Weil M H, Henning R J
Crit Care Med. 1977 Sep-Oct;5(5):215-9. doi: 10.1097/00003246-197709000-00001.
Our findings confirm that acute pulmonary edema, when caused by left ventricular failure, represents a form of acute perfusion failure (shock) with metabolic acidemia, lactacidemia, and a reduction in forward blood flow. It is associated with a marked increase in peripheral resistance and an increase in venous capacitance. Most importantly, acute pulmonary edema is associated with a reduction in the intravascular blood volume. Acute pulmonary edema is not fundamentally different from other types of shock in which the shock state is initiated by one primary defect, and during the course of its progression, other primary mechanisms are called into action. In the instance of acute cardiogenic edema, the primary defect is cardiac pump failure and the secondary defects include hypovolemia and distributive defects associated with arterial vasoconstriction and expanded venous capacitance. Furosemide reverses acute pulmonary edema by increasing rather than decreasing intravascular blood volume with consequent improvement in the distributive and hypovolemic defects. Under extreme conditions, the volume defect in acute pulmonary edema may be so great that the patient presents with primary hypovolemia. The utilization of volume repletion is warranted under these circumstances.
我们的研究结果证实，由左心室衰竭引起的急性肺水肿，表现为一种伴有代谢性酸血症、乳酸血症和前向血流减少的急性灌注衰竭（休克）形式。它与外周阻力显著增加和静脉容量增加有关。最重要的是，急性肺水肿与血管内血容量减少有关。急性肺水肿与其他类型的休克并无根本区别，在其他类型的休克中，休克状态由一个主要缺陷引发，并且在其进展过程中，其他主要机制也会发挥作用。在急性心源性水肿的情况下，主要缺陷是心脏泵衰竭，次要缺陷包括与动脉血管收缩和静脉容量扩大相关的血容量不足和分布性缺陷。呋塞米通过增加而非减少血管内血容量来逆转急性肺水肿，从而改善分布性和血容量不足性缺陷。在极端情况下，急性肺水肿中的容量缺陷可能非常严重，以至于患者表现为原发性血容量不足。在这些情况下，进行容量补充是必要的。
