A physiological study to determine the mechanism of carbon dioxide clearance during apnoea when using transnasal humidified rapid insufflation ventilatory exchange (THRIVE)

一项生理学研究,旨在确定使用经鼻湿化快速充气通气交换(THRIVE)时呼吸暂停期间二氧化碳清除的机制

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Abstract

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.

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