Changes in Ventilatory Muscle Function with Negative Pressure Ventilation in Patients: DISCUSSION

Posted by James

Our data show that in chronically stable hypercapnic patients with COPD, NPV reduces respiratory muscle activity (EMG), slightly increases muscle strength (MIP and МЕР), and improves arterial blood gas values (Pa0₂ and PaCOa). These changes were coinci­dent with significant increases in Ti, Vt, and Ti/Ttot and a decrease in RF.

In patients with COPD, increase in airway resis­tance and lung hyperinflation enhance the energy demand of the respiratory muscles; furthermore, the hypoxemia reduces the available energy supply and it is known that if energy demands are greater than supplies, the muscle will eventually fatigue.

In this study, both study group (A) and control group (B) exhibited hyperinflation (FRC) and airway obstruc­tion (FEV^, a markedly low inspiratory (MIP) and expiratory (МЕР) muscle force, and chronic hypercap­nia and hypoxia; so, consistently with the accumulating evidence that respiratory muscle fatigue and devel­opment of hypercapnia are closely related, we think that both groups A and В were in a situation of respiratory muscle fatigue. In this situation and par­ticularly in hyperinflated patients with COPD, rapid and shallow breathing has also been observed and it has been related to afferents arising from vagal pulmonary endings. More recently, a decrease in both Vt and Ti with constant Vt/Ti and increase in RF have been interpreted as a compensatory mecha­nism by which overloaded or fatigued respiratory muscles contract at optimal length without substan­tially changing their geometry. Such a mechanism theoretically postpones more severe fatigue, but the increase in PaCO_z is an unescapable consequence.

Basically, the rapid and shallow breathing, the increased neural drive, the decrease in muscle strength, and the chronic hypercapnia appeared to be concomitant in group A and В patients, consistently with the hypothesis that afferents arising from over­loaded or fatigued respiratory muscles are involved in the rapid and shallow breathing and C0₂ retention. Furthermore, our data showing an increase in EMG seem to be in contrast with the hypothesis that central inhibition plays a major role in C0₂ retention. Both chemical and mechanical afferents arising from lung and/or chest wall could be involved in the observed increase in neural inspiratory drive (EMG).
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After a seven-day period of assisted ventilation, lung volumes and FEVj showed limited changes, while muscle strength significantly improved, a pattern also noticed by others reporting on mechanical ventila­tion. It should be noted that in our study, average increase in actual MIP value, significant though it was, was less than that of another study, where, however, the average pre-NPV MIP was greater than that of our study (patients had less hyperinflation), and its percentage increase was slightly greater than that of our study. In another long-term designed study, MIP markedly increased but this increase might at least in part be due to length-tension characteristics, as expected by the reported marked VC increase. Indeed, based on length-tension and geometrical (P = T/r) characteristics, a decrease in lung volume increases the ability of the respiratory muscles to generate inspiratory pressure. Nevertheless, correc­tion of mechanical disadvantage secondary to hyper­inflation seems to be improbable in the present study since neither FRC nor FEV\ changed with NPV.

In patients with COPD, NPV has been reported to acutely suppress phasic ventilatory activity of the respiratory muscles, an observation that others have been unable to confirm. On the other hand Levy et al have more recently noticed that prolonged NPV treatment decreases EMGd activity in these patients. In the present study, a seven-day period of NPV caused both EMGd and EMGint to significantly decrease, the remaining EMGint activity being sig­nificantly lower compared with that of group В (p<0.01). So, a seven-day period of NPV resulted in a partial suppression of respiratory muscle activity. In general, our data confirm the observation of Levy et al that a short period of NPV reduces phasic activity of ventilatory muscles and extends those data for example, in patient 1 with a lower pre-NPV EMGd and a greater pre-NPV EMGint, minimal EMGd and greater EMGint decreases were observed with NPV Moreover, in patient 3 in whom both EMGd and EMGint were the lowest prior to the study, NPV caused the minimal phasic EMG suppression; the opposite occurred in patients 2 and 5, that is, those with the greater baseline EMGd and EMGint activi­ties. These data seem to indicate that the amount of phasic EMG suppression might depend on the extent of pretreatment activity. It is also well known that the degree of suppression improves with familiarity with the technique; nevertheless, in our study, the two patients (1 and 4) previously accustomed to iron lung exhibited no major decrease in EMG activity.

To our knowledge, few data have been provided until now on breathing pattern characteristics before and after a NPV study period. The latter study showed a significant increase in Vt with no consistent changes in Ti, Ttot, and Ti/Ttot. In contrast, in our study NPV resulted in significant changes in both volume (Vt) and time (Ti, RF, and Ti/Ttot) components of the respiratory cycle. These changes along with EMG changes persisted one day after discontinuation of NPV, and this indicates not merely an acute effect of NPV. The observation that these changes paralleled the consistent decrease in PaCO_z could account for the observation that the more rapid and shallower the breathing the greater the arterial C0₂ tension and vice versa.
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The answer to the question whether vagal or non- vagal afferents or both are involved in the lower Ti, Vt, and Ti/Ttot observed in patients is certainly difficult. However, we consider that (1) patients had stable tracheobronchial disease which has been sus­pected of being involved in the increase of vagal ending firing, resulting in Vt and Ti reduction, and (2) NPV is expected to modify neither tracheobronchial disease nor, as a consequence, vagal afferents from bronchial tree, while modulation in the firing of afferents arising from respiratory muscles is not un­expected with respiratory muscles resting. So, we suspect that peripheral nonvagal afferents from res­piratory muscles were at least partially involved in the observed responses.

We also found a relief of sensation of dyspnea in patients with NPV This observation could be inter­preted in the light of the recent knowledge concerning the relation between dyspnea and increased respira­tory drive.

In conclusion, patients with COPD may be in a situation of respiratory muscle fatigue characterized by decrease in muscle strength, increase in respiratory drive, and decrease in both Ti and Vt; the resulting rapid shallow breathing leads to alveolar hypoventila­tion. Negative pressure-assisted ventilation seems to partially suppress phasic ventilatory muscle activity and cause arterial blood gas values and muscle strength to improve, along with decrease in respiratory sensation of dyspnea. Change in timing seems to be linked to both EMG suppression and PaC0₂ amelio­ration. However, the evidence that change in breathing pattern, suppression of EMG phasic activity, and blood gas value improvement are closely interrelated is far from being conclusively provided.