RESUMO
INTRODUCTION: Nasal high-flow therapy (HFT) has been shown to improve daytime breathing mechanics in healthy adults as well as the lung function and quality of life in chronic obstructive pulmonary disease (COPD) patients. METHOD: We hypothesized that improved breathing mechanics with HFT may further reduce minute ventilation (i.e. decreased work of breathing) during sleep in patients with COPD. In COPD participants we examined the dose effect of HFT (within night randomization of HFT level; 0, 10, 20 and 30L/min) on minute ventilation, oxyhemaglobin saturation and transcutaneous carbon dioxide during wake and sleep. We assessed overnight polysomnography with and without HFT on two separate nights. Paired t-tests were used to compare overnight sleep quality with and without HFT. The association between ventilatory variables and HFT level was assessed using regression analysis. RESULTS: During sleep, HFT decreased minute ventilation by 0.63±0.02L/min per 10L/min nasal airflow by reducing tidal volume (37±6mL per 10L/min; p<0.001) without affecting respiratory rate (p=0.9) or arterial CO2 (p=0.7). In contrast, during wakefulness reductions in minute ventilation (0.85±0.04L/min per 10L/min) was due to respiratory rate reduction along with prolongation in expiratory time. CONCLUSION: The reduction in minute ventilation is greater with higher dead-space volumes (r=0.50; p<0.02) and during wakefulness suggesting that ventilatory responses to HFT are mediated through a reduction in dead-space ventilation. The reduction in ventilation in response to HFT is large enough to reduce respiratory loads. Reducing respiratory loads may avert muscle fatigue, preserve respiratory function, or prevent development of respiratory failure.
RESUMO
INTRODUCTION: Patients with COPD have increased respiratory loads and altered blood gases, both of which affect vascular function and sympathetic activity. Sleep, particularly rapid eye movement (REM) sleep, is known to exacerbate hypoxia and respiratory loads. Therefore, we hypothesize that nasal high flow (NHF), which lowers ventilatory loads, reduces sympathetic activity during sleep and that this effect depends on COPD severity. METHODS: We performed full polysomnography in COPD patients (n=17; FEV1, 1.6±0.6 L) and in matched controls (n=8). Participants received room air (RA) at baseline and single night treatment with O2 (2 L/min) and NHF (20 L/min) in a random order. Finger pulse wave amplitude (PWA), a measure of vascular sympathetic tone, was assessed by photoplethysmography. Autonomic activation (AA) events were defined as PWA attenuation ≥30% and indexed per hour for sleep stages (AA index [AAI]) at RA, NHF, and O2). RESULTS: In COPD, sleep apnea improved following O2 (REM-apnea hypopnea index [AHI] with RA, O2, and NHF: 18.6±20.9, 12.7±18.1, and 14.4±19.8, respectively; P=0.04 for O2 and P=0.06 for NHF). REM-AAI was reduced only following NHF in COPD patients (AAI-RA, 21.5±18.4 n/h and AAI-NHF, 9.9±6.8 n/h, P=0.02) without changes following O2 (NHF-O2 difference, P=0.01). REM-AAI reduction was associated with lung function expressed as FEV1 and FVC (FEV1: r=-0.59, P=0.001; FEV1/FVC: r=-0.52 and P=0.007). CONCLUSION: NHF but not elevated oxygenation reduces peripheral vascular sympathetic activity in COPD patients during REM sleep. Sympathetic off-loading by NHF, possibly related to improved breathing mechanics, showed a strong association with COPD severity.