Cardiopulmonary consequences of decompression stress.

Clinically undetectable venous gas emboli (VGE) can be routinely demonstrated in both animals and men undergoing clinically uneventful decompression from hyperbaric environments. The effect of VGE on gas exchange and pulmonary hemodynamics in this setting is unclear. We therefore have studied the cardiopulmonary effects of clinically uneventful decompression on unanesthetized sheep. Sheep were instrumented with a femoral arterial catheter, Swan-Ganz catheter, chronic tracheostomy, and were loosely restrained in the prone position. Following baseline measurements of pulmonary artery pressure (pPA), mean pulmonary artery wedge pressure (pPAw), cardiac output (CO), arterial and mixed venous blood gases, Doppler ultrasonic bubble detection, and V/Q scans using 133Xe, the animals were exposed to: (a) a 15-min exposure to 6.03 ATA (n = 8), (b) a 17.5-min exposure to 6.03 ATA, or (c) a 15-min control period at 1 ATA (n = 7). All measured parameters remained unchanged in the control group. VGE were detected in all animals exposed to pressure. In both exposure groups CO fell 20% (P < 0.05) and pulmonary vascular resistance (PVR) rose 60% (P < 0.05) compared to the control group. This rise in PVR was significantly in excess of that predicted for the observed fall in CO. Analysis of pPA and pPAw suggested neither right nor left ventricular failure. No significant abnormalities of gas exchange were detected. V/Q scans remained unchanged in all animals. We conclude that CO and PVR are altered by clinically uneventful decompression stress.