Implementation of closed-loop-assisted intra-operative goal-directed fluid therapy during surgery

Editor, Joosten et al.1 are to be congratulated on another elegant study using a closed-loop system to administer standardised fluid boluses to produce stroke volume (SV) maximisation for goal-directed fluid therapy in surgical patients. However, disappointingly it would appear from their Table 3 that the 30-day mortality was high at 6.7% in the closed loop group and 10% in the control group. We believe that the physiological basis of SV maximisation can be challenged as cardiac output (CO) is determined by the oxygen requirements of the tissues and not the other way round. In addition, it may lead to fluid and Na+ overload producing little benefit on reduction of complications or length of stay with no effect on mortality.2 However, this debate has been reopened by the publication of the Relief study where physiologically excessive fluids did not seem to be harmful.3 The question is can we do better and maintain the patient haemodynamic without excessive fluids and Na+? A high SV variation with fall in systemic blood pressure and CO4 is often seen postinduction and continues throughout surgery suggesting fluid depletion. In a closed loop system, as used here, this would automatically lead to administration of boluses of intravenous fluid. However, these changes are almost certainly due to fluid redistribution due to vasodilation and thus treatable by vasconstrictors5 as elective patients are unlikely to be fluid depleted at induction and thus additional fluid therapy is inappropriate. However, we believe that the generic term ‘vasodilation’ should be replaced by the more specific term ‘venodilation’ due to anaesthesia induced reduction in venous tone. The role of the venous circulation in goal-directed fluid therapy has been recently emphasised.6 Commencing phenylephrine or noradrenaline as a low-dose infusion prior to induction allows maintenance of venous tone, systemic blood pressure and CO without causing arteriolar constriction and increase of systemic vascular resistance. It also reduces the requirement for large quantities of fluid and Na+ for haemodynamic maintenance. An improved peri-operative goal-directed fluid therapy strategy would thus involve measurement of nominal or actual CO and DO2 from pre-induction using the elective high-risk patient as their own control. An infusion of phenylephrine at around 15 to 30 μg min−1 (or noradrenaline at 1 to 3 μg min−1) in the average 60 to 70 kg adult is then commenced. Induction of anaesthesia with propofol is then carefully titrated utilising a processed EEG monitor as used in the Joosten study.1 This approach results in a less profound fall in SBP and CO which can easily be corrected with an increase in phenylephrine or noradrenaline and if needed judicious use of fluids if the SV variation is greater than 10%. Fluid and Na+ requirements are markedly reduced and CO and DO2 are maintained within 10 to 15% of pre-induction values thus removing the requirement to attempt repayment of oxygen debt in the high dependency unit postoperatively. This strategy leads to improved outcome and should be tested for efficacy in a randomised controlled trial.7 Acknowledgements related to this article Assistance with the letter: none. Financial support and sponsorship: none. Conflicts of interest: none.