Domiciliary nocturnal nasal intermittent positive pressure ventilation in COPD: mechanisms underlying changes in arterial blood gas tensions

Abstract

The improvement in arterial blood gas tensions following assisted ventilation in chronic obstructive pulmonary disease (COPD) has usually been attributed to the relief of incipient or established respiratory muscle fatigue. The contribution of changes in the load placed upon and the drive to the respiratory muscle pump have not been evaluated. We have investigated the contribution of changes in respiratory muscle strength, the ventilatory response to CO2 and ventilatory function to changes in arterial blood gas tensions in eight patients with severe COPD completing six months domiciliary nasal intermittent positive pressure ventilation. Six patients showed a reduction and two an increase in arterial carbon dioxide tension (PaCO2), median (range) for eight patients, -0.9 kPa (-1.5 to +0.4) (p less than 0.05) and seven showed an improvement in arterial oxygen tension (PaO2), +0.7 kPa (-0.4 to +1.7) (p less than 0.05) during daytime spontaneous breathing. The reduction in PaCO2 was not related to increased inspiratory muscle strength but was correlated with a decrease in gas trapping (Spearman rank correlation coefficient (r(S)) 0.85, p less than 0.05) and in the residual volume (r(s) 0.78, p less than 0.05), suggesting reduced small airway obstruction and, therefore, a reduction in load. The change in PaCO2 also correlated with the increase in ventilation at an end-tidal CO2 of 8 kPa during rebreathing (r(s) -0.76, p less than 0.05) suggesting improved chemosensitivity to CO2. Our data do not support the hypothesis that improvements were due to the relief of muscle fatigue. We suggest that the contribution of changes in load and central drive warrant further investigation.

Effect of Home Noninvasive Ventilation With Oxygen Therapy vs Oxygen Therapy Alone on Hospital Readmission or Death After an Acute COPD Exacerbation

“…Such patients with chronic respiratory failure have previously been shown to benefit from noninvasive ventilation in physiological studies. 7,9 The early, within-hospital assessment of hypercapnia in the RESCUE trial may have led to the inclusion of patients with spontaneously reversible hypercapnia and conse-quently a better prognosis. 24 Consistent with this conjecture, the control group as well as the treatment noninvasive ventilation group of the RESCUE study showed a reduction in daytime PaCO 2 within 6 weeks of enrollment, 15 supporting the rationale that the trajectory of recovery for hypercapnia determines the likelihood of response to home noninvasive ventilation.…”

“…Furthermore, and unlike the RESCUE trial, the current study also required demonstration of chronic hypoxemia and thus targeted patients with more severe COPD. Such patients with chronic respiratory failure have previously been shown to benefit from noninvasive ventilation in physiological studies …”

“…One treatment option would be to use noninvasive ventilation in addition to oxygen therapy in the home setting. Small, uncontrolled studies demonstrating the physiological efficacy of home noninvasive ventilation in patients with COPD [7][8][9] have led to its prescription across Europe. 10 However, subsequent clinical studies failed to demonstrate either physiological (reduced hypercapnia) or clinical (mortality) efficacy, 11,12 and questions remain regarding whether the application of the intervention was optimized in these randomized clinical trials.…”

Ventilatory neural drive in chronically hypercapnic patients with COPD: effects of sleep and nocturnal noninvasive ventilation

“…It has been theorised that the improvements seen in NIV during sleep may also be the result of a “reset” in respiratory drive initiated by normalisation of P aCO 2 , which persists during the daytime to improve daytime P aCO 2 in addition to acutely improving nocturnal P aCO 2 during sleep ( figure 4 d). This is supported by two small studies [ 123 , 124 ] which used rebreathing protocols to measure chemosensitivity to CO 2 during the daytime, and found improvements in sensitivity after nocturnal NIV treatment and resultant decreases in daytime P aCO 2 .…”

Supplemental oxygen and noninvasive ventilation

“…This is particularly important as sleep hypoventilation and related night-to-morning change in P aCO 2 (potentially at least in part due to reduced CO 2 responsiveness) might be an additional factor in the development of pulmonary hypertension. In addition, chronic hypercapnia may further impair diaphragmatic function and have a deleterious effect on the central respiratory drive [ 105 , 108 , 109 ].…”