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ACUTE RESPIRATORY FAILURE  SMART 2001 Freefree

Minerva Anestesiologica 2001 April;67(4):198-95

Copyright © 2009 EDIZIONI MINERVA MEDICA

language: Italian

Pathophysiology of the reduction of the expiratory flow in COPD and asthma

Mergoni M., Rossi A.

Azienda Ospedaliera di Parma I Servizio di Anestesia e Rianimazione *Azienda Ospedaliera di Bergamo Unità Operativa di Pneumologia


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Asthma and chronic obstructive pulmonary diseases (COPD) lead to functional obstruction of airways, identified by increased inspiratory and expiratory resistences. Increased expiratory resistences cause, in turn, a reduction in expiratory flow. The analysis of flow-volume loops shows that, as the disease progresses, the flow generated during expiration of a tidal volume becomes very close to the flow generated during forced maximal expiration. In such condition, where there is little or no reserve of expiratory flow, higher tidal volumes need to be reached in order to increase the expiratory flow, and hyperinflation inevitably occurs. Hyperinflation, a key feature in COPD pathophysiology, is generated by two mechanisms: reduction of elastic recoil of the lung (static hyperinflation) and interruption of expiration at lung volumes still higher than FRC, due to reduction of expiratory flow (dynamic hyperinflation). When dynamic hyperinflation occurs, a residual positive pressure remains in the alveoli, which is defined as intrinsic positive end-expiratory pressure (PEEPi). Hyperinflation carries several consequences: 1) Respiratory mechanics: at lung volumes close to total lung capacity, lung compliance is physiologically reduced, and elastic work required to generate the same inspiratory volume is therefore increased; 2) Respiratory muscles: contractile properties of diaphragm deteriorate when the dome is pushed downward by an increased lung volume, inspiration is mainly performed by inspiratory muscles, and expiration becomes active; 3) Circulation: pulmonary vascular resistences increase due to compression exerted by hyperinflation on alveolar vessels and to hypoxic vasoconstriction; right ventricle afterload increases and right sided hypertrophy and dilation ensue; left ventricular afterload may increase due to increased negative intrapleural pressure which translates into an increased transmural pressure which needs to be overcome by ventricular contraction. Ventilatory support of COPD patients should decrease work of breathing and improve gas exchange without increasing hyperinflation. This target can be achieved during assisted ventilation by applying a positive pressure both during inspiration and expiration; the level of PEEP should equal PEEPi. During mechanical ventilation in sedated paralyzed patients hyperinflation should be limited by decreasing minute volume and by increasing expiratory time, eventually chosing controlled hypercapnia.

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