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Departamento de Anestesiología y Reanimación Hospital General Universitari de la Vall d’Hebron Barcelona 08035, Spain
We read with great interest Jansen et al.’s article (1), which compared the effects on the jugular bulb saturation (SjO2) of two different kinds of anesthesia (propofol versus isoflurane/nitrous oxide), under normoventilation and hyperventilation, in patients undergoing brain tumor surgery. The authors pointed out that, within the group of patients under normoventilation conditions who were anesthetized with propofol, 50% of the patients presented with SjO2 <50%, something which did not happen in patients who were anesthetized with isoflurane/nitrous oxide.
In this regard, we must observe that, recently, Schaffranietz et al. (2) published an article about patients who also underwent elective brain tumor surgery, who were anesthetized with propofol, and in which they tried to investigate the effect of different ventilation regimens on SjO2 and on other parameters of cerebral metabolism and oxygenation. In that article, they observed that PaCO2 of 31 mm Hg led to global cerebral hypoperfusion, and that the lower limit of normoventilation should be fixed at 32 mm Hg.
Taking such a remark into consideration, we do not think that the two groups under normoventilation in Jansen et al.’s article (1) can be superimposed (PaCO2 of 33 ± 3 mm Hg in the group anesthetized with propofol versus PaCO2 of 35 ± 2 mm Hg in the group anesthetized with isoflurane and nitrous oxide). It would be interesting to see how many patients in the group under normoventilation and anesthetized with propofol had PaCO2 <32 mm Hg, and out of these, the number of patients who presented with low SjO2. In Schaffranietz et al.’s article (2), patients of all different groups were anesthetized homogeneously, so before concluding that propofol can lead to global cerebral hypoperfusion, and to clarify the information given in Jansen et al.’s article (1), we should see if the SjO2 in patients who were anesthetized with isoflurane/nitrous oxide with PaCO2 of 31 mm Hg would remain within normal limits and more interestingly, which SjO2 would have patients anesthetized with such a PaCO2 and drugs without effects on cerebral blood flow.
References
Department of Anesthesiology, Academic Medical Centre, University ofAmsterdam, Amsterdam, The Netherlands Ziekenhuiscentrum Apeldoorn Apeldoorn, The Netherlands
We appreciate Olivé and Noquer’s comments regarding our article (1). From the data of our study, one may observe that of the three patients in the propofol group who had PaCO2 values <31 mm Hg, all had a jugular bulb saturation SjO2 <40%. Of the seven patients with PCO2 values >31 mm Hg, three had SjO2 of 50% and lower, whereas two of these three patients had PaCO2 values of 36 and 37 mm Hg. A broad range of PaCO2 values that are clinically acceptable during neurosurgery, thus may be responsible for low SjO2 values. The study by Schaffranietz and Heinke (2), quoted by Olivé and Noquer, shows that patients who underwent brain tumor surgery under propofol anesthesia and ventilated with oxygen in air at PaCO2 levels of <31 mm Hg, had SjO2 values <50%. From these results, the authors stated that the lower PaCO2 limit from ventilation should be fixed at 32 mm Hg, tacidly implicating that low SjO2 values, indicating global cerebral hypoperfusion, would not occur at PaCO2 levels >32 mm Hg. However, in Schaffranietz and Heinke’s (2) study of 60 brain tumor patients, a certain number of patients were excluded from further study because of primary low jugular venous oxygen saturation of <50%, probably at relative normoventilation. These excluded patients might have been exactly those patients in our study who showed SjO2 <50% at the higher PaCO2 levels of 35 mm Hg and above. Of the isoflurane/nitrous oxide group in our study, all patients had PaCO2 >31 mm Hg. No patients showed SjO2 <50%. This is also confirmed by a study of Matta et al. (3) in 12 brain tumor patients anesthesized with isoflurane (0.5%–1.0%) in an O2-air mixture. At PaCO2 values of 30 mm Hg and PaO2 values of 100 mm Hg, none of those patients had SjO2 <50%.
Thus, not only the results of our study, but also those of others, show data that suggest that during isoflurane/nitrous oxide anesthesia at PaCO2 values >31 mm Hg, SjO2 remains higher than 50%, although during propofol anesthesia, a certain number of patients consistently show SjO2 values less than 50%. Whether these SjO2 values under 50% will have any clinical consequences needs to be further investigated.
References
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