The results of this study demonstrate that NPPV can achieve, in the short term, two major goals of assisted ventilation, namely: to provide adequate ven­tilation while simultaneously allowing for a significant reduction in spontaneous inspiratory effort. Other investigators have shown that long-term intermittent NPPV can result in sustained improvements in Pco2 and clinical status, as well as increased exercise tolerance in patients with chronic respiratory fail­ure. However, the possible mechanisms for these beneficial effects have not previously been investigated. The present study demonstrates the ability of NPPV to systematically reduce inspiratory effort in the short term. This suggests that the improvements noted in the long-term studies of inter­mittent NPPV were a result of resting of chronically fatigued inspiratory muscles, as has been proposed for intermittent negative pressure ventilation. Al­ternatively, chronic nocturnal NPPV may have in­creased ventilation sufficiently to decrease Pco2, al­lowing for a gradual resetting of the respiratory control center. This possibility, however, was not explored in the present study.

During mechanical ventilation, the work of breath­ing performed by the subject is reduced as the ventilator provides an external source of work. In the present study, the respiratory muscle electromy- ograms and inspiratory intrathoracic pressure swings were used as indices of respiratory muscle energy expenditure. We did not quantify changes in the work of breathing between control and NPPV situations since the determination of this parameter requires an accurate measurement of changes in lung volume. Direct measurement of tidal volume was not possible due to the presence of unquantifiable leaks around the seal of the nasal mask, as well as through the mouth. Respiratory inductive plethysmography can be used to measure volume changes indirectly, pro­vided that the pattern of thoracic inflation remains relatively constant. During NPPy the inflation char­acteristics of the rib cage and abdomen often differed markedly from those observed during spontaneous breathing (Fig 1,2,3) which would be expected to decrease the reliability of the volume measurements obtained.
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Previous studies have demonstrated that diaphragm electrical activity is proportional to diaphragm oxygen consumption. Therefore, the observation of a systematic reduction in phasic activity of the diaphragm should reflect a decrease in energy expenditure as NPPV assumed at least part of the work of breathing. This assumption is further supported by the absence of negative inspiratory intrathoracic pressure swings observed in all subjects during NPPV, indicating that the contribution by the subject to the level of venti­lation achieved was reduced. The comparable reductions in phasic diaphragm and accessory muscle EMGs (Fig 5) confirm that NPPV suppressed the activity of all the inspiratory muscles uniformly, rather than simply altering the pattern of recruitment among different inspiratory muscle groups.

It is possible that the diaphragm EMG signal recorded from surface electrodes may not accurately reflect changes in phasic diaphragm activity for several reasons. For instance, changes in diaphragm position with reference to the surface electrodes may occur with passive inflation during positive pressure venti­lation. Furthermore, the EMG signal is presumably contaminated by the activity of other muscles in the vicinity which are active during inspiration. How­ever, these considerations do not apply to EMG signals recorded from an anchored esophageal electrode. Therefore, the comparable reductions in surface and esophageal EMGdi signals observed in the subjects in whom both were measured (Fig 4) demonstrate that the surface electrode signals adequately reflect changes in phasic diaphragm activity under the pres­ent experimental conditions.

As seen in Figure 6, oxygen saturation, end-tidal and arterial Pco2 remained stable or improved with NPPV as compared with those values obtained during spontaneous breathing. End-tidal Pco2 was used as an estimate of arterial Pco2 in order to assess changes in the level of ventilation during NPPV. While this approach may be questioned in patients with signifi­cant airways obstruction, it should be noted that similar results were obtained in normal subjects as well as patients with restrictive disease. In no subject did end-tidal or arterial Pco2 increase during NPPV The small but consistent reductions in both end-tidal and arterial Pco2 observed for the group as a whole suggest that an increase in alveolar ventilation oc­curred during NPPy as a result of either an increase in overall minute ventilation or, alternatively, improve­ment in ventilation-perfusion relationships. It would be unlikely that a decrease in anatomic dead space occurred during positive pressure ventilation. This is in keeping with the data of Henke et al which demonstrated consistent reductions in Pco2 in normal subjects during noninvasive mechanical ventilation using positive and negative pressure devices.

Although NPPV was well tolerated by most subjects, some degree of coaching, reduction of distractions and familiarity with the equipment all tended to enhance  the magnitude of the reduction in phasic EMGdi activity during assisted ventilation. One subject with severe but stable COPD (no. 12) was extremely anxious and unable to synchronize his breathing with the ventilator cycle. The failure of NPPV, however, appeared to be due to factors other than the nature or severity (Table 1) of his disease. canadian antibiotics

Initial studies of chronic NPPV were performed in patients with respiratory muscle weakness of varied etiology. Braun questioned the ability of NPPV to provide effective alveolar ventilation in patients with increased respiratory system impedance, particularly chronic obstructive pulmonary disease. The present data demonstrate that in fact NPPV can effectively assist ventilation and decrease inspiratory effort in patients with severe obstructive lung disease.