Respiration; international review of thoracic diseases · 2024
Deventilation Syndrome in Patients with Chronic Obstructive Pulmonary Disease Using Nocturnal Noninvasive Ventilation: What Are the Underlying Mechanisms?
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Elshof Judith, Oppersma Eline, Wisse Jantine J, Bladder Gerrie, Meijer Petra M, Torres Abel, Wijkstra Peter J, Duiverman Marieke L
Аннотация
INTRODUCTION: Patients with chronic obstructive pulmonary disease (COPD) commonly experience severe dyspnea after discontinuation of nocturnal noninvasive 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 (Borg 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-NIV (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-min 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.
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 (Borg 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-NIV (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-min 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.