fluid exchange Flashcards

1
Q

why is fluid exchange important? (3)

what do we need for chemical reactions?
what can abnormalities in fluid exchange lead to?
what do we try to control following heamorrhage/sepsis?

A

We need H2O for chemical reactions

Abnormalities in fluid exchange can lead to oedema/tissue swelling

Controlling blood volume, and interstitial and cell volumes are important goals in medicine following drop in blood pressure/poor end organ perfusion
e.g. haemorrhage, sepsis, during surgery, dehydration

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2
Q

Fluid movement at capillary wall

permeability of membrane? so what can pass?

what moves fluid across membrane? drivers (2)

what can’t pass?
what do they exert? effect of this?

A

Capillary wall is a semi-permeable membrane – allows H2O to pass through

Fluid moves across membrane into interstitial space due to blood flow driven by heart (Hydraulic pressure) and gravity (Hydrostatic pressure)

Large molecules (e.g. plasma proteins) cannot pass through membrane

So they exert osmotic pressure termed Oncotic pressure
which creates suction force to move
fluid from interstitial space into capillary

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3
Q

what does fluid movement at capillary wall depend upon?

what is this called?

A

Fluid movement depends on balance between Hydraulic/Hydrostatic and Oncotic pressures
across the capillary wall
- Starling’s principle of fluid exchange -

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4
Q

lumen vs interstitial space

molecules and how do they move?

what dominates moevement?

A

Hydraulic pressures
Pc = Capillary blood pressure
Pi = Interstitial fluid pressure
Easy movement across membrane

Osmotic pressures
IIp = Plasma proteins
IIi = Interstitial proteins
Movement through intercellular gaps

plasma proteins -> some can get through via intracellular gaps but larg conc still in lumen

Directions of Fluid Movements dominated by Pc and IIp

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5
Q

starling’s principle of fluid exchange

what is the equation?

what are the 3 other factors?

A

Jv = Lp A { (Pc - Pi) - σ (IIp - IIi) }
Jv (net filtration) is Hydraulic/Hydrostatic pressures difference (Pc - Pi )
- Osmotic pressure difference (IIp - IIi)

What is Lp ? Conductance of the endothelium
How leaky the endothelium is to fluid
What is A? Wall area
What is σ? Reflection coefficient – related to intercellular gaps

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6
Q

reflection coefficient

what is it?
what is it for plasma proteins? meaning of this?

A
Fraction (σ) of the osmotic pressure
is exerted by gaps
Effective osmotic pressure  = 
σ x potential osmotic pressure 
σ for plasma protein is 0.9 
i.e. 10% plasma proteins are conducted across capillary wall into interstitial space
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7
Q

σ = 1

A

small intracellular gaps mean plasma proteins can’t go through at all hence reflection via gaps and more osmotic pressure

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8
Q

what does starlings principle tell us

what is marginal?
what do we look at?

A

Pi and IIi is marginal so we really look at Pc and IIi
Pc 35 and IIp is 25
Pc but not IIp alters along length of capillary
Pc from 35 to 10 hence filtration from 35 to 25 and reabsoprtion from 25 to 10

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9
Q

What is incorrect with Starling’s principle?

what occurs throughout length of capillaries?
what doesnt occur?

what about interstitial osmotic pressure? how does this relate to plasma osmotic pressure?

what isnt taken into account but is key?

A

Fluid filtration generally occurs throughout length of capillaries
Reabsorption does not occur - important for fluid replacement

Interstitial osmotic pressure (IIi) is not small
IIp = IIi

Glycocalyx is not taken into account
This structure is now considered central to fluid exchange

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10
Q

clinical importance of incorrect starling principle - colloid fluids

colloid fluids increase osmotic pressure - how does this disprove the principle?

A

Starling’s principle states that if we increase IIp using colloid fluids (which increase osmotic pressure) we should increase blood volume by increasing reabsorption

But, colloid fluids do not significantly expand plasma volume compared to normal crystaloid fluids (e.g. 0.9% NaCl)

So, we need to revise Starling’s principle

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11
Q

revised starling’s principle of fluid exchange (including glycocalyx)

what does the glycocalyyx mean?
how do plasma proteins move into interstitial place? why?

what happens to plasma proteins in interstitial place? what does this create and how does this change the equatiuon?

A

glycocalyyx means barrier hence plasma protein can’t move into intercellular space but move via exo/endocytosis

Plasma proteins move from lumen into interstitial space via vesicle system Not via intercellular spaces as glycocalyx acts as a barrier

Stream of fluid filtration into interstitial space carries plasma proteins away from endothelium into IIi
creating low IIg (subglycocalyx region) so IIp = IIi but the IIg has lower osmotic pressure as it is washed away

Osmotic gradient is IIp - IIg (not IIp - IIi)

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12
Q

what does the revised starling’s principle mean?

in relation to filtration?
what happens when Pc decreases at venous end?
how does this affect osmotic pressure? net effect?

explain how this reduce reabsoprtion during haemorrage?

what happens if glycocalyx damaged and colloid fluids given?

A

Filtration occurs across length of capillaries
Less Pc at venous end means plasma proteins diffuse into subglycocalyx region IIi = IIg
So filtration occurs at venous end, even with low Pc

venous side has less capillary pressure so acts less like a river and less plasma protein swept away so the osmotic pressure is the same and lower gradient hence there is no drive to get fluid to lumen but continous filtration happening

Explains why a significant decrease in Pc, e.g. haemorrhage, can only produce a relatively small reabsorption

In sick patient, shedding of glycocalyx explains why colloid fluids do not expand blood volume

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13
Q

Low capillary pressure (Pc) - increased IIp

how is there low Pc?
how much is internally transfused at this point? why?
how? when does thiss top?

A

Drop in blood volume leads to drop in CO and drop in BP (BP=CO x TPR)
so Pc is reduced

500 ml interstitial fluid ‘internally transfused’ into the blood over 0.5 hr after a haemorrhage

Life-preserving: Supports CVP, Increases CO, Rises BP
Greater end organ perfusion

Only about 500 ml as this stops when IIp = IIg
(see previous slide)So even the low Pc causes filtration

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14
Q

If we have constant filtration, where does this fluid go?

where does that go?
what do these vessels have to help with flow? (2)
what else help flow?

A

Lymphatic circulation
Lymphatic circulation returns excess tissue fluid/solutes back to the cardio-vascular system

Lymph vessels have valves and smooth muscle

Spontaneous contractions of the smooth muscle contributes to lymph flow

Surrounding skeletal muscle contractions / relaxation also contributes to lymph flow

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15
Q

organisation of lymphatic system

descrive the route and organisation

A
initial lymphatic plexus
collecting lymphatic
afferent lymphatic
high endothelial venule
lymphocyte
lymph node
efferent lymphatic
cysterna chyli
lacteal
thoracic duct into left subclavian vein
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16
Q

what does overall control of extracellular fluid balance depend on?

3 things

and chnages in what?

A

Capillary filtration
Capillary reabsorption
Lymphatic system

Changes in:
Starling’s factors
Efficiency of lymphatic system
Influence fluid balance between the intravascular and interstitial spaces

17
Q

what if overall control of extracellular fluid balance is not maintained? what can it lead to?

A

Imbalance between filtration, reabsorption, lymphatic function, glycocalyx function leads to
Excess interstitial fluid – Oedema

18
Q

factors promoting filtration

A

increased Pc, IIg and Lp and decreased IIp

19
Q

factors promoting absorption

A

decreased Pc and increased IIp

20
Q

Increased capillary pressure (Pc)

3 issues

A

Gravitational oedema – ‘standing up for long periods’
Deep venous thrombosis
Cardiac failure - eject less blood hence build up of pressure in heart e.g LV + LA hence more pressure in pulmonary veins

21
Q

DVT

why? where does it occur? what causes filtration?

A

Prevention of venous return

(below clot) Increases venous pressure causes ‘back-up’ of pressure leading to:

Increased PC across capillaries therefore increased arterial pressure and more filtration

Increased filtration

22
Q

decreased plasma osmotic pressure (IIp) examples

3 examples

A

Low protein oedema
Malnutrition/malabsorption, hepatic failure, nephrotic syndrome

Nephrotic syndrome: Urinary protein loss&raquo_space;> Replaced by liver production

Liver disease (not enough endogenous albumin produced)

23
Q

decreased plasma osmotic pressure (IIp) process

what is the net result?

A
Reduced plasma protein concentration
Reduced plasma oncotic pressure (IIp) 
Greater influence of Pc
Fluid efflux from capillaries into the interstitial fluid
Leads to Oedma
24
Q

Inflammatory-mediated oedema

what causes inflammation? examples
what causes swelling?
what makes it more leaky?

what drives filtration?

A

Inflammation
e.g. Insect bites/stings, infection, trauma, autoimmune disease

Swelling is triggered by local chemical mediators of inflammation e.g increased histamine

Increase capillary permeability so its more leaky

Inflammation = increasedLp, (also decreased o, increased protein permeability (now IIp = IIg = IIi)
Enhanced filtration
as intracellular junctions are opened up so it’s easier for fluids to be filtered out therefore large proteins can move out and no oncotic gradient across + all the same therfore drives filtration

25
Q

Lymphatuc obstruction

condition? what happens?

A

Filariasis/elephantitis – nematode infestation, larvae migrate to lymphatic system grow/mate/form nests –> block lympathetic drainage

26
Q

Lymphatic removal

caused by? why?

A

Lymphoedema - caused by surgery to treat testicular cancer –> removal of lymphatics

27
Q

when glycocalyx breaksdown

what happens when you increase fluids? effect of this?

what does this drive? what does this lead to?

what is the caution?

A

It is increasingly apparent that a sick patient has a dysfunctional glycocalyx
e.g. inflammation, sepsis, following surgery

In these conditions increasing fluids (either crystalloids or colloids) also causes movement of plasma proteins through intercellular gaps as well as vesicles
So: IIp = IIg = IIi - nullifies oncotic pressures

This drives filtration as no force to drive fluid back into lumen
Pc dominants – filtration – potential oedema if the lymphatic system doesn’t reabsorb

Considerable caution must be given when giving fluid replacement therapy in an attempt to expand blood volume