Introduction
What an oversight! Fluids are drugs (1), so why has one of the most administered, and arguably beneficial, therapies employed in veterinary medicine been so inadequately investigated? Intravenous fluids (i.e., drug) can produce positive or negative effects dependent upon their dose and the circumstances (i.e., context) that exist when they are administered (2, 3). Improved understanding of the physiologic principles that determine the effects and consequences of fluid therapy in healthy and diseased animals is essential to good clinical practice (4–86). Notably, most of the “evidence” investigating fluid therapy in animals has been obtained from studies that are not randomized, properly controlled, blinded, adequately powered, or fail to identify predefined primary or secondary outcomes (73, 75, 87, 88). As a result, much of the medical literature provides, “little reliable information on the effectiveness of fluid resuscitation” in diverse clinical scenarios (2, 3, 89–93). Future studies must address these limitations since “fluid therapy might be more difficult than you think” (94), “nothing is more dangerous than conscientious foolishness” (95) and “solely the dose determines that a thing is not a poison” (96). For example, the pharmacokinetics of fluids administered to cats, dogs, horses, or cattle are largely unknown and generally not considered when designing fluid therapy trials although it has been addressed in the human medical literature for more than 20 years (31, 97–100).
This issue of Frontiers in Veterinary Science provides: (1) A review of the terms used to define or describe fluid therapy (Chow); (2) An update on body fluid compartments and the physiological concepts that guide fluid therapy (Stewart; Woodcock and Michel; Smart and Hughes; Cooper and Silverstein); (3) A discussion of fluid kinetics and its relevance to fluid administration in cats (Yiew, Bateman, Hahn, Bersenas, Muir; Yiew, Bateman, Hahn, Bersenas); (4) Contemporary recommendations for the administration of IV fluid regimens in small and large animals (Rudloff and Hopper; Crabtree and Epstein; Adamik and Yozova); (5) The effects of IV fluids on the coagulation system (Boyd et al.); (6) A discussion of fluid administration in animals with naturally occurring disorders and diseases (e.g., food deprivation, dehydration, sepsis, renal, pulmonary, trauma, hemorrhage, traumatic brain injury; Freeman; Dias et al.; Montealegre and Lyons; Constable et al.; Hall and Drobatz; Pigot and Rudloff; Langston and Gordon; Adamantos) including refractory hypotension (Valverde) and cardiopulmonary resuscitation (Fletcher and Boller); (7) The consequences of fluid overload (Hansen); (8) A description of dynamic fluid therapy monitoring techniques (Boysen and Gommeren); (9) An introduction to fluids of the future (Edwards and Hoareau); and (10) Alternative methods for fluid delivery (Gholami et al.). The information and citations contained within this collection serve as a rich resource for the design of future studies investigating the safety and efficacy of intravenous fluid therapy in animals.
Body Fluid Compartments
Water (i.e., total body water: TBW) is responsible for ~60–70% of body weight (BW) and is the primary component of all body fluids (101). The two main body fluid compartments are the intracellular fluid (ICF) and extracellular fluid (ECF). Approximately two-thirds (≈40%) of TBW is intracellular fluid (ICF) and one-third (≈20%) extracellular fluid (ECF). The ECF is comprised of four sub-compartments, the intravascular fluid volume (i.e., plasma volume: PV; 4–5% BW), the fluid that surrounds cells (i.e., interstitial fluid volume: IFV; ≈15–18% BW), lymph, and fluids contained within epithelial lined spaces (transcellular fluids) [Stewart; (101–104)]. Severe obesity can increase the relative percentage of the ECF by up to 50% of TBW (≈ 30% BW) (105). The intravascular volume (i.e., blood volume: BV) is comprised of the red cell volume (RBCV; 6–8% BW) and plasma volume (PV) (106, 107). If the packed red blood cell volume (PCV) is known BV can be determined (i.e., BV = PV × 100/100-PCV) (106). Transcellular fluids are infrequently considered when determining water and solute requirements in simple stomached animals but become important in horses and ruminants (108). Determination of the body's fluid compartments is technically challenging, time consuming, and often inaccurate (109–111). Substances used for this purpose (i.e., “dilutional tracer technique”) must be non-toxic, easily detectable and sustain a steady state concentration within the compartment (112–114).
Contemporary evidence suggests that the PV is comprised of circulating and non-circulating (15–25% of PV) components, the latter being located within an endothelial surface or glycocalyx layer (GLX) and the channels between vascular epithelial cells (115, 116). The GLX interacts freely with plasma proteins and acts as an surface layer “gatekeeper” for larger molecules selectively reducing plasma solute distribution volume dependent upon their molecular weight (MW), shape (i.e., effective molecular radius), electrical charge, and concentration (11–14, 117). Crystalloids have a shorter intravascular retention time than colloids (100, 118–121).
Blood Distribution
Blood volume is distributed between the pulmonary (18–20%) and systemic (78–80%) circulations dependent upon their (e.g., brain, heart, lung, and gut) oxygen requirements (VO2). Veins are ~30 times more compliant than arteries, contain up to five times more adrenergic receptors than arteries and normally serve as blood reservoirs (122). Some investigators have described the blood volume contained within the systemic veins as either unstressed or stressed (123, 124). The unstressed volume (Vu; ≈70% BV) is equivalent to the blood volume required to fill the veins without increasing the transmural pressure above zero mmHg and the stressed volume (Vs; ≈30% BV) as the volume of blood required to increase the transmural pressure to values above zero (123). Under normal circumstances Vu is believed to serve as a reserve volume that can be mobilized by increasing sympathetic activity (i.e., alpha 1 receptors) thereby increasing vs. (i.e., “effective” BV) (125, 126). The mean circulatory filling pressure (MCFP) is defined as the mean vascular pressure that exists in the systemic circulation after the heart is stopped and is argued to be determinant of venous return and cardiac output (127, 128). A growing number of vascular physiologists however consider this interpretation to be abstract and erroneous opting to believe that cardiac contraction is the independent variable that drives blood flow and determines cardiac output (129–136).
Water Balance
Water balance (i.e., water intake and output) is governed by a variety of neural and neuroendocrine high-gain homeostatic feedback mechanisms that include, osmoreceptors, osmotically stimulated thirst receptors, hormones [e.g., renin-angiotensin-aldosterone system (RAAS), angiotensin-converting enzyme-2 (ACE2)/angiotensin 1–7 (Ang 1–7), vasopressin (antidiuretic hormone: ADH), erythropoietin (EPO), atrial natriuretic peptide (ANP)] and membrane water channels (i.e., aquaporins), especially those located in the renal tubules (137–144). The kidney is responsible for regulating fluid, electrolyte balance and blood volume (145–147). The kidney also produces and secrets erythropoietin (e.g., low Hb, PaO2, flow) signaling bone marrow to produce more red blood cells. Activated atrial stretch receptors secrete ANP producing vasodilation and increases in glomerular filtration, salt and water excretion, and vascular permeability, thereby regulating PV and lowering arterial blood pressure (ABP) (141, 148). Therefore, the kidney is regarded as a key determinant of both PV and BV. Negatively charged glycosaminoglycans (GAGs) located in the interstitial spaces and lymphatics of the skin also function as non-renal regulators of sodium ion concentration and ECF volume (7, 8) serving as indirect controllers of arterial blood pressure (ABP) by shifting fluid from the interstitial to the intravascular space (7, 8, 149).
Blood Flow and Tissue Perfusion
The heart and vasculature deliver blood to and from the systemic and pulmonary circulations and, in conjunction with interstitial compliance and the lymphatic system, are responsible for ensuring the continuous circulation of fluid throughout the body (5, 5, 150–156). Three categories of capillaries are involved in the exchange of fluid, gases (O2, CO2), and solutes (e.g., albumin) (155, 157). Non-fenestrated or continuous capillaries nourish the tissues of the nervous system, muscle, connective tissue, skin, lung, and fat. Fenestrated (i.e., contain “pores”) capillaries perfuse the kidneys, intestinal mucosa, synovial linings, exocrine glands and sinusoidal or discontinuous capillaries with large intercellular breaks (i.e., pores) filter blood in the liver, spleen, and bone marrow (11). All three are coated to a greater or lesser extent by the semi-permeable negatively charged GLX [(11–13); [Yiew, Bateman, Hahn, Bersenas; Rudloff and Hopper; Crabtree and Epstein; Adamik and Yozova; (155, 158)]. Plasma filtration among the different types of capillaries is determined by hydrostatic (mmHg) and osmotic (mOsm/L) pressures, the number and size or their fenestrations [i.e., “pores”]), capillary surface area, the thickness of the GLX, the pre- to postcapillary vascular tone (i.e., resistance ratio), and tissue compliance (3, 159–162). Capillaries in the renal glomeruli are fenestrated (pore: 30–60 nm) but have a smaller effective pore size (pore: ≤ 15 nm) due to the influence of the GLX on the filtration of larger (>40–50 kDa) molecules (163, 164). Non-fenestrated capillaries (e.g., central nervous system blood brain barrier; ≤ 1–2 nm) with numerous endothelial transport vesicles enable transcytosis (i.e., transcellular transport of macromolecules). They are less permeable to fluid and electrolyte exchange than fenestrated capillaries, although water and small solutes pass through endothelial intercellular clefts in accordance with hydrostatic pressure differences (157). Non-fenestrated “continuous” capillaries (e.g., skin, lungs, and the blood-brain barrier) have a comparatively small effective pore size (pore: 3–5 nm) that inhibits the trans-vascular flux of fluid and most solutes (160, 163–165).
The GLX constitutes ~2% of the PV and functions as two layers: a less permeable, dense branch-like inner layer composed of heparin sulfate and glycoproteins and a more permeable porous outer later composed of plasma proteins and glycosaminoglycans (13, 104, 166). The GLX limits albumin (i.e., large molecule) and RBC access, leukocyte contact with the inner layer and endothelial surface (13, 104, 166), participates in cell signaling (i.e., nitric oxide-induced vasorelaxation), provides anti-coagulant effects and protects endothelial cells from oxidative stress (107). Small molecules, such as water, gases, small lipids, and lipid-soluble molecules diffuse freely through the GLX through endothelial intercellular clefts or by facilitated diffusion (158). Larger molecules (i.e., colloids) negligibly penetrate the GLX and distribute in a smaller intravascular volume than crystalloids which readily distribute throughout the entire intravascular space. Recent studies suggest that crystalloid-to-colloid ratios should range from 0.7 to 1.4:1 in contrast to older ratios (i.e., 1:3) (167–175) and that crystalloid-to-blood ratios > 1:1 produce perivascular edema, pulmonary parenchymal stiffness (176), impaired coagulation [Boyd et al.; (177, 178)], increased blood loss (44), and increased vasopressor requirements (43). Disagreements favoring colloids over crystalloids rest more on their delayed diffusion than on their safety [(44, 50–53); Boyd et al.; (179)], risk-benefit ratio (Adamik and Yozova) or cost.
Transvascular Fluid Flux
Traditional Theory
The dynamics of fluid flux (Jv) across capillary walls is historically attributed to Earnest Starling's observations of fluid absorption from connective tissue spaces (Starling 1896) (180). He concluded that capillary hydrostatic pressure was responsible for transudation of a small amount of fluid into the tissues (“frictional resistance of the capillary wall”), thereby forming lymph, and that the colloid osmotic pressure produced by plasma proteins was responsible for fluid absorption. He also postulated that the forces moving fluid in and out of the capillary were almost balanced. Subsequent experiments resulted in mathematical descriptions of Starling's hypothesis and suggested equations wherein Jv (i.e., transvascular fluid flux) is a balance of intravascular capillary (c) intravascular and interstitial (i) hydraulic (i.e., hydrostatic pressure: P) and oncotic [π: colloid osmotic pressure (COP)] forces (Kedem–Katchalski equations) (181). Capillary hydrostatic pressure (Pc) is a function of the hydrostatic P from the inflow (arterial: a) to the outflow (venous: v) end of the capillary and are dependent upon the pre- and post-capillary resistances (R), assuming blood flow remains constant (182–186). A decrease in Ra (e.g., arteriolar vasodilation) or an increase in Rv (venoconstriction) decreases Ra/Rv and increases both Pc and Jv (3). Under normal circumstances Pc is more sensitive to changes in Pv than Pa but during intense arterial vasoconstriction, Pc decreases rapidly (increased Ra/Rv) (3, 185). Plasma proteins are responsible for generating πc and COP is the hydrostatic pressure required to prevent fluid movement into the plasma or, alternatively, the pressure that pulls fluid across the capillary wall into the plasma. Capillary Pc (i.e., hydraulic push) is therefore opposed by capillary πc [i.e., osmotic suction: (Pc - πc)] and Pi is opposed by πi (Pi - πi). The Starling hypothesis asserts that fluid is filtered at the arterial end of the capillary because Pc predominates over all other forces, and that fluid is reabsorbed at the venous end of the capillary because πc (osmotic suction) predominates. Interstitial forces (Pi, πi) act as modulators of the rate of fluid flux and therefore the volume of Jv (14, 185). Later studies modified Starling's hypothesis to account for transvascular fluid flux rates per unit pressure (i.e., hydraulic conductance: Lp) and the macromolecular sieving properties of the microvascular barrier (Staverman's reflection coefficient: σ) [(12–14); Woodcock and Michel; (173, 187)]. Both Lp and σ vary among different types of capillaries since Lp is dependent upon the number of “pores” and σ is dependent on effective pore diameter. The σ for most plasma solutes ranges from 0 to 1 (i.e., 0 = totally permeable; 1 = totally impermeable) (187). The capillary wall osmotic and σ for water, anions, cations, and smaller soluble substances like glucose is nearly 0 (freely permeable) (160). Larger plasma solutes (>30–40 kDa), like albumin (66–69 kDa; diameter ~3.5 nm), which accounts for 80% of total plasma protein and commercial semisynthetic colloid solutions (i.e., gelatins, dextran, and hydroxyethyl starches; COP range 24–60 mm Hg) exhibit σ's ranging from 0.7 to 1.0 and are almost impermeant to most the microvascular barrier except the sinusoids of the liver. The incorporation of Lp and σ into Starlings hypothesis is the basis for what is proclaimed as the “Starling equation” that is still published in most texts [Jv = Lp [(Pc – Pi) – σ (πc – πi)]], although Starling had little to do with its derivation since the earliest form of the equation did not appear until 1927 (182).
Contemporary Theory
Recent investigations have led to a revision of the Starling hypothesis (165) and the Starling equation based upon GLX COP (πg): Jv = Lp [(Pc – Pi) – σ (πc – πg)] [(11); Woodcock and Michel; (188–193)]. It is now realized that the interstitial COP does not directly determine fluid movement across the microvascular wall, and that the effect of πc on Jv is far less than originally predicted (11, 189–195). The sieving properties of the glycocalyx modify Starling's forces by imposing an obstacle to Jv. The π difference across non-fenestrated capillaries is influenced by the πg and πi is far less important in determining Jv than originally proposed. Notably, πg is negligible compared to πc such that the osmotic pressure gradient across the glycocalyx is close to πc rather than the difference between πc and πi. Fluid that is filtered through the glycocalyx flows rapidly through narrow inter-endothelial cell breaks, thereby limiting interstitial protein back diffusion into the sub-glycocalyx space. The “Revised” Starling equation [(11); Woodcock and Michel; (189)] has proven to be more consistent with experimental and clinical observations and suggests that (1) Jv is far less than originally predicted; (2) Fluid is not normally reabsorbed from the venous end of the capillary during normal physiologic conditions (steady state no-reabsorption rule); (3) Tissue lymph drainage is the primary route for return of interstitial fluid to the circulation; (4) Interstitial fluid is reabsorbed from the interstitium when Pc decreases until a new steady state is established (14); and (5) Crystalloid is almost as effective as a colloid (Col) administration for treating hypovolemia from blood loss (11, 173–176). These revisions highlight the importance of GLX composition and integrity and the number of inter-endothelial cellular “breaks” (i.e., glycocalyx-junction-break model) in determining the effectiveness of fluid resuscitation (195). They do not negate the “importance of transcapillary refill” as suggested by some (196), but do have important implications regarding fluid selection, rate, and volume for improving fluid efficiency and effectiveness in diseased animals [Woodcock and Michel; (189, 194, 197)].
Volume Kinetics
Volume kinetics (VK) determines the volume into which an administered fluid is distributed (i.e., volume of distribution: Vd), the volume of plasma that is completely cleared of the administered fluid per unit time (i.e., clearance: Cl) and the time it takes for the total amount of administered fluid to be reduced by one-half of its original volume (i.e., half-life: t1/2) (31). Intravenous fluids are initially distributed into a central compartment (Vc) followed by diffusion into a peripheral compartment (Vt) [(31); Yiew, Bateman, Hahn, Bersenas, Muir; (179, 198–201)]. The distribution half-time for most crystalloids is relatively short (<8–10 min) implying that distribution is complete within ~30–50 min (4–5 half-lives), a range that closely coincides with the measured half-lives reported for acetated (56 min) and lactated (50 min) Ringer's solutions in humans (155). A low Cld from Vc increases the infused fluid's potency (i.e., the volume required to expand the plasma volume by 20% in 30 min) but also increases hemodilution. The Cld for colloidal solutions [i.e., hydroxyethyl starches (HES)] is much lower than crystalloids, suggesting delayed departure from Vc and prolongation of their volume expanding effects.
Rapid fluid administration rates (>40–60 ml/kg/hr) and large fluid volumes (>60–80 ml/kg) produce hemodilution, interstitial fluid accumulation (i.e., edema), and serious rebleeding in animals with uncontrolled hemorrhage (15, 78, 83, 202, 203). Most anesthetic drugs, particularly inhalant anesthetics (e.g., propofol, isoflurane), depress cardiorespiratory function, blunt homeostatic reflexes, promote vasoplegia, [Valverde; (204–206)] decrease tolerance to acute anemia [i.e., increase the critical Hb concentration: (Hbcrit)] (207, 208), promote interstitial fluid accumulation (209) and perioperative fluid retention (209–212), decrease urine output (212, 213), and depress the response to fluid administration (204, 214). In addition, vasoactive drugs are known to alter fluid volume kinetics (215–219). Stimulation of alpha1- adrenergic receptors (e.g., norepinephrine; phenylephrine) increases Vd, Cld, the accumulation of fluid in Vt, and Clr while stimulation of beta-1 adrenergic receptors (e.g., isoproterenol) increase Vc and decrease Vd, Cld, and Clr (69, 216, 217, 220). Notably, fluid accumulation in Vt is more significantly influenced by the rate of infusion (i.e., ml/kg/min) than by the infused fluid volume; higher infusion rates produce greater degrees of interstitial fluid accumulation, hemodilution, coagulation abnormalities, and organ dysfunction (79, 199, 203, 221, 222).
New Horizons
New fluids and goal directed fluid therapies (GDFT) continue to be developed for the treatment of specific naturally occurring diseases with the goals of improving tissue oxygenation and perfusion [(9); Edwards and Hoareau; (197, 223–228)], and reducing adverse events and mortality (229, 230). Damage control resuscitation (DCR) strategies limit the amount of crystalloids administered and employ balanced blood product resuscitation ratios [PRBC's-plasma-platelets ratio of 1:1:1; Hall and Drobatz; Boysen and Gommeren; (230–235)]. Isotonic and hypertonic crystalloid solutions continue to be investigated in order to rapidly restore hemodynamics, reduce the amount of fluid administered in order minimize hemodilution, and tissue edema, and lessen the development of disseminated intravascular coagulation (58–62, 236, 237). Novel therapies that mimic natural hemostatic mechanisms (68) or reduce vascular leakage (238–240) are being developed and solutions that increase tissue oxygenation (e.g., hemoglobin) and restore microcirculatory blood flow continue to evolve (241–243). Future fluids should protect or repair the endothelium (224, 228, 238, 244, 245). Methods for determining their success will be dependent upon the development of validated dynamic non or minimally invasive hemodynamic monitoring methodologies [(42); Cooper and Silverstein; Boysen and Gommeren; (20, 38–41, 235, 246–254)] in addition assessment of thromboelastographic variables (249), implementation of deep-learning algorithms (254) and development of bio-responsive drug delivery systems [Gholami et al.; (255–260)]. It is hoped that the information contained within this compendium will inspire readers to employ fluid therapy practices that improve patient outcome.
Publisher's Note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Statements
Author contributions
All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication.
Acknowledgments
We acknowledge Lincoln Memorial University College of Veterinary Medicine, Dechra Veterinary Products, and Nova Biomedical for support of this project.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
References
1.
RaghunathanKShawADBagshawSM. Fluids are drugs: type, dose and toxicity. Curr Opin Crit Care. (2013) 19:290–8. 10.1097/MCC.0b013e3283632d77
2.
JamesMFM. Context-sensitive fluid administration: what, when and how much. South Afr J Anaesth Analges. (2015) 21:38–9.
3.
TataraT. Context-sensitive fluid therapy in critical illness. J Intensive Care. (2016) 4:20. 10.1186/s40560-016-0150-7
4.
UemuraKSugimachiMKawadaTKamiyaAJinYKashiharaKet al. A novel framework of circulatory equilibrium. Am J Physiol Heart Circ Physiol. (2004) 286:H2376–85. 10.1152/ajpheart.00654.2003
5.
BreslinJWYangYScallanJPSweatRSAdderleySPMurfeeWL. Lymphatic vessel network structure and physiology. Compr Physiol. (2018) 9:207–99. 10.1002/cphy.c180015
6.
JessenNAMunkASLundgaardINedergaardM. The glymphatic system: a beginner's guide. Neurochem Res. (2015) 40:2583–99. 10.1007/s11064-015-1581-6
7.
WiigHLuftFCTitzeJM. The interstitium conducts extrarenal storage of sodium and represents a third compartment essential for extracellular volume and blood pressure homeostasis. Acta Physiol. (2018) 222:13006. 10.1111/apha.13006
8.
MinegishiSLuftFCTitzeJKitadaK. Sodium handling and interaction in numerous organs. Am J Hypertens. (2020) 33:687–96. 10.1093/ajh/hpaa049
9.
InceCErtmerC. Hemodynamic coherence: its meaning in perioperative and intensive care medicine. Best Pract Res Clin Anaesthesiol. (2016) 30:395–7. 10.1016/j.bpa.2016.11.004
10.
GuvenGHiltyMPInceC. Microcirculation: physiology, pathophysiology, and clinical application. Blood Purif. (2020) 49:143–50. 10.1159/000503775
11.
WoodcockTEWoodcockTM. Revised Starling equation and the glycocalyx model of transvascular fluid exchange: an improved paradigm for prescribing intravenous fluid therapy. Br J Anaesth. (2012) 108:384–94. 10.1093/bja/aer515
12.
JiangXZVentikosYLuoKH. Microvascular ion transport through endothelial glycocalyx layer: new mechanism and improved Starling principle. Am J Physiol Heart Circ Physiol. (2019) 317:H104–13. 10.1152/ajpheart.00794.2018
13.
GaudetteSHughesDBollerM. The endothelial glycocalyx: structure and function in health and critical illness. J Vet Emerg Crit Care. (2020) 30:117–34. 10.1111/vec.12925
14.
MichelCCWoodcockTECurryFE. Understanding and extending the Starling Principle. Acta Anaesthesiol Scand. (2020) 64:1032–7. 10.1111/aas.13603
15.
HahnRG. Fluid therapy in uncontrolled hemorrhage–what experimental models have taught us. Acta Anaesthesiol Scand. (2013) 57:16–28. 10.1111/j.1399-6576.2012.02763.x
16.
PernerAJunttilaEHaneyMHreinssonKKvåleRVandvikPOet al. Scandinavian Society of Anaesthesiology and Intensive Care Medicine: scandinavian clinical practice guideline on choice of fluid in resuscitation of critically ill patients with acute circulatory failure. Acta Anaesthesiol Scand. (2015) 59:274–85. 10.1111/aas.12429
17.
MarikPBellomoR. A rational approach to fluid therapy in sepsis. Br J Anaesth. (2016) 116:339–49. 10.1093/bja/aev349
18.
VoldbyAWBrandstrupB. Fluid therapy in the perioperative setting—a clinical review. J Intensive Care. (2016) 4:27. 10.1186/s40560-016-0154-3
19.
WiseRFaurieMMalbrainMLNGHodgsonE. Strategies for intravenous fluid resuscitation in trauma patients. World J Surg. (2017) 41:1170–83. 10.1007/s00268-016-3865-7
20.
JoostenARaj LawrenceSColesnicencoACoeckelenberghSVincentJLVan der LindenPet al. Personalized versus protocolized fluid management using noninvasive hemodynamic monitoring (clearsight system) in patients undergoing moderate-risk abdominal surgery. Anesth Analg. (2019) 129:e8–e12. 10.1213/ANE.0000000000003553
21.
RameshGHUmaJCFarhathS. Fluid resuscitation in trauma: what are the best strategies and fluids?Int J Emerg Med. (2019) 12:38. 10.1186/s12245-019-0253-8
22.
MarikPEWeinmannM. Optimizing fluid therapy in shock. Curr Opin Crit Care. (2019) 25:246–51. 10.1097/MCC.0000000000000604
23.
ZimmermanRATsaiAGIntagliettaMTartakovskyDM. A mechanistic analysis of possible blood transfusion failure to increase circulatory oxygen delivery in anemic patients. Ann Biomed Eng. (2019) 47:1094–105. 10.1007/s10439-019-02200-9
24.
KeijzersGMacdonaldSPUdyAAArendtsGBaileyMBellomoRet al. ARISE FLUIDS Observational Study Group. The Australasian Resuscitation In Sepsis Evaluation: Fluids or vasopressors in emergency department sepsis (ARISE FLUIDS), a multi-centre observational study describing current practice in Australia and New Zealand. Emerg Med Australas. (2019) 32:90–6. 10.1111/1742-6723.13223
25.
MalbrainMNGVan RegenmortelNSaugelBTavernierBVan GaalPJJoannes-BoyauOet al. Principles of fluid management and stewardship in septic shock: it is time to consider the four D's and the four phases of fluid therapy. Ann Intensive Care. (2018) 8:66. 10.1186/s13613-018-0402-x
26.
SpiegelRGordonDMarikPE. The origins of the Lacto-Bolo reflex: the mythology of lactate in sepsis. J Thorac Dis. (2020) 12:S48–53. 10.21037/jtd.2019.11.48
27.
LiraAPinskyMR. Choices in fluid type and volume during resuscitation: impact on patient outcomes. Ann Intensive Care. (2014) 4:38. 10.1186/s13613-014-0038-4
28.
AllenSJ. Fluid therapy and outcome: balance is best. J Extra Corpor Technol. (2014) 46:28–32.
29.
BennettVACecconiM. Perioperative fluid management: from physiology to improving clinical outcomes. Indian J Anaesth. (2017) 61:614–21. 10.4103/ija.IJA_456_17
30.
LewisSRPritchardMWEvansDJButlerARAldersonPSmithAFet al. Colloids versus crystalloids for fluid resuscitation in critically ill people. Cochrane Database Syst Rev. (2018) 8:CD000567. 10.1002/14651858.CD000567.pub7
31.
HahnRG. Understanding volume kinetics. Acta Anaesthesiol Scand. (2020) 64:570–8. 10.1111/aas.13533
32.
Bundgaard-NielsenMHolteKSecherNHKehletH. Monitoring of peri-operative fluid administration by individualized goal-directed therapy. Acta Anaesthesiol Scand. (2007) 51:331–40. 10.1111/j.1399-6576.2006.01221.x
33.
MarikPE. Fluid responsiveness and the six guiding principles of fluid resuscitation. Crit Care Med. (2016) 44:1920–2. 10.1097/CCM.0000000000001483
34.
MonnetXMarikPETeboulJL. Prediction of fluid responsiveness: an update. Ann Intensive Care. (2016) 6:111. 10.1186/s13613-016-0216-7
35.
MartinNDCodnerPGreeneWBraselKMichettiCAAST Critical CareCommittee. Contemporary hemodynamic monitoring, fluid responsiveness, volume optimization, and endpoints of resuscitation: an AAST critical care committee clinical consensus. Trauma Surg Acute Care Open. (2020) 5:e000411. 10.1136/tsaco-2019-000411
36.
ShiRMonnetXTeboulJL. Parameters of fluid responsiveness. Curr Opin Crit Care. (2020) 22:723. 10.1097/MCC.0000000000000723
37.
AraosJKennyJSRousseau-BlassFPangDS. Dynamic prediction of fluid responsiveness during positive pressure ventilation: a review of the physiology underlying heart-lung interactions and a critical interpretation. Vet Anaesth Analg. (2020) 4:3–14. 10.1016/j.vaa.2019.08.004
38.
SilversteinDCPruett-SaratanA2ndDrobatzKJ. Measurements of microvascular perfusion in healthy anesthetized dogs using orthogonal polarization spectral imaging. J Vet Emerg Crit Care. (2009) 19:579–87. 10.1111/j.1476-4431.2009.00488.x
39.
PeruskiAMCooperES. Assessment of microcirculatory changes by use of sidestream dark field microscopy during hemorrhagic shock in dogs. Am J Vet Res. (2011) 72:438–745. 10.2460/ajvr.72.4.438
40.
SilversteinDCCozziEMHopkinsASKeefeTJ. Microcirculatory effects of intravenous fluid administration in anesthetized dogs undergoing elective ovariohysterectomy. Am J Vet Res. (2014) 75:809–17. 10.2460/ajvr.75.9.809
41.
GommerenKAllertonFJMorinEReynaudAPeetersDSilversteinDC. Evaluation of a rapid bedside scoring system for microcirculation videos acquired from dogs. J Vet Emerg Crit Care. (2014) 24:554–61. 10.1111/vec.12212
42.
BakkerJInceC. Monitoring coherence between the macro and microcirculation in septic shock. Curr Opin Crit Care. (2020) 22:729. 10.1097/MCC.0000000000000729
43.
ByrneLObonyoNGDiabSDDunsterKRPassmoreMRBoonACet al. Unintended consequences: fluid resuscitation worsens shock in an ovine model of endotoxemia. Am J Respir Crit Care Med. (2018) 198:1043–54. 10.1164/rccm.201801-0064OC
44.
HahnRG. Adverse effects of crystalloid and colloid fluids. Anaesthesiol Intensive Ther. (2017) 49:303–8. 10.5603/AIT.a2017.0045
45.
MalbrainMLMarikPEWittersICordemansCKirkpatrickAWRobertsDJet al. Fluid overload, de-resuscitation, and outcomes in critically ill or injured patients: a systematic review with suggestions for clinical practice. Anaesthesiol Intensive Ther. (2014) 46:361–80. 10.5603/AIT.2014.0060
46.
CavanaghAASullivanLAHansenBD. Retrospective evaluation of fluid overload and relationship to outcome in critically ill dogs. J Vet Emerg Crit Care. (2016) 26:578–86. 10.1111/vec.12477
47.
JacobsRJonckheerJMalbrainMLNG. Fluid overload FADEs away! Time for fluid stewardship. J Crit Care. (2018) 48:458–61. 10.1016/j.jcrc.2018.08.027
48.
RossSWChristmasABFischerPEHolwayHSeymourRHuntingtonCRet al. Defining dogma: quantifying crystalloid hemodilution in a prospective randomized control trial with blood donation as a model for hemorrhage. J Am Coll Surg. (2018) 227:321–31. 10.1016/j.jamcollsurg.2018.05.005
49.
Van der LindenPIckxBE. The effects of colloid solutions on hemostasis. Can J Anaesth. (2006) 53(6 Suppl.):S30–9. 10.1007/BF03022250
50.
DickenmannMOettlTMihatschMJ. Osmotic nephrosis: acute kidney injury with accumulation of proximal tubular lysosomes due to administration of exogenous solutes. Am J Kidney Dis. (2008) 51:491–503. 10.1053/j.ajkd.2007.10.044
51.
Fenger-EriksenCTønnesenEIngerslevJSørensenB. Mechanisms of hydroxyethyl starch-induced dilutional coagulopathy. J Thromb Haemost. (2009) 7:1099–105. 10.1111/j.1538-7836.2009.03460.x
52.
KumarABSunejaM. Hetastarch-induced osmotic nephrosis. Anesthesiology. (2012) 117:647. 10.1097/ALN.0b013e31824de9ad
53.
GauthierV(1)HolowaychukMKKerrCLBersenasAMWoodRD. Effect of synthetic colloid administration on coagulation in healthy dogs anddogs with systemic inflammation. J Vet Intern Med. (2015) 29:276–85. 10.1111/jvim.12492
54.
BaeJSolimanMKimHKangSKimWAhnSet al. Rapid exacerbation of renal function after administration of hydroxyethyl starch in a dog. J Vet Med Sci. (2017) 79:1591–5. 10.1292/jvms.17-0196
55.
BrunoBTroìaRDondiFMaurellaCGianellaPLippiIet al. Stage 1-biomarkers of kidney injury in dogs undergoing constant rate infusion of hydroxyethyl starch 130/0.4. Animals (Basel). (2021) 11:2555. 10.3390/ani11092555
56.
SigristNEKälinNDreyfusA. Effects of hydroxyethyl starch 130/04 on serum creatinine concentration and development of acute kidney injury in nonazotemic cats. J Vet Intern Med. (2017) 31:1749–56. 10.1111/jvim.14813
57.
SchmidSMCiancioloREDrobatzKJSanchezMPriceJMKingLG. Postmortem evaluation of renal tubular vacuolization in critically ill dogs. J Vet Emerg Crit Care. (2019) 29:279–87. 10.1111/vec.12837
58.
TrefzFMConstablePDLorenzI. Effect of intravenous small-volume hypertonic sodium bicarbonate, sodium chloride, and glucose solutions in decreasing plasma potassium concentration in hyperkalemic neonatal calves with diarrhea. J Vet Intern Med. (2017) 31:907–21. 10.1111/jvim.14709
59.
WuMCLiaoTYLeeEMChenYSHsuWTLeeMGet al. Administration of hypertonic solutions for hemorrhagic shock: a systematic review and meta-analysis of clinical trials. Anesth Analg. (2017) 125:1549–57. 10.1213/ANE.0000000000002451
60.
ArifiantoMRMa'rufAZIbrahimABajamalAH. Role of hypertonic sodium lactate in traumatic brain injury management. Asian J Neurosurg. (2018) 13:971–5. 10.4103/ajns.AJNS_10_17
61.
AydogduUYildizRGuzelbektesHNaseriAAkyuzESenI. Effect of combinations of intravenous small-volume hypertonic sodium chloride, acetate Ringer, sodium bicarbonate, and lactate Ringer solutions along with oral fluid on the treatment of calf diarrhea. Pol J Vet Sci. (2018) 21:273–80.
62.
MilletACuisinierABouzatPBatandierCLemassonBStuparVet al. Hypertonic sodium lactate reverses brain oxygenation and metabolism dysfunction after traumatic brain injury. Br J Anaesth. (2018) 120:1295–303. 10.1016/j.bja.2018.01.025
63.
HonorePMBarreto GutierrezLSpapenHD. Renal protection in sepsis: is hypertonic sodium (lactate) the solution?Ann Intensive Care. (2019) 9:28. 10.1186/s13613-019-0505-z
64.
MarxGMeybohmPSchuerholzTLotzGLedinkoMSchindlerAWet al. Impact of a new balanced gelatine on electrolytes and pH in the perioperative care. PLoS ONE. (2019) 14:e0213057. 10.1371/journal.pone.0213057
65.
MackoASheppardFRNugentWHAbuchowskiASongBK. Improved hemodynamic recovery and 72-hour survival following low-volume resuscitation with a PEGylated carboxyhemoglobin in a rat model of severe hemorrhagic shock. Mil Med. (2020) 17:usz472. 10.1093/milmed/usz472
66.
CaspersMMaegeleMFröhlichM. Current strategies for hemostatic control in acute trauma hemorrhage and trauma-induced coagulopathy. Expert Rev Hematol. (2018) 11:987–95. 10.1080/17474086.2018.1548929
67.
OsekavageKEBrainardBMLaneSLAlmoslemMArnoldRDKoenigA. Pharmacokinetics of tranexamic acid in healthy dogs and assessment of its antifibrinolytic properties in canine blood. Am J Vet Res. (2018) 79:1057–63. 10.2460/ajvr.79.10.1057
68.
HickmanDAPawlowskiCLShevitzAet al. Intravenous synthetic platelet (SynthoPlate) nanoconstructs reduce bleeding and improve 'golden hour' survival in a porcine model of traumatic arterial hemorrhage. Sci Rep. (2018) 8:3118. 10.1038/s41598-018-21384-z
69.
LiYXiaozhuZGuomeiRQiannanDHahnRG. Effects of vasoactive drugs on crystalloid fluid kinetics in septic sheep. PLoS ONE. (2017) 12:e0172361. 10.1371/journal.pone.0172361
70.
ChowJHAbuelkasemESankovaSHendersonRAMazzeffiMATanakaKA. Reversal of vasodilatory shock: current perspectives on conventional, rescue, and emerging vasoactive agents for the treatment of shock. Anesth Analg. (2020) 130:15–30. 10.1213/ANE.0000000000004343
71.
HaanBJCadizMLNatavioAM. Efficacy and safety of vasopressin as first-line treatment of distributive and hemorrhagic shock states. Ann Pharmacother. (2020) 54:213–8. 10.1177/1060028019882035
72.
MeresseZMedamSMathieuCDuclosGVincentJLLeoneM. Vasopressors to treat refractory septic shock: a narrative review. Minerva Anestesiol. (2020) 2020:4. 10.23736/S0375-9393.20.13826-4
73.
FinferSMyburghJBellomoR. Intravenous fluid therapy in critically ill adults. Nat Rev Nephrol. (2018) 14:717. 10.1038/s41581-018-0044-0
74.
de KeijzerINKaufmannTScheerenTWL. Which type of fluid to use perioperatively?J Emerg Crit Care Med. (2019) 3:51. 10.21037/jeccm.2019.08.07
75.
PerelPRobertsIKerK. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev. (2013) 28:CD000567.pub6. 10.1002/14651858.CD000567.pub6
76.
BoerCBossersSMKoningNJ. Choice of fluid type: physiological concepts and perioperative indications. Br J Anaesth. (2018) 120:384–96. 10.1016/j.bja.2017.10.022
77.
MizushimaYTohiraHMizobataYMatsuokaTYokotaJ. Fluid resuscitation of trauma patients: how fast is the optimal rate?Am J Emerg Med. (2005) 23:833–7. 10.1016/j.ajem.2005.03.015
78.
RogerCLouartBLouartGBobbiaXClaretPGPerez-MartinAet al. Does the infusion rate of fluid affect rapidity of mean arterial pressure restoration during controlled hemorrhage. Am J Emerg Med. (2016) 34:1743–9. 10.1016/j.ajem.2016.05.019
79.
HoLLauLChurilovLRiedelBMcNicolLHahnRGet al. Comparative evaluation of crystalloid resuscitation rate in a human model of compensated haemorrhagic shock. Shock. (2016) 46:149–57. 10.1097/SHK.0000000000000610
80.
DohertyMBuggyDJ. Intraoperative fluids: how much is too much?Br J Anaesth. (2012) 109:69–79. 10.1093/bja/aes171
81.
MarikPEByrneLvan HarenF. Fluid resuscitation in sepsis: the great 30 mL per kg hoax. J Thorac Dis. (2020) 12:S37–47. 10.21037/jtd.2019.12.84
82.
MeyhoffTSMøllerMHHjortrupPBCronhjortMPernerAWetterslevJ. Lower vs higher fluid volumes during initial management of sepsis: a systematic review with meta-analysis and trial sequential analysis. Chest. (2020) 157:1478–96. 10.1016/j.chest.2019.11.050
83.
HirshbergAHoytDBMattoxKL. Timing of fluid resuscitation shapes the hemodynamic response to uncontrolled hemorrhage: analysis using dynamic modeling. J Trauma. (2006) 60:1221–7. 10.1097/01.ta.0000220392.36865.fa
84.
KwanIBunnFChinnockPRobertsI. Timing and volume of fluid administration for patients with bleeding. Cochrane Database Syst Rev. (2014) 3:CD002245. 10.1002/14651858.CD002245.pub2
85.
FeinmanMCottonBAHautER. Optimal fluid resuscitation in trauma: type, timing, and total. Curr Opin Crit Care. (2014) 20:366–72. 10.1097/MCC.0000000000000104
86.
GoodellGMCampbellJHoejvang-NielsenLStansenWConstablePD. An alkalinizing oral rehydration solution containing lecithin-coated citrus fiber is superior to a nonalkalinizing solution in treating 360 calves with naturally acquired diarrhea. J Dairy Sci. (2012) 95:6677–86. 10.3168/jds.2012-5605
87.
MartinGSKaufmanDAMarikPEShapiroNILevettDZHWhittleJet al. Perioperative Quality Initiative (POQI) consensus statement on fundamental concepts in perioperative fluid management: fluid responsiveness and venous capacitance. Perioper Med. (2020) 9:12. 10.1186/s13741-020-00142-8
88.
MuirWWUeyamaYNoel-MorganJKilborneAPageJ. A. Systematic review of the quality of IV fluid therapy in veterinary medicine. Front Vet Sci. (2017) 4:127. 10.3389/fvets.2017.00127
89.
RobertsIKwanIEvansPHaigS. Does animal experimentation inform human healthcare? Observations from a systematic review of international animal experiments on fluid resuscitation. BMJ. (2002) 324:474–6. 10.1136/bmj.324.7335.474
90.
MapstoneJRobertsIEvansP. Fluid resuscitation strategies: a systematic review of animal trials. J Trauma. (2003) 55:571–89. 10.1097/01.TA.0000062968.69867.6F
91.
TabbersMMBoluytNOffringaM. Implementation of an evidence-based guideline on fluid resuscitation: lessons learnt for future guidelines. Eur J Pediatr. (2010) 169:749–58. 10.1007/s00431-009-1108-8
92.
YozovaIDHowardJSigristNEAdamikKN. Current trends in volume replacement therapy and the use of synthetic colloids in small animals-an internet-based survey (2016). Front Vet Sci. (2017) 4:140. 10.3389/fvets.2017.00140
93.
HopperKGarcia RojasABarterL. An online survey of small animal veterinarians regarding current fluid therapy practices in dogs and cats. J Am Vet Med Assoc. (2018) 252:553–9. 10.2460/javma.252.5.553
94.
HahnRG. Fluid therapy might be more difficult than you think. Anesthesia Analgesia. (2007) 105:304–5. 10.1213/01.ane.0000270218.31147.67
95.
MarikPE. Lactate guided resuscitation-nothing is more dangerous than conscientious foolishness. J Thorac Dis. (2019) 15(Suppl.):S1969–72. 10.21037/jtd.2019.07.67
96.
JosephFBorzelleca. Paracelsus: herald of modern toxicology. Toxicol Sci. (2000) 53:2–4. 10.1093/toxsci/53.1.2
97.
Baxter Healthcare Corporation. Lactated Ringers (2000). Available online at: https://www.baxrerpi.com/pi-pdf/Lactated_Ringers_Injection_+viaflex_PI.pdf (accessed April 29, 2020).
98.
RawsonREDispensaMEGoldsteinRENicholsonKWVidalNK. A simulation for teaching the basic and clinical science of fluid therapy. Adv Physiol Educ. (2009) 33:202–8. 10.1152/advan.90211.2008
99.
HosteEAMaitlandKBrudneyCSMehtaRVincentJLYatesDet al. ADQI XII Investigators Group. Four phases of intravenous fluid therapy: a conceptual model. Br J Anaesth. (2014) 113:740–7. 10.1093/bja/aeu300
100.
SvensénCSjöstrandFHahnRG. Volume kinetics of intravenous fluid therapy in the prehospital setting. Prehosp Disaster Med. (2001) 16:9–13. 10.1017/S1049023X00025474
101.
BhaveGNeilsonEG. Body fluid dynamics: back to the future. J Am Soc Nephrol. (2011) 22:2166–81. 10.1681/ASN.2011080865
102.
CarlsonGP. Fluid therapy in horses with acute diarrhea. Vet Clin North Am Large Anim Pract. (1979) 1:313–29. 10.1016/S0196-9846(17)30187-8
103.
SuttonJD. Digestion and absorption of energy substrates in the lactating cow. J Dairy Sc. (1985) 68:3376–93. 10.3168/jds.S0022-0302(85)81251-0
104.
KuKanichBCoetzeeJFGehringRHubinM. Comparative disposition of pharmacologic markers for cytochrome P-450 mediated metabolism, glomerular filtration rate, and extracellular and total body fluid volume of Greyhound and Beagle dogs. J Vet Pharmacol Ther. (2007) 30:314–9. 10.1111/j.1365-2885.2007.00875.x
105.
GundersenKShenG. Total body water in obesity. Am J Clin Nutr. (1955) 19:77–83. 10.1093/ajcn/19.2.77
106.
CourticeFC. The blood volume of normal animals. J Physiol. (1943) 102:290–305. 10.1113/jphysiol.1943.sp004035
107.
LindstedtSSchaefferP. Use of allometry in predicting anatomical and physiological parameters of mammals. Lab Animals. (2002) 36:1–19. 10.1258/0023677021911731
108.
CarlsonGPBrussM. Fluid, electrolyte, and acid-base balance. In: Kaneko JJ, Harvey JW, Bruss ML, editors, Fluid, Electrolyte, and Acid-Base Balance, Clinical Biochemistry of Domestic Animals. 6th ed. New York, NY: Academic Press (2008). p. 529–59. 10.1016/B978-0-12-370491-7.00017-9
109.
LevittMFGaudinoAM. Measurement of body water compartments. Am J Med. (1950) 9:208–15. 10.1016/0002-9343(50)90024-6
110.
ZdolsekJHLisanderBHahnRG. Measuring the size of the extracellular fluid space using bromide, iohexol, and sodium dilution. Anesth Analg. (2005) 101:1770–7. 10.1213/01.ANE.0000184043.91673.7E
111.
WolfMB. Hemoglobin-dilution method: effect of measurement errors on vascular olume estimation. Comput Math Methods Med. (2017) 2017:3420590. 10.1155/2017/3420590
112.
BrandstrupB. Fluid therapy for the surgical patient. Best Pract Res Clin Anaesthesiol. (2006) 20:265–83. 10.1016/j.bpa.2005.10.007
113.
JacobMChappellDRehmM. The 'third space'–fact or fiction?Best Pract Res Clin Anaesthesiol. (2009) 23:145–57. 10.1016/j.bpa.2009.05.001
114.
ErtlACDiedrichARajSR. Techniques used for the determination of blood volume. Am J Med Sci. (2007) 334:32–6. 10.1097/MAJ.0b013e318063c6d1
115.
ReitsmaSSlaafDWVinkHvan ZandvoortMAoude EgbrinkMG. The endothelial glycocalyx: composition, functions, and visualization. Pflugers Arch. (2007) 454:345–59. 10.1007/s00424-007-0212-8
116.
CurryFE. Layer upon layer: the functional consequences of disrupting the glycocalyx-endothelial barrier in vivo and in vitro. Cardiovasc Res. (2017) 113:559–61, 10.1093/cvr/cvx044
117.
JungheinrichCNeffTA. Pharmacokinetics of hydroxyethyl starch. Clin Pharmacokinet. (2005) 44:681–99. 10.2165/00003088-200544070-00002
118.
VinkHDulingBR. Capillary endothelial surface layer selectively reduces plasma solute distribution volume. Am J Physiol Heart Circ Physiol. (2000) 278:H285–9. 10.1152/ajpheart.2000.278.1.H285
119.
MitraSKhandelwalP. Are all colloids same? how to select the right colloid?Indian J Anaesth. (2009) 53:592–607. PMID: 20640110.
120.
JiangXZLuYLuoKHVentikosY. Understanding endothelial glycocalyx function under flow shear stress from a molecular perspective. Biorheology. (2019) 56:89–100. 10.3233/BIR-180193
121.
ChappellDJacobM. Role of the glycocalyx in fluid management: small things matter. Best Pract Res Clin Anaesthesiol. (2014) 28:227–34. 10.1016/j.bpa.2014.06.003
122.
BirchDJTurmaineMBoulosPBBurnstockG. Sympathetic innervation of human mesenteric artery and vein. J Vasc Res. (2008) 45:323–32. 10.1159/000119095
123.
GelmanS. Venous function and central venous pressure: a physiologic story. Anesthesiology. (2008) 108:735–48. 10.1097/ALN.0b013e3181672607
124.
ShenTBakerK. Venous return and clinical hemodynamics: how the body works during acute hemorrhage. Adv Physiol Educ. (2015) 39:267–71. 10.1152/advan.00050.2015
125.
CannessonMJianZChenGVuTQHatibF. Effects of phenylephrine on cardiac output and venous return depend on the position of the heart on the Frank-Starling relationship. J Appl Physiol. (1985) 113:281–9. 10.1152/japplphysiol.00126.2012
126.
JacobsRLochySMalbrainMLNG. Phenylephrine-induced recruitable preload from the venous side. J Clin Monit Comput. (2019) 33:373–6. 10.1007/s10877-018-0225-1
127.
GuytonACLindseyAWAbernathyBRichardsonT. Venous return at various right atrial pressures and the normal venous return curve. Am J Physiol. (1957) 189:609–15. 10.1152/ajplegacy.1957.189.3.609
128.
MagderS. Volume and its relationship to cardiac output and venous return. Crit Care. (2016) 20:271. 10.1186/s13054-016-1438-7
129.
LevyMN. The cardiac and vascular factors that determine systemic blood flow. Circ Res. (1979) 44:739–47. 10.1161/01.RES.44.6.739
130.
RotheCF. Reflex controls of veins and vascular capacitance. Physiol Rev. (1983) 63:1281–341. 10.1152/physrev.1983.63.4.1281
131.
TybergJV. How changes in venous capacitance modulate cardiac output. Pflugers Arch. (2002) 445:10–7. 10.1007/s00424-002-0922-x
132.
ReddiBACarpenterRH. Venous excess: a new approach to cardiovascular control and its teaching. J Appl Physiol. (2005) 98:356–64. 10.1152/japplphysiol.00535.2004
133.
BeardDAFeiglEO. Understanding Guyton's venous return curves. Am J Physiol Heart Circ Physiol. (2011) 30:H629–33. 10.1152/ajpheart.00228.2011
134.
Brengelmann GLA. critical analysis of the view that right atrial pressure determines venous return. J Appl Physiol. (2003) 94:849–59. 10.1152/japplphysiol.00868.2002
135.
BrengelmannGL. Venous return and the physical connection between distribution of segmental pressures and volumes. Am J Physiol Heart Circ Physiol. (2019) 317:H939–53. 10.1152/ajpheart.00381.2019
136.
DalmauR. Venous return: a fresh start. Am J Physiol Heart Circ Physiol. (2019) 317:H1102–4. 10.1152/ajpheart.00575.2019
137.
AkramMHamidA. A comprehensive review on water balance. Biomed Nutr. (2013) 3:193–5. 10.1016/j.bionut.2012.10.003
138.
OlssonK. Fluid balance in ruminants: adaptation to external and internal challenges. Ann N Y Acad Sci. (2005) 1040:156–61. 10.1196/annals.1327.020
139.
PatelVBZhongJCGrantMBOuditGY. Role of the ACE2/angiotensin 1-7 axis of the renin-angiotensin system in heart failure. Circ Res. (2016) 118:1313–26. 10.1161/CIRCRESAHA.116.307708
140.
KnepperMAKwonTHNielsenS. Molecular physiology of water balance. N Engl J Med. (2015) 373:196. 10.1056/NEJMc1505505
141.
BieP. Natriuretic peptides and normal body fluid regulation. Compr Physiol. (2018) 8:1211–49. 10.1002/cphy.c180002
142.
BieP. Mechanisms of sodium balance: total body sodium, surrogate variables, and renal sodium excretion. Am J Physiol Regul Integr Comp Physiol. (2018) 315:R945–62. 10.1152/ajpregu.00363.2017
143.
DelpireEGagnonKB. Water homeostasis and cell volume maintenance and regulation. Curr Top Membr. (2018) 81:3–52. 10.1016/bs.ctm.2018.08.001
144.
SugieJIntagliettaMSungLA. Water transport and homeostasis as a major function of erythrocytes. Am J Physiol Heart Circ Physiol. (2018) 314:H1098–107. 10.1152/ajpheart.00263.2017
145.
BankirLBoubyNTrinh-Trang-TanMM. The role of the kidney in the maintenance of water balance. Baillieres Clin Endocrinol Metab. (1989) 3:249–311. 10.1016/S0950-351X(89)80005-9
146.
EllisonDFarrarFC. Kidney influence on fluid and electrolyte balance. Nurs Clin North Am. (2018) 53:469–80. 10.1016/j.cnur.2018.05.004
147.
DunnALoVDonnellyS. The role of the kidney in blood volume regulation: the kidney as a regulator of the hematocrit. Am J Med Sci. (2007) 334:65–71. 10.1097/MAJ.0b013e318095a4ae
148.
JacobMSallerTChappellDRehmMWelschUBeckerBF. Physiological levels of A-, B- and C-type natriuretic peptide shed the endothelial glycocalyx and enhance vascular permeability. Basic Res Cardiol. (2013) 108:347. 10.1007/s00395-013-0347-z
149.
WiigHRubinKReedRK. New and active role of the interstitium in control of interstitial fluid pressure: potential therapeutic consequences. Acta Anesthesiol Scand. (2003) 47:111–21. 10.1034/j.1399-6576.2003.00050.x
150.
GavaghanM. Cardiac anatomy and physiology: a review. AORN J. (1998) 67:802–22. 10.1016/S0001-2092(06)62644-6
151.
ReedRKRubinK. Transcapillary exchange: role and importance of the interstitial fluid pressure and the extracellular matrix. Cardiovasc Res. (2010) 8:211–7. 10.1093/cvr/cvq143
152.
SureshKShimodaLA. Lung circulation. Compr Physiol. (2016) 6:897–943. 10.1002/cphy.c140049
153.
Moore JEJrBertramCD. Lymphatic system flows. Annu Rev Fluid Mech. (2018) 50:459–82. 10.1146/annurev-fluid-122316-045259
154.
NakadaTKweeIL. Fluid dynamics inside the brain barrier: current concept of interstitial flow, glymphatic flow, and cerebrospinal fluid circulation in the brain. Neuroscientist. (2019) 25:155–66. 10.1177/1073858418775027
155.
CurryFRAdamsonRH. Vascular permeability modulation at the cell, microvessel, or whole organ level: towards closing gaps in our knowledge. Cardiovasc Res. (2010) 87:218–29. 10.1093/cvr/cvq115
156.
FrankBWKern FJr. Intestinal and liver lymph and lymphatics. Gastroenterology. (1968) 55:408–22. 10.1016/S0016-5085(19)34052-1
157.
TumaPLHubbardAL. Transcytosis: crossing cellular barriers. Physiol Rev. (2003) 83:871–932. 10.1152/physrev.00001.2003
158.
PillingerNLKamP. Endothelial glycocalyx: basic science and clinical implications. Anaesth Intensive Care. (2017) 45:295–307. 10.1177/0310057X1704500305
159.
JacobMBrueggerDRehmMWelschUConzenPBeckerBF. Contrasting effects of colloid and crystalloid resuscitation fluids on cardiac vascular permeability. Anesthesiology. (2006) 104:1223–31. 10.1097/00000542-200606000-00018
160.
SarinH. Physiologic upper limits of pore size of different blood capillary types and another perspective on the dual pore theory of microvascular permeability. J Angiogenes Res. (2010) 2:14. 10.1186/2040-2384-2-14
161.
DanzigerJZeidelML. Osmotic homeostasis. Clin J Am Soc Nephrol. (2015) 10:852–62. 10.2215/CJN.10741013
162.
RoumeliotiMEGlewRHKhitanZJRondon-BerriosHArgyropoulosCPMalhotraDet al. Fluid balance concepts in medicine: principles and practice. World J Nephrol. (2018) 7:1–28. 10.5527/wjn.v7.i1.1
163.
WeiskopfRBJamesMF. Update of use of hydroxyethyl starches in surgery and trauma. J Trauma Acute Care Surg. (2015) 78:S54–S9. 10.1097/TA.0000000000000636
164.
HeHLiuDInceC. Colloids and the microcirculation. Anesth Analg. (2018) 126:1747–54. 10.1213/ANE.0000000000002620
165.
MichelCCCurryFE. Microvascular permeability. Physiol Rev. (1999) 79:703–61. 10.1152/physrev.1999.79.3.703
166.
CurryFE. The molecular structure of the endothelial glycocalyx layer (EGL) and surface layers (ESL) modulation of transvascular exchange. Adv Exp Med Biol. (2018) 1097:29–49. 10.1007/978-3-319-96445-4_2
167.
ChoiPTYipGQuinonezLGCookDJ. Crystalloids vs. colloids in fluid resuscitation: a systematic review. Crit Care Med. (1999) 27:200–10. 10.1097/00003246-199901000-00053
168.
RaghunathanKMurrayPTBeattieWSLoboFNMyburgJSladenRet al. Choice of fluid in acute illness: what should be given? An international consensus. Br J Anaesth. (2014) 113:772–83. 10.1093/bja/aeu301
169.
ZaarMLauritzenBSecherNHKrantzTNielsenHBMadsenPLet al. Initial administration of hydroxyethyl starch vs lactated Ringer after liver trauma in the pig. Br J Anaesth. (2009) 102:221–6. 10.1093/bja/aen350
170.
HartogCSBauerMReinhartK. The efficacy and safety of colloid resuscitation in the critically ill. Anesth Analg. (2011) 112:156–64. 10.1213/ANE.0b013e3181eaff91
171.
JacobMChappellDHofmann-KieferKHelfenTSchuelkeAJacobBet al. The intravascular volume effect of Ringer's lactate is below 20%: a prospective study in humans. Crit Care. (2012) 16:R86. 10.1186/cc11344
172.
OrbegozoCortés DGamarano BarrosTNjimiHVincentJ-L. Crystalloids versus colloids. Anesthesia Analgesia. (2015) 120:389–402. 10.1213/ANE.0000000000000564
173.
FinferSBellomoRBoyceNFrenchJMyburghJNortonRet al. comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med. (2004) 350:2247–56. 10.1056/NEJMoa040232
174.
HahnRG. Why are crystalloid and colloid fluid requirements similar during surgery and intensive care?Eur J Anaesthesiol. (2013) 30:515–8. 10.1097/EJA.0b013e328362a5a9
175.
LászlóIDemeterGÖvegesNÉrcesDKaszakiJTánczosKet al. Volume-replacement ratio for crystalloids and colloids during bleeding and resuscitation: an animal experiment. Intensive Care Med Exp. (2017) 5:52. 10.1186/s40635-017-0165-y
176.
FodorGHHabreWBaloghALSüdyRBabikBPetákF. Optimal crystalloid volume ratio for blood replacement for maintaining hemodynamic stability and lung function: an experimental randomized controlled study. BMC Anesthesiol. (2019) 19:21. 10.1186/s12871-019-0691-0
177.
PassmoreMRObonyoNGByrneLBoonACDiabSDDunsterKRet al. Fluid resuscitation with 0.9% saline alters haemostasis in an ovine model of endotoxemic shock. Thromb Res. (2019) 176:39–45. 10.1016/j.thromres.2019.02.015
178.
ZiebartARuemmlerRMöllmannCKamufJGarcia-BardonAThalSCet al. Fluid resuscitation-related coagulation impairment in a porcine hemorrhagic shock model. PeerJ. (2020) 8:e8399. 10.7717/peerj.8399
179.
HahnRGLyonsG. The half-life of infusion fluids: an educational review. Eur J Anaesthesiol. (2016) 33:475–82. 10.1097/EJA.0000000000000436
180.
StarlingEH. On the absorption of fluids from the connective tissue spaces. J Physiol. (1896) 19:312–26. 10.1113/jphysiol.1896.sp000596
181.
AxelL. Flow limits of Kedem-Katchalsky equations for fluid flux. Bull Math Biol. (1976) 38:671–7. 10.1016/S0092-8240(76)80007-9
182.
LandisEM. The relationship between capillary pressure and the rate at which fluid passes through the walls of single capillaries. Am J Physiol. (1927) 82:217–38. 10.1152/ajplegacy.1927.82.2.217
183.
LandisEM. Factors controlling the movement of fluid through the human capillary wall yale. J Biol Med. (1933) 5:201–25.
184.
PappenheimerJRSoto-RiveraA. Effective osmotic pressure of the plasma proteins and other quantities associated with the capillary circulation in the hind limb of cats and dogs. Am J Physiol. (1948) 152:471–449. 10.1152/ajplegacy.1948.152.3.471
185.
PopelASJohnsonPC. Microcirculation and hemorheology. Annu Rev Fluid Mech. (2005) 37:43–69. 10.1146/annurev.fluid.37.042604.133933
186.
TaylorAE. Capillary fluid filtration. Starling forces and lymph flow. Circ Res. (1981) 49:557–75. 10.1161/01.RES.49.3.557
187.
StavermanAJ. The theory of measurement of osmotic pressure. Recueil des Travaux Chimiques des Pays-Bas. (1951) 70:344–52. 10.1002/recl.19510700409
188.
LevickJR. Revision of the Starling principle: new views of tissue fluid balance. J Physiol. (2004) 557:704. 10.1113/jphysiol.2004.066118
189.
MichelCC. Starling: the formulation of his hypothesis of microvascular fluid exchange and its significance after 100 years. Exp Physiol. (1997) 82:1–30. 10.1113/expphysiol.1997.sp004000
190.
WeinbaumSTsayRCurryFE. A three-dimensional junction-pore-matrix model for capillary permeability. Microvasc Res. (1992) 44:85–111. 10.1016/0026-2862(92)90104-W
191.
HuXAdamsonRHLiuBCurryFEWeinbaumS. Starling forces that oppose filtration after tissue oncotic pressure is increased. Am J Physiol Heart Circ Physiol. (2000) 279:H1724–36. 10.1152/ajpheart.2000.279.4.H1724
192.
AdamsonRH. Oncotic pressures opposing filtration across non-fenestrated rat microvessels. J Physiol. (2004) 557:889–907. 10.1113/jphysiol.2003.058255
193.
CurryFEAdamsonRH. Endothelial glycocalyx: permeability barrier and mechanosensor. Ann Biomed Eng. (2012) 40:828–39. 10.1007/s10439-011-0429-8
194.
ThindGSZandersSBakerJK. Recent advances in the understanding of endothelial barrier function and fluid therapy. Postgrad Med J. (2018) 94:289–95. 10.1136/postgradmedj-2017-135125
195.
GuerciPErginBUzZInceYWestphalMHegerMet al. Glycocalyx degradation is independent of vascular barrier permeability increase in nontraumatic hemorrhagic shock in rats. Anesth Analg. (2019) 129:598–607. 10.1213/ANE.0000000000003918
196.
DullROHahnRG. Transcapillary refill: the physiology underlying fluid reabsorption. J Trauma Acute Care Surg. (2021). F90:e31–9. 10.1097/TA.0000000000003013
197.
ArnemannPHHesslerMKampmeierTSeidelLMalekYVan AkenHet al. Resuscitation with hydroxyethyl starch maintains hemodynamic coherence in ovine hemorrhagic shock. Anesthesiology. (2020) 132:131–9. 10.1097/ALN.0000000000002998
198.
SvensenCHRodhePMProughDS. Pharmacokinetic aspects of fluid therapy. Best Pract Res Clin Anaesthesiol. (2009) 23:213–24. 10.1016/j.bpa.2008.11.003
199.
SvensénCHBrauerKPHahnRGUchidaTTraberLDTraberDLProughDS. Elimination rate constant describing clearance of infused fluid from plasma is independent of large infusion volumes of 09% saline in sheep. Anesthesiology. (2004) 101:666–74. 10.1097/00000542-200409000-00015
200.
SilversteinDCAldrichJHaskinsSCDrobatzKFCowgillLD. Assessment of changes in blood volume in response to resuscitative fluid administration in dogs. J Vet Emerg Crit Care. (2005) 15:185–92. 10.1111/j.1476-4431.2005.00138.x
201.
WoodcockTE. Plasma volume, tissue oedema, and the steady-state Starling principle. BJA Education. (2017) 17:74–8. 10.1093/bjaed/mkw035
202.
HirshbergAHoytDBMattoxKL. From “leaky buckets” to vascular injuries: understanding models of uncontrolled hemorrhage. J Am Coll Surg. (2007) 204:665–72. 10.1016/j.jamcollsurg.2007.01.005
203.
HahnRGDrobinDZdolsekJ. Distribution of crystalloid fluid changes with the rate of infusion: a population-based study. Acta Anaesthesiol Scand. (2016) 60:569–78. 10.1111/aas.12686
204.
ValverdeAGianottiGRioja-GarciaEHathwayA. Effects of high-volume, rapid-fluid therapy on cardiovascular function and hematological values during isoflurane-induced hypotension in healthy dogs. Can J Vet Res. (2012) 76:99–108.
205.
LambdenSCreagh-BrownBCHuntJ. Definitions and pathophysiology of vasoplegic shock. Crit Care. (2018) 22:174. 10.1186/s13054-018-2102-1
206.
LevyBFritzCTahonE. Vasoplegia treatments: the past, the present, and the future. Crit Care. (2018) 22:174. 10.1186/s13054-018-1967-3
207.
Van der LindenPDe HertSMathieuNDegrooteFSchmartzDZhangHet al. Tolerance to acute isovolemic hemodilution. Effect of anesthetic depth. Anesthesiology. (2003) 99:97–104. 10.1097/00000542-200307000-00018
208.
MoritaYChin-YeeIYuPSibbaldWJMartinCM. Critical oxygen delivery in conscious septic rats under stagnant or anemic hypoxia. Am J Respir Crit Care Med. (2003) 167:868–72. 10.1164/rccm.200205-490OC
209.
PapeAKutschkerSKertschoHSteinPHornOLossenMet al. The choice of the intravenous fluid influences the tolerance of acute normovolemic anemia in anesthetized domestic pigs. Crit Care. (2012) 16:R69. 10.1186/cc11324
210.
ConnollyCMKramerGCHahnRGChaissonNFSvensénCHKirschnerRAet al. Isoflurane but not mechanical ventilation promotes extravascular fluid accumulation during crystalloid volume loading. Anesthesiology. (2003) 98:670–81. 10.1097/00000542-200303000-00015
211.
MarikP. The physiology of fluid resuscitation. Curr Anesthesiol Rep. (2014) 4:353–9. 10.1007/s40140-014-0080-7
212.
HahnRGNemmeJ. Volume kinetic analysis of fluid retention after induction of general anesthesia. BMC Anesthesiol. (2020) 20:95. 10.1186/s12871-020-01001-1
213.
BoscanPPypendopBHSiaoKTFranceyTDowersKCowgillLet al. Fluid balance, glomerular filtration rate, and urine output in dogs anesthetized for an orthopedic surgical procedure. Am J Vet Res. (2010) 71:501–7. 10.2460/ajvr.71.5.501
214.
EganEDJohnsonKB. The influence of hemorrhagic shock on the disposition and effects of intravenous anesthetics: a narrative review. Anesth Analg. (2020) 130:1320–30. 10.1213/ANE.0000000000004654
215.
GelmanSMushlinPS. Catecholamine-induced changes in the splanchnic circulation affecting systemic hemodynamics. Anesthesiology. (2004) 100:434–43. 10.1097/00000542-200402000-00036
216.
VaneLAProughDSKinskyMAWilliamsCAGradyJJKramerGC. Effects of different catecholamines on the dynamics of volume expansion of crystalloid infusion. Anesthesiology. (2004) 101:1136–44. 10.1097/00000542-200411000-00013
217.
EwaldssonCAVaneLAKramerGCHahnRG. Adrenergic drugs alter both the fluid kinetics and the hemodynamic responses to volume expansion in sheep. J Surg Res. (2006) 131:7–14. 10.1016/j.jss.2005.09.012
218.
StephensCTUwaydahNKramerGCProughDSSalterMKinskyMP. Vascular and extravascular volume expansion of dobutamine and norepinephrine in normovolemic sheep. Shock. (2011) 36:303–11. 10.1097/SHK.0b013e318225b031
219.
AsmussenSSalterMProughDSKramerGCSvensenCSheffield-MooreMet al. Isoproternenol increases vascular volume expansion and urinary output after a large crystalloid bolus in healthy volunteers. Shock. (2014) 42:407–714. 10.1097/SHK.0000000000000233
220.
KanekoTTataraTHiroseM. Effects of anaesthesia-induced hypotension and phenylephrine on plasma volume expansion by hydroxyethyl starch: a randomised controlled study. Acta Anaesthesiol Scand. (2020) 64:620–7. 10.1111/aas.13548
221.
TataraTTsunetohTTashiroC. Crystalloid infusion rate during fluid resuscitation from acute haemorrhage. Br J Anaesth. (2007) 99:212–7. 10.1093/bja/aem165
222.
OgbuOCMurphyDJMartinGS. How to avoid fluid overload. Curr Opin Crit Care. (2015) 21:315–21. 10.1097/MCC.0000000000000211
223.
SantryHPAlamHB. Fluid resuscitation: past, present, and the future. Shock. (2010) 33:229–41. 10.1097/SHK.0b013e3181c30f0c
224.
NaumannDNBeavenADretzkeJHutchingsSMidwinterMJ. Searching for the optimal fluid to restore microcirculatory flow dynamics after haemorrhagic shock: a systematic review of preclinical studies. Shock. (2016) 46:609–22. 10.1097/SHK.0000000000000687
225.
MacDonaldNPearseRM. Are we close to the ideal intravenous fluid?Br J Anaesth. (2017) 119(Suppl.1):i63–i71. 10.1093/bja/aex293
226.
MuirW. Effect of intravenously administered crystalloid solutions on acid-base balance in domestic animals. J Vet Intern Med. (2017) 31:1371–81. 10.1111/jvim.14803
227.
ZwagerCLTuinmanPRde GroothHJ. Why physiology will continue to guide the choice between balanced crystalloids and normal saline: a systematic review and meta-analysis. Crit Care. (2019) 23:366. 10.1186/s13054-019-2658-4
228.
WilliamsATLucasAMullerCRBolden-RushCPalmerAFCabralesP. Balance between oxygen transport and blood rheology during resuscitation from hemorrhagic shock with polymerized bovine hemoglobin. J Appl Physiol. (1985). (2020) 129:97–107. 10.1152/japplphysiol.00016.2020
229.
JohanssonPIStensballeJOstrowskiSR. Shock induced endotheliopathy (SHINE) in acute critical illness - a unifying pathophysiologic mechanism. Crit Care. (2017) 21:25. 10.1186/s13054-017-1605-5
230.
BlackJAPierceVSJunejaKHolcombJB. Complications of hemorrhagic shock and massive transfusion-a comparison before and after the damage control resuscitation era. Shock. (2021) 56:42–51. 10.1097/SHK.0000000000001676
231.
HolcombJBTilleyBCBaraniukSFoxEEWadeCEPodbielskiJMet al. PROPPR Study Group. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. J Am Med Assoc. (2015) 313:471–82. 10.1001/jama.2015.12
232.
BogertJNHarvinJACottonBA. Damage control resuscitation. J Intensive Care Med. (2016) 31:177–86. 10.1177/0885066614558018
233.
SheppardFRSchaubLJCapAPMackoARMooreHBMooreEEet al. Whole blood mitigates the acute coagulopathy of trauma and avoids the coagulopathy of crystalloid resuscitation. J Trauma Acute Care Surg. (2018) 85:1055–62. 10.1097/TA.0000000000002046
234.
GuyetteFXSperryJLPeitzmanABBilliarTRDaleyBJMillerRSet al. Prehospital blood product and crystalloid resuscitation in the severely injured patient: a secondary analysis of the prehospital air medical plasma trial. Ann Surg. (2021) 273:358–64. 10.1097/SLA.0000000000003324
235.
ChongMAWangYBerbenetzNMMcConachieI. Does goal-directed haemodynamic and fluid therapy improve peri-operative outcomes? A systematic review and meta-analysis. Eur J Anaesthesiol. (2018) 35:469–83. 10.1097/EJA.0000000000000778
236.
JiangSWuMLuXZhongYKangXSongYFanZ. Is restrictive fluid resuscitation beneficial not only for hemorrhagic shock but also for septic shock? a meta-analysis. Medicine. (2021) 100:e25143. 10.1097/MD.0000000000025143
237.
PfortmuellerCASchefoldJC. Hypertonic saline in critical illness -a systematic review. J Crit Care. (2017) 42:168–77. 10.1016/j.jcrc.2017.06.019
238.
WodickaJRChambersAMSanghaGSGoergenCJPanitchA. Development of a glycosaminoglycan derived, selectin targeting anti-adhesive coating to treat endothelial cell dysfunction. Pharmaceuticals. (2017) 10:36. 10.3390/ph10020036
239.
DekkerNAMvan MeursMvan LeeuwenALIHoflandHMvan SlykePVonkABAet al. Vasculotide, an angiopoietin-1 mimetic, reduces pulmonary vascular leakage and preserves microcirculatory perfusion during cardiopulmonary bypass in rats. Br J Anaesth. (2018) 121:1041–51. 10.1016/j.bja.2018.05.049
240.
UchimidoRSchmidtEPShapiroNI. The glycocalyx: a novel diagnostic and therapeutic target in sepsis. Crit Care. (2019) 23:16. 10.1186/s13054-018-2292-6
241.
FerenzKBSteinbickerAU. Artificial oxygen carriers-past, present, and future-a review of the most innovative and clinically relevant concepts. J Pharmacol Exp Ther. (2019) 369:300–10. 10.1124/jpet.118.254664
242.
Sen GuptaA. Hemoglobin-based oxygen carriers: current state-of-the-art and novel molecules. Shock. (2019) 52:70–83. 10.1097/SHK.0000000000001009
243.
SiegemundMHollingerAGebhardECScheuzgerJDBolligerD. The value of volume substitution in patients with septic and haemorrhagic shock with respect to the microcirculation. Swiss Med Wkly. (2019) 149:w20007. 10.4414/smw.2019.20007
244.
OllerLDyerWBSantamaríaLLargoCJavidrooziMShanderA. The effect of a novel intravenous fluid (Oxsealife®) on recovery from haemorrhagic shock in pigs. Anaesthesia. (2019) 74:765–77. 10.1111/anae.14627
245.
MilfordEMReadeMC. Resuscitation fluid choices to preserve the endothelial glycocalyx. Crit Care. (2019) 23:77. 10.1186/s13054-019-2369-x
246.
EndoYKawaseKMiyashoTSanoTYamashitaKMuirWW. Plethysmography variability index for prediction of fluid responsiveness during graded haemorrhage and transfusion in sevoflurane-anaesthetized mechanically ventilated dogs. Vet Anaesth Analg. (2017) 44:1303–12. 10.1016/j.vaa.2017.07.007
247.
EndoYTamuraJIshizukaTItamiTHanazonoKMiyoshiKet al. Stroke volume variation (SVV) and pulse pressure variation (PPV) as indicators of fluid responsiveness in sevoflurane anesthetized mechanically ventilated euvolemic dogs. J Vet Med Sci. (2017) 79:1437–45. 10.1292/jvms.16-0287
248.
SanoHChambersJP. Ability of pulse wave transit time to detect changes in stroke volume and to estimate cardiac output compared to thermodilution technique in isoflurane-anaesthetised dogs. Vet Anaesth Analg. (2017) 44:1057–67. 10.1016/j.vaa.2016.11.014
249.
ChanAHughesDTennent-BrownBSBollerM. In vitro effects of lactated Ringer's solution, hypertonic saline, hydroxyethyl starch, hypertonic saline/hydroxyethyl starch, and mannitol on thromboelastographic variables of canine whole blood. J Vet Emerg Crit Care. (2020) 30:264–71. 10.1111/vec.12929
250.
Yaguiyan-ColliardLDaumasCNguyenPGrandjeanDCardotPPriymenkoNet al. Evaluation of total body water in canine breeds by single-frequency bioelectrical impedance analysis method: specific equations are needed for accuracy. BMC Res Notes. (2015) 8:336. 10.1186/s13104-015-1298-2
251.
LatmanNSKeithNNicholsonADavisM. Bioelectrical impedance analysis determination of water content and distribution in the horse. Res Vet Sci. (2011) 90:516–20. 10.1016/j.rvsc.2010.07.012
252.
MillerAMandevilleJ. Predicting and measuring fluid responsiveness with echocardiography. Echo Res Pract. (2016) 3:G1–12. 10.1530/ERP-16-0008
253.
DesaiND. Garry D. Assessing dynamic fluid-responsiveness using transthoracic echocardiography in intensive care. BJA Educ. (2018) 18: 218e226. 10.1016/j.bjae.2018.03.005
254.
MoonYJMoonHSKimDS. Deep learning-based stroke volume estimation outperforms conventional arterial contour method in patients with hemodynamic instability. J Clin Med. (2019) 8:1419. 10.3390/jcm8091419
255.
RinehartJLilotMLeeC. Closed-loop assisted versus manual goal-directed fluid therapy during high-risk abdominal surgery: a case-control study with propensity matching. Crit Care. (2015) 19:94. 10.1186/s13054-015-0827-7
256.
DaveSShriyanDGujjarP. Newer drug delivery systems in anesthesia. J Anaesthesiol Clin Pharmacol. (2017) 33:157–63. 10.4103/joacp.JOACP_63_16
257.
HundeshagenGKramerGCRibeiro MarquesNSalterMGKoutrouvelis AK LiHet al. Closed-loop- and decision-assist-guided fluid therapy of human hemorrhage. Crit Care Med. (2017) 45:e1068–74. 10.1097/CCM.0000000000002593
258.
UemuraKKawadaTZhengCLiMSugimachiM. Computer-controlled closed-loop drug infusion system for automated hemodynamic resuscitation in endotoxin-induced shock. BMC Anesthesiol. (2017) 17:145. 10.1186/s12871-017-0437-9
259.
GholamiBHaddadWMBaileyJMGeistBUeyamaYMuirWWet al. pilot study evaluating adaptive closed-loop fluid resuscitation during states of absolute and relative hypovolemia in dogs. J Vet Emerg Crit Care. (2018) 28:436–46. 10.1111/vec.12753
260.
YuJZhangYYanJKahkoskaARGuZ. Advances in bioresponsive closed-loop drug delivery systems. Int J Pharm. (2018) 544:350–7. 10.1016/j.ijpharm.2017.11.064
Summary
Keywords
physiology, fluid compartments, perfusion, volume kinetics, monitoring, novel fluids
Citation
Muir WW, Hughes D and Silverstein DC (2021) Editorial: Fluid Therapy in Animals: Physiologic Principles and Contemporary Fluid Resuscitation Considerations. Front. Vet. Sci. 8:744080. doi: 10.3389/fvets.2021.744080
Received
19 July 2021
Accepted
21 September 2021
Published
20 October 2021
Volume
8 - 2021
Edited and reviewed by
Mujeeb Ur Rehman, Livestock and Dairy Development Department, Pakistan
Updates
Copyright
© 2021 Muir, Hughes and Silverstein.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: William W. Muir monos369@gmail.com; william.muir@lmunet.edu
†These authors have contributed equally to this work and share first authorship
This article was submitted to Comparative and Clinical Medicine, a section of the journal Frontiers in Veterinary Science
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