Arterial gas emboli in altitude-induced decompression sickness

Exposure to high altitudes can result in the evolved-gas condition referred to as decompression sickness (DCS). Ultrasonic monitoring techniques have clearly demonstrated the presence of venous gas emboli (VGE) during decompression. Although important to DCS research and our understanding of the physiological mechanisms of this condition, Venus gas emboli have not been considered clinically hazardous, unless in extreme numbers. Arterial gas emboli (AGE), on the other hand, are generally viewed with great concern. Arterial gas emboli can enter the cerebral arterial circulation and arrest blood flow resulting in potentially serious injury. Left ventricular gas emboli were observed with echo imaging in five volunteer subjects during exposure to simulated altitude. These serendipitous findings occurred during altitude exposure under 3 separate research protocols involving 79 subject exposures. The voluntary, fully informed consent of the subjects used in this research was obtained as required by AFR 169-3. A Hewlett-Packard SONOS 1000 Echo Imaging System was used to monitor for precordial gas emboli. The improved resolution of the SONOS 1000 appears to account for these new findings. Four subjects had high incidence DCS and VGE during previous research flights. One subject only had one flight. The altitudes and AGE onset times for the five cases were: (1) 25,500 ft/2:23, (2) 29,000 ft/0:27, (3) 19,500 ft/3:49, (4) 29,500 ft/3:15, and (5) 29,500 ft/1:31. In all five cases, at the time of AGE onset, the VGE scores were high from all monitored locations. Four of the cases were symptomatic at the time of AGE onset (pain and skin mottling). No cerebral manifestations were observed. All subjects were immediately recompressed to ground level and successfully treated with 2 hours of post-breathing or with hyperbaric oxygen therapy. In conclusion, previously undetected AGE were demonstrated--with and without DCS symptoms--during exposure to altitude. It appears that this gas transferred from the venous side to the arterial side via either intracardiac defects or the pulmonary circulation. The clinical and operational implications of this finding are yet to be determined.