Acid/Base, Fluids, & Electrolytes Flashcards
Seminal Papers from the ACVECC Top 100 Article List (238 cards)
1
Q
In Sen et al. (2017), what study design was used to assess the impact of chloride content on survival during fluid resuscitation?
A
Retrospective observational cohort study of 1,047 adult ICU patients who received >60 mL/kg IV fluids within 24 hours.
2
Q
What was the primary endpoint evaluated in Sen et al. (2017)?
A
30-day in-hospital mortality.
3
Q
According to Sen et al. (2017), what chloride threshold defined “high-chloride” fluids?
A
Chloride content ≥109 mmol/L (e.g., 0.9% NaCl, colloids in saline).
4
Q
What mortality difference was observed between high- and low-chloride groups in Sen et al. (2017)?
A
27.8% in the high-chloride group vs. 18.8% in the low-chloride group; p = 0.003.
5
Q
What was the adjusted odds ratio for mortality in patients receiving high-chloride fluids in Sen et al. (2017)?
A
aOR = 1.73 (95% CI: 1.14–2.63); p = 0.01.
6
Q
What pathophysiologic mechanisms are proposed in Sen et al. (2017) to explain increased mortality from high-chloride fluids?
A
1) Hyperchloremic metabolic acidosis, 2) renal vasoconstriction with ↓ GFR, 3) endothelial and glycocalyx injury promoting inflammation and microvascular dysfunction.
7
Q
Did Sen et al. (2017) find a significant difference in total fluid volume administered between high- and low-chloride groups?
A
No — mortality differences were attributed to chloride content, not fluid volume.
8
Q
How did Sen et al. (2017) control for differences in illness severity between groups?
A
Used multivariate logistic regression adjusted for APACHE III score and other confounders.
9
Q
What clinical recommendation can be drawn from Sen et al. (2017) regarding fluid selection for resuscitation?
A
Preferential use of balanced crystalloids (e.g., Plasma-Lyte, LRS) over high-chloride fluids to reduce mortality in high-volume resuscitation cases.
10
Q
In Semler et al. (2018) (SMART trial), what type of study was conducted to compare balanced crystalloids vs saline?
A
A pragmatic, cluster-randomized, multiple-crossover trial conducted in 5 ICUs over 16 months.
11
Q
What was the primary composite endpoint evaluated in the SMART trial by Semler et al. (2018)?
A
MAKE-30: Major Adverse Kidney Events within 30 days (composite of death, new renal replacement therapy, or persistent renal dysfunction).
12
Q
What was the incidence of MAKE-30 in the balanced crystalloid group vs the saline group in Semler et al. (2018)?
A
14.3% in the balanced group vs 15.4% in the saline group (p = 0.04).
13
Q
According to Semler et al. (2018), what fluids were considered ‘balanced crystalloids’?
A
Lactated Ringer’s (LR) and Plasma-Lyte A.
14
Q
What subgroup of patients derived the most benefit from balanced crystalloids in Semler et al. (2018)?
A
Patients with sepsis, renal impairment, or those receiving larger fluid volumes.
15
Q
What did Semler et al. (2018) conclude about the effect of balanced crystalloids on mortality?
A
No statistically significant difference in mortality alone, but a significant reduction in MAKE-30 supports preferential use of balanced fluids.
16
Q
How many ICU patients were included in Semler et al. (2018) SMART trial?
A
15,802 patients.
17
Q
What is the clinical relevance of Semler et al. (2018) for fluid resuscitation in critical illness?
A
Balanced crystalloids are associated with fewer kidney-related complications and should be preferred over saline for ICU fluid resuscitation.
18
Q
What potential mechanism may explain the benefits of balanced crystalloids seen in Semler et al. (2018)?
A
Balanced fluids avoid hyperchloremic metabolic acidosis, thereby reducing renal vasoconstriction and inflammation.
19
Q
According to Adamantos (2021), how does pulmonary interstitial edema affect gas exchange?
A
It increases the diffusion distance for oxygen, impairs alveolar expansion, and contributes to ventilation-perfusion mismatch.
20
Q
According to Adamantos (2021), what is the most important determinant of pulmonary fluid accumulation during resuscitation?
A
The integrity of the endothelial glycocalyx and capillary permeability, not just hydrostatic pressure or volume alone.
21
Q
According to Bohrer-Clancy et al. (2021), can dogs with very high lactate levels still survive?
A
Yes. Survival was still possible even with L-lactate > 6 mmol/L, underscoring the importance of clinical context.
22
Q
According to Bohrer-Clancy et al. (2021), what was the mortality rate in dogs with an L-lactate ≥ 6.0 mmol/L?
A
29.7%, compared to 6.4% in those with lactate < 6.0 mmol/L.
23
Q
According to Boysen & Rozanski (2021), what are the risks of using large-volume bolus fluids indiscriminately?
A
Interstitial edema, hemodilution, worsening coagulopathy, and exacerbation of hypoxia via endothelial damage and glycocalyx disruption.
24
Q
According to Boysen & Rozanski (2021), what is the primary goal of triage in emergency medicine?
A
To rapidly identify life-threatening conditions and initiate prompt, targeted resuscitation before full diagnostics are available.
25
According to Gholami et al. (2021), what physiologic parameters are most commonly used as feedback signals in closed-loop systems?
Stroke volume (SV), pulse pressure variation (PPV), mean arterial pressure (MAP), and sometimes lactate clearance.
26
According to Hansen (2021), what are three patient populations at highest risk for fluid overload?
1) Oliguric/AKI patients, 2) patients receiving aggressive resuscitation, 3) hypoalbuminemic or capillary leak syndrome patients.
27
According to Hansen (2021), what percentage of body weight gained from fluid accumulation may indicate fluid overload in small animals?
A gain of >10% of body weight in fluids is often used as a threshold for fluid overload in critically ill animals.
28
According to Jaber et al. (2018), what subgroup of patients derived benefit from bicarbonate therapy?
Patients with acute kidney injury (AKI) (KDIGO stage 2–3) showed improved survival and reduced need for dialysis.
29
According to Rudloff & Hopper (2021), what is the primary difference between crystalloids and colloids?
Crystalloids are aqueous electrolyte solutions that equilibrate quickly across compartments, while colloids contain large molecules that stay within the intravascular space longer, creating oncotic pressure.
30
According to Smart & Hughes (2021), what are the two main ways fluid therapy disrupts the glycocalyx?
1) Hyperchloremia from unbalanced crystalloids, 2) Rapid fluid loading causing shear stress and atrial natriuretic peptide (ANP)-mediated degradation.
31
According to Valverde et al. (2008), what type of fluid was administered, and in what volume?
A crystalloid bolus of 30 mL/kg of Lactated Ringer’s Solution (LRS) was administered over 15 minutes.
32
According to Woodcock & Michel (2021), where does oncotic pressure primarily act under the revised Starling principle?
At the glycocalyx layer, not the interendothelial cleft, shifting the primary site of oncotic gradient control to within the vessel lumen.
33
According to Woodcock & Michel (2021), why does administering albumin not prevent edema in septic patients?
Glycocalyx degradation allows protein to leak into the interstitium, dissolving the oncotic gradient, and albumin extravasates, further increasing interstitial oncotic pressure and promoting edema.
34
Adamik & Yozova (2021): How do colloids affect Starling forces differently from crystalloids?
Colloids exert oncotic pressure that retains fluid intravascularly, whereas crystalloids equilibrate more quickly with the interstitial space.
35
Adamik & Yozova (2021): In which situations might natural colloids (like plasma or albumin) be beneficial?
In hypoalbuminemia, protein-losing diseases, and severe vasculopathy (e.g., SIRS, sepsis), natural colloids may help maintain oncotic pressure and support vascular integrity.
36
Adamik & Yozova (2021): What are potential risks associated with synthetic colloids (e.g., hydroxyethyl starch)?
Risks include coagulopathy, renal injury, tissue storage, anaphylaxis, and interference with lab tests; these have been confirmed in human studies.
37
Adamik & Yozova (2021): What are the theoretical benefits of colloids over crystalloids?
They theoretically provide greater intravascular volume expansion with smaller volumes and longer duration of effect due to larger molecule size and oncotic pressure.
38
Adamik & Yozova (2021): What does current evidence suggest about mortality and AKI risk with synthetic colloids in human ICU patients?
Human ICU trials suggest increased risk of AKI and mortality with synthetic colloids like HES, particularly in septic or critically ill patients.
39
Adamik & Yozova (2021): What is the "Gretchen question" in fluid therapy referring to?
It refers to the debate over whether colloids should still be used, given growing concerns about risks and lack of demonstrated superiority over crystalloids.
40
Adamik & Yozova (2021): What is the recommendation for colloid use in veterinary patients based on current data?
Use colloids cautiously and selectively in veterinary patients; synthetic colloids should generally be avoided, while natural colloids may be considered in certain cases.
41
Adamik & Yozova (2021): What physiologic role does albumin play aside from oncotic support?
Albumin also serves as a carrier protein for hormones and drugs, and buffers acid-base disturbances.
42
Adamik & Yozova (2021): Why is albumin supplementation controversial in veterinary medicine?
Veterinary albumin products are limited, human albumin may be immunogenic, and evidence of benefit in critically ill animals is limited or inconclusive.
43
Chow (2021): Define “colloid.”
A fluid containing large-molecule solutes (natural or synthetic) that remain in the intravascular space longer and exert oncotic pressure (e.g., plasma, HES).
44
Chow (2021): Define “fluid responsiveness.”
A physiologic state in which stroke volume or cardiac output increases following fluid administration.
45
Chow (2021): Define "insensible losses."
Fluid losses that are not readily measured, such as respiratory water loss and evaporation from the skin.
46
Chow (2021): Define "maintenance fluids" in the context of veterinary fluid therapy.
Fluids required to meet the daily physiologic needs of a patient, including insensible losses and minimal urine production, typically administered over 24 hours.
47
Chow (2021): Define "replacement fluids" as per Chow (2021).
Fluids administered to correct pre-existing deficits or ongoing pathological losses (e.g., vomiting, diarrhea, polyuria).
48
Chow (2021): Define "shock dose" fluid administration.
The volume of fluid required to restore effective circulating volume in shock: typically 80–90 mL/kg for dogs and 50–60 mL/kg for cats, titrated to effect.
49
Chow (2021): Define the term “crystalloid.”
A solution containing water and small-molecule solutes that freely cross capillary membranes (e.g., LRS, 0.9% NaCl).
50
Chow (2021): How are isotonic, hypotonic, and hypertonic fluids defined?
Based on osmolality: isotonic ≈ plasma (~300 mOsm/kg), hypotonic < 300 mOsm/kg, hypertonic > 300 mOsm/kg.
51
Chow (2021): How are maintenance fluid requirements calculated in small animals?
Estimated at 40–60 mL/kg/day, adjusted based on insensible losses, patient condition, and ongoing losses.
52
Chow (2021): How should clinicians tailor fluid therapy to patient needs?
By assessing volume status, disease process, ongoing losses, and organ function, with regular reassessment and adjustment.
53
Chow (2021): What are “resuscitation fluids”?
Fluids rapidly administered to correct intravascular volume depletion and restore tissue perfusion in shock.
54
Chow (2021): What are the advantages of intraosseous (IO) fluid administration?
Rapid access in emergencies, similar pharmacokinetics to IV, useful in neonates or patients with collapsed vessels.
55
Chow (2021): What are the common routes of fluid administration discussed?
IV (most common), IO (intraosseous, when IV inaccessible), SC (for non-critical patients), and oral (if GI function intact).
56
Chow (2021): What are the three major fluid therapy goals described?
Resuscitation (restore intravascular volume), replacement (correct deficits/losses), and maintenance (meet daily needs).
57
Chow (2021): What distinguishes resuscitation fluids from replacement fluids?
Resuscitation fluids are given rapidly to restore perfusion and intravascular volume, whereas replacement fluids are calculated to correct measured or estimated fluid losses over time.
58
Chow (2021): What does “fluid deficit” refer to?
The estimated volume of fluid loss resulting in dehydration, calculated as % dehydration × body weight (kg) × 1000.
59
Chow (2021): What fluid-related terminology standardization does this paper emphasize?
Consistent use of terms like “fluid rate,” “fluid deficit,” and “shock dose” improves clarity and minimizes miscommunication in clinical settings.
60
Chow (2021): What is meant by “ongoing losses”?
Pathologic fluid losses that continue after presentation, such as vomiting, diarrhea, or effusion drainage.
61
Chow (2021): What is the difference between dehydration and hypovolemia?
Dehydration refers to total body water deficit (interstitial/intracellular), while hypovolemia is a deficit in intravascular volume.
62
Chow (2021): Why should subcutaneous fluid administration be avoided in shock or dehydrated patients?
Peripheral vasoconstriction and poor perfusion impair absorption, delaying therapeutic effect.
63
Compare the classic vs. revised Starling hypothesis per Woodcock & Michel (2021).
Classic: Filtration at arterial end, reabsorption at venous end. Revised: Filtration throughout capillary length; no reabsorption; lymphatics clear excess fluid.
64
Define actuator in the context of Gholami et al. (2021).
The device that delivers the intervention, such as a fluid pump or syringe driver that administers resuscitation fluid.
65
Define colloid osmotic pressure (COP) based on Rudloff & Hopper (2021).
The pressure exerted by proteins or large molecules that draws water into the vasculature, maintaining intravascular volume.
66
Define fluid responsiveness as used in Boysen & Rozanski (2021).
A measurable increase in stroke volume or cardiac output after a fluid bolus, often used to justify continued fluid therapy.
67
Define R time, K time, and MA in the context of Cooper & Silverstein (2021)’s TEG analysis.
R: time to initial clot formation; K: speed of clot strengthening; MA: maximum clot strength. All are used to assess coagulation kinetics and profile.
68
Did Bohrer-Clancy et al. (2021) support using L-lactate as a sole determinant of outcome?
No. It should be used in combination with physical exam, diagnostics, and monitoring, not in isolation.
69
Did Cooper & Silverstein (2021) find correlation between platelet count and TEG hypercoagulability?
No — many hypercoagulable dogs had normal platelet counts, indicating that TEG provides more functional data than CBC alone.
70
Did sodium bicarbonate therapy reduce 28-day mortality in all patients in Jaber et al. (2018)?
No — there was no mortality benefit in the overall population, only in the AKI subgroup.
71
Edwards & Hoareau (2021): How do perfluorocarbons function as oxygen therapeutics?
They dissolve large amounts of oxygen and release it in response to tissue hypoxia but require emulsification and high inspired oxygen concentrations.
72
Edwards & Hoareau (2021): What are examples of next-generation fluids mentioned in the paper?
Novel fluids include oxygen-carrying fluids, hemoglobin-based oxygen carriers (HBOCs), perfluorocarbon emulsions, and synthetic colloids with improved safety profiles.
73
Edwards & Hoareau (2021): What broader concept does the paper encourage ECC clinicians to adopt?
The concept of precision medicine in fluid therapy: tailoring interventions based on real-time physiologic data and patient-specific goals.
74
Edwards & Hoareau (2021): What is a limitation of current fluid therapy that novel approaches aim to address?
Current fluids do not address oxygen delivery, endothelial dysfunction, or inflammation modulation, all of which are targets for novel solutions.
75
Edwards & Hoareau (2021): What is a major challenge associated with hemoglobin-based oxygen carriers (HBOCs)?
HBOCs have been associated with oxidative stress, vasoconstriction, and renal toxicity due to free hemoglobin toxicity.
76
Edwards & Hoareau (2021): What is the central thesis of "Fluids of the Future"?
The paper argues that fluid therapy must evolve from static volume replacement to a more precise, patient-specific, goal-directed therapy using novel fluids and technologies.
77
Edwards & Hoareau (2021): What role do nanotechnology and bioengineering play in the future of fluid therapy?
These fields may allow for targeted drug/fluid delivery, molecular diagnostics, and smart resuscitation systems tailored to patient needs.
78
Edwards & Hoareau (2021): Why is personalization of fluid therapy emphasized?
Individual patient physiology, disease state, and dynamic response to fluids vary significantly, necessitating individualized protocols over fixed-dose therapy.
79
How did the authors of Bohrer-Clancy et al. (2021) interpret L-lactate as a predictor?
L-lactate is an early, objective prognostic biomarker for mortality risk, particularly when markedly elevated.
80
How do balanced crystalloids help protect the glycocalyx per Rudloff & Hopper (2021)?
Their lower chloride load reduces endothelial stress, preventing hyperchloremia-mediated shedding of the glycocalyx.
81
How does atrial natriuretic peptide (ANP) contribute to glycocalyx shedding during fluid loading in Smart & Hughes (2021)?
Rapid fluid boluses stretch the atria, releasing ANP, which enzymatically cleaves proteoglycans and accelerates glycocalyx degradation.
82
How does Boysen & Rozanski (2021) recommend using point-of-care ultrasound (POCUS) during triage?
As a non-invasive tool to assess fluid responsiveness (e.g., via Vena Cava or Aorta collapsibility), identify effusions, and differentiate shock types.
83
How does Boysen & Rozanski (2021) suggest fluid resuscitation be titrated?
Using a goal-directed approach based on response: improved perfusion, lactate reduction, normalized mentation, and restoration of pulse quality.
84
How does capillary hydrostatic pressure (Pc) interact with the glycocalyx layer in Woodcock & Michel (2021)?
Pc drives filtration across the capillary wall, but its effect is modulated by the presence of the glycocalyx and the low-protein sub-glycocalyx space.
85
How does Cooper & Silverstein (2021) define disseminated intravascular coagulation (DIC) in dogs?
A continuum involving systemic inflammation, consumption of coagulation factors, platelet dysfunction, and microvascular thrombosis.
86
How does dilutional hypoproteinemia affect unmeasured anion (UA) calculations, as reported in Valverde et al. (2008)?
The decrease in weak acids (especially albumin) led to a lower calculated UA, potentially masking the presence of metabolic acidosis.
87
How does glycocalyx injury amplify systemic inflammation, as described in Smart & Hughes (2021)?
Shedding exposes the endothelial basement membrane, promotes PAMP/DAMP recognition, increases cytokine release (e.g., IL-6, TNFα), and facilitates leukocyte transmigration.
88
How does Hansen (2021) suggest clinicians monitor for fluid overload in ICU patients?
Frequent reassessment of fluid input/output, body weight, physical exam findings, and point-of-care ultrasound (lung and abdominal).
89
How does inflammation affect the Starling forces as described in Woodcock & Michel (2021)?
It disrupts the glycocalyx, increasing capillary permeability, protein leak, and interstitial oncotic pressure, reducing effective fluid return and promoting edema.
90
How does rapid volume expansion with crystalloids affect Starling forces per Woodcock & Michel (2021)?
It increases hydrostatic pressure and may damage the glycocalyx, reducing πg and favoring uncontrolled filtration and edema formation.
91
How does the revised Starling model explain the near absence of steady-state capillary reabsorption per Woodcock & Michel (2021)?
Plasma proteins cannot readily cross the glycocalyx, so fluid moves out (filtration) along most of the capillary and lymphatic return becomes the primary method of fluid balance.
92
How does the revised Starling principle affect decisions about fluid boluses in shock per Woodcock & Michel (2021)?
Suggests more conservative fluid use and preference for balanced crystalloids, as excess volume can damage the glycocalyx and worsen edema.
93
How does the traditional Starling equation differ from the revised version in Woodcock & Michel (2021)?
Traditional: Assumes net filtration at arterial end and reabsorption at venous end. Revised: Predicts filtration dominates along entire capillary length; lymphatics clear excess interstitial fluid.
94
How should fluid resuscitation be adjusted to minimize glycocalyx injury based on Smart & Hughes (2021)?
1) Use balanced crystalloids, 2) Avoid rapid, large boluses, 3) Consider early fluid de-escalation strategies, 4) Use goal-directed resuscitation tools like POCUS and lactate trends.
95
How should L-lactate ≥ 6.0 mmol/L be interpreted clinically per Bohrer-Clancy et al. (2021)?
As a poor prognostic indicator, prompting aggressive assessment, resuscitation, and close monitoring, but not necessarily an indicator for euthanasia.
96
In Adamantos (2021), what is the recommendation for fluid resuscitation in animals with concurrent pulmonary disease?
Use goal-directed, titrated fluid boluses (10 mL/kg) with frequent reassessment for signs of pulmonary compromise (e.g., respiratory effort, oxygenation, ultrasound).
97
In Boysen & Rozanski (2021), what is emphasized as the most critical parameter to evaluate during triage?
Perfusion parameters (e.g., pulse quality, mucous membranes, mentation, capillary refill time) — more than heart rate or blood pressure alone.
98
In Cooper & Silverstein (2021), what percentage of septic dogs were hypercoagulable on TEG?
Approximately 47% were hypercoagulable, while 40% were normocoagulable, and 13% were hypocoagulable.
99
In Gholami et al. (2021), what is the function of an input sensor in a closed-loop system?
It continuously measures a physiologic variable (e.g., MAP, SV, PPV) to provide real-time feedback for decision-making.
100
In Rudloff & Hopper (2021), how is a balanced crystalloid defined?
A solution with electrolyte concentrations approximating plasma, including buffers (e.g., lactate, acetate) to minimize acid-base disturbance.
101
In Valverde et al. (2008), what acid-base method was used to calculate UA?
The Strong Ion Difference (SID) model was used, accounting for Na⁺, K⁺, Cl⁻, lactate, HCO₃⁻, and A⁻ (primarily albumin and phosphate).
102
In Valverde et al. (2008), what was the primary objective of the study?
To evaluate how fluid therapy alters total protein and how this impacts the calculation of unmeasured anions (UA) in anesthetized dogs using the strong ion approach.
103
In Woodcock & Michel (2021), what is the function of the sub-glycocalyx space in transvascular exchange?
It is the key oncotic barrier where plasma proteins are largely excluded, generating a strong oncotic gradient that opposes filtration.
104
In Woodcock & Michel (2021), why does capillary reabsorption not occur in steady-state physiology?
Because plasma proteins are excluded from the sub-glycocalyx space, resulting in a persistent oncotic gradient that favors filtration, not reabsorption; lymphatics clear excess interstitial fluid.
105
Muir et al. (2021): How do the authors frame the role of evidence-based decision-making in fluid therapy?
As critical for advancing veterinary critical care, highlighting the need for standardized protocols and integration of objective data (e.g., dynamic indices, POCUS).
106
Muir et al. (2021): What are the evolving research frontiers mentioned in the editorial?
Development of closed-loop fluid delivery systems, fluid biomarkers, and refined understanding of fluid pharmacokinetics and pharmacodynamics in veterinary species.
107
Muir et al. (2021): What concept is emphasized as essential for future fluid therapy strategies?
Individualized and physiology-guided fluid therapy—tailoring fluid type, volume, and timing to patient-specific needs and responses.
108
Muir et al. (2021): What is the main purpose of this editorial?
To introduce the thematic collection on fluid therapy in animals, emphasizing a shift toward precision resuscitation guided by physiology, microcirculation, and data-driven strategies.
109
Muir et al. (2021): What pathophysiologic principles are emphasized for fluid management?
Starling forces, vascular barrier integrity, and the interplay between fluid overload and organ dysfunction, including AKI and pulmonary edema.
110
Muir et al. (2021): What systems-level goal is highlighted for fluid resuscitation?
Preservation of the endothelial glycocalyx, microcirculatory integrity, and systemic perfusion—not merely increasing blood pressure.
111
Stewart (2020): How does the structure of the interstitium influence fluid movement?
It regulates capillary filtration and reabsorption by modulating resistance and compliance based on the proteoglycan matrix and lymphatic drainage.
112
Stewart (2020): How does this paper challenge traditional views of the Starling Principle?
It supports the revised Starling model, where fluid reabsorption at the venous end of capillaries is minimal and lymphatics are the primary means of interstitial fluid clearance.
113
Stewart (2020): What are the two phases of the interstitial compartment described in this paper?
The gel phase (bound water with proteoglycans and glycosaminoglycans) and the free fluid phase (mobile water not bound to matrix components).
114
Stewart (2020): What clinical scenarios are impacted by interstitial compliance changes?
Sepsis, trauma, and fluid overload can increase interstitial compliance, allowing for significant fluid accumulation before edema is clinically apparent.
115
Stewart (2020): What is the “interstitial safety factor” and why is it important?
It is the buffering capacity of the interstitial matrix to accommodate small increases in fluid without developing edema, dependent on tissue matrix integrity.
116
Stewart (2020): What is the interstitial space, and why is it physiologically important?
The interstitium is the space between cells and vasculature, serving as a reservoir for fluid exchange, nutrient delivery, waste removal, and cellular signaling.
117
Stewart (2020): What role does the interstitial matrix play in edema formation?
Disruption or saturation of the matrix (e.g., via inflammation or fluid overload) reduces its ability to bind water, allowing accumulation of free interstitial fluid and promoting edema.
118
Stewart (2020): Why is interstitial structure relevant to critical care fluid therapy?
Understanding the limits of interstitial compliance and drainage guides fluid administration to avoid overload and preserve microvascular function.
119
Valverde (2021): How do adrenergic receptor downregulation and nitric oxide contribute to vasopressor resistance?
Chronic exposure to catecholamines leads to β-adrenergic receptor desensitization, while elevated nitric oxide in sepsis causes cGMP-mediated vasodilation, both reducing the effectiveness of vasopressors like norepinephrine.
120
Valverde (2021): How does cardiac output monitoring refine resuscitation in hypotensive patients?
It allows distinction between hypodynamic and hyperdynamic shock states, supports tailored vasopressor/inotrope use, and avoids blind fluid administration by confirming preload responsiveness or need for vasomotor support.
121
Valverde (2021): How does vasopressin help in fluid-refractory hypotension?
Acts on V1 receptors to induce vasoconstriction independent of adrenergic receptors, often effective when catecholamine resistance occurs.
122
Valverde (2021): What are the common causes of refractory hypotension in small animals?
Distributive shock (e.g., sepsis, anaphylaxis), adrenal insufficiency, hypovolemia, or cardiac dysfunction.
123
Valverde (2021): What are the dose-dependent effects of norepinephrine in veterinary patients with refractory hypotension?
Norepinephrine improves MAP via α1-mediated vasoconstriction and β1-mediated inotropy; higher doses primarily act on α1 receptors and may reduce renal perfusion if MAP overshoots target thresholds.
124
Valverde (2021): What clinical endpoints are used to guide therapy in refractory hypotension?
Target MAP ≥65 mmHg, improvement in mentation, urine output >1 mL/kg/h, improved lactate clearance (ΔLactate >10–20% in 6h), and resolution of peripheral hypoperfusion (CRT, extremity temperature, pulses).
125
Valverde (2021): What is the clinical definition of refractory hypotension?
Persistent hypotension that does not respond to adequate volume resuscitation and requires vasopressor support.
126
Valverde (2021): What is the importance of dynamic monitoring in hypotensive patients?
It allows tailored fluid and drug therapy based on changes in cardiac output, pulse pressure variation, or lactate clearance rather than fixed protocols.
127
Valverde (2021): What is the rationale for corticosteroid administration in fluid-refractory shock?
In cases of CIRCI, hydrocortisone (1–2 mg/kg/day) can restore sensitivity to vasopressors by modulating glucocorticoid receptor activity and dampening nitric oxide-mediated vasodilation.
128
Valverde (2021): What is the role of norepinephrine in managing refractory hypotension?
Acts as a first-line vasopressor for septic and distributive shock to increase vascular tone and MAP by α1-adrenergic receptor stimulation.
129
Valverde (2021): What pathophysiologic states underlie refractory hypotension in critical illness?
Refractory hypotension often results from profound vasodilation (e.g., sepsis), myocardial depression, CIRCI (critical illness-related corticosteroid insufficiency), or uncorrected hypovolemia, all contributing to impaired vascular tone and reduced effective circulating volume.
130
Valverde (2021): When should vasopressin be added to norepinephrine therapy in refractory hypotension?
Vasopressin is typically added when norepinephrine requirements exceed 0.3–0.5 μg/kg/min, or in cases of catecholamine resistance, to improve vascular tone via V1 receptor stimulation without further increasing myocardial oxygen demand.
131
Valverde (2021): Why is early, aggressive fluid resuscitation potentially harmful in refractory hypotension?
Excessive fluids can exacerbate endothelial glycocalyx damage, promote edema, and impair gas exchange, especially in septic or vasoplegic patients; fluid responsiveness should always be assessed before administration.
132
Valverde (2021): Why is hydrocortisone considered in refractory hypotension?
Used in suspected CIRCI to restore vascular responsiveness to catecholamines and improve blood pressure.
133
Valverde (2021): Why should large-volume fluid boluses be used cautiously?
To avoid fluid overload, dilutional coagulopathy, and worsening endothelial damage; especially in distributive or septic shock.
134
What are clinical consequences of glycocalyx disruption per Smart & Hughes (2021)?
Increased vascular permeability, interstitial edema, impaired oxygen delivery, leukocyte adhesion, and procoagulant signaling.
135
What are clinical implications of identifying hypocoagulable dogs early, as per Cooper & Silverstein (2021)?
These dogs may benefit from FFP, vitamin K, or careful fluid therapy, and may have poorer outcomes if unrecognized.
136
What are the clinical implications of the revised Starling principle discussed in Woodcock & Michel (2021)?
Overzealous IV fluid therapy may exacerbate interstitial edema, as capillaries do not significantly reabsorb fluid; emphasis should shift to preserving glycocalyx integrity.
137
What are the key components of a closed-loop control system for fluid therapy as described in Gholami et al. (2021)?
1) Input sensor (e.g., arterial pressure, cardiac output), 2) Controller algorithm, 3) Actuator (e.g., infusion pump), and 4) Target setpoint (e.g., MAP, SV).
138
What are the main forces in the revised Starling equation per Woodcock & Michel (2021)?
1) Capillary hydrostatic pressure (Pc), 2) Sub-glycocalyx oncotic pressure (πg), 3) Interstitial hydrostatic pressure (Pi), and 4) Interstitial oncotic pressure (πi).
139
What are the main pathophysiologic consequences of fluid overload described in Hansen (2021)?
1) Interstitial and pulmonary edema, 2) impaired oxygen diffusion, 3) reduced cardiac and renal function, 4) abdominal compartment syndrome, and 5) delayed wound healing.
140
What are the major challenges of implementing closed-loop systems per Gholami et al. (2021)?
1) Sensor accuracy and reliability, 2) inter-individual variability, 3) delays in feedback loops, and 4) lack of standard physiologic targets across species.
141
What are the primary structural components of the endothelial glycocalyx discussed in Smart & Hughes (2021)?
Proteoglycans (e.g., syndecans, glypicans), glycosaminoglycans (e.g., heparan sulfate, chondroitin sulfate), and adhesion molecules anchored to the endothelial membrane.
142
What are two suggested strategies to prevent fluid overload in critically ill veterinary patients per Hansen (2021)?
1) Early de-escalation of fluid therapy (e.g., transition to conservative or diuretic-guided therapy), 2) Use of goal-directed fluid resuscitation guided by dynamic assessments (e.g., PPV, POCUS).
143
What clinical implication does Valverde et al. (2008) highlight for interpreting acid-base status during anesthesia or shock?
Always interpret UA and acid-base data in context of total protein and albumin levels; normal UA may be misleading post-resuscitation.
144
What clinical sign is often delayed in patients with fluid overload, making early recognition difficult, according to Hansen (2021)?
Weight gain is often delayed and under-recognized until overload is severe; it is not sensitive for early detection.
145
What colloid type is considered safer according to Rudloff & Hopper (2021)?
Natural colloids like plasma and albumin are preferred due to lower risk of adverse effects compared to synthetic colloids.
146
What conditions were required in Sano et al. (2018) for PPV and PVI to be valid predictors?
1) Controlled mechanical ventilation, 2) Regular cardiac rhythm, 3) Sufficient tidal volume (~15 mL/kg), and 4) No spontaneous breathing.
147
What determines whether fluid moves across the capillary wall in Woodcock & Michel (2021)?
The net Starling force: (Pc − Pi) − σ(πg − πi), where σ = reflection coefficient. Most capillary beds exhibit a net positive pressure → filtration.
148
What diagnostic tool did Cooper & Silverstein (2021) use to evaluate hemostatic status?
Thromboelastography (TEG), which assesses whole-blood viscoelastic properties.
149
What does chloride load refer to in the context of fluid therapy as described in Rudloff & Hopper (2021)?
The total amount of chloride delivered with a fluid, which impacts acid-base status and renal perfusion.
150
What does damage to the glycocalyx cause in critically ill animals as per Woodcock & Michel (2021)?
Increased capillary permeability, protein leakage, interstitial oncotic pressure elevation, and accelerated fluid accumulation (edema).
151
What does the hypercoagulable state in septic dogs imply per Cooper & Silverstein (2021)?
An increased risk for microthrombosis, organ dysfunction, and later transition to consumption coagulopathy.
152
What effect did fluid therapy have on total protein and albumin concentrations in Valverde et al. (2008)?
It caused a significant decrease in total protein and albumin due to dilutional effects.
153
What happens to πg and πi during sepsis according to Woodcock & Michel (2021)?
πg decreases (glycocalyx shedding allows protein infiltration), πi increases, and the gradient collapses, favoring uncontrolled filtration and interstitial edema.
154
What is a key advantage of closed-loop fluid control discussed in Gholami et al. (2021)?
Real-time titration of fluids based on dynamic response, reducing under- or over-resuscitation and promoting individualized therapy.
155
What is a major clinical limitation of using PPV/PVI identified in Sano et al. (2018)?
These indices are only valid under strict ventilatory and physiologic conditions, making them unreliable in many clinical ICU scenarios.
156
What is a proposed mechanism for fluid-associated worsening of pulmonary disease in patients with intact cardiac function per Adamantos (2021)?
Glycocalyx shedding and capillary leak may allow fluid to move into the lung interstitium despite normal cardiac pressures, especially in inflammatory states.
157
What is a synthetic colloid and why is it controversial per Rudloff & Hopper (2021)?
A colloid like HES derived from starch polymers; associated with adverse effects including renal injury and coagulopathy in critical illness.
158
What is a target setpoint in closed-loop fluid resuscitation as per Gholami et al. (2021)?
A predefined goal physiologic value (e.g., MAP ≥ 65 mmHg or SV increase ≥ 10%) the system attempts to reach and maintain.
159
What is clot strength (G value) in TEG and why is it important in Cooper & Silverstein (2021)?
It reflects the firmness of the formed clot, influenced by platelets and fibrin. High G suggests hypercoagulability.
160
What is meant by goal-directed fluid therapy in Boysen & Rozanski (2021)?
A resuscitation approach where fluid administration is guided by continuous assessment of hemodynamic and clinical parameters, rather than fixed-volume dosing.
161
What is the central concept presented in Gholami et al. (2021) regarding fluid therapy?
Development and application of closed-loop fluid resuscitation systems to provide automated, precision-guided volume administration in critical illness.
162
What is the central question addressed in Adamantos (2021)?
Whether fluid therapy contributes to or exacerbates pulmonary edema in patients with respiratory disease, and how to optimize fluid management in these cases.
163
What is the clinical significance of the glycocalyx's role as a shear stress sensor in Woodcock & Michel (2021)?
It regulates nitric oxide production, vascular tone, and permeability — critical for vascular homeostasis and organ perfusion in critical illness.
164
What is the future potential of closed-loop resuscitation, according to Gholami et al. (2021)?
Precision-guided fluid therapy integrated with machine learning, multimodal monitoring, and adaptive algorithms tailored to each patient’s response profile.
165
What is the key concept presented in Woodcock & Michel (2021)?
The revised Starling principle, which incorporates the endothelial glycocalyx layer into the understanding of transvascular fluid exchange.
166
What is the mini-fluid bolus test, according to Boysen & Rozanski (2021)?
Administering small aliquots (2–5 mL/kg) of fluid and evaluating for transient improvement in perfusion as an indicator of fluid responsiveness.
167
What is the overall purpose of a closed-loop control system in critical care according to Gholami et al. (2021)?
To achieve precise, responsive, and individualized fluid resuscitation without relying solely on manual intervention by clinicians.
168
What is the primary clinical risk of unbalanced crystalloids like 0.9% NaCl per Rudloff & Hopper (2021)?
Hyperchloremic metabolic acidosis, renal vasoconstriction, and delayed recovery in critically ill patients.
169
What is the recommended first-line fluid for most emergency resuscitations in Boysen & Rozanski (2021)?
Isotonic balanced crystalloids (e.g., LRS, Plasma-Lyte A), due to safety and broad applicability.
170
What is the recommended shock dose of crystalloids per Boysen & Rozanski (2021)?
80–90 mL/kg for dogs and 40–60 mL/kg for cats, given in incremental boluses (10–20 mL/kg) and reassessed between aliquots.
171
What is the role of the controller algorithm in the system described by Gholami et al. (2021)?
It interprets the data from the input sensor, compares it to a desired setpoint, and sends instructions to the actuator to adjust therapy.
172
What is the role of the glycocalyx in the revised Starling model per Woodcock & Michel (2021)?
It forms a molecular sieve that selectively restricts protein passage, modulates capillary permeability, and generates a sub-glycocalyx oncotic gradient that governs filtration.
173
What is the suggested strategy for cats in shock per Boysen & Rozanski (2021)?
Smaller boluses (5–10 mL/kg) of crystalloids due to risk of volume overload and frequent reassessment.
174
What is the theoretical benefit of colloids discussed in Rudloff & Hopper (2021)?
They may expand plasma volume more efficiently per mL and stay intravascular longer than crystalloids.
175
What is the working definition of fluid overload according to Hansen (2021)?
A positive fluid balance resulting in interstitial edema that causes or worsens organ dysfunction.
176
What is Type A hyperlactatemia, as relevant to Bohrer-Clancy et al. (2021)?
Lactate elevation due to tissue hypoperfusion and hypoxia, commonly seen in shock states.
177
What is Type B hyperlactatemia, and why is it relevant?
Lactate elevation not related to hypoxia, often due to drugs, liver dysfunction, neoplasia, or mitochondrial disease — important for differential diagnosis of elevated lactate.
178
What L-lactate concentration was significantly associated with higher mortality in Bohrer-Clancy et al. (2021)?
Dogs with L-lactate ≥ 6.0 mmol/L had significantly higher in-hospital mortality compared to those < 6.0 mmol/L.
179
What laboratory markers may indicate glycocalyx shedding, according to Smart & Hughes (2021)?
Elevated levels of syndecan-1, hyaluronan, and heparan sulfate in plasma or interstitial fluid.
180
What monitoring strategy does Adamantos (2021) advocate to guide fluid therapy in pulmonary disease?
Use of point-of-care ultrasound (POCUS) to detect B-lines and pleural irregularities that suggest pulmonary fluid accumulation.
181
What pathophysiologic condition increases the risk of pulmonary edema with fluid administration per Adamantos (2021)?
Endothelial dysfunction (e.g., SIRS, sepsis, trauma) leads to increased vascular permeability and non-cardiogenic pulmonary edema.
182
What physiologic functions does the glycocalyx serve under normal conditions per Smart & Hughes (2021)?
1) Barrier to fluid/protein leakage, 2) Modulator of shear stress and nitric oxide signaling, 3) Inhibitor of leukocyte and platelet adhesion, 4) Regulator of vascular tone and coagulation.
183
What risks are associated with synthetic colloids (e.g., HES) according to Rudloff & Hopper (2021)?
Risk of coagulopathy, acute kidney injury, and increased mortality, especially in septic or critically ill patients.
184
What role does the glycocalyx play in fluid exchange, per Woodcock & Michel (2021)?
Acts as a selective molecular sieve, regulating protein and fluid movement, and sensing shear stress to maintain endothelial health and NO production.
185
What secondary outcome was improved in the bicarbonate group in Jaber et al. (2018)?
Reduced need for renal replacement therapy (RRT) and vasopressors in the AKI subgroup.
186
What structure is the focus of Smart & Hughes (2021), and what is its clinical relevance?
The endothelial glycocalyx, a protective carbohydrate-rich layer lining the vascular endothelium that regulates permeability, shear sensing, and anti-inflammatory signaling.
187
What type of dogs and anesthetic protocol was used in Sano et al. (2018)?
Healthy, isoflurane-anesthetized Beagle dogs undergoing mechanical ventilation.
188
What type of fluid is Plasma-Lyte, and what is its chloride content as noted in Rudloff & Hopper (2021)?
It is a balanced isotonic crystalloid with a chloride concentration of ~98 mmol/L.
189
What type of study was conducted by Bohrer-Clancy et al. (2021)?
A prospective, observational cohort study evaluating dogs upon presentation to a veterinary ER.
190
What veterinary application does Gholami et al. (2021) suggest for closed-loop resuscitation?
Integration into high-fidelity ICU monitoring for dogs and cats, especially during anesthesia, hemorrhagic shock, or sepsis, where traditional resuscitation targets are unreliable.
191
What was a key conclusion drawn in Valverde et al. (2008) regarding acid-base interpretation after fluid therapy?
UA-based acid-base interpretation may underestimate acidosis after aggressive fluid resuscitation due to dilution of weak acids like albumin.
192
What was a limitation of the BICAR-ICU trial noted in Jaber et al. (2018)?
The trial was open-label and not powered for mortality, which may limit generalizability of the findings outside AKI-specific scenarios.
193
What was the clinical implication of Jaber et al. (2018) for use of sodium bicarbonate in ICU acidosis?
Bicarbonate is not routinely indicated in all acidemic patients but may be beneficial in patients with AKI and impaired buffering capacity.
194
What was the conclusion of Sano et al. (2018) about the utility of PVI compared to PPV?
PVI had moderate predictive value, but PPV was more reliable for assessing fluid responsiveness under ideal conditions.
195
What was the PPV threshold that best predicted fluid responsiveness in Sano et al. (2018)?
PPV ≥ 13% was the most predictive cutoff for fluid responsiveness.
196
What was the primary finding of Cooper & Silverstein (2021) regarding coagulopathy in septic dogs?
A majority of dogs with sepsis showed evidence of hemostatic dysfunction, ranging from hypocoagulable to hypercoagulable states.
197
What was the primary objective of Bohrer-Clancy et al. (2021)?
To evaluate whether initial L-lactate concentration upon emergency room presentation predicts in-hospital mortality in dogs.
198
What was the primary objective of the BICAR-ICU trial in Jaber et al. (2018)?
To determine whether sodium bicarbonate administration improves outcomes in ICU patients with severe metabolic acidaemia (pH < 7.20).
199
What was the primary objective of the study by Sano et al. (2018)?
To evaluate whether pulse pressure variation (PPV) and pleth variability index (PVI) can predict fluid responsiveness in anesthetized, mechanically ventilated dogs.
200
What was the reported sensitivity and specificity of PPV ≥ 13% in Sano et al. (2018)?
Sensitivity: 85.7%, Specificity: 83.3% for predicting a ≥15% increase in stroke volume after fluid bolus.
201
What was the study design used in Jaber et al. (2018) (BICAR-ICU trial)?
A multicenter, open-label, randomized controlled phase 3 trial in 26 ICUs in France.
202
What were the inclusion criteria for severe metabolic acidaemia in Jaber et al. (2018)?
Arterial pH < 7.20, bicarbonate < 20 mmol/L, and PaCO₂ < 45 mmHg.
203
Which pressure is the main oncotic force opposing filtration in the revised model from Woodcock & Michel (2021)?
πg, the sub-glycocalyx oncotic pressure (not interstitial oncotic pressure as in the classic model).
204
Why are static preload indicators (e.g., CVP) considered less useful than PPV/PVI as shown in Sano et al. (2018)?
Static markers do not account for dynamic changes in preload, and are poor predictors of whether a patient will respond to volume expansion.
205
Why is albumin concentration important in the strong ion model as shown in Valverde et al. (2008)?
Albumin is a major weak acid contributor in the [A⁻] component of the strong ion model; its dilution reduces the apparent acid burden.
206
Why is hypotension alone not a reliable guide for fluid resuscitation in shock per Boysen & Rozanski (2021)?
Because many patients, especially cats, may maintain normal BP despite profound hypoperfusion, and conversely, hypotension may persist despite improved perfusion.
207
Why is lymphatic drainage emphasized in Woodcock & Michel (2021)?
Because reabsorption does not occur, lymphatic return is the primary route for clearing excess interstitial fluid, especially during inflammation.
208
Why is serial lactate monitoring clinically useful according to principles referenced in Bohrer-Clancy et al. (2021)?
It allows assessment of treatment response and tissue perfusion trends, with delta lactate > 2 mmol/L generally a favorable sign.
209
Why is TEG useful in septic dogs, based on Cooper & Silverstein (2021)?
It detects early or subclinical hemostatic changes, helps distinguish hypo- vs. hypercoagulability, and can guide therapy like plasma or anticoagulants.
210
Why is the glycocalyx particularly vulnerable in critically ill patients, per Smart & Hughes (2021)?
Inflammation (sepsis, trauma) upregulates protease activity, increases oxidative stress, and primes the vasculature for further injury with even modest fluid overload or ionic imbalance.
211
Why is πg (sub-glycocalyx oncotic pressure) more important than πi in Woodcock & Michel (2021)?
πg reflects the true oncotic barrier, as proteins excluded from the glycocalyx generate the primary force opposing filtration.
212
Why might synthetic colloids be ineffective or harmful, as interpreted through Woodcock & Michel (2021)?
They may fail to restore oncotic gradients if the glycocalyx is compromised and may worsen endothelial injury and coagulopathy.
213
Yiew et al. (2020): How did isotonic crystalloid behave compared to hypertonic saline and tetrastarch?
Isotonic crystalloids had rapid distribution and elimination, whereas tetrastarch had the longest intravascular persistence and hypertonic saline rapidly expanded plasma volume but had transient effects.
214
Yiew et al. (2020): How long do the effects of hypertonic saline last, according to this study?
Effects are rapid but transient, with plasma volume expansion peaking early and declining quickly due to redistribution.
215
Yiew et al. (2020): What are the limitations of using crystalloids in cats, based on this study?
Rapid redistribution out of the intravascular space and fast elimination rates suggest that crystalloids may require more frequent administration or larger volumes to maintain perfusion in cats.
216
Yiew et al. (2020): What are the safety considerations for hypertonic saline in cats?
Risk of hypernatremia, osmotic demyelination (if rapidly infused), and transient hypotension due to peripheral vasodilation following fluid shift. Frequent monitoring is essential.
217
Yiew et al. (2020): What assumptions underlie volume kinetic models in this study?
One- or two-compartment models assume homogenous mixing, consistent elimination rates, and apply first-order kinetics to predict volume behavior after bolus or infusion.
218
Yiew et al. (2020): What implication does this study have for clinical fluid therapy in cats?
Cats may experience faster redistribution and clearance of crystalloids, emphasizing the need for frequent reassessment and consideration of alternative volume expanders when appropriate.
219
Yiew et al. (2020): What is the clinical significance of volume kinetic modeling in fluid therapy?
It provides a quantitative framework to predict how fluids distribute and are eliminated in vivo, allowing for more precise and individualized fluid administration.
220
Yiew et al. (2020): What is the physiologic rationale for using hypertonic saline in volume resuscitation?
Hypertonic saline creates a strong osmotic gradient that draws water from the interstitial and intracellular compartments into the intravascular space, rapidly increasing plasma volume.
221
Yiew et al. (2020): What key parameter does volume kinetic modeling incorporate to estimate fluid behavior?
It uses central volume of distribution (Vc), rate constants for elimination (k10), and inter-compartmental exchange rates (k12, k21).
222
Yiew et al. (2020): What makes cats a unique model in fluid kinetics?
Cats have lower interstitial compliance, smaller total blood volumes, and distinct renal handling of fluids, all of which influence volume kinetics and elimination.
223
Yiew et al. (2020): What was the primary objective of this study?
To evaluate and compare the volume kinetics—distribution and elimination—of isotonic crystalloid, 5% hypertonic saline, and 6% tetrastarch in healthy conscious cats using volume kinetic modeling.
224
Yiew et al. (2020): Why is colloid (tetrastarch) volume expansion more sustained than crystalloids?
Large starch molecules exert colloid osmotic pressure and remain in the vascular space longer due to their size and slower metabolism, resulting in prolonged volume expansion.
225
Yiew et al. (2020): Why is volume kinetic modeling superior to simple fluid balance tracking?
It accounts for distribution compartments, time-dependent rates, and nonlinear elimination, offering a more accurate prediction of fluid dynamics in vivo.
226
Yiew et al. (2020): Why was tetrastarch 130/0.4 included in this study?
As a representative synthetic colloid, to evaluate its prolonged intravascular retention properties compared to crystalloids and hypertonic saline.
227
Yiew et al. (2021): Define “volume kinetics” in the context of fluid therapy.
A quantitative model used to describe the time-dependent distribution and elimination of infused fluids, analogous to drug pharmacokinetics.
228
Yiew et al. (2021): How can kinetic modeling assist in individualized fluid therapy?
It allows prediction of how much and how fast a fluid will distribute and be cleared in a given patient, enabling dose tailoring based on physiology and disease state.
229
Yiew et al. (2021): How does disease state alter volume kinetics?
In conditions like sepsis or capillary leak, increased vascular permeability leads to larger peripheral compartments and faster fluid loss from the central compartment.
230
Yiew et al. (2021): How does the concept of “half-life” apply in volume kinetics?
It refers to the time required for half the volume of infused fluid to be eliminated from the intravascular space. Shorter half-lives require more frequent fluid administration.
231
Yiew et al. (2021): What are some limitations of volume kinetic modeling?
Assumes normal physiology, doesn’t account well for third spacing or dynamic changes in capillary permeability, and limited species-specific data for veterinary patients.
232
Yiew et al. (2021): What are the key components of a volume kinetic model?
1) Input sensor (e.g., fluid infusion), 2) Central compartment (Vc), 3) Peripheral compartment (Vp), 4) Rate constants (k12, k21, k10), and 5) Actuator/infusion pump.
233
Yiew et al. (2021): What are the primary assumptions behind volume kinetic modeling?
Linear distribution and elimination (first-order kinetics), homogenous compartments, and time-invariant rate constants.
234
Yiew et al. (2021): What distinguishes crystalloid from colloid behavior in volume kinetic models?
Crystalloids distribute rapidly into the interstitium with fast elimination (short Vc half-life), while colloids have prolonged vascular retention and slower elimination.
235
Yiew et al. (2021): What is meant by “fluid responsiveness” from a kinetic perspective?
It is the increase in stroke volume or cardiac output in response to a fluid bolus, often associated with central compartment expansion and improved preload.
236
Yiew et al. (2021): What is the primary focus of this review paper?
To explain the application of pharmacokinetic modeling to fluid therapy, especially volume kinetic modeling, and how this improves understanding of fluid distribution, elimination, and efficacy.
237
Yiew et al. (2021): What is the role of pharmacokinetic modeling in evaluating novel fluids?
It helps predict distribution and retention properties of new fluid types before clinical application, improving safety and efficacy evaluation.
238
Yiew et al. (2021): What practical applications of volume kinetics exist in veterinary ECC?
Guiding fluid bolus volume and frequency, understanding colloid persistence, predicting risk of overload, and tailoring therapy in hypo- or hyperdynamic states.
