Impact of high-flow nasal oxygen therapy on esophageal pressure and cardiovascular function in healthy, anesthetized, spontaneously breathing dogs.

Abstract

Objective: To determine whether high-flow nasal oxygen therapy (HFNOT) induces changes in esophageal pressure, a surrogate for intrathoracic pressure, and to evaluate the associated cardiovascular and respiratory effects in healthy dogs.

Methods: A prospective, randomized study was conducted in 6 healthy Beagles. Anesthesia was induced and maintained using alfaxalone total IV anesthesia. High-flow nasal oxygen therapy was applied in the following 4 stages: baseline, HFNOT at 1 and 2 L/kg/min (each for 10 minutes in a randomized order), and post-HFNOT (15-minute recovery period). Measurements taken at each stage included esophageal pressure, cardiovascular parameters, and respiratory parameters.

Results: Both end-expiratory and end-inspiratory esophageal pressures increased in a flow rate-dependent manner (end-expiratory esophageal pressure: -1.2 ± 1.1, 1.3 ± 1.7, and 4.7 ± 3.0 cm H2O; end-inspiratory esophageal pressure: -7.1 ± 1.8, -4.2 ± 1.8, and -0.2 ± 3.4 cm H2O at baseline, 1 L/kg/min, and 2 L/kg/min, respectively). Cardiac index remained unchanged across flow rates, whereas mean arterial pressure increased at 2 L/kg/min compared with baseline (82.0 ± 7.2 vs 77.5 ± 7.9 mm Hg, respectively). Respiratory rate decreased at 2 L/kg/min compared with baseline (11 ± 3 vs 18 ± 6 breaths/min, respectively). Arterial blood gas values were not different across flow rates.

Conclusions: High-flow nasal oxygen therapy increased esophageal pressure without cardiovascular compromise in healthy, anesthetized, spontaneously breathing dogs. Additionally, HFNOT reduced the respiratory rate without altering arterial blood gas values.

Clinical relevance: In healthy, anesthetized dogs, HFNOT induced measurable changes in intrathoracic pressure without clinically relevant alteration in cardiovascular or respiratory function.