Alongside the kidneys and lungs, the liver has been recognised as an important regulator of
acid-base homeostasis. While
respiratory alkalosis is the most common
acid-base disorder in chronic
liver disease, various complex metabolic
acid-base disorders may occur with
liver dysfunction. While the standard variables of acid-base equilibrium, such as pH and overall base excess, often fail to unmask the underlying cause of
acid-base disorders, the physical-chemical
acid-base model provides a more in-depth pathophysiological assessment for clinical judgement of
acid-base disorders, in patients with
liver diseases. Patients with stable chronic
liver disease have several offsetting acidifying and alkalinising metabolic
acid-base disorders. Hypoalbuminaemic
alkalosis is counteracted by hyperchloraemic and dilutional
acidosis, resulting in a normal overall base excess. When patients with
liver cirrhosis become
critically ill (e.g., because of
sepsis or
bleeding), this fragile equilibrium often tilts towards
metabolic acidosis, which is attributed to
lactic acidosis and
acidosis due to a rise in unmeasured
anions. Interestingly, even though patients with
acute liver failure show significantly elevated
lactate levels, often, no overt
acid-base disorder can be found because of the offsetting hypoalbuminaemic
alkalosis. In conclusion, patients with
liver diseases may have multiple co-existing metabolic
acid-base abnormalities. Thus, knowledge of the pathophysiological and diagnostic concepts of
acid-base disturbances in patients with
liver disease is critical for therapeutic decision making.