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

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