MacIver David H, Clark Andrew L
Department of Cardiology, Taunton and Somerset Hospital, Taunton, United Kingdom; Biological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, United Kingdom; Medical Education, University of Bristol, Bristol, United Kingdom.
Department of Cardiology, Hull York Medical School, University of Hull, Castle Hill Hospital, Cottingham, United Kingdom.
Am J Cardiol. 2015 Apr 1;115(7):992-1000. doi: 10.1016/j.amjcard.2015.01.026. Epub 2015 Jan 15.
The development of acute pulmonary edema involves a complex interplay between the capillary hydrostatic, interstitial hydrostatic, and oncotic pressures and the capillary permeability. We review the pathophysiological processes involved and illustrate the concepts in a number of common clinical situations including heart failure with normal and reduced ejection fractions, mitral regurgitation, and arrhythmias. We also describe other rarer causes including exercise, swimming, and diving-induced acute pulmonary edema. We suggest a unifying framework in which the critical abnormality is a mismatch or imbalance between the right and left ventricular stroke volumes. In conclusion, we hypothesize that increased right ventricular contraction is an important contributor to the sudden increase in capillary hydrostatic pressure, and therefore, a central mechanism involved in the development of alveolar edema.
急性肺水肿的发展涉及毛细血管静水压、间质静水压、胶体渗透压以及毛细血管通透性之间复杂的相互作用。我们回顾了其中涉及的病理生理过程,并在一些常见临床情况中阐述这些概念,包括射血分数正常和降低的心力衰竭、二尖瓣反流及心律失常。我们还描述了其他较罕见的病因,包括运动、游泳和潜水诱发的急性肺水肿。我们提出了一个统一的框架,其中关键异常是左右心室每搏量之间的不匹配或失衡。总之,我们推测右心室收缩增强是毛细血管静水压突然升高的一个重要因素,因此是肺泡水肿发生的核心机制。