We appreciate the interest of Dr Alston in our review article on jugular bulb oximetry during cardiac surgery [1]. We agree with him that bench oximetry, not fibreoptic catheters, is the gold standard for the measurement of jugular bulb oxygen saturation (Sjo2) during cardiopulmonary bypass (CPB). Dr Alston provides a perfectly valid explanation of why Sjo2 less than 50% occurs during cardiopulmonary bypass and why, postoperatively, hyperventilation leads to reduced arterial carbon dioxide tension (Paco2), cerebral vasoconstriction, decreased cerebral perfusion and hence increase in oxygen extraction and reduced Sjo2. We recently studied the effect of Paco2 on Sjo2[2], but found that it explains only 34% of the variance of Sjo2 during warm CPB. Recently, Robson and colleagues found that cognitive dysfunction at 3 months after CPB was not related to jugular bulb desaturation (Sjo2 < 50%) during or after CPB [3]. In their study, the authors did not report the early cognitive changes in the first week after CPB or its relation to Sjo2, which was reported by Croughwell et al. [4]. It would be very interesting to confirm this finding because it seems that jugular bulb desaturation may affect only short-term cognitive dysfunction. Low Sjo2 is a symptom of reduced oxygen availability to the brain and if values < 50% do not lead to long-term cerebral damage, we must presume that the brain can still function under this condition. However, there must be some lower limit of Sjo2 (20%, 30%, 40%?) below which cerebral damage will occur. Another factor might be cerebral damage arising from embolism, which would be minimised by reduced cerebral perfusion. We have tried to explain in our review article that Sjo2 does reflect global cerebral oxygenation but does not detect regional cerebral oxygenation. This was confirmed in our recent paper [5] where we found that Sjo2 did not reflect impairment of regional cerebral oxygenation detected by near-infrared spectroscopy (NIRS). Therefore, if brain injury is due to regional ischaemia, it may or may not be reflected by Sjo2. Thus, in attempting to optimise cerebral oxygenation during CPB, it is important to determine whether the aim should be to maintain good oxygenation of the brain or to minimise cerebral perfusion and hence the risk of embolism (while still maintaining adequate oxygenation – whatever this may be).