肺水肿是液体在肺内蓄积而引起的一种症状。通常,心源性肺水肿的发病机理如下: 随着心功能的恶化——如在急性心肌梗塞时——左心室的排出量降低,造成左心室舒张末压升高。这一压力的升高波及到左心房、肺静脉,最终达肺毛细血管。于是,肺毛细血管“微孔”的孔径和通透性增加,肺毛细血管流体静力压亦增加,导致肺间质液体蓄积。间质神经末稍受到刺激而出现呼吸急促,肺泡和呼吸道出现水肿后,由于肺含气量减少和呼吸阻力增加,呼吸功能进一步恶化并导致低氧血症。低氧血症通过水肿液 Pulmonary edema is a symptom of fluid accumulation in the lungs. In general, the pathogenesis of cardiogenic pulmonary edema is as follows: As cardiac function worsens - as in acute myocardial infarction - a decrease in left ventricular output results in an increase in left ventricular end-diastolic pressure. This increase in pressure spreads to the left atrium, pulmonary veins, eventually reaching the pulmonary capillaries. As a result, pulmonary capillary “microporous” pore size and permeability increased, pulmonary capillary hydrostatic pressure also increased, resulting in interstitial fluid accumulation. Stimulation of the end of interstitial nerve resulting in shortness of breath, alveolar and respiratory tract edema, decreased lung volume and respiratory resistance due to increased respiratory function worsened and lead to hypoxemia. Hypoxemia through the edema fluid