New insights into pharyngo-esophageal bolus transport revealed by pressure-impedance measurement

Authors


Address for Correspondence
Taher Omari, NH & MRC Senior Research Fellow, Gastroenterology Unit, Women’s and Children’s Health Network, 72 King William Rd, North Adelaide, SA 5006, Australia.
Tel: +61 8 8161 6880; fax: +61 8 8161 6088;
e-mail: taher.omari@adelaide.edu.au

Abstract

Background  Pharyngeal propulsion, strength of peristalsis and esophago–gastric junction (EJG) resistance are determinants of esophageal bolus transport. This study used pressure-impedance methods to correlate pharyngo-esophageal function with the esophageal bolus trajectory pathway and pressures generated during bolus transport.

Methods  Pharyngo-esophageal pressure-impedance measurements were performed in 20 healthy adult controls. Pharyngeal automated impedance manometry (AIM) analysis was performed to derive pharyngeal swallow function variables. The esophageal time of nadir impedance (TZn) was used to track bolus trajectory pathway. The inflection, or flow stasis point (FSP), of the trajectory curve was determined as were the pressures within the bolus (PZn) above and below the FSP. The size of 20 mmHg isocontour defect (20 mmHg IC defect) measured the integrity of the peristaltic wave.

Key Results  For viscous boluses, weaker pharyngeal bolus propulsion correlated with the FSP being located higher in the esophagus. Pressure within the bolus was observed to increase at the FSP and below the FSP in a manner that correlated with the magnitude of esophageal peak pressures. Larger 20 mmHg IC defects were associated with lower pressures within the bolus at the FSP and below.

Conclusions & Inferences  The FSP of the bolus trajectory pathway appears to represent a switch from bolus propulsion due to pharyngeal mechanisms to bolus propulsion due to esophageal mechanisms. 20 mmHg IC defects significantly reduce bolus driving pressure at or below the FSP.

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