{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T17:28:09Z","timestamp":1787160489001,"version":"build-2736575974"},"reference-count":55,"publisher":"Georg Thieme Verlag KG","issue":"05","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Semin Respir Crit Care Med"],"published-print":{"date-parts":[[2023,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Disorders of acid-base status are common in the critically ill and prompt recognition is central to clinical decision making. The bicarbonate\/carbon dioxide buffer system plays a pivotal role in maintaining acid-base homeostasis, and measurements of pH, PCO2, and HCO3\n          - are routinely used in the estimation of metabolic and respiratory disturbance severity. Hypoventilation and hyperventilation cause primary respiratory acidosis and primary respiratory alkalosis, respectively. Metabolic acidosis and metabolic alkalosis have numerous origins, that include alterations in acid or base intake, body fluid losses, abnormalities of intermediary metabolism, and renal, hepatic, and gastrointestinal dysfunction. The concept of the anion gap is used to categorize metabolic acidoses, and urine chloride excretion helps define metabolic alkaloses. Both the lungs and kidneys employ compensatory mechanisms to minimize changes in pH caused by various physiologic and disease disturbances. Treatment of acid-base disorders should focus primarily on correcting the underlying cause and the hemodynamic and electrolyte derangements that ensue. Specific therapies under certain conditions include renal replacement therapy, mechanical ventilation, respiratory stimulants or depressants, and inhibition of specific enzymes in intermediary metabolism disorders.<\/jats:p>","DOI":"10.1055\/s-0043-1770341","type":"journal-article","created":{"date-parts":[[2023,6,27]],"date-time":"2023-06-27T18:39:58Z","timestamp":1687891198000},"page":"612-626","source":"Crossref","is-referenced-by-count":8,"title":["Arterial Blood Gases and Acid\u2013Base Regulation"],"prefix":"10.1055","volume":"44","author":[{"given":"Sarah F.","family":"Sanghavi","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Washington, Puget Sound Veterans Affairs Healthcare System, Seattle, Washington"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik R.","family":"Swenson","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, University of Washington, Puget Sound Veterans Affairs Healthcare System, Seattle, Washington"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"194","published-online":{"date-parts":[[2023,6,27]]},"reference":[{"issue":"04","key":"ref1","doi-asserted-by":"crossref","first-page":"595","DOI":"10.1152\/physrev.1967.47.4.595","article-title":"Carbonic anhydrase: chemistry, physiology, and inhibition","volume":"47","author":"T H Maren","year":"1967","journal-title":"Physiol Rev"},{"key":"ref2","doi-asserted-by":"crossref","first-page":"427","DOI":"10.1126\/science.413195","article-title":"Acceleration of plasma bicarbonate conversion to carbon dioxide by pulmonary carbonic anhydrase","volume":"199","author":"R M Effros","year":"1978","journal-title":"Science"},{"issue":"01","key":"ref3","doi-asserted-by":"crossref","first-page":"50","DOI":"10.1038\/nrm2820","article-title":"Sensors and regulators of intracellular pH","volume":"11","author":"J R Casey","year":"2010","journal-title":"Nat Rev Mol Cell Biol"},{"issue":"01","key":"ref4","doi-asserted-by":"crossref","first-page":"119","DOI":"10.4187\/respcare.04556","article-title":"Circumstances when arterial blood gas analysis can lead us astray","volume":"61","author":"T J Albert","year":"2016","journal-title":"Respir Care"},{"issue":"20","key":"ref5","doi-asserted-by":"crossref","first-page":"1312","DOI":"10.1056\/NEJM198905183202004","article-title":"Assessing acid-base status in circulatory failure. 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