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减压应激的心肺后果。

Cardiopulmonary consequences of decompression stress.

作者信息

Neuman T S, Spragg R G, Wagner P D, Moser K M

出版信息

Respir Physiol. 1980 Aug;41(2):143-53. doi: 10.1016/0034-5687(80)90048-1.

DOI:10.1016/0034-5687(80)90048-1
PMID:6776599
Abstract

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.

摘要

临床上无法检测到的静脉气体栓塞(VGE)在接受高压环境下临床平稳减压的动物和人类中都能常规检测到。在这种情况下,VGE对气体交换和肺血流动力学的影响尚不清楚。因此,我们研究了临床平稳减压对未麻醉绵羊心肺的影响。给绵羊植入股动脉导管、 Swan - Ganz导管、进行慢性气管切开,并将其俯卧位轻度约束。在对肺动脉压(pPA)、平均肺动脉楔压(pPAw)、心输出量(CO)、动脉血和混合静脉血气进行基线测量、使用多普勒超声气泡检测以及用133Xe进行V/Q扫描后,将动物暴露于:(a)6.03ATA下15分钟(n = 8),(b)6.03ATA下17.5分钟,或(c)1ATA下15分钟的对照期(n = 7)。对照组中所有测量参数均保持不变。在所有暴露于压力的动物中均检测到VGE。与对照组相比,两个暴露组的CO均下降20%(P < 0.05),肺血管阻力(PVR)上升60%(P < 0.05)。PVR的这种升高明显超过了根据观察到的CO下降所预测的值。对pPA和pPAw的分析表明,左右心室均未衰竭。未检测到气体交换的明显异常。所有动物的V/Q扫描均保持不变。我们得出结论,临床平稳减压应激会改变CO和PVR。

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