Numerical Modelling of Respiratory Gas Concentrations During Nasal High Flow Therapy

Abstract

This thesis aims to examine the role of anatomical dead-space flushing as a proposed mechanism for the enhancement of gas exchange observed in nasal high flow therapy. Airway computational fluid dynamics models were created to simulate and quantify changes in flow patterns and CO2 distributions upon application of the therapy during breathing and apnea. Transient airflow, representing breathing, was simulated through open and closed mouth upper airway models. The numerical models were validated using measurements from physical airway models. The therapy replaced the upper airway deadspace with gas containing a low CO2 concentration. A non-linear relationship was observed between inspired CO2 and therapy flow rate. Applying 60 L min−1 NHF reduced the inspired CO2 volume, relative to natural breathing, by 71% when the mouth was open and by 54% with a closed mouth. The effect of therapy on airway and blood gas concentrations during apnea was investigated using three models, which included the effects of: flow generated by cardiac mechanical activity, lower airway impedance and a ventilatory mass flow. In the first model, the combination of NHF therapy and cardiogenic flow resulting in greater transport of CO2 out of the airway than from either therapy or cardiogenic flow alone, or from a linear combination of these two flows. After a 10 s apneic period, the CO2 at the carina was reduced by 31% of the initial concentration when the therapy and cardiogenic flows interacted, whereas a 3% reduction occurred when only cardiogenic flow was present. The therapy alone did not cause any reduction in carinal CO2 concentration. In the second apneic model, various pressure conditions applied to the truncated airway boundaries were compared. Applying an impedance boundary condition, to the truncated bronchi of a 3D airway with seven branching generations, was found to influence the upstream pharyngeal flow. As a result, the extent to which the therapy flushes the airway was altered. The last apneic model coupled the 3D upper airway to a compartmental model which allowed analysis of blood gas tensions and aventilatory mass flow. Aventilatory mass flow did not affect the upper airway flow fields and NHF did not significantly reduce the blood CO2 tensions over the apneic periods simulated.