Metabolic alkalosis resident survival guide: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{| class="infobox" style="margin: 0 0 0 0; border: 0; float: right; width: 100px; background: #A8A8A8; position: fixed; top: 250px; right: 21px; border-radius: 0 0 10px 10px;" cellpadding="0" cellspacing="0"; | |||
|- | |||
! style="padding: 0 5px; font-size: 85%; background: #A8A8A8" align=center| {{fontcolor|#2B3B44|Metabolic alkalosis Resident Survival Guide Microchapters}} | |||
|- | |||
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Metabolic alkalosis resident survival guide#Overview|Overview]] | |||
|- | |||
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Metabolic alkalosis resident survival guide#Causes|Causes]] | |||
|- | |||
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Metabolic alkalosis resident survival guide#Diagnosis|Diagnosis]] | |||
|- | |||
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Metabolic alkalosis resident survival guide#Treatment|Treatment]] | |||
|- | |||
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Metabolic alkalosis resident survival guide#Do's|Do's]] | |||
|- | |||
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align=left | [[Metabolic alkalosis resident survival guide#Don'ts|Don'ts]] | |||
|} | |||
{{WikiDoc CMG}}; {{AE | {{WikiDoc CMG}}; {{AE}} | ||
{{SK}} Approach to | {{SK}} Approach to Metabolic alkalosis, Metabolic alkalosis management, Metabolic alkalosis Work-up | ||
==Overview== | ==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 buffer|pH]] buffers in maintaining [[chemical equilibrium]] of physiological [[Blood pH]] are [[alkaline]] [[Bicarbonate|Bicarbonate ions(HCO3]]) and [[acidic]] [[Carbon dioxide|carbon dioxide(CO2)]]. When there is increase amount of [[Bicarbonate|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|Bicarbonate ions]] (HCO3) or loss of [[hydrogen ions]] in body due to some [[metabolic]] causes for example- [[Gastrointestinal|gastrointestinal loss]] of [[hydrogen ions]], [[Intracellular|intracellular shifting]] of [[hydrogen ions]], [[renal]] [[hydrogen]] loss, increased [[Bicarbonate|bicarbonate ions]] in [[extracellular]] [[Compartments|compartment]], [[Diuretic|diuretic i]]<nowiki/>nduced [[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|chloride depletion]], [[hypokalemia]], [[hyperaldosteronism]], reduced [[Glomerular filtration rate|glomerular function rate]], reduced [[Effective circulating volume|effective arterial blood volume]] ([[EABV|EABV)]]) in [[heart failure]] or [[cirrhosis]] will lead to [[metabolic alkalosis]]. When the [[physiologic]] [[blood pH]] is above 7.45, it triggers [[Respiratory centre of the medulla|respiratory center]] to cause [[hypoventilation]], thus decreased [[Carbon dioxide|PCO2]] leading to [[Compensatory responses for acid-base disorders|compensatory]] [[respiratory acidosis]]. The [[Carbon dioxide|PCO2]] increases about 0.5 to 0.7 mmHg to every 1.0 mM increase in [[Bicarbonate|plasma bicarbonate concentration]]. In severe [[Metabolic alkalosis]] [[Carbon dioxide|PCO2]] can reach 60 mmHg. The [[mortality rate]] with [[metabolic alkalosis]] is 45% with [[Arterial blood ph|arterial blood pH]] 7.55 to 80% with arterial blood pH of 7.65. [[Treatment]] is usually supportive based on cause of the [[Disease|disease.]] | 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 buffer|pH]] buffers in maintaining [[chemical equilibrium]] of physiological [[Blood pH]] are [[alkaline]] [[Bicarbonate|Bicarbonate ions(HCO3]]) and [[acidic]] [[Carbon dioxide|carbon dioxide(CO2)]]. When there is increase amount of [[Bicarbonate|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|Bicarbonate ions]] (HCO3) or loss of [[hydrogen ions]] in body due to some [[metabolic]] causes for example- [[Gastrointestinal|gastrointestinal loss]] of [[hydrogen ions]], [[Intracellular|intracellular shifting]] of [[hydrogen ions]], [[renal]] [[hydrogen]] loss, increased [[Bicarbonate|bicarbonate ions]] in [[extracellular]] [[Compartments|compartment]], [[Diuretic|diuretic i]]<nowiki/>nduced [[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|chloride depletion]], [[hypokalemia]], [[hyperaldosteronism]], reduced [[Glomerular filtration rate|glomerular function rate]], reduced [[Effective circulating volume|effective arterial blood volume]] ([[EABV|EABV)]]) in [[heart failure]] or [[cirrhosis]] will lead to [[metabolic alkalosis]]. When the [[physiologic]] [[blood pH]] is above 7.45, it triggers [[Respiratory centre of the medulla|respiratory center]] to cause [[hypoventilation]], thus decreased [[Carbon dioxide|PCO2]] leading to [[Compensatory responses for acid-base disorders|compensatory]] [[respiratory acidosis]]. The [[Carbon dioxide|PCO2]] increases about 0.5 to 0.7 mmHg to every 1.0 mM increase in [[Bicarbonate|plasma bicarbonate concentration]]. In severe [[Metabolic alkalosis]] [[Carbon dioxide|PCO2]] can reach 60 mmHg. The [[mortality rate]] with [[metabolic alkalosis]] is 45% with [[Arterial blood ph|arterial blood pH]] 7.55 to 80% with arterial blood pH of 7.65. [[Treatment]] is usually supportive based on cause of the [[Disease|disease.]] | ||
| Line 40: | Line 56: | ||
**[[Acetate]] containing [[Colloid|colloid sollution]]. | **[[Acetate]] containing [[Colloid|colloid sollution]]. | ||
**[[Exogenous]] [[alkali]] admintration. | **[[Exogenous]] [[alkali]] admintration. | ||
**Combined [[antacid]] and cation exchange resin | **Combined [[antacid]] and cation exchange resin administration. | ||
**Sodium [[Penicillin|penicillins]]. | **Sodium [[Penicillin|penicillins]]. | ||
| Line 67: | Line 83: | ||
==Do's== | ==Do's== | ||
*Maintenance of Airway, breathing, circulation if there is unstable patient. | *Maintenance of Airway, breathing, circulation if there is an unstable patient. | ||
*Correction of underlying cause for [[Bicarbonate|HCO3]] production. | *Correction of the underlying cause for [[Bicarbonate|HCO3]] production. | ||
*Removal of inciting factors | *Removal of inciting factors that reabsorb [[Bicarbonate|HCO3]]. | ||
*Patient should be monitored carefully with [[Oxygen saturation|SaO2]], Vital signs monitor and [[The electrocardiogram|EKG]]. | *Patient should be monitored carefully with [[Oxygen saturation|SaO2]], Vital signs monitor and [[The electrocardiogram|EKG]]. | ||
*Consider [[Respiratory|respiratory suppor]]<nowiki/>t in hypoxemic patient. | *Consider [[Respiratory|respiratory suppor]]<nowiki/>t in hypoxemic patient. | ||
| Line 80: | Line 96: | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Resident survival guide]] | [[Category:Resident survival guide]] | ||
Revision as of 17:52, 9 December 2020
| Metabolic alkalosis Resident Survival Guide Microchapters |
|---|
| Overview |
| Causes |
| Diagnosis |
| Treatment |
| Do's |
| Don'ts |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Synonyms and keywords: Approach to Metabolic alkalosis, Metabolic alkalosis management, Metabolic alkalosis Work-up
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 increases about 0.5 to 0.7 mmHg to every 1.0 mM increase 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. Treatment is usually supportive based on cause of the disease.
Causes
Life Threatening Causes
Life threatening causes of severe metabolic alkalosis (pH 7.55 to 7.65) may result in death (45% to 80%) or permanent disability within 24 hours if left untreated.[1]
Common Causes
- Chloride depletion or Gastrointestinal loss of hydrogen
- GI loss: Vomiting (most commonly seen in pyloric stenosis), NG suction , Zollinger-ellison syndrome, Bulimia.[2]
- Diuretics: Loop and thiazide diuretics.
- Diarrhea: Villous adenoma[3], congenital chloride diarrhea[4]
- Cystic fibrosis.[5]
- Chloride deficient infant formula.
- Gastrocystoplasty [6]
- Post hypercapneic metabolic alkalosis.
- Potassium depletion or Mineralocorticoids excess or Renal loss of hydrogen
- Dietary potassium depletion.[7]
- 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.[8] [9]
- Bartter and Gitelman syndrome. [10]
- Laxative
- Reduced Glomerular filtration rate
- ECF volume depletion/ Volume contraction
- Hypovolemia or massive diuresis with loop diuretics.
- Miscellanous
- Hypercalcemia due to 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.
Diagnosis
Shown below is an algorithm summarizing the diagnosis and treatment of Metabolic Alkalosis.
Do's
- Maintenance of Airway, breathing, circulation if there is an unstable patient.
- Correction of the underlying cause for HCO3 production.
- Removal of inciting factors that reabsorb HCO3.
- Patient should be monitored carefully with SaO2, Vital signs monitor and EKG.
- Consider respiratory support in hypoxemic patient.
Don'ts
- Avoid hyperventilation as it will worsen alkalemia.
References
- ↑ Tripathy S (October 2009). "Extreme metabolic alkalosis in intensive care". Indian J Crit Care Med. 13 (4): 217–20. doi:10.4103/0972-5229.60175. PMC 2856150. PMID 20436691.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Sabatini S (March 1996). "The cellular basis of metabolic alkalosis". Kidney Int. 49 (3): 906–17. doi:10.1038/ki.1996.125. PMID 8648937.
- ↑ 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.
- ↑ 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.
- ↑ 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.