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Closing volume 1967-2007 : implicazioni cliniche della ciclica apertura-chiusura delle vie aeree
Pathophysiology of chronic obstructive pulmonary disease
In normal animals, cyclic airway closure and reopening during prolonged mechanical ventilation at low lung volumes causes histological damage of small airways, characterized by epithelial sloughing and lesion and/or rupture of alveolar-bronchiolar attachments, with a concurrent increase in airway resistance that persists after restoration of physiological end-expiratory lung volume. Peripheral airway injury should be therefore expected to occur when the closing capacity exceeds the functional residual capacity and tidal airway closure is regularly present during spontaneous breathing. On these basis, it is proposed that in smokers the transition from peripheral airway disease to chronic obstructive pulmonary disease is characterized by three sequential stages: Stage I, during which the closing capacity eventually exceeds the functional residual capacity, i.e. airway closure and reopening occur cyclically with breathing; Stage II, during which tidal expiratory flow limitation is eventually exhibited; and Stage III, during which dynamic hyperinflation progressively increases leading to dyspnea and exercise limitation. In this perspective, it is tidal airway closure and, probably, tidal expiratory flow limitation that promote peripheral airway injury, accelerate the abnormalities of lung function, and may determine which smoker is destined to develop chronic obstructive pulmonary disease
Interrupter technique for measurement of respiratory mechanics in anesthetized humans
Flow (V), volume (V), and tracheal pressure (Ptr) were measured throughout a series of brief (100 ms) interruptions of expiratory V in six patients during anesthesia (halothane-N2O) and anesthesia-paralysis (succinylcholine). For the latter part of spontaneous expiration and throughout passive deflation during muscle paralysis, a plateau in postinterruption Ptr was observed, indicating respiratory muscle relaxation. Under these conditions, passive elastance of the total respiratory system (Ers) was determined as the plateau in postinterruption Ptr divided by the corresponding V. The pressure-flow relationship of the total system was determined by plotting the plateau in Ptr during interruption against the immediately preceding V. Ers averaged 23.5 +/- 1.9 (SD) cmH2O X l-1 during anesthesia and 25.5 +/- 5.4 cmH2O X l-1 during anesthesia-paralysis. Corresponding values of total respiratory system resistance were 2.0 +/- 0.8 and 1.9 +/- 0.6 cmH2O X l-1 X s, respectively. Respiratory mechanics determined during anesthesia paralysis using the single-breath method (W.A. Zin, L. D. Pengelly, and J. Milic-Emili, J. Appl. Physiol. 52: 1266-1271, 1982) were also similar. Early in spontaneous expiration, however, Ptr increased progressively during the period of interruption, reflecting the presence of gradually decreasing antagonistic (postinspiratory) pressure of the inspiratory muscles. In conclusion, the interrupter technique allows for simultaneous determination of the passive elastic as well as flow-resistive properties of the total respiratory system. The presence of a plateau in postinterruption Ptr may be employed as a useful and simple criterion to confirm the presence of respiratory muscle relaxation
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