Matching the two groups for a given level of PetCQ2 (65 mm Hg) (Table 5) showed in patients a greater absolute value of both P01 (p<0.Ql) and diaphragmatic XP/Ti (p<0.01). The Vt (p<0.05) and Ti (p<0.01) were lower in patients, while Vr/Ti (p<0.05) and f (p<0.01) were greater than in the normal control group; in contrast, Ve and Tj/Ttot were similar in the two groups. To assess neuromuscular inspiratory coupling, both in individual normal subjects and in patients (Fig 2), the P01 response slope was plotted against EMGd response slope to PetC02. In the normal subjects but not in patients, this relationship was significant (Y = 0.065+ 0.25 PetC02, r = 0.862, and p<0.001).

Figure 2 shows that in eight of the 12 patients, for a given EMGd response slope, the P01 response slope fell below the normal regression line, and in six patients it was below the 95 percent confidence interval. As a mean AP0 /AEMGd was 0.33 cm H20/ %TLC-s±0.09 SD in normal subjects and 0.21 cm H20/%TLC*s J±0.09 SD in patients, with p<0.01 (Table 4). For a PetC02 of 65 mm Hg (Table 5), the P01/EMGd ratio was (0.31 cm H20/%TLC*s ±0.15 SD) significantly lower in patients (p<0.05) than in normal subjects (0.50 cm H20/%TLC*s±0.22 SD). Plotting the P01/EMGd response slopes of patients with hypercapnia against the estimated duration of the disease showed no significant relationship.
In three normal subjects and in three patients, we compared EMGd activity as recorded by surface electrodes (EMGds) and EMGd activity as recorded by e$ophageal electrodes (EMGde) during C02 rebreathing. Comparison between intraindividual slopes (by covariance analysis) is shown in Table 6. In both normal subjects and in patients there were no significant differences between the EMGds and EMGde response slopes to increasing PetC02. No substantial change in heart rate during C02 rebreathing was observed in any patient. While breathing room air, the average heart rate was 78 ± 20 beats/ min, and during rebreathing, the average maximal heart rate was 82 ± beats/min (p = NS).

Table 5-Breathing Pattern, P0>1, EMGd, ami P0 JEMGd at 65 mm HgofpETCOtin the Two Groups of Subjects

Group Ve,L-s f,cycles’* Vt,L Ti,s Ti/tot Vt/Ti,L’s* Po„ cm H20 EMGd, % TLC’s Pai/EMGd, cm HaO/% TLC-s
Normalsubjects 23.6 15.7 1.59 1.76 0.43 0.86 4.9 13.6 0.50
(6.2) (3.9) (0.30) (0.43) (0.06) (0.28) (2.5) (8.1) (0.22)
t X t * t t *
Patients 30.10 28.20 1.20 1.03 0.40 1.24 10.80 42.28 0.31
(9.70) (10.90) (0.54) (0.56) (0.05) (0.44) (4.20) (31.80) (0.15)

Table 6—Intraindividual Comparisons Between EMGd Response to Increasing PejCO% as Recorded by Esophageal and Surface Electrodes (Covariance Analysis) in 3 Patients with C1LD and in 3 Normal Subjects 

Group Case Esophageal AEMGd/APETCO*, %TLC*s~‘/mm Hg Surface AEMGd/APErrC02, %TLC*s _1/mm Hg f P
Normal 1 1.24 0.80 3.035 NS
subjects 2 1.26 1.30 0.001 NS
3 1.15 1.24 0.080 NS
5 3.24 2.19 1.15 NS
Patients 7 9.35 7.20 1.13 NS
8 1.38 1.30 0.27 NS

Ficure 2. Representation of neuromuscular coupling assessed by plotting P0, change per change in PetCOs against EMGd change per change in PetC02 of the same sitting. Solid and broken lines, the mean slope and 95% confidence intervals, respectively, of this relationship in 21 normal subjects. Individual data points for normal subjects (•) and patients (X).

Figure 2. Representation of neuromuscular coupling assessed by plotting P0, change per change in PetCOs against EMGd change per change in PetC02 of the same sitting. Solid and broken lines, the mean slope and 95% confidence intervals, respectively, of this relationship in 21 normal subjects. Individual data points for normal subjects (•) and patients (X).