This chapter is has bsome borderline relevance to Section I1(i) of the 2017 CICM Primary Syllabus, which expects the exam candidate to "explain the ...movement of body fluids". Any mention of fluid movement must sound dangerously circulatory in character, and it is true that the bulk of these discussions takes place wherever the circulatory system is discussed. Still, the college wants what it wants, and so this chapter is left here as a brief summary of the forces that govern transvascular fluid movement. Let's call them Starling forces.
Starling, in 1896, published a paper on the absorption of fluids from the connective tissue spaces. The basis of his work were a series of experiments injecting serum or saline solution into the hindlimb of a dog, to track the movement of extravascular fluid. From his findings, Starling deduced that the capillaries and post-capillary venules behave as semi-permeable membranes absorbing fluid from the interstitial space. Thereafter, the true "classical model" of Starling's Principle finally took its modern form in the hands of Krogh, Landis and Turner (1931):
- The movement of fluid between capillaries and tissues is governed by the balance of the hydrostatic pressure and oncotic pressure.
- Where capillary hydrostatic pressure and blood oncotic pressure are equal, no net fluid movement occurs.
- When capillary hydrostatic pressure is higher than oncotic pressure, fluid is ultrafiltered out of the capillaries and into the tissues
- When oncotic pressure is higher than intravascular hydrostatic pressure, tissue oedema fluid should be attracted back into the circulation.
- The classic model of the Starling principle holds that hydrosatic pressure is higher than oncotic pressure in the post-arteriolar capillary segments, but as the pressure in the capillary decreases along its length, oncotic pressure "wins" and attracts some of the ultrafiltered water back into the pre-venule capillaries.
- In reality, there is likely no movement of ultrafiltered water back into the capillaries, and it returns back into the systemic circulation by means of the lymphatics.
This is consistent with the current data:
- There is no clinical benefit in correcting hypoalbuminaemia in most ICU patients
- Hyperoncotic albumin does not improve oxygenation in patients with interstitial pulmonary oedema due to ARDS. Specifically, increasing the oncotic pressure difference does not improve oxygenation in ARDS patients (but "drying" them with diuretics does help).
- The colloid oncotic pressure of grossly oedematous septic patients is the same as that of non-septic, non-oedematous patients.
(It is now thought that the intravascular volume increase which occurs with the administration of hyperoncotic albumin is likely the result of water moving into the circulation out of the non-circulating glycocalyx, which contributes about 25% to the total intravascular volume).