Swiss Cardiovascular Center Bern, University Hospital, Bern, Switzerland.
Prog Cardiovasc Dis. 2009 Nov-Dec;52(3):249-59. doi: 10.1016/j.pcad.2009.10.002.
Flash pulmonary edema (FPE) is a general clinical term used to describe a particularly dramatic form of acute decompensated heart failure. Well-established risk factors for heart failure such as hypertension, coronary ischemia, valvular heart disease, and diastolic dysfunction are associated with acute decompensated heart failure as well as with FPE. However, endothelial dysfunction possibly secondary to an excessive activity of renin-angiotensin-aldosterone system, impaired nitric oxide synthesis, increased endothelin levels, and/or excessive circulating catecholamines may cause excessive pulmonary capillary permeability and facilitate FPE formation. Renal artery stenosis particularly when bilateral has been identified has a common cause of FPE. Lack of diurnal variation in blood pressure and a widened pulse pressure have been identified as risk factors for FPE. This review is an attempt to delineate clinical and pathophysiological mechanisms responsible for FPE and to distinguish pathophysiologic, clinical, and therapeutic aspects of FPE from those of acute decompensated heart failure.
暴发性肺水肿(Flash pulmonary edema,FPE)是用于描述一种特别剧烈的急性失代偿性心力衰竭形式的通用临床术语。高血压、冠状动脉缺血、瓣膜性心脏病和舒张功能障碍等已确立的心力衰竭风险因素与急性失代偿性心力衰竭以及 FPE 相关。然而,内皮功能障碍可能继发于肾素-血管紧张素-醛固酮系统过度活跃、一氧化氮合成受损、内皮素水平升高和/或循环儿茶酚胺过多,可能导致肺毛细血管通透性增加并促进 FPE 的形成。肾动脉狭窄,特别是双侧肾动脉狭窄,是 FPE 的常见病因。缺乏血压的昼夜变化和脉压增宽已被确定为 FPE 的危险因素。本综述旨在阐述导致 FPE 的临床和病理生理机制,并将 FPE 的病理生理、临床和治疗方面与急性失代偿性心力衰竭区分开来。