Deventilation syndrome in patients with chronic obstructive pulmonary disease using nocturnal non-invasive ventilation: what are the underlying mechanisms?

Introduction: Patients with chronic obstructive pulmonary disease (COPD) commonly experience severe dyspnea after discontinuation of nocturnal non-invasive ventilation (NIV), known as deventilation syndrome (DVS), which negatively affects quality of life. Despite various hypotheses, the precise mechanisms of DVS remain unknown.

Methods: An observational pilot study was performed monitoring 16 stable COPD patients, before, during and after an afternoon nap on NIV. Seven patients experienced DVS (Borge dyspnea scale ≥ 5), while nine served as controls (Borg Dyspnea Scale ≤ 2). Hyperinflation was evaluated through inspiratory capacity (IC) measurements and end-expiratory lung impedance (EELI) via electrical impedance tomography. Respiratory muscle activity was assessed by diaphragmatic surface electromyography (sEMG).

Results: Post-NIV dyspnea scores were significantly higher in the DVS group (5[3-7] vs. 0[0-1.5], p<0.001). IC values were lower in the DVS group compared to controls, both pre- (54[41-63] vs. 88[72-94] %pred., p=0.006) and post-NIV (45[40-59] vs. 76[65-82] %pred., p=0.005), while no intergroup difference was seen in IC changes pre- and post-NIV. EELI values after NIV indicated a tendency towards lower values in controls and higher values in DVS patients. sEMG amplitudes were higher in the DVS group within the first 5 minutes post-NIV (221[112-294] vs. 100[58-177]% of baseline, p=0.030).

Conclusion: This study suggests that it is unlikely that DVS originates from the inability to create diaphragmatic muscle activity after NIV. Instead, NIV-induced hyperinflation in individuals with static hyperinflation may play a significant role. Addressing hyperinflation holds promise in preventing DVS symptoms in COPD patients.