Colloid Supplementation during Induction of Anesthesia

Abstract

The present paper puts forward the hypothesis that infusion of colloid during induction will prevent the development of an oxygen debt. The reasoning behind this hypothesis depends on there being a drop in venous tone during induction, as a result of reduced sympathetic drive. The resulting venous relaxation leads to blood volume loss from the arterial side of the circulation into the venous side. The loss of arterial volume is responsible for the reduction in arterial blood pressure. The lowered value of Mean Arterial Pressure (MAP) results in a fall in Cardiac Output (CO) below normal, in the face of little if any change in Systemic Vascular Resistance (SVR). Most clinical assessments to date have emphasised changes in Stroke Volume (SV), whereas the fall in CO is the important variable since it determines Oxygen Delivery to the tissues (DO2). When DO2 is lower than normal it is responsible for the development of oxygen debt, and this is the main reason for development of the complications commonly found following anesthesia. The present hypothesis is that addition of carefully titrated colloid fluid during induction can be scaled to reduce or prevent the fall in MAP and CO. Although this means the presence of extra fluid in the circulation previous work suggests this will be eliminated readily during recovery. An alternative, giving phenylephrine over the induction period reduces the anesthetic induced venous wall relaxation. Phenylephrine is already being utilised successfully and is likely to be a useful adjunct to colloid supplementation. By maintaining normal or near normal pressure, as assessed prior to induction, and hence sustaining normal blood flow, normal DO2
will be sustained. Avoidance of an oxygen debt should reduce or even eliminate the complications which result from tissue ischaemia during anesthesia. Vasopressor administration may raise arterial pressure but will worsen the cardiac output and hence increase oxygen debt.