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Post-Hypercapnic Alkalosis: A Brief Review
Metabolic alkalosis is a common acid-base imbalance frequently observed in intensive care unit (ICU) patients and is associated with increased mortality. Post-hypercarbia alkalosis (PHA) is a type of metabolic alkalosis caused by sustained high serum bicarbonate levels following a rapid resolution o...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Korean Society of Electrolyte Metabolism
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10329906/ https://www.ncbi.nlm.nih.gov/pubmed/37434801 http://dx.doi.org/10.5049/EBP.2023.21.1.18 |
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author | Yi, Yongjin |
author_facet | Yi, Yongjin |
author_sort | Yi, Yongjin |
collection | PubMed |
description | Metabolic alkalosis is a common acid-base imbalance frequently observed in intensive care unit (ICU) patients and is associated with increased mortality. Post-hypercarbia alkalosis (PHA) is a type of metabolic alkalosis caused by sustained high serum bicarbonate levels following a rapid resolution of hypoventilation in patients with chronic hypercapnia due to prolonged respiratory disturbance. Common causes of chronic hypercapnia include chronic obstructive pulmonary disease (COPD), central nervous system disorders, neuromuscular disorders, and narcotic abuse. Rapid correction of hypercapnia through hyperventilation leads to a swift normalization of pCO(2), which lacks renal compensation, consequently causing an increase in plasma HCO(3-) levels and severe metabolic alkalosis. Most of PHA occurs in the ICU setting requiring mechanical ventilation and can progress severe alkalemia due to secondary mineralocorticoid excess from volume depletion or decreased HCO(3-) excretion from decreased glomerular filtration rate and increased proximal tubular reabsorption. PHA is associated with increased ICU stay, ventilator dependency, and mortality. Acetazolamide, a carbonic anhydrase inhibitor, has been utilized for managing PHA by inducing alkaline diuresis and reducing tubular reabsorption of bicarbonate. While acetazolamide effectively improves alkalemia, its impact on hard outcomes may be limited by factors such as patient complexity, co-administered medications, and underlying conditions contributing to alkalosis. |
format | Online Article Text |
id | pubmed-10329906 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | The Korean Society of Electrolyte Metabolism |
record_format | MEDLINE/PubMed |
spelling | pubmed-103299062023-07-11 Post-Hypercapnic Alkalosis: A Brief Review Yi, Yongjin Electrolyte Blood Press Review Article Metabolic alkalosis is a common acid-base imbalance frequently observed in intensive care unit (ICU) patients and is associated with increased mortality. Post-hypercarbia alkalosis (PHA) is a type of metabolic alkalosis caused by sustained high serum bicarbonate levels following a rapid resolution of hypoventilation in patients with chronic hypercapnia due to prolonged respiratory disturbance. Common causes of chronic hypercapnia include chronic obstructive pulmonary disease (COPD), central nervous system disorders, neuromuscular disorders, and narcotic abuse. Rapid correction of hypercapnia through hyperventilation leads to a swift normalization of pCO(2), which lacks renal compensation, consequently causing an increase in plasma HCO(3-) levels and severe metabolic alkalosis. Most of PHA occurs in the ICU setting requiring mechanical ventilation and can progress severe alkalemia due to secondary mineralocorticoid excess from volume depletion or decreased HCO(3-) excretion from decreased glomerular filtration rate and increased proximal tubular reabsorption. PHA is associated with increased ICU stay, ventilator dependency, and mortality. Acetazolamide, a carbonic anhydrase inhibitor, has been utilized for managing PHA by inducing alkaline diuresis and reducing tubular reabsorption of bicarbonate. While acetazolamide effectively improves alkalemia, its impact on hard outcomes may be limited by factors such as patient complexity, co-administered medications, and underlying conditions contributing to alkalosis. The Korean Society of Electrolyte Metabolism 2023-06 2023-06-27 /pmc/articles/PMC10329906/ /pubmed/37434801 http://dx.doi.org/10.5049/EBP.2023.21.1.18 Text en Copyright © 2023 Korean Society for Electrolyte and Blood Pressure Research https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Yi, Yongjin Post-Hypercapnic Alkalosis: A Brief Review |
title | Post-Hypercapnic Alkalosis: A Brief Review |
title_full | Post-Hypercapnic Alkalosis: A Brief Review |
title_fullStr | Post-Hypercapnic Alkalosis: A Brief Review |
title_full_unstemmed | Post-Hypercapnic Alkalosis: A Brief Review |
title_short | Post-Hypercapnic Alkalosis: A Brief Review |
title_sort | post-hypercapnic alkalosis: a brief review |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10329906/ https://www.ncbi.nlm.nih.gov/pubmed/37434801 http://dx.doi.org/10.5049/EBP.2023.21.1.18 |
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