• acidosis;
  • albumin;
  • alkalosis;
  • chloride;
  • complications of cirrhosis


Background and Aims: Conflicting results exist with regard to metabolic acid–base status in liver cirrhosis, when the classic concept of acid–base analysis is applied. The influence of the common disturbances of water, electrolytes and albumin on acid–base status in cirrhosis has not been studied. The aim of this study was to clarify acid–base status in cirrhotic patients by analyzing all parameters with possible impact on acid–base equilibrium.

Patients and Methods: Fifty stable cirrhotic patients admitted to a university hospital. Arterial acid–base status was analyzed using the principles of physical chemistry and compared with 10 healthy controls.

Results: Apart from mild hypoalbuminemic alkalosis, acid–base state was normal in Child–Pugh A cirrhosis. Respiratory alkalosis was the net acid–base disorder in Child–Pugh B and C cirrhosis with a normal overall metabolic acid–base state (Base excess−1.0 (−3.6 to 1.6) vs 1.1 (−0.2 to 1.1) mmol/l, P=0.136, compared with healthy controls, median (interquartile range)). Absence of an apparent metabolic acid–base disorder was based on an equilibrium of hypoalbuminemic alkalosis and of dilutional acidosis and hyperchloremic acidosis.

Conclusion: A balance of offsetting acidifying and alkalinizing metabolic acid–base disorders leaves the net metabolic acid–base status unchanged in cirrhosis.