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1. Tidal pressure/volume and flow/volume respiratory loops were constructed from records obtained during 98 studies on 48 neonates of various ages and gestations. Records were obtained with a total body plethysmograph and an oesophageal balloon. Total pulmonary resistance was computed at five separate levels in the breathing cycle and results were expressed graphically as tidal resistance profiles by plotting total pulmonary resistance against percentage tidal volume above functional residual capacity. 2. Values obtained for standard pulmonary mechanical measurements and thoracic gas volume were similar to those of other workers. In addition six distinctive resistance profile patterns were found and related to different breathing patterns. 3. The technique appeared to be particularly useful in identifying air trapping and also demonstrated that total pulmonary resistance is open to misinterpretation when measured only at the mid-tidal-volume level, as is the present convention.

Simple clinical measurements were performed on a group of 23 very low birth weight babies (< 1500 g and < 32 weeks gestation), and combined with pulmonary function studies in 13 cases. The studies included a special single-breath analysis, or Tidal Resistance Profile, which enabled us to detect air trapping. 2 infants developed classical Wilson-Mikity syndrome and 2 further infants exhibited a milder, shorter form of the same disorder. All 4 survived. Results suggest that all infants in this maturity group are at risk of developing Wilson-Mikity syndrome, and that it comprises a wide spectrum of respiratory dysfunction.

Lung function tests were carried out in the first 6 hours of life on 26 babies born by vaginal delivery and 10 born by caesarean section. The babies born by caesarean section had a mean thoracic gas volume of only 19.7 ml/kg body weight compared with 32.7 ml/kg for the babies born vaginally. We conclude that this is owing to an excess of lung fluid in the babies born by caesarean section.

Measurements of tidal flow, volume, and oesophageal pressure were recorded on a group of 8 severely preterm infants with periodic respiration. Analysis of the flow trace for evidence of cardiac artefact, and the tidal volume trace to identify at what point of the tidal cycle apnoea starts, indicated that upper airways obstruction was associated with about half these attacks. It is surmised that this is produced by glottic closure.

Within the first 6 hours of life a consistent difference can be demonstrated between the TGV measured plethysmographically and the FRC measured using a helium dilution technique. This difference persists despite oxygen administration which has little or no effect on the lung volumes in this group of babies.

Pulmonary mechanics were measured in 22 normal, full-term babies as soon as quiet, regular breathing was established. The method included construction of tidal resistance profiles, by which it was demonstrated that ‘air trapping’ is probably not the major factor in establishing and maintaining the functional residual capacity immediately after birth.

Serial measurements of thoracic gas volume revealed no evidence of air trapping in maintenance of functional residual capacity (FRC) in healthy term babies in the first days of life. Tidal pressure/volume and flow/volume analysis demonstrated intermittent air trapping in only 2 of 19 such babies. Artificial FRC reduction by continuous positive external pressure of 7 cm H 2 O induced grunting in 4 babies, but otherwise had no effect on spontaneous breathing pattern or on dynamic compliance. Group mean total pulmonary resistance rose by 52.9% but only one baby demonstrated evidence of air trapping. Our findings suggest that FRC is maintained in the immediate neonatal period by some means other than air trapping.

We have studied the effect of continuous positive airways pressure (CPAP) on the lung mechanics and thoracic gas volumes on 15 occasions in 12 healthy neonates. As expected, the thoracic gas volume rose and total pulmonary resistance fell. The dynamic compliance fell on all occasions. 43% of the applied pressure was transmitted through to the mediastinal structures.

Total obstruction of the airways caused all respiratory efforts to stop on 15 occasions in 10 preterm babies. This was not seen in 60 studies on 38 term babies. These findings suggest that failure to achieve an oral airway may not be the only mechanism by which upper airway obstruction might cause the cot death syndrome.