FLUID THERAPY Flashcards
Describe TBW distribution
~60% TBW water.
- age, gender, species and body condition.
- 2 compartments.
ECF/ICF
• ICF fluid within cell
largest fluid compartment
40% of total body weight or ~ 66% of total body water. Cell membrane separatesICF from ECF
ECF(33% TBW) - comprised of
• INSTL fluid between the cells, includes lymph.
~75% of the extracellular fluid compartment volume and approximately 15% of total body weight.
• IV: plasma (the fluid in the blood vessels) ~25% of the ECF volume and ~5% of TB weight
Transcellular fluid: joint, csf, gastro = ~1%
Describe plasma volume in relation to TBW
Total blood volume dog vs cat?
Plasma volume~50 mL/kg.
TBV - PCV
TBV (i.e. plasma and cells)
Dog:80- 90 mL/kg
Cat: ~ 50-60 mL/kg
What is the 60:40:40 rule?
60% of body weight is water
40% of body weight is intracellular fluid
20% of body weight is extracellular fluid.
Difference between hypovolaemia and dehydration?
Hypovolaemia - loss of water from the IVC
Dehydration-loss of total body water across ALL compartments.
- does not always lead to hypovolaemia as fluid shifts from the extravascular to the intravascular compartment to maintain normovolaemia in the face of dehydration.
With severe dehydration hypovolaemia will also occur.
Describe fluid dynamics
Water moves freely between body compartments, however body fluids contain not only water but various concentrations of solutes and proteins.
membranes separating compartments and the concentration of these solutes and proteins in the different compartments that govern the dynamics of fluid movement.
Describe fluid movement from the IV to Intersitital space
traditionally explained by the hydrostatic and oncotic forces that govern the movement of fluid across a capillary membrane.
According to the Starling equation –> Fluid movement between the intravascular and interstitial compartments (transcapillary fluid dynamics), is governed by hydrostatic pressure and oncotic pressure.
Hydrostatic pressure: fluid pressure that pushes against a membrane
Oncotic pressure: pressure created by the colloid osmotic gradient.
Increased COP or decreased capillary HP favors resorption of fluid into the intravascular space whereas increased capillary HP and decreased capillary COP favors fluid filtration out of the vascular space.
High interstitial HP, due to the relatively non-distensible nature of the interstitial compartment, and low interstitial OP, due to the relative impermeability of the capillary membrane to proteins, favour fluid retention in the intravascular compartment.
Large differences in membrane permeability and tissue compliance occur throughout the body. This leads to great variation in fluid flux between vascular beds thus adding to the complexity and intricacy of body fluid movement.
Define starlings equation (write it down and explain)
Jv ≈Kf ([Pc – Pi] – 𝝈 [πc – π i])
where
- Jv is the net fluid movement between compartments
- Kf([Pc–Pi]–𝝈[πc–πi]isthenetdrivingforce
- Pc is the capillary hydrostatic pressure
- Pi is the interstitial hydrostatic pressure
- πc is the capillary oncotic pressure
- π i is the interstitial oncotic pressure
- Kf is the filtration coefficient – a proportionality constant • 𝝈𝝈 is the reflection coefficient
Describe vascular endothelial permeability
Vascular endothelium is freely permeable to water and solutes, –> concentrations are almost the same in the intravascular and interstitial spaces.
However, endothelium is relatively IMpermeable to blood cells and plasma proteins (maintained within the intravascular space) –> creates a difference in protein concentration between the vasculature and the interstitial compartment and consequently a colloid osmotic gradient between the two compartments.
Oncotic pressure moves fluid in the opposite direction to hydrostatic pressure. I.e. fluid moves towards the highest value of oncotic pressure. For this reason it can be useful to think of oncotic pressure as oncotic “pull”.
Describe EC to IC fluid movement
Cell membrane governs fluid distribution between the ICF & ECF space
Cell membrane is permeable to water but impermeable to most solutes.
Concentrations of various solutes (osmolality) in each space determine the volume of fluid within the space.
Ion channels and solute pumps govern solute movement into and out of the cell.
Most important pump sodium-potassium ATPase pump.
extrudes 3 sodium ions from the cell in exchange for bringing in 2 potassium ions.
Responsible for maintaining high intracellular potassium and high extracellular sodium concentrations and thus generating a concentration gradient across the cell membrane.
Discuss transfluid flux
The traditional Starling equation may not hold true for transcapillary fluid flux.
The importance of the membrane glycocalyx in the regulation of fluid movement increasingly recognised.
Glycocalyx is a gel matrix layer that is secreted by the endothelial cells and lines blood vessels. Beneath the glycocalyx is the subglacial space.
Suspected that it is the relative concentrations of proteins and fluid in the intravascular space, the membrane glycocalyx, the subglyceal layer and the interstitium which govern the movement of fluids.
The colloid osmotic pressure (COP) in the intravascular space is thought to only oppose outward movement of fluid.
Thus movement of fluid from the capillaries is likely to be predominantly dependent on the capillary hydrostatic pressure. Increasing the COP by administering synthetic colloids is likely to draw water out of the glycocalyx, dehydrating and damaging it.
Disease states that alter vascular permeability cause abnormal fluid and protein movement out of the vascular space.
LEADS to interstitial oedema which interrupts normal tissue and organ homeostasis and can prove challenging to regulate.
Lymphatic vessels play a pivotal role in the prevention of oedema by returning interstitial protein and fluid to the vascular compartment.
Define osmosis, osmolarity and osmolality
ne mole of any substance contains the same number of particles (Avogradro’s number = 6.023 x 1023) regardless of their weight, size or valence. The osmotic effect exerted by solutes is dependent on the number of particles they dissociate into. One osmole is equivalent to the amount of solute that dissociates in solution to form one mole of particles. Osmolality is the number of osmoles per kilogram of solvent and is expressed as mOsm/ kg. Osmolarity is the number of osmoles per litre of solution and is expressed as mOsm/L. In the body there is very little difference between the two measurements and so ongoing I will use the term osmolality. The number of osmotically active molecules in each space and their relative permeability across membranes determine the volumes of fluid in the intracellular and extracellular spaces.
What is calculated osmolality?
The calculated osmolality (in Osm) is based on the formula: 2(Na+ + K+)+ urea + glucose The reason for multiplying the electrolytes by two is to take into account the contribution of chloride and bicarbonate in the serum. This assumes the serum is electrically neutral (the concentrations of all major anions and cations are equal).
What is effective osmolality?
Urea is a small molecule which readily diffuses across most membranes. As a result, it exerts very little effective osmolality. As the potassium concentration in extracellular fluid is relatively low, its effect on osmolality is negligible. This allows us to simplify the equation above to the ‘effective’ osmolality which is: 2(Na+) + glucose
What is a normal osmolality in dog vs cat?
he normal osmolality in dogs ranges from 290 to 310 mOsm/kg and in cats from 290 to 330 mOsm/kg. Isotonic fluids generally have an osmolarity in the range of 270–310 mOsm/L.
Why do we measure osmolality?
Measurement of osmolality with an osmometer allows you to calculate the osmolar gap, the difference between the measured and calculated osmolality. This can be useful to determine the presence of osmotically active agents not accounted for by the equation. For example, in ethylene glycol toxicity an increased osmolar gap alerts you to the presence of measured osmoles that are not included in your calculation of osmolality.
Describe control of osmolality?
Osmolality is controlled by hypothalamic osmoreceptors. These receptors primarily detect changes in serum sodium concentration. Increased plasma osmolality stimulates osmoreceptors leading to the release of ADH (antidiuretic hormone, also known as vasopressin) from the posterior pituitary and increased thirst. Antidiuretic hormone acts on the V2 receptors in the renal collecting ducts of the kidney, leading to insertion of aquaporins in the collecting duct and increased water resorption by the kidney. This resorption of water occurs without concurrent sodium resorption thus the result is a decrease in serum sodium concentration (decreased osmolality).
Describe fluid loss and their effect on osmolality?
In many disease states water and solutes are lost from the body. The nature of fluid loss will determine the effect on osmolality. Tonicity is a measure of the effective osmolality of two solutions that are separated by a semipermeable membrane. In the case of the body tonicity refers to the relative osmolality when compared to the intra and extra cellular fluid compartments.
Desc isotonic fluid loss
Isotonic fluid losses: There is proportional loss of fluid and solutes. If we use Starling’s equation to explain inter-compartmental fluid flux: a decreased capillary hydrostatic pressure results in movement of fluid from the interstitial compartment into the vascular compartment without any change in the intracellular fluid volume. In this way the body preferentially maintains intravascular volume over interstitial fluid volume. Hypovolaemia should not result unless losses are severe or not replaced i.e. initially dehydration will occur without hypovolaemia. If volume depletion does occur along with isotonic fluid loss, the body will activate systems that act to correct hypovolaemia despite normal osmolality. Hypovolaemia leads to activation of the renin-angiotensin-aldosterone system (RAAS). The resulting production of angiotensin II leads to increased thirst and release of ADH. This means that there will be increased water intake orally and free water retention by the kidneys. Whilst these processes will correct hypovolaemia, they will result in hyponatraemia (and a hypo-osmolar state). Isotonic fluid losses are the most commonly encountered losses. Examples of isotonic fluid loss include vomiting and diarrhoea. Isotonic crystalloids should be used to replace isotonic fluid losses.
Desc hypotonic fluid loss
Hypotonic fluid losses: Hypotonic losses occur with diabetes insipidus and excessive panting. This results in increased osmolarity of the extracellular fluid. Water moves along this concentration gradient with a net movement occurring from the cellular compartment into the extracellular compartment. Cell shrinkage occurs as a result. Changes in osmolality are further discussed in the tutorial ‘Electrolyte disturbances’ under the section on sodium as this electrolyte is primarily responsible for extracellular osmolality.
Desc hypertonic fluid loss
Hypertonic fluid losses: These occur infrequently in small animals as a result of excessive loss of solutes in the urine or from the gastrointestinal tract. Examples include use of diuretics, hypoadrenocorticism and haemorrhagic gastroenteritis in dogs. Hypertonic fluid losses cause hypo-osmolality of the extracellular compartment. A rapid decrease in extracellular osmolality will favour net movement of water into the cells (cell swelling). Hypovolaemia will occur as fluid moves out of the hypotonic vascular compartment into the interstitium. For this reason, hypertonic fluid loss that is not replaced is likely to lead to a rapid onset of shock.
Describe normal regulation of ECF volume
Fluid balance depends on the daily intake and losses of water, nutrients and minerals. Animals in homeostasis are said to be in zero balance when there is no net gain or loss of fluid, i.e., the volume of water consumed in food and water plus the water produced by metabolism equals that lost in urine, faeces, saliva, respiratory and cutaneous secretions. The intravascular volume is prioritised above interstitial and intracellular volumes to maintain tissue perfusion. This fine balance of intravascular volume is intricately associated with total body sodium which is regulated by the renin-angiotensin-aldosterone system (RAAS). This system along with baroreceptors and volume receptors of the atria are responsible for this balance. Baroreceptors are located in the walls of the carotid sinus and aortic arch (arterial side of vasculature). The arterial baroreceptors respond rapidly to acute changes in blood pressure. They play a key role in rapid, short-term regulation of blood pressure. Baroreceptors respond to changes in blood pressure by increasing or decreasing their rate of firing. In this way they send input to the cardiac and vasopressor centres of the medulla through the afferent vagal and glossopharyngeal nerves. The result of baroreceptor input is altered parasympathetic (vagal) and therefore increased sympathetic outflow. Baroreceptor input also alters release of ADH (antidiuretic hormone, vasopressin) secretion from the pituitary. Arterial baroreceptors are very sensitive to a fall in arterial blood pressure. A fall in blood pressure will lead to decreased firing of the baroreceptors and thus a decreased vagal response (and increased sympathetic response) from the medulla. At the same time there will be increased release of ADH/vasopressin from the pituitary resulting in vasoconstriction and water retention. Volume receptors (volureceptors) are located in the cardiac atria, right ventricle and the large pulmonary vessels. These receptors detect stretch and are capable of modulating sympathetic outflow and ADH release. Volume receptors are particularly sensitive to increased stretch (due to increased blood volume). Activation from increased stretch leads to decreased sympathetic outflow with ensuing vasodilation and increased renal blood flow (thus increased glomerular filtration). Increased stretch will also result in decreased ADH release from the pituitary and the release of A-type (ANP) and B-type (BNP) natriuretic peptides. ANP and BNP result in increased sodium and water excretion. All of these processes lead to increased urine output and thus result in reduced blood volume. Example A dog has been anorexic and vomiting for 12 hours. His fluid losses have caused a negative fluid balance and a decreased intravascular volume. This decreased intravascular volume leads to a reduction in blood pressure. This activates his baroreceptors and results in increased sympathetic output and vasoconstriction. In the short term this will lead to a normalisation of blood pressure for the dog despite ongoing losses and inadequate water intake.
Desc regulation of total body sodium
Regulation of total body sodium (and thus total body water) is under the control of the renin-angiotensin-aldosterone system. Renin is released by the juxtaglomerular apparatus in the kidney and converts angiotensinogen to angiotensin I. This is further converted to angiotensin II and aldosterone. Aldosterone leads to Na+ resorption and thus water resorption in the kidney.
How is RAAS activated?
The RAAS is activated via the following mechanisms: • reduced blood flow to the kidneys • increased sympathetic nerve activity • decreased delivery of sodium chloride to the juxtaglomerular apparatus. Renin is released by the juxtaglomerular apparatus in the kidney and converts angiotensinogen to angiotensin I. Angiotensin I is further converted to angiotensin II by the endothelium. Angiotensin II causes increased synthesis and release of aldosterone by the adrenal glands.The end result of RAAS activation is increased intravascular volume and total body water.
What does Angiotensin II result in?
Angiotensin II results in: • systemic vasoconstriction • aldosterone release • vasopressin (ADH) release • increased thirst • activation of the sympathetic nervous system.