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Methods for Assessing Expiratory Flow Limitation during Tidal Breathing in COPD Patients

DOI: 10.1155/2012/234145

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Abstract:

Patients with severe COPD often exhale along the same flow-volume curve during quite breathing as during forced expiratory vital capacity manoeuvre, and this has been taken as indicating expiratory flow limitation at rest ( E F L T ). Therefore, E F L T , namely, attainment of maximal expiratory flow during tidal expiration, occurs when an increase in transpulmonary pressure causes no increase in expiratory flow. E F L T leads to small airway injury and promotes dynamic pulmonary hyperinflation with concurrent dyspnoea and exercise limitation. In fact, E F L T occurs commonly in COPD patients (mainly in GOLD III and IV stage) in whom the latter symptoms are common. The existing up-to-date physiological methods for assessing expiratory flow limitation ( E F L T ) are reviewed in the present work. Among the currently available techniques, the negative expiratory pressure (NEP) has been validated in a wide variety of settings and disorders. Consequently, it should be regarded as a simple, non invasive, most practical, and accurate new technique. 1. Introduction Some experts use the term chronic airflow limitation as a synonym for chronic obstructive pulmonary disease (COPD) to indicate the reduction in maximum expiratory flow that occurs in this disease (and indeed in other pulmonary diseases). Patients with severe COPD often exhale along the same flow-volume curve during quite breathing as during forced expiratory vital capacity manoeuvre, and this has been taken as indicating flow limitation at rest ( E F L T ). Consequently, the term tidal expiratory flow limitation ( E F L T ) is used to indicate that maximal expiratory flow is achieved during tidal breathing at rest or during exercise. This is characteristic of intrathoracic flow obstruction. The former term does not imply that E F L T actually occurs during tidal breathing [1]. The location of expiratory flow limitation is considered to be in the central airways (4th–7th generation) and move to the periphery during forced expiratory manoeuvres. It is located beyond the 7th (i.e., from the 8th onwards) generation during tidal breathing [2–4]. Tidal expiratory flow limitation ( E F L T ) [5–8] plays a central role according to a recent hypothesis [5] on the transition from small airways disease (SAD) to overt COPD in smokers. E F L T implies inhomogeneity of ventilation distribution with concurrent impairment of gas exchange and unevenly distributed stress and strain within the lung, which is amplified by tissue interdependence [6, 7] and may lead to small airway injury [5–8]. Initially, the latter is

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