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Accordingly, it is essential to explore in greater depth the pathophysiology of the fluid overload to optimize and individualize its management.2,3 The current evidence suggests that fluid overload exhibits considerable variability in terms of severity, quantity, and distribution.3 This is due to the complex pathophysiology of the condition, with multiple interconnecting mechanisms: cardiac anatomy and function and changes in pulmonary and systemic venous capacitance, vascular endothelial barrier function, neurohormonal activation, interaction between hydrostatic and oncotic pressures in the capillary and interstitial compartments, and lymphatic system integrity and distensibility.3 All of the above can result in a disconnection between the pressure and fluid overloads and give rise to distinct clinical and hemodynamic patterns.4 Thus, volume redistribution from the splanchnic to pulmonary vascular territory predominates in some patients while endovascular/interstitial fluid overload predominates in others