## 1 Introduction  
Heart failure (HF) is a clinical syndrome characterized by structural or functional cardiac abnormalities that impair ventricular filling or the ejection of blood [1], triggering a cascade of compensatory neurohormonal and inflammatory responses [2, 3, 4]. The estimated prevalence of HF is around 2% among adults in developed countries and exceeds 10% in those over 70 years old, making it a major healthcare concern [3]. In Spain, the prevalence is similar [3] and HF remains a leading cause of hospitalization in older adults, primarily due to signs and symptoms of congestion [3; 5]. To better understand the clinical course and guide treatment, HF is classified according to left ventricular ejection fraction (LVEF) into three main phenotypes: reduced (HFrEF, \(\leq\)40%), mildly reduced (HFmrEF, 41-49%), and preserved (HFpEF, \(\geq\)50%) [3]. This classification is clinically significant, as it reflects different underlying etiologies, comorbidities, and, most importantly, variable responses to treatment [5]. HFrEF is characterized predominantly by neurohormonal activation and structural remodeling, whereas HFpEF involves endothelial and microvascular dysfunction and presents a heterogeneous biological profile [5]. Despite these distinctions, decongestive treatment strategies in acute settings often do not differ across these phenotypes [5]. Accurate congestion assessment remains one of the most critical and challenging aspects of HF management. Persistent congestion after hospital discharge is strongly associated with poor prognosis [6]. Hemodynamic congestion, or elevated ventricular filling pressures, often precedes clinical signs by days to weeks [6]. Unfortunately, a reliable non-invasive method for determining volume status is lacking, posing a significant diagnostic challenge when physical examination and standard laboratory tests are inconclusive [7; 8]. To address this issue, several tools have emerged, including congestion biomarkers, such as N-terminal pro-B-type natriuretic peptide (NT-proBNP) and Carbohydrate Antigen 125 (CA125) [9; 10], and point-of-care ultrasound (POCUS), which has become increasingly integrated into clinical practice across internal medicine units worldwide. Bedside ultrasound has proven to be a valuable diagnostic tool that complements history and physical examination [11; 12; 13; 14] and is now considered the fifth pillar of physical examination in HF [15]. Lung ultrasound (LUS) helps detect extravascular pulmonary water through B-lines, which correlate with worse prognosis [13; 14]. Inferior vena cava (IVC) diameter assessment provides a simple estimate of right atrial pressure and is associated with changes in pulmonary capillary wedge pressure [12]. Therapy guided by IVC diameter in hospitalized HF patients has been shown to lead to reductions in rehospitalizations and mortality [11; 12; 13; 14]. A recent pilot study (CAVAL US-AHF) combining a Doppler assessment of cardiac filling pressures, IVC, and LUS demonstrated that this approach is safe and reliable for guiding therapy [12]. In line with these advances, the recent consensus on the management of fluid overload in acute HF by [PERSON] et al. [16] proposes two distinct congestion phenotypes and recommends a multiparametric approach that integrates clinical symptoms, biomarkers, and ultrasound findings to guide treatment. To further refine the quantification of congestion, [PERSON] et al. proposed the Venous Excess Ultrasound (VExUS) score, a protocol based on Doppler flow patterns in three abdominal veins--hepatic, portal, and intrarenal--that classifies patients into three levels of congestion: none, mild, or severe [17]. The VExUS protocol begins by assessing the IVC. If the diameter is <2 cm, venous congestion is ruled out. If it is \(\geq\)2 cm, a further Doppler evaluation is performed. The hepatic vein waveform, portal vein pulsatility, and intrarenal vein pattern are analyzed and integrated into a severity score (grades 0-3).