No abstract

Intravenous midazolam (mean dose of 6.3 mg) was given to 100 consecutive patients coming to endoscopy. All patients had an ear oximeter attached throughout the procedure to record continuously their levels of oxygen saturation. Eighty‐five of the 100 patients had pre‐ endoscopy respiratory function tests measured, and 82 wore an induction plethysmograph vest to get a continuous qualitative estimate of respiratory rate and excursion throughout the procedure. Following intravenous midazolam a reduction in respiratory excursion was observed in 80% of patients. The initial baseline oxygen saturation of 95.4% fell 3.3% (P less than 0.0005) following intravenous midazolam to 92.1%. During the endoscopic procedure there was a further 3.1% decrease in oxygen saturation to 89.0% (P less than 0.0005) and in 7% the level fell to below 80%. Age, sex, dose of midazolam given and pre‐ endoscopy respiratory function tests failed to identify those patients at risk of hypoxia during the endoscopy.

No abstract

1 One hundred and two consecutive patients undergoing upper gastrointestinal endoscopy were randomised to be sedated with either intravenous diazepam (Diazemuls-Kabi Vitrum) or intravenous midazolam (Hypnovel-Roche). It was assumed that midazolam was likely to be approximately twice as potent as diazepam on the basis of previous work. 2 All patients had an ear oximeter attached throughout the procedure to record continuously their level of oxygen saturation. 3 All 102 patients had pre-endoscopy respiratory function tests measured and 100 wore an induction plethysmograph vest to allow continuous estimation of respiratory rate and excursion. The plethysmograph was calibrated using a pneumotachygraph, so baseline, post-injection and post-endoscopy minute volumes could be estimated. 4 The age, sex ratio and pre-endoscopy respiratory function tests of the 51 patients given intravenous diazepam in a mean dose (s.d.) of 11.5 (5.8) mg over a mean of 3.4 (0.9) min) were similar to that of the 51 patients sedated with intravenous midazolam (mean dose 6.0 (2.8) mg over 3.3 (0.9) min. 5 Both drugs significantly reduced minute volume (P < 0.001) and oxygen saturation (P < 0.001). Midazolam appeared to produce slightly greater hypoxaemia with 57% having falls in oxygen saturation of greater than 2.5% compared with only 35% given an equivalent dose of diazepam. 6 Ventilation was still less than baseline when re-checked some minutes after removal of the gastroscope. The speed of recovery appeared faster after diazepam sedation which is in contrast to its longer pharmacological half-life. 7 Potentially dangerous falls in oxygen saturation were observed in five cases (three following diazepam and two midazolam), necessitating supplementary oxygen administration. The implications of these findings are discussed.

Intravenous midazolam was given to 17 patients coming to upper G.I. endoscopy. All patients had an ear oximeter and calibrated induction plethysmograph attached to record oxygen saturation and minute volume continuously. Midazolam induced significant depression of respiration. Following removal of the endoscope, a new base line was obtained before giving intravenous flumazenil in an attempt to reverse the sedative and ventilatory effects of midazolam. When 0.5 mg of flumazenil was given over 20 s, followed by 0.1 mg every minute, up to a total of 1.0 mg, all patients were apparently awake in under 2 min. Although the flumazenil had clearly reversed the sedative effects of midazolam, the ventilatory effects were largely uninfluenced. The implications are discussed.