IV fluids Flashcards
Body water distribution and ml/kg for cats and dogs
- Total body water is 60% of body weight (BW).
- Intracellular fluid (ICF) is 66% (2/3) of body water
- Extracellular fluid (ECF) is 33% (1/3) of body water and is divided into:
- The interstitial compartment: ¾ of ECF.
- The intravascular compartment: ¼ of ECF. This is estimated at:
50-60 mls/kg of bodyweight (or 6-7 % of BW) for cats
60-80 mls/kg of bodyweight (8-9% of BW) for dogs
Fluid moves between the intravascular, interstitial and intracellular spaces due to:
- Hydrostatic pressure gradients
- Colloidal pressure gradients
- Osmotic gradients
- Membrane channels and paracellular flow (between endothelial cells)
What is the Glycocalyx?
gel matrix layer, made up of glycoproteins and proteoglycans.
It covers the endothelium of all blood vessels.
What does the proteins of the glycolax do? and what does it mean?
The proteins that make up the matrix of this ‘endothelial surface layer’ differ within the capillaries of various organs, resulting in the capillaries in different organs having different permeability.
Between the endothelial surface layer and the endothelium is a space called the subglyceal space, which contains fluid and is relatively impermeable to proteins. The oncotic pressure of the fluid in this space is low and contributes to the direction of fluid movement between the intravascular and interstitial space.
What is the role of the glycocalyx?
- Provides resistance to the filtration of water and macro-molecules
- The subglyceal oncotic pressure is normally low because:
- The glycocalyx prevents protein passing into the subglyceal space from the lumen of the blood vessel.
- High rates of hydrostatically driven fluid flow from the lumen to the subglyceal space and then through endothelial clefts into the interstitium, limit the influx of proteins from interstitium to subglyceal space.
- This low subglyceal oncotic pressure means the oncotic gradient across the glycocalyx opposes capillary hydrostatic pressure.
- Fluid does not shift from the interstitium into the plasma down an oncotic gradient as previously thought.
Effect of glycocalyx on fluid flux and Starling’s Law
With the glycocalyx intact, the oncotic pressure difference between the capillary and the subglyceal space is what affects fluid flow (not the difference between the capillary and interstitial space oncotic pressure).
This essentially means hydrostatic pressure has a more significant role on net flow across the endothelium than the original Starling’s Law theory suggests.
Destruction of glycocalyx can occur due to:
- Hypervolaemia
- Hyperglycaemia
- Surgery/trauma
- Ischaemia or reperfusion injury
- Cytokines
If the glycocalyx is destroyed, what will happen with the filtration rate?
The drivers of filtration rate will then return to:
- Hydrostatic gradient between lumen and interstitial space
- Oncotic gradient between lumen and interstitial space
Interstitial oedema - what is it and what does it affect?
- Abnormal accumulation of fluid in the interstitial space.
- Impedes oxygen diffusion to cells therefore affecting cellular function and healing.
Interstitial oedema occurs due to:
- Venous hypertension (as may occur with overzealous fluid administration)
- Severe hypoproteinaemia
- Increased microvascular permeability (endothelial damage) e.g. sepsis, SIRs
- Impaired lymph flow
- Inflammatory oedema
Interstitial oedema can be prevented by:
Prevented by:
- Decreased hydrostatic gradient between lumen and interstitial space
- Increased interstitial volume = increased interstitial hydrostatic pressure and therefore decreased fluid extravasation
* Increased lymph drainage - Increased interstitial hydrostatic pressure = increased driving pressure for lymphatic drainage
- Decreased colloidal osmotic pressure gradient
- Interstitial oedema generally occurs due to low protein fluid accumulation.
- This results in reduced interstitial oncotic pressure which should create opposition to further oedema formation
Glycocalyx changes how we think about interstitial oedema - how?
- Fluid is returned to the vascular system mainly through lymphatics (except in acute hypovolaemia where there may be an autotransfusion effect – see other question)
- There is no significant movement of fluid from the interstitial space to the intravascular space across the endothelium due to oncotic pressure gradients
- This means colloid therapy does not prevent or improve interstitial oedema
- If membrane permeability increases (due to vascular endothelial damage), colloids will be lost into the interstitial fluid from the intravascular space and may exacerbate oedema
- Oedematous states require more than just hypoproteinaemia
- Destruction of glycocalyx
- Inflammation of blood vessels leading to increased endothelial permeability
Autotransfusion -In fluid physiology, hypovolaemia -> capillary hydrostatic pressure decrea. below interstitial hydrostatic pressure.
How can you give clotting factors?
- Fresh frozen plasma
- whole blood
What are colloids?
Colloids (synthetic colloids e.g. Dextran, Voluven) are fluids that contain high molecular weight molecules that DON’T pass through semi-permeable membranes and therefore help hold fluid in the intravascular space.
Risks of colloid administration?
- Anaphylactic reactions
- Prolonged coagulation times and increased risk of bleeding (need to monitor coagulation times – PTT)
- Initiation or exacerbation of acute kidney injury
- Increased risk of death in SEPSIS – now considered to be contraindicated in sepsis
