NITROUS OXIDE SEDATION CAUSES POST-HYPERVENTILATION APNOEA

We have studied, in six normal subjects, the effect of nitrousoxide sedation on the ventilatory pattern and oxygen saturationusing pulse oximetry (Sp_O2) after hyperventilation to an endtidalcarbon dioxide partial pressure (P_CO2) of 3 kPa. This valueof P_CO2 was shown to be less than the apnoeic threshold of allthese subjects when their ventilation vs P_CO2 response curveswere plotted. All subjects became apnoeic when told to relaxfollowing hyperventilation while breathing 75% nitrous oxidefor 90 s. Apnoea was defined as cessation of breathing for 20s or more. The mean duration of apnoea was 78 s (range 29–130s). All subjects demonstrated arterial desaturation (mean Sp_O275%, range 44–87%). In contrast, following hyperventilationwith air, no apnoea was seen in any subject, although therewas some evidence of desaturation (mean Sp_O2 92.5%, range 88–98%).It was concluded that subjects who are sedated with nitrousoxide behave similarly to those who are anaesthetized ratherthan to those who were fully conscious, in that they becomeapnoeic below the apnoeic threshold point. The reduction inSp_O2 after hyperventilation was explained almost entirely byapnoea and may explain abnormalities of respiratory controland hypoxaemia in patients recovering from general anaesthesiaor sedation accompanied by hypocapnia. This mechanism may beof importance in obstetric patients after breathing Entonox,when apnoea and hypoxaemia may reduce oxygen delivery to thefetus. This work was presented to the Anaesthetic Research Societyat the Nottingham Meeting in July 1990. ^*Present address: Doncaster Royal Infirmary, Doncaster.     

MODIFICATION BY ALFENTANIL OF THE HAEMODYNAMIC RESPONSE TO TRACHEAL INTUBATION IN ELDERLY PATIENTS: A Dose-Response Study

Fifty-five elderly patients undergoing elective ophthalmologicalsurgery were randomly allocated to four groups. Following theinduction of anaesthesia with thiopentone (given over 2 min)and the administration of atracurium 0.6 mg kg^–1, patientsreceived alfentanii 400, 600, 800 or 1000 µg. Intubationof the trachea was performed 90 s later. Heart rate was monitoredcontinuously and systolic arterial pressure was measured at1-min intervals for 3 min before induction, and both variableswere monitored until 10 min had elapsed after tracheal intubation.In each of the groups there was a significant decrease in systolicarterial pressure and a significant increase in heart rate oninduction of anaesthesia. In those patients who received either400 or 600 µg of alfentanii, arterial pressure increasedimmediately after tracheal intubation, whereas in those receivingalfentanii 800 or 1000 µg, arterial pressure decreasedimmediately after tracheal intubation, and when measured 10min after intubation. It is suggested that alfentanil 600 µg(10 µg kg^–1) constitutes the optimal dose with whichto obtund the haemodynamic response to tracheal intubation inelderly patients, and to minimize cardiovascular depressionafter tracheal intubation.