**2. Physiologic mechanism of NPPV effect in patients with COPD**

Severe COPD places the respiratory muscles at a mechanical disadvantage (Rochester, Braun, & Arora 1979). During COPD exacerbation, this situation becomes catastrophic. Exacerbations of COPD increase the respiratory load in these patients, exceeding their ability to adequately ventilate through a variety of mechanisms, including increasing hyperinflation with decreased diaphragmatic excursion and strength, increasing intrinsic positive end-expiratory pressure (PEEP), changes in respiratory patterns and increased respiratory frequency leading to ineffective or inadequate tidal volume generation. NPPV effectively unloads the respiratory muscles by increasing tidal volume, decreasing the respiratory rate, and decreasing the diaphragmatic work of breathing, which translates into an improvement in oxygenation, a reduction in hypercapnia, and an improvement in dyspnea. NPPV treatment counterbalances auto-PEEP, assists inspiration, reduces transdiaphragmatic pressure, lowers respiratory rate, rests the accessory muscles, increases functional residual capacity, decreases respiratory load and work of breathing and leads to favorable changes in the ventilation/perfusion ratio as well as the respiratory center and the sensivity of chemoreceptors (Mansfield & Naughton 1999; de Miguel et al. 2002). Expiration positive airway pressure (EPAP) counterbalances intrinsic PEEP. Inspiration positive airway pressure (IPAP) is capable of increasing tidal volume and subsequently decreasing the elevated levels of PC02.
