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PO 1.47 essential features of the microciculation including fluid exchange and its control


intro microcirculation - roles, mechanism of exchange

Roles of microcirculation
- resistance – small arteries and arterioles
- capacitance – venules and small veins
- passage of leukocytes from blood into extravascular space
- exchange of gases, nutrients, wastes, thermal energy between blood and tissues. Also drugs

  • capillaries are the site where the intravascular volume is in contact with the interstitial fluid which bathes all the cells in the body


Mechansims of exchange (diffusion, bulk flow, vesicular transport, active transport)

Microcirculation uses:

- diffusion for O2 and CO2 via Ficks law of diffusion, J = Dx A(change concentration/diffusion distance) image 82. 

- diffusion of water is high 80,000L/day but no net movement as no water osmotic gradient across capillary wall. hydrostatic and oncotic forces not involved

Bulk transport for fluid:

o water, electrolytes and lipid insoluble substances
o happens between intercellular clefts/pores between endothelial cells
o can’t happen if continuous capillary (tight epithelium) – skeletal muscle, skin, lung, brain
o happens more if fenestrated capillaries(have perforations) – renal glomeruli, intestinal mucosa, exocrine glands
o happens most in discontinuous capillaries (large intracellular gaps in endothelium and basement membrane) – liver, spleen, bone marrow

Flow via Poisuille’s equation, flow = change P/R

J = NDF x Kf x A

 flow = J, change p = NDF, resistance or capacitance (its reciprocal) = Kf


PO 1.47 essential features of the microciculation including fluid exchange and its control


Filtrate = reabsorption + lymphatics 

if filtrate > resorption = lymphatics get oedema

filtrate = 20ml/min for whole body – 18ml/min reabsorbed, 2ml/min lymphatics

o Similar size to venules, endothelium has interceullalar gaps and highly permeable basement membrane
o Large lymphatics have smooth muscle cells

  • spontaneous vasomotion (myogenic) to pump lymph
  • Sympathetic can modulate
  • One way valves, muscle pump from movement, negative intrathoracic pressure, gravity, all help
  • Empty into thoracic duct and subclavian veins

o Lymph – fluid, electrolytes, macromolecules, 2-4L/day


PO 1.47 essential features of the microciculation including fluid exchange and its control


J = NDF x Kf x A

J - rate of net fluid flow

Kf - filtration constant, permeability of cap wall to water, hydraulic conductivity

A - surface area

NDF - net driving force

NDF = (Pc- Pi) - σ (πc -πi)

P - hydrostatic pressure

π - oncotic pressure (osmotic pressure from non permeable proteins

c - capillary

i - interstitium

σ - reflection consant (how permeable the capillary is to the proteins)

- if NDF pos get filtration, if neg get resportion

- if rate of filtration > rate of resorption + lymphatic drainage get oedema. This happens if P, π,σ or lymphatic drainage move away from normal

- Pc 35mmHg arteriole end, 15mmH venous end, Pi 0mmHg, πc 25mmHg, πi 5mmHg, σ 0-1


PO 1.47 essential features of the microciculation including fluid exchange and its control

hydrostatic pressure

• Net hydrostatic pressure is intracapillary – interstial hydrostatic pressure, Pc – Pi
• Pc highest at arteriolar end and lowest at venous end, drops differing degrees in different organs due to resistance. Means get more filtration at arteriolar end
• normally 30mmHg arterial and 15mmHg venous ends
• Average intracapillary pressure depends on arterial and venous pressure and resistance at either end

  • Elevating venous pressure has greater effect cos its resistance is lower than high arterial resistance which blunts the effect of increased arterial pressure. 
  • Means that increased venous pressure (RVF, cirrhosis DVT) cause oedema by increasing capillary hydrostatic pressure and fluid filtration

• Pi determined by interstial fluid volume and compliance of tissue (change p = V/C), so pressure less in dehydration and more in oedema, normally 0mmHg


PO 1.47 essential features of the microciculation including fluid exchange and its control

oncotic pressure

• Is osmotic pressure due to non diffusible particles
• Net oncotic pressure is intracapillary – interstial hydrostatic pressure πc- πi
• Πc determined by impermeable proteins (not permeable electrolytes), promotes reabsorption

  • Albumin, globulin, fibrinogen
  • Normally 25mmHg
  • Increases as go along capillary
  • In reality some proteins are permeable in some walls, or not effectve at retaining water, so need reflection co-effiecnt (σ=1 if impermeable like glomerulus, = 0 if freely permeable like hepatic, normally = .9)

• πi determined by interstitial protein concentration (determined by how much fluid in it) and σ

  • so as get filtration protein less concentrated so exerts less oncotic force and fluid stays in vessel
  • normally 5mmHg


PO 1.47 essential features of the microciculation including fluid exchange and its control

model for capillary fluid exchange

o Balance of oncotic and hydrostatic pressure is by the starling equation

o Assumes the following remain constant

  • Pi 1mmHg, πc 25mmHg, πi 6mmHg, σ 1

o So get filtration at start (where Pc is high~30mmHg) and resorption at end (where Pc is low `15mmHg), crosses over where NDF = 0
o The rate of this filtration depends on Kf and A
o In reality as fluid leaves beginning of capillary, Pi increases, πc increases and πi decreases to oppose filtration.

  • But fluid leaving is only 1% of fluid in so change these factors is small except:
    • in kidneys where it is 20%, so get significant changes in oncotic pressure
    • in disease, eg venous occlusion or heart failure increase capillary hydrostatic pressure so increased filtration so big changes in these values

o when net filtration increases lymphatic flow increases


PO 1.47 essential features of the microciculation including fluid exchange and its control


- when filtration exceeds reabsorption plus lymphatic flow
- can be localized or generalized (increased total ECF volume)
- oedema always caused by one of factors in eqn or lymph

  • Pc - increased capillary hydrostatic pressure – most common
  • increased venous pressure – DVT, RHF
  • decreased arterial resistance – vasodilation
  • decreased Pi – negative pressure pulm oedema
  •  πc - decreased plasma oncotic pressure – malnutrition, decreased synthesis in liver failure, increased loss in nephropathy
  • • or increased interstitial oncotic from burns, infam
  • o Kf, σ - increased capillary permeability – injury and inflamation causes histamine/bradykinin/leukotriene release -localized edema
  • o lymphatic obstruction – immobile, damage, node removal surgery

o increased diffusion distance for O2 into mitochondria and waste products to leave
o in muscle decreased efficiency of excitation contraction coupling as less overlap of fibres
o increase in interstitial pressure

  • depends on compliance (change p = change v/compliance) - high in brain as not compliant subcut tissue is compliant so increases greatly in volume
  • can compress capillaries and cause cell death, even in tissues if severe enough
  • can compress lymphatics and worsen oedema

o Diuretics to reduced blood volume and venous pressure and therefore hydrostatic pressure
o Elevation to decrease hydrostatic pressure
o Bandage to increase tissue hydrostatic pressure
o Antihistamine to block paracrine substances


PO 1.47 essential features of the microciculation 


o Lipid soluble so diffuses through tissue by Ficks law
o Used by mitochondria of first cell it enters so if tissue has high O2 demand it needs lots of capillaries so O2 goes only short distances
o Capillaries have high diffusion constant for O2
o Normally systemic arterial blood is fully saturated with pO2 95mmHg, but in small arterioles its 25-35mmHg cos it diffuses out before get to capillary
o Can increase rate of diffusion by

  • increasing arterial pO2- breath pure O2
  • dilating vessel cos more O2 delivered to capillary and increase capillary surface area. Precapillary phincters and metarterioles relax (normall contract and relax in vasomotion causeing intermittent capillary flow)
  • decreasing tissue pO2 - increased consumption
  • other things are fixed


PO 1.47 essential features of the microciculation including fluid exchange and its control

Diff in kidney

- in whole body, filtration is 2-4L/day in XS of reabsorption
- in glomerulus it is 180L/day
- high filtration coefficient (water permeability)
- high reflection coefficient (impermeable to protein), so filtrate has 0 oncotic pressure
- hydrostatic pressure in capillary is high and doesn’t decrease down the capillary, because of this get large fluid loss and oncotic pressure increases down the capillary (important later for reabsorption of water from prox tumule into the peritubular capillaries)



 PO 1.47 essential features of the microciculation including fluid exchange and its control

cerebral circulation

- normally only proteins can exert oncotic force because low molecular solues can pass through the wall
- in cerebral capillaries even low weight solutes are impermeable (Na+, Cl-) so exert osmotic force
- oncotic force extremely low compared to osmotic so now the starlings forces are hydrostatic and osmotic
- still get small leak of solutes – reflection co-effiecnt
- 1 miliosmale increased in osmotic gradient between blood and brain interstial fluid can exerte a force of 17-20mmHg


 PO 1.47 essential features of the microciculation including fluid exchange and its control

pulmonary microcirculation differences

- balance is to resorption
- lower capillary hydrostatic pressure due to lower pressure in pulomary arteries and low pulmonary vascular resistance.

  • Changes with gravity – less pressure at apex, 30cm higher than base, 23mmHg difference
  • Max pressure in PA usually 25mmHg, if 23mmHg less than that nearly wont perfuse
  • Low pulmonary vascular resistance as no muscle in pulmonary cap walls so cap hydrostatic pressure quickly affected by change in PAP and LAP – usualy small net flow out to lymph 10-20ml/hr

- higher interstial oncotic pressure as significant protein leak across thin capillary walls normally, σ is low, 0.5. So net oncotic gradient small (given low reflection coeffient and typical values) and favours resorption
- interstial pressure is that of alveoli and slightly negative, even more neg close to hilum and favours flow from interstitium into pulmonary lymphatics
- very large capillary surface area

Pc 13mmHg arteriole end, 6mmHg venous end - change with gravity

Pi ommHg

πc 25mmHg

πi 17mmHg

σ 0.5


 PO 1.47 essential features of the microciculation including fluid exchange and its control

pulmonary oedema

detetction clinicially or with starlings?

o Cap hydrostatic pressure can triple before get oedema
o To get oedema xs fluid must go into interstitium then alveoli
o Resisted by increased lymphatic flow
o Decrease in interstial oncotic pressure by lymph washout of albumin and as filtrate increases albumin loss decreases
o High compliance of interstium, don’t get alveolar flooding until interstium full
o surfactant


- starling not useful clinically as can only measure plasma proteins and maybe capillary hydrostatic pressure with pulm artery catheter, can’t measure interstitium – use CXR and auscultation