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Department of Anesthesiology and Intensive Care Medicine, University of Leipzig, Leipzig, Germany
To the Editor:
We have read with great interest the article of Muñoz et al. (1), which compared the effect of propofol or sevoflurane in combination with nitrous oxide on jugular bulb oxygen saturation (Sjo2) in neurosurgical patients undergoing resection of brain tumors. The authors could demonstrate in their investigation that N2O did not reduce the incidence of low Sjo2 values (50%) in patients anesthetized with propofol.
Comparable results in neurosurgical patients were found by Jansen et al. (2). Both, (1) and (2) described low Sjo2 values in patients anesthetized with propofol and ventilated at relative low Paco2 values (30 respective 32 mmHg). We think that the patients of both studies have been moderately hyperventilated. The low Sjo2 values were the result of propofol administration, but were additionally induced by moderate hyperventilation.
We could find in our study a reduction of Sjo2 values from 67% to 50% in neurosurgical patients anesthetized with propofol and moderately hyperventilated from Paco2 40 mmHg to 29 mmHg (3). With our latest study, we could demonstrate that hyperventilation (from Paco2 38 mmg to 30 mmHg) in patients with a propofol-based anesthesia and additional N2O leads to a reduction of Sjo2values from 68% to 50% (4).
Our results correlate with studies from De Baerdemaeker et al. (5,6). The authors recommend that forced hyperventilation (Paco2 < 25 mmHg) should be reconsidered. Moderate hyperventilation (Paco2 30 mmHg) can cause cerebral hypoperfusion associated with low Sjo2(< 50%) and increased AJDo2values (> 9 ml/dl) in some patients.
We agree with Muñoz et al. (1), that additional N2O cannot prevent low Sjo2 values in hyperventilated patients under propofol-based anesthesia. In normocapnic patients (Paco2 38 mmHg) anesthetized with propofol and additional N2O we have not seen low Sjo2 values (4).
References
Department of Anesthesiology, School of Medicine, Catholic University of Chile, Santiago, Chile
In Response:
We appreciate the comments by Schaffranietz and colleagues and agree that moderately hyperventilated neurosurgical patients (PaCO2 2832 mm Hg) receiving propofol (and to a lesser extent inhalational agents, too) can present low SjO2 values (1,2). However, although Schaffranietz et al. did not find SjO2 values compatible with brain hypoperfusion in normoventilated neurosurgical patients receiving propofol either with or without nitrous oxide (3,4), preliminary results of recent studies show that this happens. Indeed, in patients with brain tumors under normoventilation, De Keersmaeker et al. found a higher incidence of jugular bulb desaturation with propofol/nitrous oxide compared with sevoflurane/nitrous oxide (5) and De Deyne et al. also found episodes of low SjO2 values with propofol (6). Moreover, while at PaCO2 of 2829 mm Hg, we found that mean SjO2 was not affected by the addition of 67% nitrous oxide during propofol anesthesia (SjO2 of 52% and 50% with and without N2O, respectively); mean SjO2 increased from 56% to 66% with N2O in patients receiving sevoflurane (2). In contrast, under normoventilation, the addition of 65% nitrous oxide increased mean SjO2 during both propofol (from 49.5% to 57.5%) and sevoflurane (from 57.6% to 67.2%) anesthesia (6). This increase points out the difficulties in making predictions on the final effect of nitrous oxide, which is highly variable and clearly determined by the basal condition of the patients, mainly including the type of anesthesia and the arterial blood pressure of CO2.
References
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