Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Aug 6;48(12):1781–1786. doi: 10.1007/s00134-022-06761-7

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.

PMC Copyright notice

Fig. 1 — The 4 phases conceptual model and deleterious effects of fluid accumulation syndrome. Panel A The four-hit model of shock with evolution of patients’ cumulative fluid volume status over time during the five phases of resuscitation: Resuscitation (R), Optimization (O), Stabilization (S), and Evacuation (E) (ROSE), followed by a possible risk of Hypoperfusion in case of too aggressive deresuscitation. On admission patients are often hypovolemic, followed by normovolemia after fluid resuscitation (escalation or EAFM, early adequate fluid management), and possible fluid overload, again followed by a phase returning to normovolemia with de-escalation via achieving zero fluid balance or late conservative fluid management (LCFM) and followed by late goal directed fluid removal (LGFR) or deresuscitation. In case of hypovolemia, O₂ cannot get into the tissue because of convective problems, in case of hypervolemia O₂ cannot get into the tissue because of diffusion problems related to interstitial and pulmonary edema, gut edema (ileus and abdominal hypertension). *Volumetric preload indicators like GEDVI, LVEDAI, or RVEDVI are preferred over barometric ones like CVP or PAOP. **Vasopressor can be started or increased to maintain MAP/APP above 55/45 during deresuscitation phase. ^#Can only be measured via Swan-Ganz pulmonary artery catheter (PAC) and became obsolete. Panel B Potential consequences of fluid accumulation syndrome (formerly known as fluid overload) and GIPS (global increased permeability syndrome) on end-organ function. Figures adapted from Malbrain et al. with permission, according to the Open Access CC BY Licence 4.0 [2, 7]. ACS abdominal compartment syndrome, APP abdominal perfusion pressure = MAP-IAP, BIA bio-electrical impedance analysis, CARS cardio-abdominal-renal syndrome, CI cardiac index, CLI capillary leak index (serum CRP divided by serum albumin), CO cardiac output, COP colloid oncotic pressure, CPP cerebral perfusion pressure, CS compartment syndrome, CVP central venous pressure, ECW/ICW extracellular/intracellular water, EVLWI extra-vascular lung water index, FAS fluid accumulation syndrome, GEDVI global end-diastolic volume index, GEF global ejection fraction, GFR glomerular filtration rate, IAH intra-abdominal hypertension, IAP intra-abdominal pressure, ICG-PDR indocyanine green plasma disappearance rate, ICH intracranial hypertension, ICP intracranial pressure, ICS intracranial compartment syndrome, IOP intra-ocular pressure, IVCCI inferior vena cava collapsibility index, LVEDAI left ventricular end-diastolic area index, MAP mean arterial pressure, OCS ocular compartment syndrome, PAOP pulmonary artery occlusion pressure, PF P_aO₂ over FiO₂ ratio, pHi gastric tonometry, PLR passive leg raising, PPV pulse pressure variation, PVPI pulmonary vascular permeability index, RVEDVI right ventricular end-diastolic volume index, RVR renal vascular resistance, S_cvO₂ central venous oxygen saturation, SSCG surviving sepsis campaign guidelines, S_vO₂ mixed venous oxygen saturation, SV stroke volume, SVV stroke volume variation, V_E volume excess (from baseline body weight), VExUS venous congestion by ultrasound

Fig. 1 — The 4 phases conceptual model and deleterious effects of fluid accumulation syndrome. Panel A The four-hit model of shock with evolution of patients’ cumulative fluid volume status over time during the five phases of resuscitation: Resuscitation (R), Optimization (O), Stabilization (S), and Evacuation (E) (ROSE), followed by a possible risk of Hypoperfusion in case of too aggressive deresuscitation. On admission patients are often hypovolemic, followed by normovolemia after fluid resuscitation (escalation or EAFM, early adequate fluid management), and possible fluid overload, again followed by a phase returning to normovolemia with de-escalation via achieving zero fluid balance or late conservative fluid management (LCFM) and followed by late goal directed fluid removal (LGFR) or deresuscitation. In case of hypovolemia, O₂ cannot get into the tissue because of convective problems, in case of hypervolemia O₂ cannot get into the tissue because of diffusion problems related to interstitial and pulmonary edema, gut edema (ileus and abdominal hypertension). *Volumetric preload indicators like GEDVI, LVEDAI, or RVEDVI are preferred over barometric ones like CVP or PAOP. **Vasopressor can be started or increased to maintain MAP/APP above 55/45 during deresuscitation phase. ^#Can only be measured via Swan-Ganz pulmonary artery catheter (PAC) and became obsolete. Panel B Potential consequences of fluid accumulation syndrome (formerly known as fluid overload) and GIPS (global increased permeability syndrome) on end-organ function. Figures adapted from Malbrain et al. with permission, according to the Open Access CC BY Licence 4.0 [2, 7]. ACS abdominal compartment syndrome, APP abdominal perfusion pressure = MAP-IAP, BIA bio-electrical impedance analysis, CARS cardio-abdominal-renal syndrome, CI cardiac index, CLI capillary leak index (serum CRP divided by serum albumin), CO cardiac output, COP colloid oncotic pressure, CPP cerebral perfusion pressure, CS compartment syndrome, CVP central venous pressure, ECW/ICW extracellular/intracellular water, EVLWI extra-vascular lung water index, FAS fluid accumulation syndrome, GEDVI global end-diastolic volume index, GEF global ejection fraction, GFR glomerular filtration rate, IAH intra-abdominal hypertension, IAP intra-abdominal pressure, ICG-PDR indocyanine green plasma disappearance rate, ICH intracranial hypertension, ICP intracranial pressure, ICS intracranial compartment syndrome, IOP intra-ocular pressure, IVCCI inferior vena cava collapsibility index, LVEDAI left ventricular end-diastolic area index, MAP mean arterial pressure, OCS ocular compartment syndrome, PAOP pulmonary artery occlusion pressure, PF P_aO₂ over FiO₂ ratio, pHi gastric tonometry, PLR passive leg raising, PPV pulse pressure variation, PVPI pulmonary vascular permeability index, RVEDVI right ventricular end-diastolic volume index, RVR renal vascular resistance, S_cvO₂ central venous oxygen saturation, SSCG surviving sepsis campaign guidelines, S_vO₂ mixed venous oxygen saturation, SV stroke volume, SVV stroke volume variation, V_E volume excess (from baseline body weight), VExUS venous congestion by ultrasound