Mechanisms of hypoxemia during panendoscopy

Abstract

Hypoxemia during esophagogastroduodenoscopy (EGD), or panendoscopy has been generally attributed to sedation. We studied 49 patients ranging in age from 17 to 71 years with normal or nearly normal lung function undergoing EGD to determine the effects of sedation and the effects of the endoscope on arterial oxygen saturation (SaO2). All patients received intravenous diazepam and 41 also received meperidine. EGD was delayed 10.7 +/- 7.5 min after intravenous diazepam administration in the 42 group 1 patients. Seven patients underwent EGD within 2 min of receiving intravenous diazepam (group 2). Ventilation decreased after diazepam, recovered, then decreased immediately after endoscope insertion in the group 1 patients. Periods of hypopnea, up to 39 s long, were observed during EGD. The average decrease in SaO2 was 4.0% after diazepam (p less than 0.0001). SaO2 returned to the pre-EGD level, then decreased 2.4% during EGD (p less than 0.0005). Maximum SaO2 decrease occurred 27 +/- 6 s after insertion of the endoscope then rapidly recovered. There was a linear correlation between the duration of hypopnea and maximum SaO2 decrease (r = 0.84, p less than 0.001). All group 2 patients experienced a period of hypopnea (13.3 +/- 9.6 s) and SaO2 declined 9.0%. The SaO2 decline was significantly greater in the group 2 subjects (p less than 0.0001). Our results confirm previous findings that intravenous sedation causes hypoventilation and hypoxemia. Moreover, hypoventilation and further arterial oxygen desaturation are caused by either the mechanical effect of the endoscope or a reflex stimulated by it.