S2: Capillaries - Fluid Movement Flashcards

1
Q

Importance of fluid exchange

A
  • Fluid exchange is important for normal physiological function
  • H2O is needed 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

Explain fluid movement at the capillary wall

What pressure is exerted?

A

Capillary wall is a semi permeable membrane and it allows H2O to pass through

  • Fluid moves across membrane into interstitial space due to blood flow which exerts hydraulic pressure (pressure trying to move fluid out of capillaries)
  • Large molecules (e.g. plasma proteins) cannot pass through membrane
    These in the capillary exert an osmotic pressure/oncotic pressure which creates a suction force (trying to move fluid from interstitial space into capillary)
  • Fluid movement depends on balance between Hydraulic and Oncotic pressures across the capillary wall
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3
Q

What are the two types of hydrostatic pressures and osmotic pressures?

A

Hydrostatic:
- Pc = Capillary blood pressure
- Pi = Intersititial fluid pressure
Easy movement across membrane

Osmotic:
- π p = Plasma Proteins
- πi- Interstitial proteins
Movement through intracellular gaps

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4
Q

What is Starlings Principle of Fluid exchange

A

Jv = Lp A [(Pc - Pi ) - σ (πp - πi)]
Jv is the net filtration (flux)

Pc - Pi is hydraulic pressure difference
πp - πi is the osmotic pressure difference

Lp = Hydraulic conductance of the endothelium (how leaky it is to fluid)

A = wall area

σ = reflection coefficient - related to intracellular gaps so how much osmotic pressure molecules can exert ( smaller σ , larger gap, higher the JV)

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5
Q

What does starling’s principle tell us about fluid exchange at capillaries?

A
  • There us a pressure drop across capillaries from arterial to venous end
  • If Pc is larger than πp there will be filtration
  • As capillary pressure drops πp becomes more dominant
  • Filtration on the arterial side as hydraulic pressure is higher
  • Re absorption of the venous side as hydraulic pressure is less
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6
Q

What is incorrect with starling’s principle?

A
  • Fluid filtration generally occurs throughout the length of capillaries and reabsorption does not occur even though it is important for fluid replacement.
  • Interstitial osmotic pressure is not small so sometimes πp= πi
  • The glycocalyx is not taken into account
  • · Starling’s principle states that increasing πp and reabsorption with colloid fluids should increase blood volume
    But, colloid fluids do not significantly expand plasma volume so, we need to revise Starling’s principle
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7
Q

What is the revised starling’s principle of fluid exchange?

A

Jv = Lp A [(Pc - Pi ) - σ (πp - πg)]

  • Includes glycocalyx (lumen side)
  • Plasma proteins move from lumen into interstitial space via vesicle system not via intracellular space as glycocalyx acts as a barrier
  • Stream of fluid filtration into interstitial carries plasma proteins away from endothelium into πi creating low πg region - now πp equals πi
  • πg is plasma proteins in endothelium
  • · Osmotic gradient is πp - πg (not πp - πi)
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8
Q

What does revised starling’s principle tell us about fluid exchange at capillaries?

A
  • Filtration occurs across the length of capillaries
  • Less Pc at venous end means πi moves into πg – less (πp - πg) gradient promoting filtration at venous end
  • This explains why a significant decrease in Pc e.g. haemorrhage will initially produce reabsorption in an attempt to maintain blood volume.
  • In sick patient, shedding of glycocalyx explains why colloid fluid do not expand blood volume
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9
Q

What is hypovolemia?

A

It is a state of decreased blood volume or more specifically, decrease in volume of blood plasma

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10
Q

Describe the relationship between low capillary pressure pc and hypovolemia

A

Big drop in BP as blood volume is lost e.g. in injury. Also sympathetic medicated vasoconstriction causes larger pressure drop so Pc is reduced

  • Plasma protein levels are much higher
  • Larger oncotic drive so little filtration and more reabsorption (balance shifts)
  • πp will reduce in concentration if blood volume increases and then filtration will occur again
  • This small window of reabsorption period is a life saving mechanism (maintains CO, starlings law, perfusion of major organs)
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11
Q

Where does the fluid from constant filtration go to?

A

The lymphatic circulation

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12
Q

Describe the lymphatic circulation

A
  • Lymphatic circulation returns excess tissue fluid/solutes back to the CVS (same amount of fluid is just shifted to a different part of the body).
  • 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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13
Q

What controls ECF balance?

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

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14
Q

What happens if balance of ECFV is not maintained?

A

Imbalance between filtration, reabsorption, lymphatic function, glycocalyx function

Excess interstitial fluid – Oedema

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15
Q

Factors from starlings principle promoting filtration and reabsorption

A

Factors promoting filtration:

  • Increase Pc
  • Increase πg
  • Increase Lp
  • Increase A

Factors promoting reabsorption:
- Increase πp

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16
Q

Clinical scenarios where there is increased capillary pressure (Pc)

A
  • Dependent (gravitational) oedema – ‘standing up for long periods’ Deep venous thrombosis
  • Cardiac failure
17
Q

Describe deep vein thrombosis

A
  • Prevention of venous return
  • (coagulation process –> clot –> thrombosis –> blockage)
  • Pressure below clot will increase (in venous return)

Increases venous pressure causes ‘back-up’ of pressure leading to:

  • Increased PC across capillaries
  • Increased­ filtration
18
Q

What can cause decreased Plasma Osmotic Pressure (πp)?

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)
Kwashiokor - excess filtration to interstitial space as plasma proteins oncotic pressure is not enough the keep fluid in capillaries

19
Q

Describe inflammatory mediated oedema

A
  • inflammation e.g. Insect bites/stings, infection, trauma, autoimmune disease
  • Swelling is triggered by local chemical mediators of inflammation
  • Mediators increase capillary permeability (e.g. histamine). They become more leaky increasing fluid and protein movement which can equilibrate oncotic pressure very quickly so just filtration occurs.

Inflammation = increased ­Lp, increased s, increased­protein permeability (now πp = πg = πi)
More pronounced Pc – enhanced filtration

20
Q

What are some lymphatic problems?

A
  • Lymphatic obstruction:
    Filariasis/elephantitis – nematode infestation, larvae migrate to lymphatic system grow/mate/form nests – block lympathetic drainage
  • Lymphatic removal:
    Lymphoedema - caused by surgery to treat testicular cancer – removal of lymphatics.
    Continued Pc/filtration leads to build up of fluid in interstitial space
21
Q

What happens in glycocalyx breakdown?

A

e.g. inflammation, sepsis, during surgery

In these conditions increasing fluids (either crystalloids or colloids) means movement of plasma proteins through intercellular gaps (πp aren’t held in lumen through glycocalyx barrier)
So: πp = πg = πi - nullifies oncotic pressures as they equilibrate (no gradient). Increasing plasma proteins will have no effect as they will just naturally equilibrate.

Pc dominants – filtration – potential oedema

Considerable caution must be given when giving fluid replacement therapy in an attempt to expand blood volume. In the lungs, this can lead to pulmonary oedema which is a life threatening condition.