Detection of Arterial Gas Embolism by Increased End-Tidal Nitrogen in Dogs

Abstract

Increased end-tidal (ET) nitrogen in a patient being ventilated with a nitrogen-free gas mixture through a leak-free circuit has been considered a specific sign of venous air embolism. We hypothesized that increased ETN2 would occur after arterial air emboli, just as following venous air emboli, and that clinically relevant arterial air emboli could be detected with respiratory gas monitoring by mass spectrometry. After approval from the institutional Animal Utilization Committee, eight mongrel dogs were studied. All were anesthetized with pentobarbital and ventilated with room air by a volume ventilator. Each animal was monitored by a femoral artery and a pulmonary artery catheter for systemic and pulmonary blood pressures, respectively, an electrocardiograph, pulse oximetry, and inspired and expired respiratory gas measurements by mass spectrometry. Arterial blood gas analysis was undertaken after one series of air emboli. Air boluses (containing the nonradioactive nitrogen isotope N2) of 50, 100, 200, and 500 mul/kg were injected slowly into the distal aorta through a second arterial catheter advanced 35 cm above the inguinal ligament. All emboli >/=100 mul/kg and 60% of the 50 mul/kg emboli were detected by increased ETN2 within 30 s, reaching peak levels in <2.75 min. The washout time for the N2 was longer for larger emboli, ranging from 2.9 +/- 2.8 min for 50 mul/kg emboli to 17.3 +/- 3.2 min for the 500 mug/kg emboli. There were no significant changes in end-tidal carbon dioxide, pulmonary or systemic blood pressures, or arterial blood gases. Increased ETN2 can no longer be considered pathognomonic for venous air embolism; arterial air embolism may have occurred.