Antonelli D, Barzilay E, Lev A, Dar H
Minerva Med. 1985 Oct 13;76(39):1819-22.
Pulmonary oedema is caused by an excessive accumulation of interstitial fluid in the lungs: in the case of left ventricular failure, oedema arises due to an increase in capillary hydrostatic pressure. Non-cardiac oedema, on the other hand, is brought about by a change in alveolar capillary membrane permeability. Although the causes are different, namely respiratory distress syndrome in adults, altitude-induced pulmonary oedema, oxygen toxicity, medication, metabolic changes, etc., the result is the same, i.e. damage to the alveolar capillary membrane. This damage appears to be brought about by two factors: complement activation and damage to the blood clotting mechanism. The difference between cardiac and non-cardiac pulmonary oedema is difficult to gauge. If pulmonary cone pressure is normal or low, and if the oedematous fluid/plasma protein ratio is greater than 0.7, the oedema is non-cardiac in origin. Treatment is carried out with the aim of repairing the alveolar capillary membrane and preventing extension of the damage. Respiratory insufficiency is treated by a mechanical respirator, applying positive pressure at the end of expiration. Fluid administration is adjusted according to pulmonary cone pressure levels. Opinions are still divided over whether to administer crystalline or colloidal solutions, steroids or protease inhibitors.
在左心室衰竭的情况下,水肿是由于毛细血管静水压升高所致。另一方面,非心源性水肿是由肺泡毛细血管膜通透性改变引起的。尽管病因不同,如成人呼吸窘迫综合征、高原性肺水肿、氧中毒、药物、代谢变化等,但结果是相同的,即肺泡毛细血管膜受损。这种损伤似乎是由两个因素引起的:补体激活和凝血机制损伤。心源性和非心源性肺水肿之间的差异很难判断。如果肺楔压正常或偏低,且水肿液/血浆蛋白比值大于0.7,则水肿为非心源性。治疗的目的是修复肺泡毛细血管膜并防止损伤扩大。呼吸功能不全通过机械通气治疗,在呼气末施加正压。根据肺楔压水平调整液体输入量。对于是否给予晶体或胶体溶液、类固醇或蛋白酶抑制剂,仍存在分歧。