Davis H H, Schwartz D J, Lefrak S S, Susman N, Schainker B A
Chest. 1978 Apr;73(4):507-11. doi: 10.1378/chest.73.4.507.
Hypoxemia is a frequent occurrence in patients with severe hepatic disease. Multiple mechanisms have been implicated in the production of such hypoxemia. The case of a 35-year-old man with cyanosis, clubbing, and cirrhosis is presented. Physiologic data from this patient revealed normal pulmonary function, except for a low diffusing capacity and a 28 percent shunt while the patient was breathing 100 percent oxygen. A perfusion scan with radioactive 99mtechnetium-labelled macroaggregated albumin revealed 67 percent of the labelled macroaggregated albumin in the systemic circulation. Post-mortem examination demonstrated normal pulmonary parenchyma, markedly dilated intraparenchymal capillaries and arterioles, subpleural angiomata, and cirrhosis. No anatomic arteriovenous connections were demonstrated before or after death. We conclude that the arterial hypoxemia of some patients with hepatic cirrhosis results from dilated gas-exchanging blood vessels. These widened vessels prevent end pulmonary capillary oxygen tension from reaching equilibrium with alveolar gas, perhaps because of the widened distance for diffusion.
低氧血症在重症肝病患者中很常见。多种机制与这种低氧血症的产生有关。本文介绍了一名35岁患有发绀、杵状指和肝硬化的男性病例。该患者的生理数据显示，除了在呼吸100%氧气时弥散能力低和分流率为28%外，肺功能正常。用放射性99m锝标记的大颗粒白蛋白进行的灌注扫描显示，67%的标记大颗粒白蛋白存在于体循环中。尸检显示肺实质正常，实质内毛细血管和小动脉明显扩张，胸膜下血管瘤，以及肝硬化。生前和死后均未发现解剖学上的动静脉连接。我们得出结论，一些肝硬化患者的动脉低氧血症是由扩张的气体交换血管引起的。这些增宽的血管阻止肺终末毛细血管氧张力与肺泡气体达到平衡，可能是因为扩散距离增宽。
