Aronson Doron
Department of Cardiology, Rambam Health Care Campus, B. Rappaport Faculty of Medicine, Technion Medical School, Haifa, Israel.
Front Cardiovasc Med. 2022 Aug 17;9:933384. doi: 10.3389/fcvm.2022.933384. eCollection 2022.
Congestion is the single most important contributor to heart failure (HF) decompensation. Most of the excess volume in patients with HF resides in the interstitial compartment. Inadequate decongestion implies persistent interstitial congestion and is associated with worse outcomes. Therefore, effective interstitial decongestion represents an unmet need to improve quality of life and reduce clinical events. The key processes that underlie incomplete interstitial decongestion are often ignored. In this review, we provide a summary of the pathophysiology of the interstitial compartment in HF and the factors governing the movement of fluids between the interstitial and vascular compartments. Disruption of the extracellular matrix compaction occurs with edema, such that the interstitium becomes highly compliant, and large changes in volume marginally increase interstitial pressure and allow progressive capillary filtration into the interstitium. Augmentation of lymph flow is required to prevent interstitial edema, and the lymphatic system can increase fluid removal by at least 10-fold. In HF, lymphatic remodeling can become insufficient or maladaptive such that the capacity of the lymphatic system to remove fluid from the interstitium is exceeded. Increased central venous pressure at the site of the thoracic duct outlet also impairs lymphatic drainage. Owing to the kinetics of extracellular fluid, microvascular absorption tends to be transient (as determined by the revised Starling equation). Therefore, effective interstitial decongestion with adequate transcapillary plasma refill requires a substantial reduction in plasma volume and capillary pressure that are prolonged and sustained, which is not always achieved in clinical practice. The critical importance of the interstitium in the congestive state underscores the need to directly decongest the interstitial compartment without relying on the lowering of intracapillary pressure with diuretics. This unmet need may be addressed by novel device therapies in the near future.
充血是导致心力衰竭(HF)失代偿的最重要单一因素。HF患者体内多余的液体大部分潴留在间质腔隙。充血不充分意味着间质持续充血,并与更差的预后相关。因此,有效的间质去充血是改善生活质量和减少临床事件的一项未被满足的需求。间质去充血不完全的关键机制常常被忽视。在这篇综述中,我们总结了HF中间质腔隙的病理生理学以及控制液体在间质和血管腔隙之间流动的因素。细胞外基质致密化的破坏会随着水肿发生,使得间质顺应性增高,容积的大幅变化只会轻微增加间质压力,并允许液体持续从毛细血管滤入间质。需要增加淋巴液流动以防止间质水肿,并且淋巴系统能够将液体清除量增加至少10倍。在HF中,淋巴系统重塑可能变得不足或适应不良,以至于淋巴系统从间质清除液体的能力被超越。胸导管出口处中心静脉压升高也会损害淋巴引流。由于细胞外液的动力学特性,微血管吸收往往是短暂的(由修正的Starling方程决定)。因此,要通过充足的跨毛细血管血浆再充盈实现有效的间质去充血,需要大幅且持续地降低血浆量和毛细血管压力,而这在临床实践中并不总能实现。间质在充血状态中的关键重要性凸显了直接消除间质充血的必要性,而不依赖利尿剂降低毛细血管内压力。在不久的将来,新型设备疗法可能满足这一未被满足的需求。