Pathophysiology
Clinical meaning
Successful ventilator weaning requires adequate respiratory muscle strength, gas exchange capability, and absence of factors that increase ventilatory demand. The diaphragm, the primary muscle of inspiration, generates 60-80% of tidal volume. Mechanical ventilation causes ventilator-induced diaphragmatic dysfunction (VIDD) through diaphragmatic disuse atrophy, occurring within 18-69 hours of controlled mechanical ventilation through proteolytic pathways (calpain and caspase-3 activation). Critical illness polyneuromyopathy further impairs respiratory muscle function. The rapid shallow breathing index (RSBI = respiratory rate / tidal volume in liters) is the most validated weaning predictor: RSBI <105 predicts successful weaning with 97% sensitivity. Spontaneous breathing trials (SBT) assess the patient's ability to breathe independently using either T-piece (complete ventilator disconnection), CPAP (5 cmH2O), or pressure support (5-8 cmH2O) for 30-120 minutes. Weaning failure occurs in 20-30% of patients, most commonly from cardiac dysfunction (increased preload from negative intrathoracic pressure), respiratory muscle weakness, or excessive respiratory load.