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.