BACKGROUND: Decompression to simulated altitude causes super-saturation of nitrogen desolved in body tissues and can result in venous gas emboli (VGE), which are usually "cleared" in the lung. Large intravenous boli of air administered to animals increase pulmonary artery pressure (PAP), and may induce cross-over of gas to the left side of the heart (creating dangerous arterial gas emboli). This study was conducted to determine whether high VGE grades induced at simulated altitude elevate PAP in humans. METHODS: Eight human subjects with subclinical tricuspid regurgitation were exposed to simulated altitude of > or = 24,000 ft (7315 m) for up to 4 h. Systolic PAP was derived from Doppler ultrasound echo imaging measurements of peak flow velocity of the regurgitant jet. VGE was rated using the Spencer scale. A technique of "bubble titration" was employed with changes in exercise and altitude to maintain sufficient bubbles without decompression sickness. RESULTS: All subjects developed grade III-IV VGE, but 3 developed decompression sickness, resulting in earlier termination. Pre-exposure systolic PAP averaged 24.4 +/- 1.3 (SE) mm Hg. After 1, 2, 3 and 4 h, systolic PAP was 23.7 +/- 1.2 (n = 8), 23.4 +/- 1.1 (n = 8), 23.3 +/- 1.0 (n = 6), and 25.9 +/- 0.6 (n = 5) mm Hg, respectively. Systolic PAP remained unchanged, in spite of bubble grades III-IV for up to 4 h. CONCLUSION: As systolic PAP did not increase with hypobaric exposures that created substantial VGE, the bubble loading was not sufficient to overwhelm the lung clearing capacity. The risk of high PAP resulting in VGE cross-over is low during typical operational altitude exposures.
BACKGROUND: Decompression to simulated altitude causes super-saturation of nitrogen desolved in body tissues and can result in venous gas emboli (VGE), which are usually "cleared" in the lung. Large intravenous boli of air administered to animals increase pulmonary artery pressure (PAP), and may induce cross-over of gas to the left side of the heart (creating dangerous arterial gas emboli). This study was conducted to determine whether high VGE grades induced at simulated altitude elevate PAP in humans. METHODS: Eight human subjects with subclinical tricuspid regurgitation were exposed to simulated altitude of > or = 24,000 ft (7315 m) for up to 4 h. Systolic PAP was derived from Doppler ultrasound echo imaging measurements of peak flow velocity of the regurgitant jet. VGE was rated using the Spencer scale. A technique of "bubble titration" was employed with changes in exercise and altitude to maintain sufficient bubbles without decompression sickness. RESULTS: All subjects developed grade III-IV VGE, but 3 developed decompression sickness, resulting in earlier termination. Pre-exposure systolic PAP averaged 24.4 +/- 1.3 (SE) mm Hg. After 1, 2, 3 and 4 h, systolic PAP was 23.7 +/- 1.2 (n = 8), 23.4 +/- 1.1 (n = 8), 23.3 +/- 1.0 (n = 6), and 25.9 +/- 0.6 (n = 5) mm Hg, respectively. Systolic PAP remained unchanged, in spite of bubble grades III-IV for up to 4 h. CONCLUSION: As systolic PAP did not increase with hypobaric exposures that created substantial VGE, the bubble loading was not sufficient to overwhelm the lung clearing capacity. The risk of high PAP resulting in VGE cross-over is low during typical operational altitude exposures.