Summary Clinical observations suggest that compared with standard apnoeic oxygenation, transnasal humidified rapid‐insufflation ventilatory exchange using high‐flow nasal oxygenation reduces the rate of carbon dioxide accumulation in patients who are anaesthetised and apnoeic. This suggests that active gas exchange takes place, but the mechanisms by which it may occur have not been described. We used three laboratory airway models to investigate mechanisms of carbon dioxide clearance in apnoeic patients. We determined flow patterns using particle image velocimetry in a two‐dimensional model using particle‐seeded fluorescent solution; visualised gas clearance in a three‐dimensional printed trachea model in air; and measured intra‐tracheal turbulence levels and carbon dioxide clearance rates using a three‐dimensional printed model in air mounted on a lung simulator. Cardiogenic oscillations were simulated in all experiments. The visualisation experiments indicated that gaseous mixing was occurring in the trachea. With no cardiogenic oscillations applied, mean (SD) carbon dioxide clearance increased from 0.29 (0.04) ml.min−1 to 1.34 (0.14) ml.min−1 as the transnasal humidified rapid‐insufflation ventilatory exchange flow rate was increased from 20 l.min−1 to 70 l.min−1 (p = 0.0001). With a cardiogenic oscillation of 20 ml.beat−1 applied, carbon dioxide clearance increased from 11.9 (0.50) ml.min−1 to 17.4 (1.2) ml.min−1 as the transnasal humidified rapid‐insufflation ventilatory exchange flow rate was increased from 20 l.min−1 to 70 l.min−1 (p = 0.0014). These findings suggest that enhanced carbon dioxide clearance observed under apnoeic conditions with transnasal humidified rapid‐insufflation ventilatory exchange, as compared with classical apnoeic oxygenation, may be explained by an interaction between entrained and highly turbulent supraglottic flow vortices created by high‐flow nasal oxygen and cardiogenic oscillations.

A method for the construction of both rigid and compliant (flexible) transparent flow phantoms of biological flow structures, suitable for PIV and other optical flow methods with refractive-index-matched working fluid is described in detail. Methods for matching the in vivo compliance and elastic wave propagation wavelength are presented. The manipulation of MRI and CT scan data through an investment casting mould is described. A method for the casting of bubble-free phantoms in silicone elastomer is given. The method is applied to fabricate flexible phantoms of the carotid artery (with and without stenosis), the carotid artery bifurcation (idealised and patient-specific) and the human upper airway (nasal cavity). The fidelity of the phantoms to the original scan data is measured, and it is shown that the cross-sectional error is less than 5% for phantoms of simple shape but up to 16% for complex cross-sectional shapes such as the nasal cavity. This error is mainly due to the application of a PVA coating to the inner mould and can be reduced by shrinking the digital model. Sixteen per cent variation in area is less than the natural patient to patient variation of the physiological geometries. The compliance of the phantom walls is controlled within physiologically realistic ranges, by choice of the wall thickness, transmural pressure and Young's modulus of the elastomer. Data for the dependence of Young's modulus on curing temperature are given for Sylgard 184. Data for the temperature dependence of density, viscosity and refractive index of the refractiveindex-matched working liquid (i.e. water-glycerol mixtures) are also presented.

No abstract

Background Nasal High Flow (NHF) therapy delivers flows of heated humidified gases up to 60 LPM (litres per minute) via a nasal cannula. Particles of oral/nasal fluid released by patients undergoing NHF therapy may pose a cross-infection risk, which is a potential concern for treating COVID-19 patients. Methods Liquid particles within the exhaled breath of healthy participants were measured with two protocols: (1) high speed camera imaging and counting exhaled particles under high magnification (6 participants) and (2) measuring the deposition of a chemical marker (riboflavin-5-monophosphate) at a distance of 100 and 500 mm on filter papers through which air was drawn (10 participants). The filter papers were assayed with HPLC. Breathing conditions tested included quiet (resting) breathing and vigorous breathing (which here means nasal snorting, voluntary coughing and voluntary sneezing). Unsupported (natural) breathing and NHF at 30 and 60 LPM were compared. Results Imaging: During quiet breathing, no particles were recorded with unsupported breathing or 30 LPM NHF (detection limit for single particles 33 μm). Particles were detected from 2 of 6 participants at 60 LPM quiet breathing at approximately 10% of the rate caused by unsupported vigorous breathing. Unsupported vigorous breathing released the greatest numbers of particles. Vigorous breathing with NHF at 60 LPM, released half the number of particles compared to vigorous breathing without NHF. Chemical marker tests: No oral/nasal fluid was detected in quiet breathing without NHF (detection limit 0.28 μL/m3). In quiet breathing with NHF at 60 LPM, small quantities were detected in 4 out of 29 quiet breathing tests, not exceeding 17 μL/m3. Vigorous breathing released 200–1000 times more fluid than the quiet breathing with NHF. The quantities detected in vigorous breathing were similar whether using NHF or not. Conclusion During quiet breathing, 60 LPM NHF therapy may cause oral/nasal fluid to be released as particles, at levels of tens of μL per cubic metre of air. Vigorous breathing (snort, cough or sneeze) releases 200 to 1000 times more oral/nasal fluid than quiet breathing (p < 0.001 with both imaging and chemical marker methods). During vigorous breathing, 60 LPM NHF therapy caused no statistically significant difference in the quantity of oral/nasal fluid released compared to unsupported breathing. NHF use does not increase the risk of dispersing infectious aerosols above the risk of unsupported vigorous breathing. Standard infection prevention and control measures should apply when dealing with a patient who has an acute respiratory infection, independent of which, if any, respiratory support is being used. Clinical trial registration ACTRN12614000924651

Nasal high flow (NHF) therapy is used to treat a variety of respiratory disorders to improve patient oxygenation. A CO2 washout mechanism is believed to be responsible for the observed increase in oxygenation. In this study, experimentally validated Computational Fluid Dynamics simulations of the CO2 concentration within the upper airway during unassisted and NHF assisted breathing were undertaken with the aim of exploring the existence of this washout mechanism. An anatomically accurate nasal cavity model was generated from a CT scan and breathing was reproduced using a Fourier decomposition of a physiologically measured breath waveform. Time dependent CO2 profiles were obtained at the entrance of the trachea in the experimental model, and were used as simulation boundary conditions. Flow recirculation features were observed in the anterior portion of the nasal cavity upon application of the therapy. This causes the CO2 rich gas to vent from the nostrils reducing the CO2 concentration in the dead space and lowering the inspired CO2 volume. Increasing therapy flow rate increases the penetration depth within the nasal cavity of the low CO2 concentration gas. A 65% decrease in inspired CO2 was observed for therapy flow rates ranging from 0 to 60 L min(-1) supporting the washout mechanism theory.