Abstract
Routine anaesthesia monitoring until the mid-1980s often consisted of just a finger on the pulse, primitive ECG and intermit-tent blood pressure (MAP) measurement using a cuff and aneroid gauge or me-chanical oscillotonometer. Then in quick succession an explosion of new monitors was introduced including pulse oximetry (SpO2), end tidal carbon dioxide (EtCO2) and anaesthetic agent monitoring as well as automated non-invasive blood pres-sure (NIBP) machines. These were all rou-tinely in place in many hospitals by the late 1980’s, but then progress came to a halt with no advances in routine anaesthetic monitoring for over 25 years. This paper concentrates on three classes of non- or minimally invasive monitors which have become additionally avail-able in the last 10 to 15 years and if used in combination their potential impact on improving outcome following surgery in high risk patients:tary information which should improve perioperative haemodynamic manage-ment and outcome and form part of a multi-modal monitoring (MMM) strategy which is the subject of this article. 
Highlights
mean arterial pressure (MAP) fall following induction of anaesthesia is often ascribed to peripheral vasodilation with a fall in systemic vascular resistance (SVR)
MAP fall following induction of anaesthesia is often ascribed to peripheral vasodilation with a fall in SVR
In a review of perioperative haemodynamic therapy the authors stated that “once an individualised approach will be identified, the terms of liberal, restrictive and supranormal values could eventually be replaced by adequate haemodynamic support that fits every patient’s own needs”. [4] The question is, can we identify a better individualised approach to further improve outcomes and in particular reduce mortality in this high risk patient group? The goal should be directed towards avoiding the build-up of oxygen debt as this has been shown by Shoemaker et al to contribute to poor outcome
Summary
[20] It seems that liberal fluid replacement in surgery (see above) was given historically to overcome the effects of increase in venous capacitance rather than a true loss of functional extracellular fluid. Phenylephrine, in low dose infusion commenced pre-induction, with the effect monitored by the LiDCOrapid (see later), can maintain venous tone (without increasing SVR), venous capacitance SV, CO and MAP without the need for liberal fluid administration. This excess fluid can lead to complications in the later postoperative period. The Optimise trial, did not reduce a composite outcome of complications or 30 day mortality. [5] A recent editorial concluded that SV optimisation/maximisation provides “no marginal benefit in aerobically fit patients having elective surgery within a contemporary enhanced recovery pathway”. [25]
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