[Hemodynamic responses to nitrous oxide during isoflurane anesthesia in humans]

Isoflurane often produces tachycardia during clinical anesthesia. We examined the effect of a stepwise increase of isoflurane concentration on hemodynamic parameters in the absence or presence of nitrous oxide (N2O). After induction with thiamylal (3 mg.kg-1), isoflurane in oxygen or in 66% N2O-oxygen was administered with mask ventilation. Inspired isoflurane concentration was increased in a stepwise fashion (1, 2, 3 and 4%) every 5 minutes and manual ventilation was performed to maintain ETCO2 within 35-40 mmHg. Blood pressure (BP), heart rate (HR) and cardiac output (CO) were measured before and at every minute after isoflurane administration until 20 minutes. Systolic BP decreased gradually with increasing isoflurane concentration, but was transiently elevated for 3%. HR increased in a dose-related manner. CO decreased significantly at 1-3%. N2O and this seemed to magnify the isoflurane-induced decrease in BP and increase in HR at 1% and 2%. CO increased from baseline at 4%. Isoflurane tended to increase HR in a dose-related manner and induced a hyperdynamic response during rapid increasing of isoflurane concentration. This response may have beed caused by the irritating effect of isoflurane on the airways. Addition of N2O attenuated this response because it increases the speed of induction and the depth of anesthesia.