Acute and chronic influences of obstructive sleep apnoea on the pulmonary circulation

Obstructive sleep apnoea (OSA) produces immediate effects on pulmonary haemodynamics during sleep in all subjects. In addition, in some subjects, OSA is accompanied by chronic abnormalities of the pulmonary circulation. During sleep, pressure in the main pulmonary artery oscillates within each apnoea, in synchrony with intrathoracic pressure changes; in addition, it may increase progressively as a consequence of prolonged severe hypoxaemia. Pulmonary capillary wedge pressure may increase during inspiratory efforts, possibly reflecting a mechanical limitation of left ventricular function. Cardiac output decreases at apnoea resolution as an effect of a decreased right ventricular stroke volume, despite increased cardiac frequency. During wakefulness, postcapillary pulmonary hypertension occurs on exercise in many OSA patients, whilst pulmonary hypertension at rest is precapillary and occurs in patients with an altered daytime respiratory function. Development of right ventricular hypertrophy and a decrease in right ventricular ejection fraction appear to be related to the severity of respiratory alterations during sleep, whilst an overt right heart failure requires an altered daytime respiratory function. Long-term treatment of the obstructive sleep apnoea syndrome is more effective in increasing right ventricular ejection fraction than in decreasing pulmonary artery pressure during wakefulness.