Jugular bulb oximetry

The review of jugular bulb oximetry and cardiac surgery is timely and welcome (Shaban Ali et al. Anaesthesia 2001; 56: 24–37). Being amongst one of the first groups to recognise the phenomenon of jugular bulb oxyhaemoglobin desaturation (Sjo2 < 50%) during cardiac surgery [1, 2], we have had a long-standing interest in the area and I wish to contribute some information and comments. Even after a combined experience of jugular bulb oximetry in almost 300 patients undergoing cardiac surgery, we are still unable to obtain reliable results with fibreoptic catheters during cardiopulmonary bypass (CPB) when compared to isolated blood sampling from the jugular bulb and bench oximetry [1, 3-6]. Although we have found the bias between the methods during CPB to be small, the limits of agreement are wide [5]. So the gold standard for the measurement of Sjo2 during CPB should remain bench oximetry. In the early postoperative period following cardiac surgery, by contrast, we have found the limits of agreement between the methods to be reasonable [5, 6]. However, even in this setting I would recommend that studies using fibreoptic oximetry include method comparison with bench oximetry to confirm the reliability of the technique. To my knowledge, only the eminent group of researchers from Duke University have found Sjo2 < 50% to be associated with cognitive decline following coronary artery bypass grafting (CABG) surgery and that only short-term decline (one week postoperatively) [7]. Our recent work has failed to demonstrate any important association between Sjo2 during CPB and long-term cognitive outcome at 3 months following CABG surgery [7]. Moreover, we were also unable to demonstrate an association between Sjo2 < 50% and neurological outcome 3 months following surgery (unpublished data). So whilst Sjo2 < 50% during CPB may be involved in the aetiology of the short-term brain damage, it does not appear to be associated with long-term damage. Following CABG surgery, we have observed Sjo2 < 50% in many patients during the early postoperative period following CABG surgery using fibreoptic oximetry and confirmed this observation with isolated blood sampling and bench oximetry [4, 8]. The duration of postoperative Sjo2 < 50% is in excess of six times longer than that ever reported during CPB [4]. Therefore, if Sjo2 < 50% during CPB is associated with cognitive decline, the far more prolonged episodes in the postoperative period should consequently be associated with more cerebral damage. However, we have been unable to find any important association between postoperative Sjo2 < 50% and either cognitive or neurological outcome 3 months after CABG surgery (unpublished data) [6]. If many patients are experiencing Sjo2 < 50% during CPB and in the early postoperative period after CABG surgery, what is causing the phenomenon, and why is this cerebral hypoperfusion not associated with adverse neurological or cognitive outcome? I can offer a singularly important reason, and that is arterial carbon dioxide tension (Paco2). During CPB and following surgery, Sjo2 is highly influenced by Paco2[8]. Moreover, changes in Sjo2 are not reciprocated by changes in the concentration of jugular bulb lactate (unpublished data). Therefore, Sjo2 < 50% in this setting does not represent cerebral ischaemia as there would have been an increase in cerebral lactate production. Rather Sjo2 < 50% appears to be largely the result of hypocapnia, caused by mechanical hyperventilation, inducing cerebral vasoconstriction. This in turn decreases cerebral blood flow, and any decrement in cerebral oxygen delivery is compensated for by increased oxygen extraction. Therefore, Sjo2 < 50% during CPB and following CABG surgery is largely artefactual, and is not a valuable predictor of cerebral outcome. Future research investigating the causes of cerebral damage that is associated with CABG surgery should examine putative factors other than Sjo2 < 50%.