Anesth Analg 2002;94:1041-1042
© 2002 International Anesthesia Research Society
LETTERS TO THE EDITOR
Searching the Preferred Anesthetic Technique During One-Lung-Ventilation
I. Garutti, MD, and
L. Olmedilla, MD
Service of Anesthesiology and Reanimation, Hospital General "Gregorio Marañón", Madrid, Spain
To the editor: We appreciate that there is someone interested in studying the potential intraoperative effects of an anesthetic technique that, when continued in the postoperative period, reduces morbidity and mortality (1). However, we question the conclusion of the study of Von Dossow et al. (2) that the preferred technique for thoracic surgery is a thoracic epidural anesthesia (TEA) combined with isoflurane. We are concerned with an insufficient anesthetic depth because they used an end-tidal concentration of isoflurane of 0.3%–0.5% (equivalent to <0.5 MAC). Because the inhibition of hypoxic pulmonary vasoconstriction (HPV) produced by isoflurane is dose-dependent, an adequate anesthetic concentration could decrease arterial oxygenation and increase the intrapulmonary shunt of the TEA group.
In our experience and in the literature, it is unusual to find a PaO2>300 mm Hg during one-lung ventilation (OLV). The nerve supply of the pulmonary vasculature corresponds to T2-4 level of the sympathetic nervous system. A sympathetic block produces pulmonary vasodilatation and blocks activated pulmonary vasoconstriction. Von Dossow et al. (2) used a dose of bupivacaine of 6–8 mL injected at T6-7 or T7-8, so they probably did not achieve a block of T2-4. Hyperexcitability of the adjacent segments that are not blocked could cause vasoconstriction (3). This situation could explain the high PaO2 observed in these patients. In our study (4), we used larger doses of epidural bupivacaine, so T2 was blocked. That is probably why we had a lower PaO2 during OLV in the TEA group.
We would like to know the values of PaCO2 and airway pressure, as they can also affect HPV during OLV. With regard to the time of tracheal extubation and its possible effect on postoperative morbidity, we would like to know whether the anesthesiologist who extubated the trachea knew the purpose of the study and the group in which each patient was included. This, in our opinion, could bias the study. On the other hand, it is not likely that the difference in time to extubation (13 min versus 45 min), although statistically significant, could have a clinically relevant effect (i.e., fewer pneumonias or shorter stays in the hospital).
It would be interesting to continue this investigation combining TEA with the doses used by Von Dossow et al. (2) plus more intense general anesthesia.
References
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Rodgers A, Walker N, Schug S, et al. Reduction of postoperative mortality and morbidity with epidural or spinal anaesthesia: Results from overview of randomised trials. BMJ 2000; 321: 1493–7.[Abstract/Free Full Text]
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Von Dossow V, Welte M, Zaune U, et al. Thoracic epidural anesthesia combined with general anesthesia: the preferred anesthetic technique for thoracic surgery. Anesth Analg 2001; 92: 848–54.[Abstract/Free Full Text]
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Taniguchi M, Kasaba T, Takasaki M. Epidural anesthesia enhances sympathetic nerve activity in the unanesthetized segments in cats. Anesth Analg 1997; 84: 391–7.[Abstract]
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Garutti I, Quintana B, Olmedilla L, et al. Arterial oxygenation during one-lung ventilation: combined versus general anesthesia. Anesth Analg 1999; 88: 494–9.[Abstract/Free Full Text]
Response
C. D. Spies, MD
Department of Anesthesiology and Intensive Care, Humboldt-University, Campus Mitte Charité, Berlin, Germany
In Response: We thank Drs. Garutti and Olmedilla for the discussion about the preferred anesthetic technique for lung resections during one-lung ventilation.
Whether thoracic epidural anesthesia in combination with general anesthesia reduces the anesthetic dosage remains to be determined. However, reduction of anesthetic doses for older patients is considered without signs of awareness (1).
Carlsson et al. (2) studied the effect of isoflurane anesthesia with different concentrations of end-tidal 1% and 1.5% on the hypoxia-induced pulmonary vasoconstriction in eight patients before elective surgery. There were no changes in pulmonary vascular resistance or in any other circulatory variables; arterial blood gases remained essentially unaltered. In addition, a decrease in cardiac output and mixed venous oxygen partial pressure is associated with an increased response of hypoxic pulmonary vasoconstriction (3). Kellow et al. (4) showed an increased shunt fraction but no change in cardiac output with isoflurane anesthesia, whereas propofol anesthesia caused a decrease of cardiac output which was associated with a lower shunt fraction. Therefore, changes in cardiac output might be the reason for these controversial results in many clinical studies.
We do not agree with Dr. Garutti’s opinion that hypoxic pulmonary vasoconstriction is influenced by sympathetic nerve activity. Neither sympathetic nerve activity (5) nor chemical sympathectomy (6) influenced the hypoxic pulmonary vasoconstriction response (3,7). Thoracic epidural anesthesia had no influence on the primary hypoxic-induced increase in vascular tone (3).
According to clinical routine (8) the individual dose for every patient was titrated depending on the initial required dose, age (0.1 mL/age), and size, i.e., 30–40 mg epidural bupivacaine were sufficient to spread epidural anesthesia up to the Th1–Th4 segments. In addition, for older patients (>50 yr) and those with coronary artery disease it is recommended to reduce the dosage for 30%–50% with respect to extensive arterial hypotonia (8). In comparison to the study of Garutti et al. (9) no differences were found with respect to the age (60 [43–75]/60 ± 11) and the thoracic placement of the epidural catheter (Th6–7/7–8).
Arterial carbon dioxide partial pressure values were kept constant between 35 mm Hg and 45 mm Hg throughout the study period and differences between groups were not found. In addition, the extubation time was not the primary aim of this study because of methodological reasons: as stable conditions were required until the patient was returned in the supine position, propofol infusion as well as the application of isoflurane were only stopped afterward. Therefore, it cannot be ruled out that this might have biased the longer extubation time in the TIVA group.
References
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Schwender D, Faber-Zullig E, Klasing S, et al. Motor signs of wakefullness during general anesthesia with propofol, isoflurane, and flunitrazepam/fentanyl and midlatency auditory evoced potentials. Anesthesia 1994; 49: 476–8.[Web of Science][Medline]
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Carlsson AJ, Bindslev L, Hedenstierna G. Hypoxia-induced vasoconstriction in the human lung: the effect of isoflurane anesthesia. Anesthesiology 1987; 66: 312–6.[Web of Science][Medline]
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Ishibe Y, Shiokawa Y, Umeda T, et al. The effect of thoracic epidural anesthesia on hypoxic pulmonary vasoconstriction in dogs: an analysis of the pressure-flow curve. Anesth Analg 1996; 82: 1049–55.[Abstract]
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Kellow NH, Draper EA, Wagner DP, et al. Comparison of the effects of propofol and isoflurane anesthesia on right ventricular function and shunt fraction during thoracic surgery. Br J Anaesth 1995; 75: 578–82.[Abstract/Free Full Text]
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Naeije R, Lambert M, Lejeune P, et al. Cardiovascular and blood gas responses to inhaled anesthetics in normoxic and hypoxic dogs. Acta Anaesthesiol Scand 1986; 30: 538–44.[Medline]
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Lodato RF, Michael JR, Murray PA. Absence of neural modulation of hypoxic pulmonary vasoconstriction in conscious dogs. J Appl Physiol 1988; 65: 1481–7.[Abstract/Free Full Text]
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Brimouille S, Vachiery JL, Brichant JF, et al. Sympathetic modulation of hypoxic pulmonary vasoconstriction in intact dogs. Cardiovasc Res 1997; 34: 384–92.[Abstract/Free Full Text]
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Jancovic D. Thorakale epiduralanaesthesie regionalblockaden in klinik und praxis. Berlin, Wien: Blackwell-Wissenschafts-Verlag, 1999: 257.
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Garutti I, Quintana B, Olmedilla L, et al. Arterial oxygenation during one-lung ventilation: combined versus general anesthesia. Anesth Analg 1999; 88: 494–9.
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