PubMed1995
This study primarily examined the effect of three endtidal isoflurane concentrations (0.2, 1.0 and 1.4%) on the isocapnic hypoxic ventilatory response (HVR), as well as the hypercapnic ventilatory response (HCVR), in 18 women (ASA I) who were all in the follicular phase of their menstrual cycle. Capnography was used, together with pulseoximetry to indicate desired levels of hypoxia (SpO2 75-80%). This hypoxic challenge resulted, after 3-4 min, in a stable ventilation, and ventilation measurements were then taken during a 90 s period. The HCVR provocation (inhalation of 4.5% CO2 in air) and measurements were conducted using a similar time frame as for HVR. Isoflurane 0.2% did not affect any ventilatory parameter. Isoflurane 1.0 and 1.4% dose-dependently increased endtidal CO2 and respiratory rate, while tidal volumes decreased. Minute ventilation was not reduced. HVR, as well as HCVR, were both uninfluenced by isoflurane 0.2%. HVR was reduced by 60-70% at isoflurane 1.4% (P < 0.01), and was parallelled by a similar depression of HCVR (P < 0.01). The HVR during anaesthesia was accomplished by a respiratory rate response, while the increase in tidal volume, seen in the awake state, was abolished. The HCVR during anaesthesia was, on the other hand, the result of a dose-dependently depressed tidal volume response, without any increase in respiratory rate. In conclusion, isoflurane 0.2% did not affect the ventilatory response to mild isocapnic hypoxia, nor to mild hypercapnic challenge. During anaesthesia with isoflurane (1.0 and 1.4%), there was a parallel reduction of HVR and HCVR.