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Dyspnea (respiratory difficulty) and activity limitation are the primary symptoms of chronic obstructive pulmonary disease (COPD) and progress relentlessly as the disease advances, contributing to reduced quality of life. In COPD, the mechanisms of dyspnea are multifactorial, but abnormal dynamic ventilatory mechanics are believed to play a central role. In flow-limited patients with COPD, dynamic lung hyperinflation (DH) occurs during exercise and has serious sensory and mechanical consequences. In several studies, indices of DH strongly correlate with ratings of dyspnea intensity during exercise, and strategies that reduce resting hyperinflation (either pharmacological or surgical) consistently result in reduced exertional dyspnea. The mechanisms by which DH gives rise to exertional dyspnea and exercise intolerance are complex, but recent mechanistic studies suggest that DH-induced inspiratory muscle loading, restriction of tidal volume expansion during exercise, and consequent neuromechanical uncoupling of the respiratory system are key components. This review examines the specific derangements of ventilatory mechanics that occur in COPD during exercise and attempts to provide a mechanistic rationale for the attendant respiratory discomfort and activity limitation.

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QOL in survivors of ARDS appears to be influenced by the mechanism of lung injury (primary vs. secondary), lending support to the concept that ARDS is a heterogeneous condition.