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

Authors Fricke K, Schneider H, Biselli P, Hansel NN, Zhang ZG, Sowho MO, Grote L

Received 21 February 2018

Accepted for publication 15 June 2018

Published 2 November 2018 Volume 2018:13 Pages 3635—3643


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Richard Russell

K Fricke,1,2 H Schneider,1 P Biselli,1,3 NN Hansel,1 ZG Zhang,1,4 MO Sowho,1 L Grote1,5,6

1Department of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, MD, USA; 2Department for Pulmonary, Sleep, and Intensive Care Medicine, Helios Klinikum, Wuppertal, Germany; 3Intensive Care Unit, Medical Division, University Hospital, University of Sao Paolo, Sao Paolo, Brazil; 4Department for Geriatrics, Peking University First Hospital, Beijing, China; 5Sleep Disorders Center, Department for Pulmonary Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden; 6Center for Sleep and Wake Disorders, Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden

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

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