The lungs are “downstream” from the liver. The effects of venous blood (flow and constituents) arising in the liver and portal system and which subsequently traverses the pulmonary arterial and capillary system, seem to be quite subtle in the “normal” situation. Dysfunction of either the lungs or liver may dramatically alter this steady state condition and affect the other organ. For example, severe arterial pathology originating within the lungs, as seen in primary pulmonary hypertension, can have a profound “backflow” vascular impact on the normal liver, with resultant hepatic congestion and ascites. Alternatively, liver disorders causing portal hypertension (cirrhotic or non-cirrhotic) may result in a high flow, hyperdynamic circulatory state and an imbalance between vasoconstrictors, vasodilators, and other mediators metabolised or synthesised by the liver. The pulmonary consequences of hepatic dysfunction may have dramatic clinical relevance and have been considered hepatopulmonary syndromes. Such pathophysiologies of recent interest are the focus of this article (table1).