Alkalosis

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List of terms related to Alkalosis

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

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.

Respiratory Alkalosis

  • It is thought that the respiratory alkalosis is the result of hyperventilation. The causes of hyperventilation can be due to increased stimulation of the medullary respiratory center, low oxygen tension in blood, lung pathologies, and iatrogenic. The stimulation of the respiratory center occurs due to stroke, head injury, metabolic disease like hyperthyroidism, emotional stress, panic attack, and side effect of medications like aspirin. The low oxygen tension in the blood causes stimulation of the respiratory center resulting in hyperventilation and hypocapnia. The acute attack of asthma, COPD, pulmonary embolism can cause tachypnea with increase loss of carbon dioxide.

Epidemiology and Demographics

  • The prevalence of alkalosis ranges from 32,727 to 80,000 per 100,000 in hospitalized patients with an acid-base metabolic disorder. [3][4]
  • The prevalence of alkalosis is approximately 44,046 per 100,000 in acute heart failure patients. [5]

Differential Diagnosis

Differential diagnosis of metabolic alkalosis is as follow:

Disease Clinical Paraclinical Gold standard diagnosis Other findings
Symptoms Signs Lab data
ABG Chemistry Enzyme Renal function
fatigability Muscle weakness Muscle paresthesia Cardiac arrythmia Hypotension Dehydration HCO3− paCO2 O2 Cl− K+ Na+ Ca+ Mg+ Renin Bun Cr Urine Cl−
Vomiting[6] + + + - + + ↑ ↑ Nl ↓ ↓ ↑ Nl Nl ↑ Nl to ↑ Nl ↓ Clinical manifestations
  • Not applicable
Nasogastric tube suction[7] + + + - + + ↑ ↑ Nl ↓ ↓ ↑ Nl Nl ↑ Nl to ↑ Nl ↓ Clinical manifestations
Chronic laxative abuse + − − - + + ↑ ↑ Nl ↓ ↓ ↓ ↓ ↓ ↓ Nl to ↑ Nl ↓ Medication history  Abdominal cramps, large volume diarrhea
Villous adenoma[8] + + + + + + ↑ ↑ Nl ↓ ↓ ↓ ↓ ↓ ↑ Nl to ↑ Nl ↑ Colonoscopy
Loop diuretics[9] + ± - - + − ↑ ↑ Nl ↓ ↓ ↓ ↓ ↓ ↑ ↑ ↑ ↑ Medication history Not applicable
Hypomagnesemia[10] − − − − Nl − ↑ ↑ Nl ↓ ↓ ↑ Nl Nl ↑ Nl Nl Nl Lab findings
  • Not applicable
Hypokalemia[11] − − − − Nl − ↑ ↑ Nl ↓ ↓ ↑ Nl Nl ↑ Nl Nl Nl Lab findings
  • Not applicable
Bartter's syndrome[12] − − − − Nl + ↑ ↑ Nl ↓ ↓↓ ↓ ↓ Nl ↑ Nl to ↑ Nl to ↑ Nl Genetic testing
Gitelman’s syndrome[13][14] − − − − ↓ + ↑ ↑ Nl ↓ ↓↓ ↓ Nl ↓ ↑ Nl Nl Nl Genetic testing
Renal artery stenosis[15] − + + + ↑ + ↑ ↑ ↓ ↓ ↑ ↓ ↑ Nl ↑ ↑ ↑ Nl Clinical manifestations+ imaging
Liddle syndrome[16] − − − − ↑ + ↑ ↑ Nl ↓ ↓↓ ↓ Nl ↓ ↑ Nl Nl Nl Genetic testing
  • Not applicable
Renal tumors[17] − + + + ↑ + ↑ ↑ ↓ ↓ ↑ ↓ ↑ Nl ↑ ↑ ↑ Nl Biopsy
  • Not applicable
Endocrine Cushing's syndrome[18] − − + − ↑ + ↑ ↑ Nl ↓ ↑ ↓ ↑ Nl ↓ ↑ ↑ Nl 24−hour urinary cortisol excretion + low−dose dexamethasone suppression test
Hyperaldosteronism Primary[19] − − + − ↑ + ↑ ↑ Nl ↓ Nl to ↓ ↓ ↑ Nl ↓ ↑ ↑ Nl Lab findings
Secondary[20] − + + + ↑ + ↑ ↑ Nl ↓ ↓ ↑ Nl ↓ ↑ ↑ ↑ Nl Lab findings
Congenital adrenal hyperplasia 11β−Hydroxylase deficiency[21] − − + − ↑ + ↑ ↑ Nl ↓ ↓ ↓ ↑ Nl ↓ Nl Nl Nl Genetic testing
17α−Hydroxylase deficiency[22] − − + − ↑ + ↑ ↑ Nl ↓ ↓ ↓ ↑ Nl ↓ Nl Nl Nl Genetic testing
Systemic Cystic fibrosis[23] − + − + ↓ + ↑ ↑ Nl ↓ ↓ Nl Nl Nl ↑ Nl to ↑ Nl ↑ Genetic testing
Category Disease Fever Dyspnea Edema Toxic/ill BP Dehydration HCO3− paCO2 O2 Cl− K+ Na+ Ca+ Mg+ Renin Bun Cr Urine Cl− Gold standard diagnosis Other findings

References

  1. ↑ 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.
  2. ↑ 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.
  3. ↑ Palange P, Carlone S, Galassetti P, Felli A, Serra P (1990). "Incidence of acid-base and electrolyte disturbances in a general hospital: a study of 110 consecutive admissions". Recenti Prog Med. 81 (12): 788–91. PMID 2075281.
  4. ↑ Hodgkin JE, Soeprono FF, Chan DM (1980). "Incidence of metabolic alkalemia in hospitalized patients". Crit Care Med. 8 (12): 725–8. doi:10.1097/00003246-198012000-00005. PMID 6778655.
  5. ↑ Park JJ, Choi DJ, Yoon CH, Oh IY, Lee JH, Ahn S; et al. (2015). "The prognostic value of arterial blood gas analysis in high-risk acute heart failure patients: an analysis of the Korean Heart Failure (KorHF) registry". Eur J Heart Fail. 17 (6): 601–11. doi:10.1002/ejhf.276. PMID 26096207.
  6. ↑ Gan, Tong J.; Meyer, Tricia; Apfel, Christian C.; Chung, Frances; Davis, Peter J.; Eubanks, Steve; Kovac, Anthony; Philip, Beverly K.; Sessler, Daniel I.; Temo, James; Tram??r, Martin R.; Watcha, Mehernoor (2003). "Consensus Guidelines for Managing Postoperative Nausea and Vomiting". Anesthesia & Analgesia: 62–71. doi:10.1213/01.ANE.0000068580.00245.95. ISSN 0003-2999.
  7. ↑ Gilbertson, Heather Ruth; Rogers, Elizabeth Jessie; Ukoumunne, Obioha Chukwunyere (2011). "Determination of a Practical pH Cutoff Level for Reliable Confirmation of Nasogastric Tube Placement". Journal of Parenteral and Enteral Nutrition. 35 (4): 540–544. doi:10.1177/0148607110383285. ISSN 0148-6071.
  8. ↑ Gennari, F. J.; Weise, W. J. (2008). "Acid-Base Disturbances in Gastrointestinal Disease". Clinical Journal of the American Society of Nephrology. 3 (6): 1861–1868. doi:10.2215/CJN.02450508. ISSN 1555-9041.
  9. ↑ Kataoka H (2018). "Dynamic changes in serum chloride concentrations during worsening of heart failure and its recovery following conventional diuretic therapy: A single-center study". Health Sci Rep. 1 (11): e94. doi:10.1002/hsr2.94. PMC 6242367. PMID 30623047.
  10. ↑ Elisaf M, Milionis H, Siamopoulos KC (1997). "Hypomagnesemic hypokalemia and hypocalcemia: clinical and laboratory characteristics". Miner Electrolyte Metab. 23 (2): 105–12. PMID 9252977.
  11. ↑ Galla JH (February 2000). "Metabolic alkalosis". J. Am. Soc. Nephrol. 11 (2): 369–75. PMID 10665945.
  12. ↑ Simon, David B.; Karet, Fiona E.; Hamdan, Jahed M.; Pietro, Antonio Di; Sanjad, Sami A.; Lifton, Richard P. (1996). "Bartter's syndrome, hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the Na–K–2CI cotransporter NKCC2". Nature Genetics. 13 (2): 183–188. doi:10.1038/ng0696-183. ISSN 1061-4036.
  13. ↑ Fremont, Oliver T.; Chan, James C. M. (2012). "Understanding Bartter syndrome and Gitelman syndrome". World Journal of Pediatrics. 8 (1): 25–30. doi:10.1007/s12519-012-0333-9. ISSN 1708-8569.
  14. ↑ Colussi G, Macaluso M, Brunati C, Minetti L (1994). "Calcium metabolism and calciotropic hormone levels in Gitelman's syndrome". Miner Electrolyte Metab. 20 (5): 294–301. PMID 7700218.
  15. ↑ Safian, Robert D.; Textor, Stephen C. (2001). "Renal-Artery Stenosis". New England Journal of Medicine. 344 (6): 431–442. doi:10.1056/NEJM200102083440607. ISSN 0028-4793.
  16. ↑ Salih, Mahdi; Gautschi, Ivan; van Bemmelen, Miguel X.; Di Benedetto, Michael; Brooks, Alice S.; Lugtenberg, Dorien; Schild, Laurent; Hoorn, Ewout J. (2017). "A Missense Mutation in the Extracellular Domain ofαENaC Causes Liddle Syndrome". Journal of the American Society of Nephrology. 28 (11): 3291–3299. doi:10.1681/ASN.2016111163. ISSN 1046-6673.
  17. ↑ Lasseigne, Brittany N.; Brooks, James D. (2018). "The Role of DNA Methylation in Renal Cell Carcinoma". Molecular Diagnosis & Therapy. doi:10.1007/s40291-018-0337-9. ISSN 1177-1062.
  18. ↑ Araujo Castro, Marta; Marazuela Azpiroz, Mónica (2018). "Two types of ectopic Cushing syndrome or a continuum? Review". Pituitary. doi:10.1007/s11102-018-0894-2. ISSN 1386-341X.
  19. ↑ Martell-Claros, Nieves; Abad-Cardiel, María; Alvarez-Alvarez, Beatriz; García-Donaire, José A.; Pérez, Cristina Fernández (2015). "Primary aldosteronism and its various clinical scenarios". Journal of Hypertension. 33 (6): 1226–1232. doi:10.1097/HJH.0000000000000546. ISSN 0263-6352.
  20. ↑ Monticone S, Losano I, Tetti M, Buffolo F, Veglio F, Mulatero P (May 2018). "Diagnostic approach to low renin hypertension". Clin. Endocrinol. (Oxf). doi:10.1111/cen.13741. PMID 29758100.
  21. ↑ Baş F, Toksoy G, Ergun-Longmire B, Uyguner ZO, Abalı ZY, Poyrazoğlu Ş, Karaman V, Avcı Ş, Altunoğlu U, Bundak R, Karaman B, Başaran S, Darendeliler F (April 2018). "Prevalence, clinical characteristics and long-term outcomes of classical 11 β-hydroxylase deficiency (11BOHD) in Turkish population and novel mutations in CYP11B1 gene". J. Steroid Biochem. Mol. Biol. doi:10.1016/j.jsbmb.2018.04.001. PMID 29626607.
  22. ↑ Goldsmith, Oliver; Solomon, David H.; Horton, Richard (1967). "Hypogonadism and Mineralocorticoid Excess". New England Journal of Medicine. 277 (13): 673–677. doi:10.1056/NEJM196709282771302. ISSN 0028-4793.
  23. ↑ Bates CM, Baum M, Quigley R (February 1997). "Cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent". J. Am. Soc. Nephrol. 8 (2): 352–5. PMID 9048354.

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