Not all fluid overloads are the same: some practical considerations for better decongestion

This article refers to ‘Contributions of cardiac dysfunction and volume status central haemodynamics in chronic heart failure’ by W.L. Miller et al., published this issue on pages 1097–1105. Fluid overload with and/or peripheral congestion is the cardinal feature characterizing syndrome failure (HF). The pathophysiology underlying fluid retention complex multifactorial but it seems that process develops at early stage disease, being related augmented reflex sympatho-excitation (in response transient elevations intracardiac pressures) an impairment renal sodium water control.1 In parallel, myocardial resulted reduced output causes arterial underfilling, sensed as a reduction effective circulating blood (BV) baroreceptors unloading neurohormonal activation, which also leads further deterioration (retention) handling.2 Although mechanisms link between spiraling progression HF are not clearly understood, association presence more severe symptoms higher risk adverse clinical outcomes documented.3 Congestion remains main reason for hospital admission acute its persistence discharge contributes readmission predicts poor outcomes.4, 5 Thus, safe decongestion major goal challenge optimal management patients chronic, stable settings even those admitted signs HF. Additionally, prevention overload, identification risk, detection monitoring during entire natural course essential improve patients' quality life outcomes. accumulation starts intravascular compartment comprises venous systems – latter much complaint store increasing blood.5, 6 particular, splanchnic veins low vascular resistance high capacitance receive ?25% serve functional reservoir able accumulate 20–50% total BV.6, 7 With time, hydrostatic pressure vessels increases expands extravascular, interstitial space compliant capacity 3–4 times bigger than compartment.5, Clinically, manifests multi-organ congestion. compartments separated highly permeable membranes amounts distributed them mainly colloid osmotic pressures across capillary membranes. Typically, symptomatic HF, despite overall increase body majority patients, can be characterized equilibrium distribution extracellular (interstitial intravascular) (Figure 1A). magnitude one determinants symptom severity target decongestive therapy.5 multiple triggering factors, clinically manifesting worsening leading decompensation, often diagnosis Patterns development (i.e. gradual vs. rapid), localization congestion, therapy all important elements evaluation patterns decompensated associated different treatment response, short-term long-term outcomes.8 Such heterogeneity result relative predominance type either or 1B 1C, respectively). former presents rapid involvement filling (haemodynamic congestion) sudden 1B). pattern referred congestion5, 9 pulmonary oedema due hypertensive emergency most illustrative results from sympathetically-driven redistribution circulation, rather accumulation.7 These may present excessive explains absence any detectable changes weight BV preceding decompensation.7 contrast, (referred 9) constant tissues, gradually slower deterioration, (often multi-kilogram magnitude), 1C). Of note, balance level interstitium strongly dependent lymphatic system removal 10- 50-fold when rises.5 However, drainage deteriorated case significantly elevated right decreased perfusion gradient thoracic duct lead relation above considerations, al.10 provide interesting relevant piece information. authors aimed study simultaneously: (using radiolabel indicator-dilution technique assess plasma volume), catheterization (RHC), measures function detailed echocardiographic assessment, explore contributions each component Patients were divided according value into hypervolaemia (defined >+8% referenced normal volume) euvolaemia (total ?+8%). conclusion was only combined analysis (intravascular), (intracardiac), provides comprehensive picture consequences guide individualized therapy.10 We believe there some additional findings particular interest. Firstly, including moderate-severe [New York Heart Association (NYHA) class III–IV], less 40% presented (euvolaemia). carefully evaluated resting reported 20% had ventricular 24% left pressures.10 It reassures us advanced (NYHA III–IV), neither excess nor pressures. Here, want refer seminal work Prof. Phillip Poole-Wilson, who three decades ago teaching dyspnoea typically atrial pressure, almost always improvement symptoms.11 tend report corrected diuretics shortness breath under these circumstances simply determined interaction respiratory metabolic exercising skeletal muscle.11 Secondly, assessment using sophisticated accurate methods (not readily available practice) does tell everything about As depicted Figure 1, misleading proper interpretation (e.g. compartment). Total poorly correlates physical natriuretic peptide levels, meaningful information reservoir.7 has been documented stimulation nerves resultant pool significant preload within minutes, entirely unrelated change BV.12 forms strong background based development. For predominant ‘cardiac type’ diuretics, aquaretics ultrafiltration resistant forms) preferable recommended 1D).5, Other (although thoroughly investigated) include hypertonic saline infusion compression Interestingly, reports sodium–glucose co-transporter 2 (SGLT2) inhibitors facilitate volume-overloaded via mechanisms, diuresis13 potentially places SGLT2 therapy. vasodilators (with diuretics) recommended5, recent have shown neural control novel form 1E).7, 9, 14 Last, least, (cardiac) should equated (intravascular) volumes therapeutic decisions. study, euvolaemic 70% displayed 63% pressures; conversely, among hypervolaemia, around 15% confirms although RHC-derived indices gold standard used up/down-titration diuretics/vasodilators haemodynamic goal, applicable. ESCAPE trial, RHC addition routine better exercise tolerance life, mortality hospitalizations.15 To achieve (both settings) challenging (one my say impossible) numerous reasons. A reliable, reproducible, universal simple tool our diagnostic armamentarium still lacking.16, 17 described above, factors complex, cases unidentifiable. An through prism volume. Dynamic interplay determines move extravascular maintain appropriate required output. rate exchanged called refilling (PRR). if removed too fast (a greater PRR), output/renal hypoperfusion subsequent activations intrarenal cause detrimental consequences. what really matters characterization evaluate components function. Unfortunately, do how (and if) translates so we remain continuous search elusive object Conflict interest: none declared.