Investigating a novel tracheostomy high-flow therapy device interface in COPD models: design and preclinical validation

Abstract Background High-flow tracheal oxygen (HFTO) lacks a positive end-expiratory pressure (PEEP) effect, limiting its use in patients with chronic obstructive pulmonary disease (COPD), who often require PEEP to counteract intrinsic PEEP and prevent dynamic hyperinflation or atelectasis. We developed a novel high-flow tracheal interface (nHFTI) and compared its PEEP and respiratory effects with those of the traditional high-flow tracheal interface (tHFTI) at varying flow rates in a bench model of COPD with tracheostomy. Methods A randomized crossover benchtop experiment was conducted, with a size 8 cuffed tracheostomy tube connected to the high-flow therapy device via two different interfaces. A high-fidelity lung simulator was used to simulate the lungs of patients with COPD. Gas flow rates were set from 10 to 80 L/min in increments of 10 L/min, with randomization of the flow sequence. In each step, the following parameters were collected: PEEP, peak inspiratory pressure (PIP), peak expiratory pressure (PEP), end-inspiratory transpulmonary pressure (Ptp-EI), end-expiratory transpulmonary pressure (Ptp-EE), end-inspiratory cardiac pressure (PEIC), end-expiratory cardiac pressure (PEEC), functional residual capacity (FRC), tidal volume (Vt), and fraction of inspired oxygen (FiO 2 ). Results Increasing flow rates significantly elevated PEEP with both tHFTI and nHFTI ( P < 0.001). Compared with tHFTI at all flow rates, the nHFTI generated significantly higher PEEP (e.g., 4.1 vs. 2.2 cmH 2 O at 40 L/min; 8.1 vs. 4.1 cmH 2 O at 60 L/min). This was accompanied by significant increases in FRC ( P < 0.01) and Ptp-EE ( P < 0.05), and a slight reduction in Vt with nHFTI. Exploratory variables—including PIP, PEP, Ptp-EI, PEIC, and PEEC—also showed consistent differences favoring nHFTI. FiO 2 did not differ significantly between interfaces. Conclusions The nHFTI was observed to generate modest PEEP, increase FRC, and slightly reduce Vt at 40–60 L/min in a bench model of COPD, with these mechanical effects potentially contributing to counteraction of intrinsic PEEP and support of lung expansion. However, these in vitro findings should not be interpreted as evidence of clinical benefit. In vivo studies are warranted to evaluate whether any potential physiological effect translates into meaningful patient-centered outcomes—particularly in COPD patients requiring prolonged mechanical ventilation and weaning support.