The hepatopulmonary syndrome results from the formation of microscopic intrapulmonary arteriovenous dilatations in patients with both chronic, and far less commonly acute liver failure.

[1] The dilation of these blood vessels causes overperfusion relative to ventilation, leading to ventilation-perfusion mismatch and hypoxemia.

[2] Additionally, late in cirrhosis, it is common to develop high output failure, which would lead to less time in capillaries per red blood cell, exacerbating the hypoxemia.

[citation needed] The hepatopulmonary syndrome is suspected in any patient with known liver disease who reports dyspnea (particularly platypnea).

[citation needed] Hepatopulmonary syndrome (HPS) consists of the triad of liver dysfunction, otherwise unexplained hypoxemia, and intrapulmonary vascular dilation (IPVD).