Acid-base abnormalities and liver dysfunction

In addition to the kidneys and lungs, the liver also plays an important role in the regulation of the Acid-Base Equilibrium (ABE). The involvement of the liver in the regulation of ABE is crucial because of its role in lactic acid metabolism, urea production and in protein homeostasis. The main acid-base imbalance that occurs in patients with liver cirrhosis is Respiratory Alkalosis (RAlk). Due to the fact that in these patients additional pathophysiological mechanisms that affect the ABE are present, other disorders may appear which compensate or enhance the primary disorder. Conventional ABE reading models fail to identify and assess the underlying disorders in patients with liver cirrhosis. This weakness of the classical models led to the creation of new physicochemical mathematical models that take into account all the known parameters that develop and affect the ABE. In addition to the RAlk, in patients with liver cirrhosis, metabolic alkalosis (due to hypoalbuminemia), hyponatremic metabolic acidosis, hyperchloremic metabolic acidosis, lactic acidosis and metabolic alkalosis due to urea metabolism are some of the pathophysiological mechanisms that affect the ABE. (c) 2022 Fundacion Clinica Medica Sur, A.C. Published by Elsevier Espana, S.L.U. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Automated summary

In addition to the kidneys and lungs, the liver also plays a crucial role in regulating Acid-Base Equilibrium (ABE). Patients with liver cirrhosis may experience various acid-base imbalances, including Respiratory Alkalosis (RAlk) and other pathophysiological mechanisms such as metabolic alkalosis, hyponatremic metabolic acidosis, hyperchloremic metabolic acidosis, lactic acidosis, and metabolic alkalosis due to urea metabolism. Traditional ABE reading models fail to identify and assess these underlying disorders, leading to the development of new physicochemical mathematical models.