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急性失代偿性心力衰竭中充血的机制

Mechanisms of Congestion in Acute Decompensated Heart Failure.

作者信息

Karimi Ashkan, Mathew Kristen, Pourafshar Negiin

机构信息

Carient Cardiovascular Medicine, Vienna, Virginia, USA.

Georgetown University School of Medicine, Washington, DC, USA.

出版信息

Cardiorenal Med. 2025;15(1):544-551. doi: 10.1159/000544929. Epub 2025 Jun 28.


DOI:10.1159/000544929
PMID:40582349
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12306954/
Abstract

BACKGROUND: Acute decompensated heart failure (ADHF) poses a challenging paradox of renal and cardiac pathophysiology, with volume excess or "congestion" being a key player. Understanding the mechanisms of congestion is crucial for effectively managing fluid overload and improving patient prognosis. SUMMARY: In this review, we evaluate the physiology of congestion and explore its implications for management in clinical practice. Mechanisms of congestion can largely be broken down under the subtext of fluid accumulation and fluid redistribution. Fluid accumulation develops as a consequence of neurohormonal dysregulation, physiologic maladaptive mechanisms, and detrimental crosstalk between the heart and the kidney. On the other hand, fluid redistribution evolves due to progressive overriding of compensatory vascular mechanisms, renal injury, and hormonal feedback. KEY MESSAGES: Understanding the complex pathophysiology of congestion in ADHF is crucial for effective volume management and protection against long-term mortality and morbidity risks. By targeting both fluid accumulation and redistribution mechanisms, clinicians can optimize treatment strategies to alleviate congestion and restore hemodynamic stability in patients with ADHF.

摘要

背景:急性失代偿性心力衰竭(ADHF)在肾脏和心脏病理生理学方面构成了一个具有挑战性的矛盾,容量超负荷或“充血”是一个关键因素。了解充血机制对于有效管理液体超负荷和改善患者预后至关重要。 总结:在本综述中,我们评估了充血的生理学,并探讨了其在临床实践中对管理的影响。充血机制在很大程度上可以在液体蓄积和液体重新分布的背景下进行分解。液体蓄积是神经激素失调、生理适应不良机制以及心脏与肾脏之间有害相互作用的结果。另一方面,液体重新分布是由于代偿性血管机制的逐渐失效、肾损伤和激素反馈而演变的。 关键信息:了解ADHF中充血的复杂病理生理学对于有效进行容量管理以及预防长期死亡和发病风险至关重要。通过针对液体蓄积和重新分布机制,临床医生可以优化治疗策略,以减轻ADHF患者的充血并恢复血流动力学稳定性。

相似文献

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[2]
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[6]
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[7]
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本文引用的文献

[1]
Angiotensin II and the Renal Hemodynamic Response to an Isolated Increased Renal Venous Pressure in Rats.

Front Physiol. 2021-11-16

[2]
Diuretic Resistance Treated with Low-Dose Hydralazine: A Case Report and Review of the Literature.

Case Rep Nephrol Dial. 2021-8-12

[3]
Renal negative pressure treatment as a novel therapy for heart failure-induced renal dysfunction.

Am J Physiol Regul Integr Comp Physiol. 2021-10-1

[4]
Estimated Glomerular Filtration Rate Is Associated With an Increased Risk of Death in Heart Failure Patients With Preserved Ejection Fraction.

Front Cardiovasc Med. 2021-4-26

[5]
Pathophysiology of Hypertension: The Mosaic Theory and Beyond.

Circ Res. 2021-4-2

[6]
Renal Denervation for Patients With Heart Failure: Making a Full Circle.

Circ Heart Fail. 2021-3

[7]
Systematic Review of the Association Between Worsening Renal Function and Mortality in Patients With Acute Decompensated Heart Failure.

Kidney Int Rep. 2020-7-2

[8]
SGLT2 inhibitors in patients with heart failure with reduced ejection fraction: a meta-analysis of the EMPEROR-Reduced and DAPA-HF trials.

Lancet. 2020-8-30

[9]
Sympathetic Overactivity in CKD Disrupts Buffering of Neurotransmission by Endothelium-Derived Hyperpolarizing Factor and Enhances Vasoconstriction.

J Am Soc Nephrol. 2020-10

[10]
Pulmonary artery pressure-guided therapy in ambulatory patients with symptomatic heart failure: the CardioMEMS European Monitoring Study for Heart Failure (MEMS-HF).

Eur J Heart Fail. 2020-10

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