Tracheal Wall Collapse Produced by Esophageal Detector Devices in a Porcine Cardiac Arrest Model

Abstract

To the Editor Schuh et al.1 compared 3 esophageal detector devices (EDDs) for detecting tracheal and esophageal intubation in pigs, before and after inducing cardiac arrest. They concluded that false-negative results (no reinflation of the bulb with the tracheal tube in the trachea) with one of the devices were caused by decreased tone of the posterior tracheal wall during cardiac arrest. We have 2 issues regarding their interpretation of these results. First, among the factors affecting the performance of EDDs are (a) whether the self-inflating bulb (SIB) is compressed before or after being attached to the tracheal tube, and (b) a decreased functional residual capacity.2 Schuh et al. did not specify whether the bulb was compressed before or after being attached to the tracheal tube.1 In our investigation of the efficacy of the EDD in confirming tracheal intubation in morbidly obese patients, we found that compressing the SIB after connection to the tracheal tube decreased the occurrence of false-negative results (from 24% to 4%).3 Second, an altered functional residual capacity/closing capacity relationship after anesthetic induction in supine patients results in decreased caliber of airways. In addition, excessive negative pressure generated by an SIB (more negative than −36.7 mm Hg) can result in collapse of large airways, invagination of the posterior tracheal wall, and consequently no reinflation of the SIB.3 SIBs used clinically in prior studies generate negative pressures between −55 and −68 mm Hg,4,5 whereas the SIBs used by Schuh et al.1 generate greater negative pressures in excess of −100 mm Hg. The authors' findings do not support their proposed mechanism for the false-negative results. If decreased tone was an important factor, then there should have been more false-negative results as the postarrest phase progressed. We propose that their false-negative results were caused by the excessive negative pressure generated by Bulb #2 (−110.2 mm Hg). David J. Lang, DO M. Ramez Salem, MD Department of Anesthesiology Advocate Illinois Masonic Medical Center University of Illinois College of Medicine Chicago, Illinois [email protected]