Ricardo Castro

La sobrecarga de fluidos después de la reanimación es una condición frecuente en el paciente crítico y se asocia de forma independiente con lesión renal aguda, recuperación renal incompleta, ventilación mecánica prolongada y mayor mortalidad (Malbrain et al., 2014). En este escenario, la ultrafiltración durante la terapia de reemplazo renal se ha transformado en una herramienta habitual de desresucitación. Sin embargo, remover fluido no equivale simplemente a corregir un balance positivo. La ultrafiltración es una intervención hemodinámica, con beneficios potenciales, riesgos inmediatos y un margen terapéutico estrecho. La pregunta clínica relevante no debería limitarse a cuánto fluido debe retirarse, sino a cuánto fluido puede tolerar ese paciente, en ese momento, con su reserva cardiovascular, endotelial e intersticial disponible.

The vascular waterfall phenomenon, rooted in Starling resistor principles, describes how blood flow becomes independent of downstream pressure when intraluminal pressure falls below a critical closing pressure (Pcrit). This review first introduces the classic arterial vascular waterfall, where local Pcrit enables organ-specific autoregulation of blood flow despite varying metabolic demands. Building on this framework, we extend the concept to the venous side, where similar mechanisms govern venous return and protect against congestion. The pulmonary vascular waterfall serves as a prototype, illustrating how alveolar pressures redefine downstream limits, shaping the effects of mechanical ventilation and positive end-expiratory pressure (PEEP). In valveless venous beds such as the hepatic veins, a reverse vascular waterfall may occur when elevated downstream pressure, typically right atrial pressure, causes brief, localized backflow buffered by vessel collapse and the emergence of a new Pcrit. These mechanisms explain organ-specific vulnerabilities to venous congestion: organs with effective venous waterfalls, such as the liver and intestine, can partially buffer overload, whereas the kidney, lacking such protection, is highly susceptible to venous pressure-dependent injury. Clinical implications include refined approaches to PEEP titration, fluid management balancing responsiveness with tolerance, and congestion assessment through Doppler ultrasound. Reframing congestion as a dynamic Starling resistor process explains why similar CVP elevations produce heterogeneous organ effects and provides a mechanistic basis for individualized, physiology-guided critical care.

The concept of fluid tolerance was recently introduced by our group. Here we review the major organ systems affected by potential venous congestion (cardiovascular, pulmonary, abdominal, renal, central nervous system and dermal tissue) as well as the pathophysiological findings that may lead them to be more vulnerable to detrimental effects of overzealous fluid administration. We thus propose an organ system-based framework for clinicians to assess their patient’s fluid tolerance by different means ranging from the traditional physical examination to the more invasive and technology-based methods. Hopefully this can lead to further study and eventual validation of a fluid tolerance score.

In response to the recent proposal by Monares-Zepeda et al. to estimate mean systemic filling pressure (MSFP) using cardiac power (CP) as a surrogate for the venous return pressure gradient (VRg), we raise concerns regarding the physiological validity and generalizability of the reported correlation. We demonstrate through simulation that the relationship between CP and VRg arises from structural mathematical coupling due to shared dependence on cardiac output (CO), and that this correlation weakens significantly (r = 0.54) when realistic physiological variability is introduced. We further argue that CP and VRg reflect distinct hemodynamic domains, and caution against interpreting their empirical correlation as evidence of physiological interchangeability. We call for broader validation of the model across diverse circulatory conditions. Comment on: ‘Presentation of a novel method to estimate analog mean systemic filling pressure based on cardiac power’ —on Correlation, Coupling, and Physiological Meaning.