RESUMEN
Ernest Starling first presented a hypothesis about the absorption of tissue fluid to the plasma within tissue capillaries in 1896. In this Chapter we trace the evolution of Starling's hypothesis to a principle and an equation, and then look in more detail at the extension of the Starling principle in recent years. In 2012 Thomas Woodcock and his son proposed that experience and experimental observations surrounding clinical practices involving the administration of intravenous fluids were better explained by the revised Starling principle. In particular, the revised or extended Starling principle can explain why crystalloid resuscitation from the abrupt physiologic insult of hypovolaemia is much more effective than the pre-revision Starling principle had led clinicians to expect. The authors of this chapter have since combined their science and clinical expertise to offer clinicians a better basis for their practice of rational fluid therapy.
RESUMEN
The Starling Principle states that fluid movements between blood and tissues are determined by differences in hydrostatic and colloid osmotic (oncotic) pressures between plasma inside microvessels and fluid outside them. The Revised Starling Principle recognizes that, because microvessels are permeable to macromolecules, a balance of pressures cannot halt fluid exchange. In most tissues, steady oncotic pressure differences between plasma and interstitial fluid depend on low levels of steady filtration from plasma to tissues for which the Revised Principle provides the theory. Plasma volume is normally maintained by fluid losses from filtration being matched by fluid gains from lymph. Steady state fluid uptake into plasma only occurs in tissues such as intestinal mucosa and renal peri-tubular capillaries where a protein-free secretion of adjacent epithelia contributes significantly to interstitial fluid volume and keeps interstitial oncotic pressure low. Steady filtration rates in different tissues are disturbed locally by reflex changes in capillary pressure and perfusion. The rapid overall decline in capillary pressure after acute blood loss initiates rapid fluid uptake from tissue to plasma, that is, autotransfusion. Fluid uptake is transient, being rapid at first then attenuating but low levels may continue for more than an hour. The Revised Principle highlights the role of oncotic pressure of small volumes of interstitial fluid within a sub-compartment surrounding the microvessels rather than the tissue's mean interstitial fluid oncotic pressure. This maximizes oncotic pressure differences when capillary pressure are high and enhances initial absorption rates when pressures are low, accelerating short-term regulation of plasma volume.
