Reductions in dead space ventilation with nasal high flow depend on physiological dead space volume: metabolic hood measurements during sleep in patients with COPD and controls

Abstract

Nasal high flow (NHF) reduces minute ventilation and ventilatory loads during sleep but the mechanisms are not clear. We hypothesised NHF reduces ventilation in proportion to physiological but not anatomical dead space.11 subjects (five controls and six chronic obstructive pulmonary disease (COPD) patients) underwent polysomnography with transcutaneous carbon dioxide (CO2) monitoring under a metabolic hood. During stable non-rapid eye movement stage 2 sleep, subjects received NHF (20 L·min-1) intermittently for periods of 5-10 min. We measured CO2 production and calculated dead space ventilation.Controls and COPD patients responded similarly to NHF. NHF reduced minute ventilation (from 5.6±0.4 to 4.8±0.4 L·min-1; p<0.05) and tidal volume (from 0.34±0.03 to 0.3±0.03 L; p<0.05) without a change in energy expenditure, transcutaneous CO2 or alveolar ventilation. There was a significant decrease in dead space ventilation (from 2.5±0.4 to 1.6±0.4 L·min-1; p<0.05), but not in respiratory rate. The reduction in dead space ventilation correlated with baseline physiological dead space fraction (r2=0.36; p<0.05), but not with respiratory rate or anatomical dead space volume.During sleep, NHF decreases minute ventilation due to an overall reduction in dead space ventilation in proportion to the extent of baseline physiological dead space fraction.

Conflict of interest statement

Conflict of interest: P. Biselli reports grants from the National Institutes of Health (NIH) (HL105546), and grants from the Brazilian funding agencies FAPESP and CNPq, during the conduct of the study. K. Fricke reports grants from the NIH (HL105546), during the conduct of the study. L. Grote reports grants from ResMed Foundation and Philips Foundation, grants, personal fees and nonfinancial support from ResMed (speaker's bureau and study support), personal fees from Philips (speaker's bureau), personal fees from Itamar (speaker's bureau and study support), and personal fees from Weinmann (for consultancy), outside the submitted work. A.T. Braun reports grants from the NIH (HL105546), during the conduct of the study. J. Kirkness has received grants from the NIH (HL105546), and is director of clinical affairs for Fisher & Paykel Healthcare, during the conduct and publication of the study. P. Smith reports grants from the NIH (HL105546), during the conduct of the study. A. Schwartz reports grants from the NIH (HL105546), during the conduct of the study. H. Schneider reports grants from the NIH (HL105546), personal fees for consulting and nonfinancial support with devices in patients with CF from Fisher & Paykel Healthcare, grants from ResMed (for sponsored research on the effect of NHF in COPD), and personal fees from TNI Medical (for consultancy; high flow in COPD), during the conduct of the study; personal fees for consultancy from Fisher & Paykel Healthcare and TNI Medical, outside the submitted work; in addition, H. Schneider has a US patent: 7,080,645 issued to TNI Medical (anti-snoring device, method for reducing snoring, and a nasal air cannula).

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