Nasal high flow, but not supplemental O₂, reduces peripheral vascular sympathetic activity during sleep in COPD patients

Abstract

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.

Keywords:

• COPD
• sleep
• nasal high flow
• oxygen therapy
• sympathetic activity
• pulse wave amplitude

Acknowledgments

This study was supported by the Swedish Heart and Lung Foundation (HLF 20130488, 20150313, and 20160584), by grants from the Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement (ALFGBG 725601), and the National Institute of Health (R01 HL105546). This article was submitted as an abstract for the American Thoracic Society 2016 International Conference; May 13–18, 2016; San Francisco, CA, USA.

Author contributions

HS and LG take responsibility for the content of the manuscript, including the data and data analysis. All authors contributed to data analysis, drafting and revising the article, gave final approval of the version to be published, and agree to be accountable for all aspects of the work.

Disclosure

The authors report no conflicts of interest in this work.