University of Groningen, Department of Cardiology, University Medical Center Groningen, Groningen, Netherlands.
Center for Clinical Medicine, University Faculty of Health, University of Witten Herdecke, Witten, Germany.
Nat Rev Cardiol. 2020 Oct;17(10):641-655. doi: 10.1038/s41569-020-0379-7. Epub 2020 May 15.
Congestion is the main reason for hospitalization in patients with acute decompensated heart failure and is an important target for therapy. However, achieving complete decongestion can be challenging. Furthermore, residual congestion before discharge from hospital is associated with a high risk of early rehospitalization and death. An improved understanding of the pathophysiology of congestion is of great importance in finding better and more personalized therapies. In this Review, we describe the two different forms of congestion - intravascular congestion and tissue congestion - and hypothesize that differentiating between and specifically treating these two different forms of congestion could improve the outcomes of patients with acute decompensated heart failure. Although the majority of these patients have a combination of both intravascular and tissue congestion, one phenotype can dominate. Each of these two forms of congestion has a different pathophysiology and requires a different diagnostic approach. We provide an overview of novel and established biomarkers, imaging modalities and mechanical techniques for identifying each type of congestion. Treatment with loop diuretics, the current cornerstone of decongestive treatment, reduces circulating blood volume and thereby reduces intravascular congestion. However, the osmolality of the circulating blood decreases with the use of loop diuretics, which might result in less immediate translocation of fluid from the tissues (lungs, abdomen and periphery) to the circulation when the plasma refill rate is exceeded. By contrast, aquaretic drugs (such as vasopressin antagonists) predominantly cause water excretion, which increases the osmolality of the circulating blood, potentially improving translocation of fluid from the tissues to the circulation and thereby relieving tissue congestion.
充血是急性失代偿性心力衰竭患者住院的主要原因，也是治疗的重要目标。然而，实现完全充血消退可能具有挑战性。此外，出院前仍存在充血与早期再住院和死亡的风险增加有关。深入了解充血的病理生理学对于寻找更好和更个性化的治疗方法非常重要。在这篇综述中，我们描述了两种不同形式的充血——血管内充血和组织充血，并假设区分和专门治疗这两种不同形式的充血可以改善急性失代偿性心力衰竭患者的预后。尽管这些患者大多数都同时存在血管内和组织充血，但有一种表型可能占主导地位。这两种充血形式中的每一种都有不同的病理生理学，需要不同的诊断方法。我们概述了用于识别每种充血类型的新型和已建立的生物标志物、成像方式和机械技术。袢利尿剂是目前充血治疗的基石，可减少循环血量，从而减轻血管内充血。然而，袢利尿剂的使用会降低循环血液的渗透压，当血浆再填充率超过时，可能会导致从组织（肺部、腹部和外周）向循环中转移的液体量减少。相比之下， aquaretic 药物（如血管加压素拮抗剂）主要引起水排泄，增加循环血液的渗透压，可能改善从组织向循环中转移液体，从而缓解组织充血。
