Venous air embolism, hypotension, and end-tidal nitrogen.

The most sensitive method of venous air embolism (VAE) detection in clinical use is the precordial Doppler detector. Because the Doppler detector may provide false-positive and false-negative data, many clinicians rely on end-tidal gas measurements for verification of VAE in the operating room. End-tidal nitrogen (ETN2) increases soon after experimental VAE are small enough to cause minimal changes in blood pressure; however, decreases in end-tidal CO2 (ETCO2) are more sensitive. A large VAE causes hemodynamic instability, and the effect of low cardiac output on ETN2 has not been evaluated. This study was done to compare the changes in ETN2 and ETCO2 during large bolus and infusion VAE. Five mongrel dogs were anesthetized, intubated, and ventilated (FIO2 1.0, PaCO2 38 +/- 4 (SD) mm Hg). The animals were studied in the supine position; anesthesia and paralysis were maintained with a constant infusion of thiamylal and pancuronium. Maintenance fluids were administered at 5 ml kg-1 h-1. Mean arterial and pulmonary arterial pressures (PAP) and ETN2 and ETCO2 were displayed on a strip chart recorder. The dogs underwent both bolus and infusion VAE in separate experiments 10 to 14 days apart. The air emboli were given in random order by automated syringe over 1 minute (infusion) (1 to 2.5 ml kg-1 min-1) or by hand injection over 5 seconds (bolus) (1 to 2.5 ml kg-1). Changes in precordial Doppler sounds occurred in all animals at all doses. The peak increase in PAP and decrease in ETCO2 were significant after all air doses. ETN2 changes were biphasic. The peak increase was significant after all air doses; the peak decrease was significant in 37 of 40 bolus and infusion VAE episodes, occurred within 1 to 3 minutes, and lasted 20 to 30 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)