Effect of an inhaled β‐2 adrenergic receptor agonist on arterial partial pressure of oxygen in hypoxemic anesthetized horses

All too commonly, and despite high inspired oxygen concentration, anesthetized horses develop low arterial oxygen tension, potentially compromising oxygen delivery. Traditional methods of addressing hypoxemia have proven inadequate. This clinical evaluation was designed to test the hypothesis that a specific β-2 adrenergic receptor agonist, albuterol sulfate, when delivered by metered-dose inhaler (MDI) would affect arterial partial pressure of oxygen in hypoxemic anesthetized horses, and demonstrate a safe, effective alternative medical approach to treatment. Client owned animals (n = 22; 16 males, six female) which approached (PaO2 < 90 mm Hg, < 12 kPa and declining) or became hypoxemic (PaO2 < 60 mm Hg, < 8 kPa) under anesthesia were administered albuterol sulfate at 2 µg kg−1 (rounded to the nearest 45 kg) through a MDI connected to a linear aerosolization chamber, after all other treatment modalities were attempted. Blood gases were drawn following MDI therapy (mean 24.6 ± 2.2 minutes). The mean and standard error of the mean (mean ± SEM) were calculated for all data and a t-test for paired samples was calculated to evaluate significance of differences. A p-value less than 0.05 was adopted as significant. The collective increase in PaO2 was 54.9 ± 11.4 mm Hg (7.3 ± 1.5 kPa). This difference was statistically and clinically significant. Evaluation of only those horses with unequivocal hypoxemia (PaO2 < 60 mm Hg) demonstrated a larger mean increase in PaO2 (61.7 ± 14.9 mm Hg, 8.2 ± 2 kPa) than those horses with merely low PaO2 (< 90 mm Hg, < 12 kPa and declining) (50.2 ± 16.7 mm Hg, 6.7 ± 2.2 kPa). A second evaluation of client owned animals (n = 42; 17 males, eight geldings, 17 females; 8.7 ± 0.9 year; 495.1 ± 16.8 kg; dorsal recumbency, n = 36; right lateral recumbency, n = 3; left lateral recumbency, n = 3) determined to be hypoxemic (PaO2 = 63.9 ± 2.8 mm Hg, 8.5 ± 0.4 kPa) under anesthesia were administered 900 µg of albuterol sulfate by MDI. Arterial pH, PaCO2, HCO3–, and BE did not change significantly with treatment. A statistically significant increase (48.2 ± 7.7 mm Hg, 6.4 ± 1 kPa) in PaO2 from 63.9 ± 2.8 mm Hg (8.5 ± 0.4 kPa) to 112.2 ± 9.1 mm Hg (15 ± 1.2 kPa) was detected. Careful monitoring of heart rate, ECG, blood pressure and electrolytes revealed no deleterious side-effects of the therapy, with the exception of sweating. Albuterol sulfate delivered by MDI inhalation therapy was an effective means of increasing arterial oxygen concentration. A controlled study including measurement of cardiac output will be necessary to define the mechanism and support these clinical findings.