Abstract
Abstract
Background
Acute heart failure (AHF) is a significant cardiovascular syndrome characterized by either new-onset heart failure (HF) or acutely decompensated heart failure (ADHF), typically presenting with systemic and pulmonary congestion. The European Society of Cardiology has reinforced the importance of early guideline-directed medical therapy (GDMT) initiation and individualized decongestive strategies. This article explores current knowledge of AHF pathophysiology. The simplified hemodynamic paradigm previously used to explain AHF has been replaced over the past few decades by a more complex network of interacting mechanisms.
Main text
The clinical presentation of AHF reflects a heterogeneous combination of cardiac abnormalities and systemic pathophysiological processes rather than a single disease entity. Despite overlapping clinical presentations, AHF arises from diverse underlying conditions and pathophysiological mechanisms. Left ventricular systolic or diastolic dysfunction elevates filling pressures, contributing to increased preload and afterload, which in turn promotes pulmonary congestion. End-organ dysfunction may result from the combined effects of venous congestion, impaired perfusion, and neurohormonal and inflammatory activation. Despite advances, limited progress in acute management may contribute to persistently poor outcomes in AHF patients.
Conclusion
Initial management of AHF commonly includes intravenous diuretics for patients with congestion, while vasodilators and other therapies are selected according to congestion status, perfusion, blood pressure, hemodynamic profile, clinical phenotype, and the predominant underlying pathophysiological mechanism. This review examines pathophysiological processes contributing to AHF onset and progression, highlighting clinical implications and therapeutic targets.