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Correspondence  |   March 1995
Measurements of Occlusion Pressure during Anesthesia with Volatile Anesthetics in Humans
Author Notes
  • Department of Anaesthetics University of Edinburgh, Royal Infirmary, Edinburgh EH3 9YW Scotland.
Article Information
Correspondence
Correspondence   |   March 1995
Measurements of Occlusion Pressure during Anesthesia with Volatile Anesthetics in Humans
Anesthesiology 3 1995, Vol.82, 798. doi:
Anesthesiology 3 1995, Vol.82, 798. doi:
To the Editor:—Recently, Canet et al., [1 ] reporting on changes in occlusion pressure and ventilation with different depths of anesthesia using either halothane or isoflurane, suggested that only one study previously analyzed occlusion pressure in humans, at increasing concentrations of a halogenated anesthetic agent and that studies of the occlusion pressure wave are scarce.
In an analysis of the occlusion pressure wave and inspiratory flow patterns of patients anesthetized with enflurane and nitrous oxide, [2 ] I found that ventilatory depression caused by an increase in inspired enflurane concentration was related solely to a reduction in central drive and not to the peripheral factors more favored by Canet et al. in their discussion. The same study also reported changes in the occlusion pressure and inspiratory flow pattern caused by opioid administration. There was no marked change in estimates of active elastance and impedance, again suggesting that the depression was central. Occlusion pressure also was used in a further study, investigating the findings of Wahba and Sadkova, [3 ] who found that atropine increased ventilation during anesthesia with enflurane. The effects of atropine administration were studied in patients anesthetized with enflurane and halothane, using occlusion pressure to distinguish central effects from peripheral, mechanical effects. The findings suggested a minor effect after premedication with meperidine, consistent with the possibility of bronchodilation: Atropine caused an increase in inspiratory flow, although occlusion pressure was unlatered. [4 ].
These observations support the suggestion of Canet et al that further analysis of occlusion pressure waveform in spontaneously breathing anesthetized patients can be helpful to investigate the neural mechanisms of respiratory depression.
G. B. Drummond, M.B.Ch.B., Department of Anaesthetics University of Edinburgh, Royal Infirmary, Edinburgh EH3 9YW Scotland.
(Accepted for publication December 9, 1994.)
REFERENCES
Canet J. Sanchis J. Zegri A, Llorente C, Navajas D, Casan P. Effects of halothane and isoflurane on ventilation and occlusion pressure. ANESTHESIOLOGY 81:563-571, 1994.
Drummond GB: Comparison of decreases in ventilation caused by enflurane and fentanyl during anaesthesia. Br J Anaesth 55:825-835, 1983.
Wahba WM, Sadkova J: Atropine reversal of hypercarbia during enflurane anaesthesia. Br J Anaesth 51:221-226, 1979.
Drummond GB: Atropine increases inspiratory flow during enflurane anaesthesia after pethedine premedication. Br J Anaesth 56: 565-572, 1984.