Detection and hemodynamic consequences of venous air embolism. Does nitrous oxide make a difference?

Volume expansion of intravascular air by nitrous oxide (N2O) may improve the sensitivity of monitors used to detect venous air embolism (VAE) and/or exacerbate hemodynamic changes following VAE. The purpose of this study was to determine if the administration of N2O alters the sensitivity (i.e., threshold of detection) of monitors used to detect VAE or the hemodynamic consequences of VAE. Twenty-one dogs were monitored for VAE with precordial Doppler ultrasound, transesophageal echocardiography (TEE), changes in end-tidal carbon dioxide tension (ETCO2), and changes in pulmonary artery pressure (PAP). Venous air was infused at rates between 0.005 and 0.4 ml.kg-1.min-1 during 1 MAC (total anesthetic level) of isoflurane with and without 50% N2O (group 1, n = 7) or isoflurane with and without 75% N2O (group 2, n = 7). The mean quantity of infused air necessary to elicit a positive response in both the presence and absence of N2O was calculated for each monitor. Positive responses were defined as follows: unmistakable audible change in frequency on Doppler ultrasound, visualization of densities consistent with air bubbles in the right cardiac chambers or outflow tract on TEE, a decrease in ETCO2 greater than or equal to 2 mmHg, and an increase in mean PAP greater than or equal to 3 mmHg. In group 3 (n = 7), venous air was infused at rates between 0.1 and 0.8 ml.kg-1.min-1 during 1 MAC (total anesthetic level) of isoflurane with and without 50% N2O. In group 3, N2O administration was discontinued immediately upon Doppler detection of VAE and air infusion continued until mean arterial pressure (MAP) decreased by 10 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)