In patients with obstructive sleep apnoea syndrome (OSAS), pulmonary haemodynamics can show both transient perturbations during sleep and permanent alterations. During sleep, repeated fluctuations in pulmonary artery pressure and pulmonary wedge pressure, coincident with apnoeas, can be observed. Calculation of transmural pressure values is preferable to intravascular pressures in OSAS, due to the marked swings in intrathoracic pressure associated with obstructive apnoeas. Pulmonary artery pressure may progressively increase during sleep, particularly in close sequences of highly desaturating apnoeas. Apnoea-induced hypoxia appears as the most important determinant of this pulmonary artery pressure behaviour. Stroke volume and cardiac output during obstructive apnoeas show changes mainly related to intrathoracic pressure variations. Permanent precapillary pulmonary hypertension at rest is observed in <50% OSAS patients, and is poorly reversible after OSAS treatment. It correlates best with diurnal respiratory function parameters. However, the finding of pulmonary hypertension in some patients with near normal diurnal lung function led to suggest that sleep respiratory disorders may contribute to permanent pulmonary haemodynamic impairment in predisposed subjects. Knowledge on right ventricle hypertrophy in OSAS is inconsistent. As to right ventricle failure, it is clinically evident in subjects with associated lung disease or morbid obesity, while it may be detected instrumentally in subjects without such alterations, presumably as effect of apnoeas themselves. Besides, it appears more fully reversible after long-term OSAS treatment than pulmonary hypertension.