Abstract
Introduction and Objective: Evidence demonstrates that there are many errors and misconceptions on fluid therapy. Starling’s law underlies it all. This report gives the complete evidence that Starling’s law is wrong on both forces and the correct replacement is hydrodynamic of the G tube. New physiological evidence is provided with clinical relevance and significance. Material and Methods: The physics proof is based on G tube hydrodynamic. The physiological proof is based on a study of the hind limb of sheep: running plasma and later saline through the artery compared to that through the vein as regards the formation of oedema. The clinical significance is based on 2 studies one prospective and a 23 case series on volumetric overload shocks (VOS). The recent clinical studies on albumin and hydroxyethyl starch versus saline and also that on plasma proteins partly affirm that Starling’s law is wrong. My physics and physiological research completes this evidence. Results: Hydrodynamics of G tube showed that proximal, akin to arterial, pressure induces suction “absorption”, not “filtration”. In Poiseuille’s tube side pressure is all positive causing filtration based on which Starling proposed his hypothesis. The physiological evidence proves that the capillary works as G tube not Poiseuille’s tube: Oedema occurred when fluids are run through the vein but not through the artery. There was no difference using saline or plasma proteins, neither in physiological nor in clinical studies. The wrong Starling’s law dictates the faulty rules on fluid therapy misleading physicians into giving too much fluid during shock resuscitation and surgery inducing VOS and ARDS. Conclusion: Hydrodynamic of the G tube challenges the role attributed to arterial pressure as filtration force in Starling’s law. A literature review shows that oncotic pressure does not work either. The new hydrodynamic of G tube is proposed to replace Starling’s law which is wrong on both forces. The physiological proof and relevance to clinical importance on the pathogenesis of clinical syndromes are discussed.