Mark Rogers

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Phase II collaborative pilot study: preliminary analysis of central neural effects from exposure to volatile anesthetics in the PACU.

Keary A Cope; William T Merritt; Dina A Krenzischek; John Schaefer; James Bukowski; W Michael Foster; Edward Bernacki; Todd Dorman; Terence H Risby (Profiled Authors: Edward Bernacki; Todd Dorman; Terence Risby; William Merritt)

Department of Environmental Health Sciences, Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, MD 21205, USA.
Journal of perianesthesia nursing : official journal of the American Society of PeriAnesthesia Nurses / American Society of PeriAnesthesia Nurses 2002;17(4):240-50.

Nurses working in the PACU are occupationally exposed to volatile anesthetics that are exhaled by patients. Few studies have quantified this exposure using breath analysis or have characterized biological effects associated with this exposure. Isoflurane is a widely used anesthetic and is a strong respiratory depressant. Exposure to isoflurane has been shown to cause changes in breathing patterns at low doses. However, biological effects of isoflurane exposure have never been addressed in the occupational setting. This study investigates whether occupational exposure to anesthetic gases has a depressive effect on central neural control of breathing. In this study, concentrations of halogenated anesthetics were quantified in pre- and postshift breath samples of nurses working in the PACU on a Friday and the following Monday. After each breath sample was collected, an occlusion pressure measurement was taken as an indicator of central inspiratory drive. Cumulative nitrous oxide and halogenated anesthetics exposure was measured each day using personal sampling monitors placed close to the nurse's mouth. Exposure to nitrous oxide and isoflurane was significantly higher on Monday than on Friday (P <.001). Monday breath isoflurane concentrations (mean +/- SD) increased significantly from 43 +/- 30 parts per billion (ppb) in preshift breath samples to 124 +/- 57 ppb in postshift breath samples (P <.002). On Monday, there was a significant decrease in occlusion pressure from 1.2 +/- 0.37 cm H(2)O in preshift samples to 0.85 +/- 0.43 cm H(2)O in postshift samples (P =.05). There was no statistical difference in pre- versus postbreath isoflurane or occlusion pressure on Friday. These data indicate that after increased exposure to isoflurane, central neurorespiratory activity was depressed.

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