Pulmonary arterial hypertension (PAH) is characterised by increased pulmonary vascular resistance and results in increased morbidity and mortality due to right heart failure and a progressive decline in cardiac output [1, 2]. The latter disturbs oxygen delivery to the periphery and may lead to pathological changes in tissue oxygenation. The balance between global oxygen supply and demand is reflected in mixed venous oxygen saturation (SvO2), an index that is generally reduced in patients with PAH . SvO2 at baseline is one of the strongest predictors of survival in PAH [4–6]; this is also true for changes in SvO2 during follow-up . Cut-off values of 60%  and 65%  have been used to distinguish between prognostic groups suggesting that these may be suitable treatment goals. SvO2 is measured invasively in the pulmonary artery, where venous blood mixes after circulating through the superior and inferior vena cava, coronary sinuses and the right-heart chambers.