Effects of subanaesthetic sevoflurane on ventilation. 1: Response to acuteand sustained hypercapnia in humans

We have determined the influence of 0.1 minimum alveolar concentration (MAC ) of sevoflurane on ventilation, the acute ventilatory response to a step c hange in end-tidal carbon dioxide and the ventilatory response to sustained hypercapnia in 10 healthy adult volunteers. Subjects undertook a prelimina ry 10-min period of breathing air without sevoflurane to determine their no rmal ventilation and natural end-tidal PCO2. This 10-min period was repeate d while breathing 0.1 MAC of sevoflurane. Subjects then undertook Mo proced ures: end-tidal PO2 was maintained at 13.3 kPa and end-tidal PCO2 at 1.3 kP a above the subject's normal value for 30 min of data collection, first wit h and then without 0.1 MAC of sevoflurane. A dynamic end-tidal forcing syst em was used to generate these gas profiles. Sevoflurane did not significant ly change ventilation: 10.1 (SEM 1.0) litre min(-1) without sevoflurane, 9. 6 (0.9) litre min(-1) with sevoflurane. The response to acute hypercapnia w as also unchanged: mean carbon dioxide response slopes were 20.2 (2.7) litr e min(-1) kPa(-1) without sevoflurane and 18.8 (2.7) litre min(-1) kPa(-1) with sevoflurane. Sustained hypercapnia caused a significant gradual increa se in ventilation and tidal volume over time and significant gradual reduct ion in inspiratory and expiratory times. Sevoflurane did not affect these t rends during sustained hypercapnia. These results suggest that 0.1 MAC of s evoflurane does not significantly affect the acute ventilatory response to hypercapnia and does not modify the progressive changes in ventilation and pattern of breathing that occur with sustained hypercapnia.