Sisakian Hamayak S, Tavaratsyan Ani R
Department of Cardiology and Clinic of General and Invasive Cardiology, University Hospital 1, Yerevan State Medical University Yerevan, Armenia.
Erebouni Medical Centre, Yerevan State Medical University Yerevan, Armenia.
Am J Cardiovasc Dis. 2024 Apr 15;14(2):81-89. doi: 10.62347/YGQQ8696. eCollection 2024.
The current traditional pathophysiologic concept of pulmonary edema of cardiogenic origin explains its development by a hydrostatic effect due to increased pulmonary capillary pressure resulting in fluid flux to alveolar and interstitial areas from capillaries. However, several experimental studies and clinical data of poor response to hemodynamic and diuretic treatment in many scenarios provide further evidence of the involvement of several other contributing factors to the development of cardiogenic pulmonary edema. Several experimental and clinical studies have found that sympathetic overactivity with elevated plasma catecholamine concentrations may play an important role in the development of cardiovascular-associated pulmonary edema. Catecholamine-induced pulmonary injury may be one of the key mechanisms in acute cardiogenic pulmonary edema triggering proinflammatory cytokine overactivation, oxidative stress and myocardial injury. In the everyday treatment of acute heart failure, physicians should consider the possibility of other noncardiogenic mechanisms involved in the progression of acute pulmonary edema, particularly catecholamine overactivity, lymphatic drainage, inflammatory and oxidative stress, high surfactant protein. The classic, hemodynamic treatment approach in pulmonary edema with the coexistence of other contributing factors may not provide adequate clinical benefit during treatment.
目前关于心源性肺水肿的传统病理生理概念认为，其发展是由于肺毛细血管压力升高产生的流体静力效应，导致液体从毛细血管流向肺泡和间质区域。然而，多项实验研究以及许多情况下对血流动力学和利尿剂治疗反应不佳的临床数据，进一步证明了其他几个促成因素在心源性肺水肿发展过程中的作用。多项实验和临床研究发现，交感神经过度活跃以及血浆儿茶酚胺浓度升高，可能在心源性相关肺水肿的发展中起重要作用。儿茶酚胺诱导的肺损伤可能是急性心源性肺水肿引发促炎细胞因子过度激活、氧化应激和心肌损伤的关键机制之一。在急性心力衰竭的日常治疗中，医生应考虑其他非心源性机制参与急性肺水肿进展的可能性，特别是儿茶酚胺过度活跃、淋巴引流、炎症和氧化应激、高表面活性蛋白。在存在其他促成因素的情况下，经典的血流动力学治疗方法用于肺水肿时，可能在治疗期间无法提供足够的临床益处。
