British Journal of Anaesthesia, Vol 78, Issue 6 707-713, Copyright © 1997 by The Board of Management and Trustees of the British Journal of Anaesthesia
B. Nagyova, K. L. Dorrington, M. J. Poulin and P. A. Robbins
To determine the influence of 0.2 minimum alveolar concentration (MAC) of
enflurane on the time course of ventilation during sustained hypoxia, we
studied 10 healthy adult volunteers with and without enflurane. The
following design was used: end-tidal Po2 was maintained at 13.3 kPa for 8
min, at 6.7 kPa for 20 min and at 13.3 kPa for 8 min. End-tidal Pco2 was
held constant throughout at 0.67 kPa above the subject's natural value.
Control experiments were conducted with no hypoxia imposed. During the
experiment subjects breathed via a mouthpiece from an automated gas mixing
system which controlled end- tidal values. Enflurane reduced baseline
(euoxic) ventilation from 20.9 (SEM 2.0) litre min-1 to 10.1 (1.0) litre
min-1 (ANOVA, P < 0.001). Enflurane reduced the acute ventilatory
response to hypoxia (AHVR) from 20.1 (3.3) litre min-1 to 5.0 (1.3) litre
min-1 (ANOVA, P < 0.01), and the ventilatory off-response at cessation
of hypoxia from 11.7 (2.4) litre min-1 to 1.8 (0.5) litre min-1 (ANOVA, P
< 0.02). There was no significant difference in hypoxic ventilatory
decline (HVD) without and with enflurane (8.9 (2.4) litre min-1 vs 5.5
(1.1) litre min-1; ANOVA, ns). These results confirm that 0.2 MAC of
enflurane suppressed the acute ventilatory response to hypoxia, but had no
significant effect on the subsequent ventilatory decline during sustained
hypoxia.
CLINICAL INVESTIGATIONS
Influence of 0.2 minimum alveolar concentration of enflurane on the ventilatory response to sustained hypoxia in humans
University Laboratory of Physiology, Parks Road, Oxford OX1 3PT
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