To Örebro University

BACKGROUND: Face mask ventilation (FMV) during induction of anaesthesia is associated with risk of gastric insufflation that may lead to gastric regurgitation and pulmonary aspiration. A continuous positive airway pressure (CPAP) has been shown to reduce gastric regurgitation. We therefore hypothesised that CPAP followed by FMV with positive end-expiratory pressure (PEEP) during induction of anaesthesia would reduce the risk of gastric insufflation.

OBJECTIVE: The primary aim was to compare the incidence of gastric insufflation during FMV with a fixed PEEP level or zero PEEP (ZEEP) after anaesthesia induction. A secondary aim was to investigate the effects of FMV with or without PEEP on upper oesophageal sphincter (UES), oesophageal body and lower oesophageal sphincter (LES) pressures.

DESIGN: A randomised controlled trial.

SETTING: Single centre, Department of Anaesthesia and Intensive Care, Örebro University Hospital, Sweden.

PARTICIPANTS: Thirty healthy volunteers.

INTERVENTIONS: Pre-oxygenation without or with CPAP 10 cmH2O, followed by pressure-controlled FMV with either ZEEP or PEEP 10 cmH2O after anaesthesia induction.

MAIN OUTCOME MEASURES: A combined impedance/manometry catheter was used to detect the presence of gas and to measure oesophageal pressures. The primary outcome measure was the cumulative incidence of gastric insufflation, defined as a sudden anterograde increase in impedance of more than 1 kΩ over the LES. Secondary outcome measures were UES, oesophageal body and LES pressures.

RESULTS: The cumulative incidence of gastric insufflation related to peak inspiratory pressure (PIP), was significantly higher in the PEEP group compared with the ZEEP group (log-rank test P < 0.01). When PIP reached 30 cmH2O, 13 out of 15 in the PEEP group compared with five out of 15 had shown gastric insufflation. There was a significant reduction of oesophageal sphincter pressures within groups comparing pre-oxygenation to after anaesthesia induction, but there were no significant differences in oesophageal sphincter pressures related to the level of PEEP.

CONCLUSION: Contrary to the primary hypothesis, with increasing PIP the tested PEEP level did not protect against but facilitated gastric insufflation during FMV. This result suggests that PEEP should be used with caution after anaesthesia induction during FMV, whereas CPAP during pre-oxygenation seems to be safe.

TRIAL REGISTRATION: ClinicalTrials.gov, identifier: NCT02238691.

Background: Remifentanil impairs swallowing, and disturbed accommodation to bolus volume may be one of the underlying causes. It is not fully understood whether remifentanil-induced swallowing dysfunction is mediated by peripheral or central mechanisms.

Aims: To investigate if remifentanil-induced swallowing dysfunction is dependent on the bolus volume and whether the effect of remifentanil could be counteracted by methylnaltrexone, a peripherally acting opioid antagonist.

Methods: Nineteen healthy volunteers were included in this double-blinded, randomized, placebo-controlled, crossover study. Study participants received target-controlled remifentanil infusions and placebo infusions in a randomized order. Methylnaltrexone was administered by intravenous injection of doses of 0.3 mg/kg. Recordings of pressure and impedance data were acquired using a combined manometry and impedance solid state catheter. Data was analyzed from three series of bolus swallows, baseline, during remifentanil exposure, and 15 min after methylnaltrexone.

Results: Remifentanil induced significant effects on multiple pharyngeal and esophageal function parameters. No significant differences in remifentanil-induced swallowing dysfunction related to different bolus volumes were found. Pharyngeal effects of remifentanil were not significantly counteracted by methylnaltrexone, whereas on the distal esophageal level, effects on distension pressures were counteracted. Conclusions Changes in pharyngeal and esophageal pressure flow variables were consistent with previous results on remifentanil-induced swallowing dysfunction, and uniform across all bolus volumes. The effects of remifentanil on the pharyngeal level and on the proximal esophagus appear to be predominantly centrally mediated, whereas the effects of remifentanil on the distal esophagus may be mediated by both central and peripheral mechanisms.

NEW & NOTEWORTHY: In this randomized controlled trial, we used the "Swallow Gateway" online platform to analyze the effects of remifentanil on pharyngeal and esophageal swallowing. It is not fully understood whether remifentanil-induced swallowing dysfunction is mediated by peripheral or central mechanisms. By using methylnaltrexone, we demonstrated that effects of remifentanil on pharyngeal swallowing were predominantly centrally mediated, whereas its effects on the distal esophagus may be mediated by both central and peripheral mechanisms.

BACKGROUND: Sedative agents increase the risk of pulmonary aspiration, where an intact swallowing function is an important defense mechanism. Dexmedetomidine is an α2 -adrenoceptor agonist widely used during procedural sedation due to beneficial properties with minimal respiratory effects. The effects of dexmedetomidine on pharyngeal swallowing and esophageal motility are not known in detail.

METHODS: To determine the effects of dexmedetomidine on pharyngeal swallowing and esophageal motility, nineteen volunteers were included in this double-blinded, randomized placebo-controlled cross-over study. Study participants received target-controlled dexmedetomidine and placebo infusions. Recordings of pressure and impedance data were acquired using a manometry and impedance solid-state catheter. Data were analyzed from three bolus swallows series: baseline, during dexmedetomidine/placebo infusion at target plasma concentrations 0.6 ng ml-1 and 1.2 ng ml-1 . Subjective swallowing difficulties were also recorded.

KEY RESULTS: On pharyngeal swallowing, dexmedetomidine affected the upper esophageal sphincter with decreased pre- and post-swallow contractile pressures and an increase in residual pressure during swallow-related relaxation. On esophageal function, dexmedetomidine decreased contractile vigor of the proximal esophagus and increased velocity of the peristaltic contraction wave. Residual pressures during swallow-related esophagogastric junction (EGJ) relaxation decreased, as did basal EGJ resting pressure. The effects on the functional variables were not clearly dose-dependent, but mild subjective swallowing difficulties were more common at the higher dose level.

CONCLUSIONS AND INFERENCES: Dexmedetomidine induces effects on pharyngeal swallowing and esophageal motility, which should be considered in clinical patient management and also when a sedative agent for procedural sedation or for manometric examination is to be chosen.