CVS: Fluid Movement and Oedema Flashcards
Describe fluid movement at the capillary wall
Fluid moves across membrane into interstitial space due to capillary blood pressure
Large molecules (plasma proteins) can't pass thru the membrane **so they exert oncotic pressure.** This creates suction force to move fluid from interstitial space into capillary
So, Fluid movement depends on balance between capillary bp and oncotic pa across the capillary wall: Starling’s principle of fluid exchange
What is starling’s principle of fluid exchange?
What does Starling’s principle tell us?
Greater pressure at the arterial end when blood first enters the capillary. This pressure decreases as you move to the venous end, so hay a Pa gradient
At the arterial end, capillary pressure is greater than oncotic pressure, so you have filtration rather than reabsorption
At the venous end, oncotic pa is greater than capillary pa so you have reabsorption
What is incorrect with Starling’s principle?
- Interstitial osmotic pressure (πi) is not small.
- Glycocalyx is not taken into account
- usually no hay reabsorption, only constant filtration even w low capillary pressure.
Starling’s principle states that if we increase πp using colloid fluids we increase reabsorption and reduce filtration, increasing blood vol
But colloid fluids (albumin/dextran solutions) don’t significantly expand plasma vol compared to normal crystalloid fluids (NaCl). So hay que revise Starling’s principle
What is the revised Starling’s principle of fluid exchange?
Basically Osmotic gradient is πp - πg (not πp - πi)
Plasma proteins move into interstitial space via vesicles, not via intercellular spaces as glycocalyx acts as a barrier
Stream of fluid filtration into interstitial space pushes plasma proteins away from the membrane walls, so oncotic pa decreases. endothelium into πi – creating low πg (subglycocalyx region) - πp = πi
What does Starling’s revised principle mean?
Less πc at venous end means plasma proteins diffuse into subglycocalyx region. πi= πg. So filtration occurs at venous end of capillaries, even w low Pc
This explains why a significant decrease in πc, e.g. haemorrhage, can only produce a relatively small reabsorption
And in sick patients, shedding of glycocalyx explains why colloid fluids do not expand blood volume
How does starling’s revised fluid law apply to hypovolemia?
In hypovolemia, drop in blood volume=drop in CO and BP so Pc is reduced to < oncotic pa (plasma protein levels don’t change in hypovolemia).
This means less filtration and more reabsorption. Reabsorption increases blood vol, BP, CO and causes greater end organ perfusion. BUT, this is only about 500 ml as this stops when πp = πg
So even the v low Pc will cause filtration
If we have constant filtration, where does this fluid go?
- Lymphatic circulation returns excess fluid/solutes back to the cvs
- Lymph vessels have valves and smooth muscle
- Spontaneous smooth muscle contraction, as well as surrounding skeletal muscle contractions / relaxation contribute to lymph flow
Excessive fluid in interstitial space forms= oedema.
This is caused by factors that promote excessive filtration and reabsorption
How can increased capillary pressure cause oedema?
Hay prevention of venous return which increases venous pressure.
This causes ‘back-up’ of pressure, increasing Pc across capillaries. This in turn increases filtration. Excess filtration causes oedema
Clinical scenarios inc:
- Gravitational oedema – ‘standing up for long’
- DVT= prevents venous return
- Left side cardiac failure= less CO, so more blood vol remaining in LA, causing pulmonary oedema
How can decreased plasma osmotic pressure (πp) cause oedema?
Reduced plasma protein conc means less plasma oncotic pa (πp), so
More Pc leads to excessive fluid filtration from capillaries into the ICF. This causes oedema. Clinical causes inc:
- Nephrotic syndrome: Protein loss in urine > Protein made by liver due to leaky kidneys
- Liver disease (not enough albumin made by liver)
- Protein malnutrition/absorption
How can inflammation cause oedema?
Swelling is triggered by local chemical mediators of inflammation. These increase capillary permeability, they get leaky and cause oedema.
Leaky capillaries also reduce oncotic pressure and increase Lp, which causes enhanced filtration and thus oedema
How can lymphatic obstruction/removal lead to oedema?
How can glyocalyx breakdown cause oedema?
Sick patients usually have dysfunctional glycocalyx e.g. sepsis
Here, increasing crystalloid or colloid fluids will cause movement of plasma proteins through intercellular gaps, reducing oncotic pa so
Pc dominant- excess filtration= oedema
So caution must be given when giving fluids to expand blood volume bc u can instead expand the interstial space and cause pulmonary oedema
