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Clinical Journal of the American... Dec 2020Metabolic alkalosis is a very commonly encountered acid-base disorder that may be generated by a variety of exogenous and/or endogenous, pathophysiologic mechanisms.... (Review)
Review
Metabolic alkalosis is a very commonly encountered acid-base disorder that may be generated by a variety of exogenous and/or endogenous, pathophysiologic mechanisms. Multiple mechanisms are also responsible for the persistence, or maintenance, of metabolic alkalosis. Understanding these generation and maintenance mechanisms helps direct appropriate intervention and correction of this disorder. The framework utilized in this review is based on the ECF volume-centered approach popularized by Donald Seldin and Floyd Rector in the 1970s. Although many subsequent scientific discoveries have advanced our understanding of the pathophysiology of metabolic alkalosis, that framework continues to be a valuable and relatively straightforward diagnostic and therapeutic model.
Topics: Acid-Base Equilibrium; Alkalosis; Animals; Bicarbonates; Biomarkers; Chlorides; Humans; Hydrogen-Ion Concentration; Models, Biological; Prognosis
PubMed: 32586924
DOI: 10.2215/CJN.16041219 -
American Journal of Kidney Diseases :... Oct 2022Metabolic alkalosis is a widespread acid-base disturbance, especially in hospitalized patients. It is characterized by the primary elevation of serum bicarbonate and... (Review)
Review
Metabolic alkalosis is a widespread acid-base disturbance, especially in hospitalized patients. It is characterized by the primary elevation of serum bicarbonate and arterial pH, along with a compensatory increase in Pco consequent to adaptive hypoventilation. The pathogenesis of metabolic alkalosis involves either a loss of fixed acid or a net accumulation of bicarbonate within the extracellular fluid. The loss of acid may be via the gastrointestinal tract or the kidney, whereas the sources of excess alkali may be via oral or parenteral alkali intake. Severe metabolic alkalosis in critically ill patients-arterial blood pH of 7.55 or higher-is associated with significantly increased mortality rate. The kidney is equipped with sophisticated mechanisms to avert the generation or the persistence (maintenance) of metabolic alkalosis by enhancing bicarbonate excretion. These mechanisms include increased filtration as well as decreased absorption and enhanced secretion of bicarbonate by specialized transporters in specific nephron segments. Factors that interfere with these mechanisms will impair the ability of the kidney to eliminate excess bicarbonate, therefore promoting the generation or impairing the correction of metabolic alkalosis. These factors include volume contraction, low glomerular filtration rate, potassium deficiency, hypochloremia, aldosterone excess, and elevated arterial carbon dioxide. Major clinical states are associated with metabolic alkalosis, including vomiting, aldosterone or cortisol excess, licorice ingestion, chloruretic diuretics, excess calcium alkali ingestion, and genetic diseases such as Bartter syndrome, Gitelman syndrome, and cystic fibrosis. In this installment in the AJKD Core Curriculum in Nephrology, we will review the pathogenesis of metabolic alkalosis; appraise the precipitating events; and discuss clinical presentations, diagnoses, and treatments of metabolic alkalosis.
Topics: Aldosterone; Alkalies; Alkalosis; Bicarbonates; Calcium; Carbon Dioxide; Curriculum; Diuretics; Humans; Hydrocortisone
PubMed: 35525634
DOI: 10.1053/j.ajkd.2021.12.016 -
American Journal of Kidney Diseases :... Sep 2023The respiratory system plays an integral part in maintaining acid-base homeostasis. Normal ventilation participates in the maintenance of an open buffer system, allowing... (Review)
Review
The respiratory system plays an integral part in maintaining acid-base homeostasis. Normal ventilation participates in the maintenance of an open buffer system, allowing for excretion of CO produced from the interaction of nonvolatile acids and bicarbonate. Quantitatively of much greater importance is the excretion of CO derived from volatile acids produced from the complete oxidation of fat and carbohydrate. A primary increase in CO tension of body fluids is the cause of respiratory acidosis and develops most commonly from one or more of the following: (1) disorders affecting gas exchange across the pulmonary capillary, (2) disorders of the chest wall and the respiratory muscles, and/or (3) inhibition of the medullary respiratory center. Respiratory alkalosis or primary hypocapnia is most commonly caused by disorders that increase alveolar ventilation and is defined by an arterial partial pressure of CO <35 mm Hg with subsequent alkalization of body fluids. Both disorders can lead to life-threatening complications, making it of paramount importance for the clinician to have a thorough understanding of the cause and treatment of these acid-base disturbances.
Topics: Humans; Acidosis, Respiratory; Alkalosis, Respiratory; Carbon Dioxide; Hypocapnia; Bicarbonates; Alkalosis; Hydrogen-Ion Concentration; Acid-Base Equilibrium
PubMed: 37341662
DOI: 10.1053/j.ajkd.2023.02.004 -
Journal of the American Society of... Sep 1997In summary, the kidney possesses numerous mechanisms that help to prevent metabolic alkalosis. Maintenance of metabolic alkalosis for any length of time means that renal... (Review)
Review
In summary, the kidney possesses numerous mechanisms that help to prevent metabolic alkalosis. Maintenance of metabolic alkalosis for any length of time means that renal homeostatic mechanisms for HCO3- excretion have been disrupted. Understanding the mechanisms that may perturb the kidney's ability to correct alkalosis will lead to improved clinical approaches to differential diagnosis and treatment of the patient. Although metabolic alkalosis is frequently not dangerous, in certain settings metabolic alkalosis may contribute to mortality and should be treated aggressively.
Topics: Alkalosis; Humans; Kidney; Syndrome
PubMed: 9294840
DOI: 10.1681/ASN.V891462 -
Journal of Nephrology 2006Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney... (Review)
Review
Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney preserves normal acid-base balance by two mechanisms: bicarbonate reclamation mainly in the proximal tubule and bicarbonate generation predominantly in the distal nephron. Bicarbonate reclamation is mediated mainly by a Na-H antiporter and to a smaller extent by the H-ATPase. The principal factors affecting HCO 3 reabsorption include effective arterial blood volume, glomerular filtration rate, chloride, and potassium. Bicarbonate regeneration is primarily affected by distal Na delivery and reabsorption, aldosterone, arterial pH, and arterial pCO2. To generate metabolic alkalosis, either a gain of base or a loss of acid, must occur. The loss of acid may be via the GI tract or by the kidney. Excess base may be gained by oral or parenteral HCO 3 administration or by lactate, acetate, or citrate administration. Factors that help maintain metabolic alkalosis include decreased glomerular filtration rate (GFR), volume contraction, hypokalemia, hypochloremia, and aldosterone excess. Clinical states associated with metabolic alkalosis are vomiting, mineralocorticoid excess, the adrenogenital syndrome, licorice ingestion, diuretic administration, and Bartter's and Gitelma's Syndromes. The effects of metabolic alkalosis on the body are varied and include effects on the central nervous system, myocardium, skeletal muscle, and the liver. Treatment of this disorder is simple, once the pathophysiology of the cause is delineated. Therapy consists of reversing the contributory factors promoting alkalosis and in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis.
Topics: Acid-Base Equilibrium; Alkalosis; Bicarbonates; Glomerular Filtration Rate; Humans; Potassium; Prognosis
PubMed: 16736446
DOI: No ID Found -
Respiratory Care Apr 2001Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney... (Review)
Review
Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney preserves normal acid-base balance by two mechanisms: bicarbonate reclamation, mainly in the proximal tubule, and bicarbonate generation, predominantly in the distal nephron. Bicarbonate reclamation is mediated mainly by a Na(+)-H(+) antiporter and to a smaller extent by the H(+)-ATPase (adenosine triphosphate-ase). The principal factors affecting HCO3(-) reabsorption include effective arterial blood volume, glomerular filtration rate, chloride, and potassium. Bicarbonate regeneration is primarily affected by distal Na(+) delivery and reabsorption, aldosterone, arterial pH, and arterial partial pressure of carbon dioxide. To generate metabolic alkalosis, either a gain of base or a loss of acid must occur. The loss of acid may be via the gastrointestinal tract or via the kidney. Excess base may be gained by oral or parenteral HCO3(-) administration or by lactate, acetate, or citrate administration. Factors that help maintain metabolic alkalosis include decreased glomerular filtration rate, volume contraction, hypokalemia, hypochloremia, and aldosterone excess. Clinical states associated with metabolic alkalosis are vomiting, mineralocorticoid excess, the adrenogenital syndrome, licorice ingestion, diuretic administration, and Bartter's and Gitelman's syndromes. The effects of metabolic alkalosis on the body are variable and include effects on the central nervous system, myocardium, skeletal muscle, and liver. Treatment of this disorder is simple, once the pathophysiology of the cause is delineated. Therapy consists of reversing the contributory factors that are promoting the alkalosis and, in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis.
Topics: Alkalosis; Bicarbonates; Chlorides; Diuretics; Glomerular Filtration Rate; Humans; Hydrochloric Acid; Hydrogen-Ion Concentration; Hypertension; Kidney; Mineralocorticoids; Potassium; Protons; Quaternary Ammonium Compounds
PubMed: 11262555
DOI: No ID Found -
Journal of the American Society of... Feb 2000
Review
Topics: Alkalosis; Chlorides; Humans; Mineralocorticoids; Potassium Deficiency
PubMed: 10665945
DOI: 10.1681/ASN.V112369 -
Wiadomosci Lekarskie (Warsaw, Poland :... 2013An elevation of arterial blood pH called alkalosis remains an underestimated condition in hospitalized patients. Serious alkalosis can be associated with high risk of... (Review)
Review
An elevation of arterial blood pH called alkalosis remains an underestimated condition in hospitalized patients. Serious alkalosis can be associated with high risk of death. The disorder can be caused by increased concentration of bicarbonate (metabolic alkalosis) or decreased concentration of carbon dioxide (respiratory alkalosis). In most cases of metabolic alkalosis it is generated by vomiting or diuretic use, whereas respiratory alkalosis is provoked by hyperventilation associated with respiratory or neurological disorder. Maintenance of metabolic alkalosis is possible only in patients with impaired renal base excretion which is most often produced by hypochloremia. In both respiratory and metabolic alkaloses treatment depends on the underlying factor. In hyperventilation syndrome is based on behavioral therapy. In most cases of metabolic alkalosis the administration of sodium and potassium chloride forms a substantial part of therapy.
Topics: Alkalosis; Alkalosis, Respiratory; Bicarbonates; Carbon Dioxide; Diagnosis, Differential; Diuretics; Humans; Hyperventilation; Nervous System Diseases; Vomiting
PubMed: 24490489
DOI: No ID Found -
The Veterinary Clinics of North... Mar 2017Respiratory alkalosis, or primary hypocapnia, occurs when alveolar ventilation exceeds that required to eliminate the carbon dioxide produced by tissues. Concurrent... (Review)
Review
Respiratory alkalosis, or primary hypocapnia, occurs when alveolar ventilation exceeds that required to eliminate the carbon dioxide produced by tissues. Concurrent decreases in Paco, increases in pH, and compensatory decreases in blood HCO levels are associated with respiratory alkalosis. Respiratory alkalosis can be acute or chronic, with metabolic compensation initially consisting of cellular uptake of HCO and buffering by intracellular phosphates and proteins. Chronic respiratory alkalosis results in longer-lasting decreases in renal reabsorption of HCO; the arterial pH can approach near-normal values.
Topics: Acid-Base Equilibrium; Acid-Base Imbalance; Algorithms; Alkalosis, Respiratory; Animals
PubMed: 27939863
DOI: 10.1016/j.cvsm.2016.10.005 -
The Veterinary Clinics of North... Mar 2017Metabolic alkalemia is characterized by an increase in bicarbonate concentration and base excess, an increase in pH, and a compensatory increase in carbon dioxide... (Review)
Review
Metabolic alkalemia is characterized by an increase in bicarbonate concentration and base excess, an increase in pH, and a compensatory increase in carbon dioxide pressure. This article outlines indications for analysis, reference ranges, causes, and clinical signs of metabolic alkalosis. Algorithms for evaluation of patients with acid-base disorders and metabolic alkalosis are included.
Topics: Acid-Base Imbalance; Alkalosis; Animals; Bicarbonates; Cat Diseases; Cats; Dog Diseases; Dogs
PubMed: 27914757
DOI: 10.1016/j.cvsm.2016.10.007