There is normally a compensatory response to a decrease in Ve by an increase in either respiratory frequency or an increase in abdominal volume displacement, as measured by the Iabd. An increase in respiratory rate did occur during mild and moderate distortion when the tcPco2 was less than 45 mm Hg. With severe CWD and a tcPco2 greater than 50 mm Hg, however, there was a decrease in respiratory frequency. Previous work has suggested that, as an adaptive response to severe inspiratory flow limitation (markedly decreased Vt/Ti), there will be a compensatory increase in inspiratory time (Ti), and thus decrease in frequency as an alternate strategy to achieve gas exchange. Concomitant with the fall in frequency, there was a small increase in the Iabd that partially compensated for the fall in Irc and the decrease in respiratory frequency. These mechanisms failed to adequately defend alveolar ventilation and the increase in tcPco2 occurred. With recovery, as the Ve increased, there was a concomitant increase in Irc.
The factors determining CWD in these infants were not specifically studied. We speculated that inspiratory CWD was the result of an imbalance in the opposing forces applied to the chest wall during inspiration. Normally, the chest wall is supported during inspiration by the bony structures and the intercostal muscle groups that act to both anchor and expand the chest wall in synchrony with the diaphragmatic contraction during inspiration. In the infant, the static chest wall compliance is greater than lung compliance, implying that support by contraction of intercostal muscle groups is necessary to augment the rigidity for the chest wall to function normally. Diaphragmatic contraction would tend to collapse the lower chest wall because the large horizontal vector from its insertion into the lower ribs must favor CWD. As well, the large swing in negative pleural pressure associated with partial upper airway obstruction must increase the transmural pressure to augment collapse of the chest wall. Finally, fatigue of the small intercostal muscles of the chest wall may occur, leading to failure to fixate or expand the chest wall during inspiration. Alteration of one or more of these determining factors would potentially result in the failure of the chest wall to withstand the inward forces during inspiration, and thus promote development of CWD.
In summary, this study shows that, during the recovery from severe LTB, chest wall movement shows a predictable progression in pattern of distortion, associated with a decreased Ve and alveolar hypoventilation. The normal compensatory mechanisms of increasing Vt and frequency do not suffice to defend Ve when there is severe distortion, resulting in an increase in tcPco2 secondary to alveolar hypoventilation. Furthermore, in this restricted group of patients, within a very narrow age range, the temporal relationship of the chest and abdominal wall results in a phase angle of motion, rapidly measured from the Lissajous figure, that is directly related to the Ve and the tcPco2. We therefore find that the repeated measurement of phase angle provides a simple and reliable technique of objectively assessing both severity and progression of LTB, and postulate that the phase angle can be used as a noninvasive means of following the severity of obstruction within the same patient.