonate, baking soda, citrate, lactate, or acetate.
Transport of H+ into IC(Intracellular) space
- Occurs in hypokalemia. Decreased extracellular K+, potassium transports from the cells, and to keep electrical potential in a balanced state, H+ transports into the cells, leaving behind bicarbonate.
Contraction alkalosis
- This results from a loss of water in the extracellular space which is poor in bicarbonate, typically from diuretic use. Since water is lost while bicarbonate is retained, the concentration of bicarbonate increases.
Compensation for Metabolic Alkalosis
- The body attempts to compensate for the increase in pH by retaining carbon dioxide (CO2) through hypoventilation (respiratory compensation). CO2 combines with elements in the bloodstream to form carbonic acid, thus decreasing pH.
- The pCO2 rises 0.5 - 1 for every 1 unit increase in serum HCO3 from a baseline of 24.
- The maximum pCO2 in compensation is 55-60.
- Renal compensation for metabolic alkalosis consists of increased excretion of HCO3- (bicarbonate), because the filtered load of HCO3- exceeds the ability of the renal tubule to reabsorb it.
Genetics
- Genes involved in the pathogenesis of Metabolic Alkalosis include CFTR, SCNN1A/SCNN1B/SCNN1G[10], NKCC2[11] SLC12A3/CLCNKB[12] and SLC26A3 [13] causing Cystic Fibrosis, Liddle Syndrome, Bartter syndrome, Gitelman syndrome and Congenital Chloride Diarrhhea respectively.
Associated Conditions
Conditions associated with metabolic alkalosis :
- Vomiting (most commonly seen in pyloric stenosis
- NG suction
- Zollinger-ellison syndrome
- Bulimia.[1]
- Diuretics: Loop and thiazide diuretics.
- Villous adenoma[2]
- congenital chloride diarrhea[3]
- Cystic fibrosis[4]
- Chloride deficient infant formula.
- Gastrocystoplasty [5]
- Post hypercapneic metabolic alkalosis.
- Dietary potassium depletion.[6]
- Primary hyperaldosteronism: Conn syndrome or adenoma, hyperplasia, carcinoma, renin or glucocorticoid responsive.
- Secondary hyperaldosteronism: Reno vascular hypertension, edema (cirrhosis, heart failure, nephrotic syndrome), juxtaglomerular cell(renin producing) tumor, renal cell carcinoma, hemangiopericytoma, nephroblastoma
- Mineralocorticoid excess due to primary decorticosterone excess (11 beta, 17 alpha hydroxylase deficiency), licorice(glycyrrhetinic acid), liddle syndrome.[7] [8]
- Bartter and Gitelman syndrome. [9]
- Laxative
- Chronic kidney disease
- Hypovolemia or massive diuresis with loop diuretics.
- Milk-alkali syndrome or bone metastasis.
- Massive blood transfusion.
- Acetate containing colloid sollution.
- Exogenous alkali admintration.
- Combined antacid and cation exchange resin administration.
- Sodium penicillins.
Gross Pathology
- There is no specific gross pathological finding related to metabolic alkalosis. Gross characteristics are dependent on specific cause of metabolic alkalosis.
Microscopic Pathology
- There is no specific microscopic pathological finding related to metabolic alkalosis. Gross characteristics are dependent on specific cause of metabolic alkalosis.
References
- ↑ 1.0 1.1 Galla JH, Gifford JD, Luke RG, Rome L (October 1991). "Adaptations to chloride-depletion alkalosis". Am J Physiol. 261 (4 Pt 2): R771–81. doi:10.1152/ajpregu.1991.261.4.R771. PMID 1928424.
- ↑ 2.0 2.1 Babior BM (October 1966). "Villous adenoma of the colon. Study of a patient with severe fluid and electrolyte disturbances". Am J Med. 41 (4): 615–21. doi:10.1016/0002-9343(66)90223-3. PMID 5927076.
- ↑ 3.0 3.1 Höglund P, Haila S, Socha J, Tomaszewski L, Saarialho-Kere U, Karjalainen-Lindsberg ML, Airola K, Holmberg C, de la Chapelle A, Kere J (November 1996). "Mutations of the Down-regulated in adenoma (DRA) gene cause congenital chloride diarrhoea". Nat Genet. 14 (3): 316–9. doi:10.1038/ng1196-316. PMID 8896562.
- ↑ 4.0 4.1 Pedroli G, Liechti-Gallati S, Mauri S, Birrer P, Kraemer R, Foletti-Jäggi C, Bianchetti MG (1995). "Chronic metabolic alkalosis: not uncommon in young children with severe cystic fibrosis". Am J Nephrol. 15 (3): 245–50. doi:10.1159/000168839. PMID 7618650.
- ↑ 5.0 5.1 Plawker MW, Rabinowitz SS, Etwaru DJ, Glassberg KI (August 1995). "Hypergastrinemia, dysuria-hematuria and metabolic alkalosis: complications associated with gastrocystoplasty". J Urol. 154 (2 Pt 1): 546–9. doi:10.1097/00005392-199508000-00066. PMID 7609133.
- ↑ 6.0 6.1 Sabatini S (March 1996). "The cellular basis of metabolic alkalosis". Kidney Int. 49 (3): 906–17. doi:10.1038/ki.1996.125. PMID 8648937.
- ↑ 7.0 7.1 Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, Lalouel JM (January 1992). "A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension". Nature. 355 (6357): 262–5. doi:10.1038/355262a0. PMID 1731223.
- ↑ 8.0 8.1 Warnock DG (January 1998). "Liddle syndrome: an autosomal dominant form of human hypertension". Kidney Int. 53 (1): 18–24. doi:10.1046/j.1523-1755.1998.00728.x. PMID 9452995.
- ↑ 9.0 9.1 Kurtz I (October 1998). "Molecular pathogenesis of Bartter's and Gitelman's syndromes". Kidney Int. 54 (4): 1396–410. doi:10.1046/j.1523-1755.1998.00124.x. PMID 9767561.
- ↑ Tetti M, Monticone S, Burrello J, Matarazzo P, Veglio F, Pasini B, Jeunemaitre X, Mulatero P (March 2018). "Liddle Syndrome: Review of the Literature and Description of a New Case". Int J Mol Sci. 19 (3). doi:10.3390/ijms19030812. PMC 5877673. PMID 29534496.
- ↑ Simon DB, Karet FE, Rodriguez-Soriano J, Hamdan JH, DiPietro A, Trachtman H, Sanjad SA, Lifton RP (October 1996). "Genetic heterogeneity of Bartter's syndrome revealed by mutations in the K+ channel, ROMK". Nat Genet. 14 (2): 152–6. doi:10.1038/ng1096-152. PMID 8841184.
- ↑ Vargas-Poussou R, Dahan K, Kahila D, Venisse A, Riveira-Munoz E, Debaix H, Grisart B, Bridoux F, Unwin R, Moulin B, Haymann JP, Vantyghem MC, Rigothier C, Dussol B, Godin M, Nivet H, Dubourg L, Tack I, Gimenez-Roqueplo AP, Houillier P, Blanchard A, Devuyst O, Jeunemaitre X (April 2011). "Spectrum of mutations in Gitelman syndrome". J Am Soc Nephrol. 22 (4): 693–703. doi:10.1681/ASN.2010090907. PMC 3065225. PMID 21415153.
- ↑ Kamal NM, Khan HY, El-Shabrawi M, Sherief LM (May 2019). "Congenital chloride losing diarrhea: A single center experience in a highly consanguineous population". Medicine (Baltimore). 98 (22): e15928. doi:10.1097/MD.0000000000015928. PMC 6709049 Check
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