Ventilatory muscle

One subject (no. 12) with COPD was extremely anxious and unable to synchronize his breathing with the ventilator. There were no evident clinical charac­teristics which distinguished him from others in the obstructive group (Table 1). This subject was not included in further analysis. The other 11 subjects tolerated NPPV well without discomfort or complica­tions.

Figure 1 is a representative tracing from a subject with COPD (no. 10). During spontaneous breathing (Fig 1A), large negative deflections in Pes and nent EMGdi activity were evident on inspiration. The RIP demonstrated dyscoordinated thoracoabdominal motion, with the abdomen moving inward during inspiration (abdominal paradox). Application of NPPV with a mask pressure of 12 cmHaO produced a substantial reduction in phasic EMGdi activity (Fig IB) which was accompanied by a less negative deflec­tion of Pes during inspiration. Abdominal paradox was eliminated during NPPy with the rib cage and abdom­inal compartments inflating synchronously. Further increasing Pmask to 15 cmH20 (Fig 1С) almost com­pletely abolished phasic diaphragmatic EMG activity and only positive Pes swings were recorded during inspiration. End-tidal Pco2 (PetCCKj) fell to 42 mm Hg with NPPV from a control value of 47 mm Hg during spontaneous breathing.

Ficuar 1. Tracings from a

FIGURE 1. Tracings from a subject with COPD (no. 10) during spontaneous breathing (A) and during NPPV with mask pressure (Pmask) of 12 (B) and 15 (C) cmHsO. NPPV was associated with a reduction of spontaneous inspiratory efforts demonstrated by suppression of the pha¬sic surface diaphragm EMG (EMGdi) and only positive inspiratory esophageal pressure (Pes) swings. The paradoxic abdominal (ABD) motion seen during spontaneous breathing (A) became synchronous with the rib cage (RC) during NPPV (B and C).

Tracings froitt a restrictive subject (no. 6) ate shown in Figure 2. During spontaneous breathing (Fig 2A), inspiratory EMG activity of the diaphragm and ster­nocleidomastoid muscles was evident, in association with a negative deflection of Ptrach. Paradoxic abdom­inal wall motion was also present. During NPPV with a Pmask of 6 cmH20 (Fig 2B), phasic EMG activity was markedly reduced and only positive Ptrach de­flections were recorded. Thoracoabdominal motion became synchronous during assisted ventilation. When Pmask was further increased to 11 cmH20 (Fig 2C), inspiratory EMGdi activity was no longer evident. Comparable reductions in phasic sternocleidomastoid EMG activity were also observed with NPPV The higher Pmask resulted in more positive inspiratory Ptrach and a greater outward abdominal excursion during inspiration.
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Table 2—Effects cfNPPV on Inspiratory Effort

Group

NPPV Rate (breaths/min)

Peak Mask Pressure (cmHaO)

Inspiratory Pressure Swingt (cmHaO)

control NPPV

EMGdi (% control)

Normal

16.6 ±2.3

16.6± 1.4

— 5.5±0.7

6.5 ±0.8*

6.7 ±0.7*

Restrictive

19.5 ±3.3

17.0±1.8

— 3.8±0.7

13.0 ±0.9*

6.4 ±3.2*

Obstructive

18.8 ±1.6

13.3 ±1.8

-12.8± 1.4

5.5 ±0.4*

8.3±5.1*

Ficuas 2. Recordings from a restrictive

FIGURE 2. Recordings from a restrictive subject (no. 6) during spontaneous breathing (A) and with NPPV (B and C). Increasing levels of mask pressure (Pmask) resulted in progressive reductions in phasic diaphragm EMG. Comparable decreases in the EMG of the sternocleidomastoid were observed. Only positive inspiratory tracheal pressure (Ptrach) swings were noted with NPPV. The paradoxic abdominal (ABD) motion seen during spontaneous breathing became synchronous with the rib cage (RC) during NPPV.

The time course of the effects of NPPV on inspira­tory efforts is seen in Figure 3 (subject no. 10). Within five to six NPPV breaths, there was almost complete suppression of both phasic diaphragm and parasternal EMG activity, an absence of negative inspiratory Pes swings, and resolution of paradoxic abdominal motion. A transient increase in the spontaneous inspiratory effort several breaths later (arrow, Fig 3) was associ­ated with an initial negative deflection of Pes and phasic activation of the EMG signals. The application of NPPV did not result in the development of hyper­inflation in any subject, as demonstrated by stable end-expiratory position of Pes (Fig 3).
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FIGURE 3. This tracing illustrates

FIGURE 3. This tracing illustrates the time course of the effects of NPPV on indices of inspiratory effort (subject no. 10). Suppression of phasic EMC activity of the diaphragm and parasternal muscles, as well as the development of positive inspiratory Pes deflections, occurred within several breaths of the initiation of NPPV (broken line). A breath with substantial sponta¬neous effort seen later (arrow) was associated with increased inspiratory muscle EMC activity and a negative inspiratory Pes deflection.