Unveiling the Systemic Impact of Congestion in Heart Failure: A Narrative Review of Multisystem Pathophysiology and Clinical Implications

Figure 1. Mechanisms of congestion: volume overload vs. redistribution. This figure illustrates the two main mechanisms of congestion in acute heart failure. Volume overload results from excess fluid retention (RAAS activation, increased preload), leading to pulmonary (interstitial/alveolar edema) and systemic venous congestion (hepatic congestion, renal dysfunction). Redistribution occurs via a venous pressure shift, increasing capillary hydrostatic pressure and causing pulmonary congestion without fluid excess.

Figure 2. Congestion in heart failure. Congestion in heart failure results from increased venous pressure and fluid retention, leading to multisystem involvement. Pulmonary congestion manifests as pulmonary edema, dyspnea, and impaired oxygenation. Renal dysfunction occurs due to reduced glomerular filtration rate (GFR), sodium and water retention, and activation of the renin-angiotensin-aldosterone system (RAAS). Hepatic congestion can lead to hepatomegaly, liver dysfunction, and fibrosis. Peripheral congestion contributes to pitting edema and venous stasis dermatitis. Meanwhile, structural and functional cardiac changes, including remodeling, valve dysfunction, and ischemia, further exacerbate heart failure progression.