In acute respiratory failure interstitial oedema, alveolar collapse, and multiple atelectasis are the main mechanisms which lead to increased venous admixture and impaired oxygenation. Thus the lung volume available for pulmonary gas exchange is considerably reduced. Since there is strong evidence that alveolar overdistension causes lung damage ('barotrauma/volutrauma') large tidal volumes and high airway pressures in mechanical ventilation have to be strictly avoided, even allowing hypoventilation ('permissive hypercapnia'). Recruitment of the collapsed alveoli by external or intrinsic PEEP, or by changing body position, is often possible. However, alveolar recruitment takes much longer than previously assumed: instead of occurring within one respiratory cycle ('inflection point'), it seems to take hours. This slow recruitment process can be effectively supported by a deliberate use of intrinsic PEEP as with inverse ratio ventilation, either in volume or pressure controlled mode. Assisted spontaneous breathing makes ventilatory support less invasive and offers considerable advantages for many patients, but there are still some restrictions. Individual adaptation may be difficult in some patients. New principles of assistance control ('proportional assist ventilation') may improve individual adaptation. New concepts for weaning in COPD patients seem to offer better clinical strategies.