背景:肺动脉栓塞(AE)和血栓栓塞会导致严重的通气灌注缺陷。肺灌注功能障碍的空间分布在两种肺栓塞病理中存在很大差异,以及对呼吸力学的影响,气体交换,和通气-灌注匹配尚未在研究中进行比较。因此,我们比较了反映气道和呼吸组织力学的指标变化,气体交换,当通过静脉注入空气作为气体栓塞的模型或通过夹住主肺动脉以模拟严重的血栓栓塞而诱发肺栓塞时,和二氧化碳图。
方法:在通过将0.1mL空气注入股静脉并在闭塞左肺动脉(LPAO)后诱导肺AE后,在基线条件下测量麻醉和机械通气的大鼠(n=9)。通过强制振荡来评估机械参数的变化,以测量气道阻力,肺组织阻尼,和弹性。通过血气分析确定氧气(PaO2)和二氧化碳(PaCO2)的动脉分压。还通过测量潮气末CO2浓度(ETCO2)来评估气体交换指数,形状因素,和死空间参数的体积二氧化碳图。
结果:在两种栓塞模型中ETCO2均有降低的情况下,LPAO后发现支气管张力明显升高和肺组织力学受损,而AE不影响肺力学。相反,只有AE使PaO2和PaCO2恶化,而LPAO不影响这些结局.AE和LPAO均未引起解剖或生理死腔的变化,而两种栓塞模型均导致肺泡死腔指数升高,并伴有肺内分流。
结论:我们的研究结果表明,LPAO后严重的局灶性低碳酸血症会引发支气管收缩,将气流重定向到灌注良好的肺区域,从而维持正常的氧合,和肺部的二氧化碳消除能力。然而,AE后弥漫性肺灌注的低碳酸血症可能达不到诱导肺力学变化的阈值水平;因此,使通气与灌注匹配的代偿机制激活效率较低。
BACKGROUND: Pulmonary air embolism (AE) and thromboembolism lead to severe ventilation-perfusion defects. The spatial distribution of pulmonary perfusion dysfunctions differs substantially in the two pulmonary embolism pathologies, and the effects on respiratory mechanics, gas exchange, and ventilation-perfusion match have not been compared within a study. Therefore, we compared changes in indices reflecting airway and respiratory tissue mechanics, gas exchange, and capnography when pulmonary embolism was induced by venous injection of air as a model of gas embolism or by clamping the main pulmonary artery to mimic severe thromboembolism.
METHODS: Anesthetized and mechanically ventilated rats (n = 9) were measured under baseline conditions after inducing pulmonary AE by injecting 0.1 mL air into the femoral vein and after occluding the left pulmonary artery (LPAO). Changes in mechanical parameters were assessed by forced oscillations to measure airway resistance, lung tissue damping, and elastance. The arterial partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) were determined by blood gas analyses. Gas exchange indices were also assessed by measuring end-tidal CO2 concentration (ETCO2), shape factors, and dead space parameters by volumetric capnography.
RESULTS: In the presence of a uniform decrease in ETCO2 in the two embolism models, marked elevations in the bronchial tone and compromised lung tissue mechanics were noted after LPAO, whereas AE did not affect lung mechanics. Conversely, only AE deteriorated PaO2, and PaCO2, while LPAO did not affect these outcomes. Neither AE nor LPAO caused changes in the anatomical or physiological dead space, while both embolism models resulted in elevated alveolar dead space indices incorporating intrapulmonary shunting.
CONCLUSIONS: Our findings indicate that severe focal
hypocapnia following LPAO triggers bronchoconstriction redirecting airflow to well-perfused lung areas, thereby maintaining normal oxygenation, and the CO2 elimination ability of the lungs. However,
hypocapnia in diffuse pulmonary perfusion after AE may not reach the threshold level to induce lung mechanical changes; thus, the compensatory mechanisms to match ventilation to perfusion are activated less effectively.