Commentary on transfusion triggers

Abstract

In this review article Bunker et al. present their approach to the clinical conundrum regarding the use of red cell transfusion triggers. The impetus to use numerical values of haemoglobin concentration as transfusion triggers has been driven by several factors that have been clearly outlined by the authors. Whilst public perception may differ, blood itself has never been safer and currently the most pressing problem associated with this pharmacological product is the reduction in the donor pool and the exponential rise in cost due to even more sensitive screening tools and pathogen inactivation methods. This has to be tempered with the fact that decisions at the bedside will depend ultimately on the rapidity of blood loss that leads to anaemia and the co morbidities of the patient that may affect their compensatory reflexes such as ischaemic heart disease. As highlighted, the compensatory mechanisms to acute anaemia aim to preserve global oxygen delivery and involve an increase in cardiac output and an increased oxygen extraction ratio. Clearly there will be considerable variation between individuals dependant upon co-morbidities. At the bedside this translates to ‘how low is safe’ when delineating the limits of haemodilution and the concept of the ‘critical point’ emerges. This is the haemoglobin threshold at which compensatory mechanisms are overwhelmed and the sacrosanct oxygen delivery becomes inadequate to meet the oxygen demands of the individual. At present there is no way of knowing this value for an individual and therefore making clinical decisions in advance to allow a reasonable margin of safety. What is more common is the scenario that exists when the ‘critical point’ has been passed when markers of tissue hypoperfusion such as metabolic acidosis and increased lactate occur. The problem is however, that these markers are not specifically related to the requirement for a transfusion. The anxiety related to the adoption of low transfusion triggers in the latter group revolve around the provocation of coronary ischaemia be that overt or covert silent myocardial ischaemia. This is related to the high oxygen extraction ratio of the myocardium which therefore little capacity to increase this further in response to reduced arterial oxygen content. Figs. 1 and 2 serve to highlight the complex interrelationship between haemoglobin concentration, its fall, the concomitant rise in cardiac output to compensate for drop in haemoglobin and the ‘critical point’. A more pertinent point is that the ‘critical point’ is reached