Weaning covers the entire process of liberating the patient from mechanical support and from the endotracheal tube. Many controversial questions remain concerning the best methods for conducting this process. An International Consensus Conference was held in April 2005 to provide recommendations regarding the management of this process. An 11-member international jury answered five pre-defined questions. 1) What is known about the epidemiology of weaning problems? 2) What is the pathophysiology of weaning failure? 3) What is the usual process of initial weaning from the ventilator? 4) Is there a role for different ventilator modes in more difficult weaning? 5) How should patients with prolonged weaning failure be managed?The main recommendations were as follows. 1) Patients should be categorised into three groups based on the difficulty and duration of the weaning process. 2) Weaning should be considered as early as possible. 3) A spontaneous breathing trial is the major diagnostic test to determine whether patients can be successfully extubated. 4) The initial trial should last 30 min and consist of either T-tube breathing or low levels of pressure support. 5) Pressure support or assist–control ventilation modes should be favoured in patients failing an initial trial/trials. 6) Noninvasive ventilation techniques should be considered in selected patients to shorten the duration of intubation but should not be routinely used as a tool for extubation failure.

Continuous positive airway pressure therapy significantly improves subjective and objective measures of sleepiness in patients with OSA across a diverse range of populations. Patients with more severe apnea and sleepiness seem to benefit the most.

Previous studies have demonstrated that lung volume during wakefulness influences upper airway size and resistance, particularly in patients with sleep apnea. We sought to determine the influence of lung volume on the level of continuous positive airway pressure (CPAP) required to prevent flow limitation during non-REM sleep in subjects with sleep apnea. Seventeen subjects (apnea-hypopnea index, 42.6 Ϯ 6.2 [SEM]) were studied during stable non-REM sleep in a rigid head-out shell equipped with a positive/negative pressure attachment for manipulation of extrathoracic pressure. An epiglottic pressure catheter plus a mask/pneumotachometer were used to assess flow limitation. When lung volume was increased by 1,035 Ϯ 22 ml, the CPAP level could be decreased from 11.9 Ϯ 0.7 to 4.8 Ϯ 0.7 cm H 2 O (p Ͻ 0.001) without flow limitation. The decreased CPAP at the same negative extrathoracic pressure yielded a final lung volume increase of 421 Ϯ 36 ml above the initial value. Conversely, when lung volume was reduced by 732 Ϯ 74 ml (n ϭ 8), the CPAP level had to be increased from 11.9 Ϯ 0.7 to 17.1 Ϯ 1. Obstructive sleep apnea (OSA) syndrome is a common disorder that occurs in approximately 4% of middle-aged men and 2% of women (1). OSA is characterized by repetitive pharyngeal collapse during sleep, leading to sleep disruption, arousals, and arterial oxygen desaturation. However, the mechanisms leading to pharyngeal collapse are not completely understood. Previous investigators have suggested that this airway collapse involves a combination of anatomic narrowing of the upper airway by pharyngeal structures and sleep-induced decrements in pharyngeal dilator muscle activity (2-5).During sleep, in normal subjects, upper airway resistance increases and functional residual capacity (FRC) decreases (6-8). These sleep-induced decrements in lung volume are believed to increase upper airway collapsibility and contribute to inspiratory flow limitation, although the exact mechanisms are not entirely clear. Animal data, using mongrel dogs, have suggested that thoracic inflation increases upper airway pharyngeal size and

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