Fluid exchange in capillaries Flashcards

1
Q

Learning objectives

A

Describe the basic structure & function of capillaries
Describe the structure of the microcirculation
Describe briefly the different types of capillary
Describe briefly the mechanisms responsible for capillary exchange
Explain the Starling forces acting across the capillary wall
Describe the cause & consequence of oedema

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2
Q

Structure and functions of capillaries

A

-Smallest blood vessels (5-10 μm)
- Function - Exchange between blood & interstitial fluid
-Structure: Thin walls -Endothelium & a basement membrane
-No smooth muscle
-Highly permeable
-Numerous –Large surface area
Capillaries >Capillary beds >Microcirculation

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3
Q

Structure of the microcirculation

A

Capillary bed- network of vessels within a tissue
See diagram- precapillary arteriole> postcapillary venule
precapillary sphincters open to allow blood flow through true capillaries
Capillary blood flow controlled by: vasomotion in precapillary sphincters & metarterioles

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4
Q

Types of capillaries

A

3 different types
Continous-Location:muscle, skin, lung, CNS
Permeability: Low (<10nm)

Fenestrated-Location: exocrine & endocrine glands, renal glomeruli, intestinal mucosa
Permeability: relatively high (<100nm)

Discontinuous/Sinusoidal- Location: liver, spleen, bone marrow
Permeability: extremely high (<600-3000nm)

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5
Q

Exchange across the capillary wall

A
Can occur in 3 ways
1.Diffusion (most important) 
2.Vesicular transport
3.Bulk flow (ultrafiltration &amp; reabsorption)
1 and 2 Regulate fluid composition
3 Regulates fluid volume
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6
Q

Why are capillaries suited to enhanced diffusion?

A

-Thin walls (0.5mm thick)- ↓diffusion distance
-small diameters (7μm)- ↓diffusion distance
-close proximity to all cells- ↓diffusion distance
-distributed in large numbers (est. 10-40 billion)- ↑surface area
possesss paces - intercellular clefts- ↑permeability

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7
Q

Exchange across the cap’ wall

A
Bulk flow (ultrafiltration and reabsorption)
UF- Fluid leaves intravascular compartment of capillary bed, enters the interstitium and it is reabsorbed into capillary in venular end

Is dependent on a balance between hydrostatic & osmotic pressures – Starling’s forces

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8
Q

Starling forces and regulation of movement of fluid across capillary wall

A

Capillary hydrostatic pressure (capillary BP)
Arteriolar: 37mmHg, venular: 17mmHg, mean: 20 mmHg

Plasma oncotic pressure (colloid osmotic pressure)- forces fluid from interstitium back into capillary
Due to plasma proteins that remain in the capillary (too large to be filtered: albumin): 25mmHg

Interstitial fluid oncotic pressure (colloid osmotic pressure)Very low: 0mmHg

Interstitial fluid hydrostatic pressure
Pressure exerted on outside of capillary wall by IFEither at, slightly above or slightly below atmospheric pressuree.g. 1mmHg

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9
Q

Bulk flow across capillary wall

A

Net exchange pressure =(PC + πIF) – (πP+ PIF)
Outward Inward

Capillary hydrostatic pressure (PC)
Plasma oncotic pressure (πp)
Interstitial fluid hydrostatic pressure (PIF)
Interstitial fluid oncotic pressure (πIF)

Slightly more fluid filtered than reabsorbed- this fluid is picked up in lympathic system and returned to blood

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10
Q

Significance of bulk flow

A

Normal conditions- plasma oncotic pressure 25mmHg
Capillary BP- 35mmHg A, 15mmHg V
Loss from plasma almost equals gain to plasma

Other conditions- Increased capillar pressure, e.g vasodilation
Much more ultrafiltration occurs than reabsorbed
Result- net loss of fluid from plasma and expansion of interstitial fluid in tissue- OEDEMA

Increased venous pressure e.g.Congestive heart failure
Result: oedema
More ultrafiltration, small amount of reabsorption- fluid collecting in interstitium

Decreased oncotic pressure e.g.Protein deficiency & tissue damage
Result: oedema
Longer length across which UF occurs, reduced inward driving force back into capillary

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11
Q

Some causes of oedema

A

↑ capillary pressure e.g. vasodilation, heart failure, venous obstruction by clot or tumour: stagnant blood in lower limbs
-prolonged standing, flight, pregnancy

↓ plasma oncotic pressure e.g. liver disease, dietary deficiency in protein, kidney disease- kwashiorkor disease

↑ capillary permeability e.g. inflammation
Inflammation, burns

↑ interstitial fluid oncotic pressure e.g. lymphatic failure/obstruction - lymphoedema often called elephantiasis

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12
Q

Why is oedema life threatening?

A

limits exchanges of O2, CO2, nutrients & end products of metabolism.
How? increased diffusion distances

Simple test for oedema- skin stays hollow for a few seconds afterbeing pressed (pitting oedema)

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