Measurement of closing volume (CV) allows detection of presence or absence of tidal airway closure, i.e. cyclic opening and closure of peripheral airways with concurrent (1) inhomogeneity of distribution of ventilation and impaired gas exchange; and (2) risk of peripheral airway injury. Tidal airway closure, which can occur when the CV exceeds the end-expiratory lung volume (EELV), is commonly observed in diseases characterised by increased CV (e.g. chronic obstructive pulmonary disease, asthma) and/or decreased EELV (e.g. obesity, chronic heart failure). Risk of tidal airway closure is enhanced by ageing. In patients with tidal airway closure (CV > EELV) there is not only impairment of pulmonary gas exchange, but also peripheral airway disease due to injury of the peripheral airways. In view of this, the causes and consequences of tidal airway closure are reviewed, and further studies are suggested. In addition, assessment of the "open volume", as opposed to the "closing volume", is proposed because it is easier to perform and it requires less equipment.

Pulmonary function tests were performed on 62 transfusion-dependent patients with thalassemia major, ranging in age from 8 to 33 years, and receiving chelation therapy with desferrioxamine or deferiprone. Percent predicted values for FVC, FEV1, and PEF were significantly reduced, whereas FEV1/FVC and maximal expiratory flow at 25% FVC were within normal limits, indicating a restrictive disease. Both FVC and FEV1 were negatively correlated with transfusional iron burden as indexed by age. Single-breath carbon monoxide transfer factor was reduced, even after correction for low hemoglobin concentration, and was negatively correlated with iron burden and iron overload, as indexed by serum ferritin levels. Owing to low hemoglobin concentration, blood-diffusing capacity was reduced, in spite of increased lung capillary blood volume, which was, however, adequate to normalize blood diffusing capacity when hemoglobin concentration was only partially restored by transfusion. The diffusing capacity of the alveolar-capillary membrane was substantially decreased and negatively correlated with age and serum ferritin, the fall being primarily attributed to increased membrane thickness. These findings suggest that lung fibrosis and/or interstitial edema related to iron overload are the main cause of pulmonary dysfunction observed in patients with thalassemia major.

The effects of inspiratory flow rate and inflation volume on the resistive properties of the total respiratory system were investigated in 16 anesthetized paralyzed humans by using the technique of rapid airway occlusion during constant flow inflation. This allowed measurement of the intrinsic resistance (Rmin,rs) and of the effective additional resistance (delta Rrs) as the result of viscoelastic pressure dissipations within the pulmonary and chest wall tissues. We observed that 1) at fixed inflation volume, Rmin,rs increased linearly with increasing flow although delta Rrs decreased according to an exponential function; 2) at fixed inflation flow, Rmin,rs decreased with increasing inflation volume although there was a concomitant increase in delta Rrs. This behavior could be explained in terms of a spring-and-dashpot model incorporating 1) the standard resistance and elastance and 2) a spring-and-dashpot in parallel with standard elastance, reflecting the stress adaptation units within the thoracic tissues.

Pulmonary and chest wall mechanics were studied in 18 anesthetized paralyzed supine humans by use of the technique of rapid airway occlusion during constant-flow inflation. Analysis of the changes in transpulmonary pressure after flow interruption allowed partitioning of the overall resistance of the lung (RL) into two compartments, one (Rint,L) reflecting airway resistance and the other (delta RL) representing the viscoelastic properties of the pulmonary tissues. Similar analysis of the changes in esophageal pressure indicates that chest wall resistance (RW) was due entirely to the viscoelastic properties of the chest wall tissues (delta RW = RW). In line with previous measurements of airway resistance, Rint,L increased with increasing flow and decreased with increasing volume. The opposite was true for both delta RL and delta RW. This behavior was interpreted in terms of a viscoelastic model that allowed computation of the viscoelastic constants of the lung and chest wall. This model also accounts for frequency, volume, and flow dependence of elastance of the lung and chest wall. Static and dynamic elastances, as well as delta R, were higher for the lung than for the chest wall.

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