CIRCULATING BLOOD VOLUME
Hypovolaemia has been documented in up to 70% of surgical patients following anaesthesia induction (i.e., they respond positively to a fluid challenge), despite ERAS interventions to better prepare them for surgery (e.g., reduced preoperative fasting, no bowel preparations) . One of the major causes of this hypovolaemia is anaesthesia-induced vasodilatation, which increases the functional volume of the vascular system [2-4].
The consequence of an impaired circulating blood volume and subsequent oxygen debt across the perioperative period was first identified by Shoemaker et al.  in the early 1990s. The authors demonstrated that patients who maintained higher oxygen delivery across the perioperative period, were more likely to survive when compared to those with impaired oxygen delivery. This has been further established in the many studies published since (see outcome studies).
The poorer patient outcome associated with hypovolaemia can be attributed to the following physiological changes [6, 7]:
- Splanchnic bed vessels vasoconstrict to ensure adequate flow is directed towards the ‘vital’ organs (i.e., the heart and brain).
- This hypoperfusion and resulting hypoxia can cause necrosis of the gut mucosa.
- Damage to the mucosa allows bacteria and endotoxins to ‘leak’ from the gut lumen into the bloodstream.
- Toxins unable to be broken down by the liver may enter the systemic circulation, potentially resulting in multiple organ dysfunction syndrome.
Studies that have involved the administration of a standardised fluid bolus have not demonstrated the same favourable outcomes as those using ODM to guide fluid management. Parker et al.  found no reduction in mortality or length of hospital stay following the preoperative infusion of 500 mL of colloid in patients undergoing hip fracture repair. Likewise, the preoperative administration of 25 mL/kg of crystalloid does not reduce postoperative morbidity and does not significantly reduce length of hospital stay .
- Bundgaard-Nielsen, M., et al., Functional intravascular volume deficit in patients before surgery. Acta Anaesthesiol Scand, 2010. 54(4): p. 464-9.
- Dale, O. and B.R. Brown, Jr., Clinical pharmacokinetics of the inhalational anaesthetics. Clin Pharmacokinet, 1987. 12(3): p. 145-67.
- Akata, T., General anesthetics and vascular smooth muscle: direct actions of general anesthetics on cellular mechanisms regulating vascular tone. Anesthesiology, 2007. 106(2): p. 365-91.
- Veering, B.T., Cardiovascular and pulmonary effects of epidural anaesthesia. Minerva Anestesiol, 2003. 69(5): p. 433-7.
- Shoemaker, W.C., P.L. Appel, and H.B. Kram, Role of oxygen debt in the development of organ failure sepsis, and death in high-risk surgical patients. Chest, 1992. 102(1): p. 208-15.
- Fiddian-Green, R.G., Splanchnic ischaemia and multiple organ failure in the critically ill. Ann R Coll Surg Engl, 1988. 70(3): p. 128-34.
- Deitch, E.A., The role of intestinal barrier failure and bacterial translocation in the development of systemic infection and multiple organ failure. Arch Surg, 1990. 125(3): p. 403-4.
- Parker, M.J.G., R.; Boyle, A., Preoperative saline versus gelatin for hip fracture patients; a randomized trial of 396 patients. Br J Anaesth, 2004. 92(1): p. 67-70.
- Cuthbertson, B.H., et al., A pragmatic multi-centre randomised controlled trial of fluid loading in high-risk surgical patients undergoing major elective surgery – the FOCCUS study. Crit Care, 2011. 15(6): p. R296.