The ventilatory volumes obtained for the six infants with LTB were normalized for body weight. The Ve increased from a minimum of 0.28 ± 0.06 L*min ~ ukg at a tcPco2 of 64 mm Hg to 0.63 ±0.09 L’min’Hcg at a tcPco2 of 28 mm Hg. The relationship of tcPco2 to Ve is shown in Figure 2 (lowest panel), and included in Table 1.
Further, the increase in Ve resulted principally through improvement in Vt which increased from 5.6 ± 0.6 mbkg with the most severe airflow obstruction (tcPco2 of 64 mm Hg) to 15.7 ±0.4 mbkg with clinical resolution when the tcPco2 was 28 mm Hg (Fig 2, center panel). Simultaneous with the increase in Vt, there was an initial increase in respiratory frequency from 50 breaths-min” at a tcPco2 of 64 mm Hg to a maximum of 69 breaths’min at 42 mm Hg, and then subsequently decreasing to 50 breaths*min“ at 28 mm Hg (Fig 2).
This fall in tcPco2 and increase in Ve was due, primarily, to the progressive recruitment of outward (positive) chest wall excursion during inspiration. The change in Irc increased from a negative impedance change of — 4 mV ± 3 mV to 75 mV ± 4 mV over the same range of tcPco2. The excursion of the abdominal compartment, measured as the Iabd, mimicked that of respiratory frequency. The Iabd fell from the initial value of 70 mV ± 7 mV at 64 mm Hg, to a nadir value of 43 mV ± 4 mV at 50 mm Hg, and then subsequently rose to the maximum of 82 mV ±6 mV at a tcPco2 of 28 mm Hg. The changes in tcPco2 with Vt and frequency were significant by a second-order polynomial regression (^ = 0.87, p<0.05, and r2 = 0.60, p<0.05, respectively) but correlated linearly with Ve (1^ = 0.932, p<0.005). As was expected, there was an inverse linear relationship between the tcPco2 and the rib cage inductance (r2 0.828, p<0.005), and directly with the phase angle (r2 0.842, p<0.005) as illustrated in Figure 3.