Esophageal detector devices (EDDs) impose negative pressure on the trachea or esophagus to verify endotracheal tube (ETT) position. In cardiac arrest, the smooth muscle of the lower esophageal sphincter relaxes in a time-dependent and irreversible manner. If relaxation also occurs in the muscular posterior tracheal wall, it could predispose tracheal invagination or collapse with negative pressure, potentially yielding false-negative (tracheal ETT, EDD indicates esophagus) results. We compared 3 different EDDs in their ability to correctly discriminate tracheal and esophageal intubation.

ETTs were placed into the trachea and esophagus of 5 domestic swine, and bronchoscopy was used to visualize the trachea while 3 EDDs were tested. Tracheal wall activity was observed before and after induced cardiac arrest. Tracheal ETTs were aspirated with increasing negative force and pressures at initial wall movement and >50% tracheal lumen obliteration were recorded. Measurements were repeated at 4, 8, and 12 minutes postarrest and pressures at tracheal wall collapse pre- and postarrest were determined. EDDs were also tested on esophageal ETTs prearrest and at 6 and 10 minutes postarrest.

In a closed system, each EDD generated more than –100 cm H₂O pressure. Average prearrest pressure at tracheal collapse was –112 cm H₂O. Average postarrest collapse pressures were –68, –66, and –54 cm H₂O at 4, 8, and 12 minutes postarrest. One EDD consistently gave equivocal results; the remaining 2 gave accurate results in all subjects. Most observed movement was insufficient to cause device failure although tracheal wall movement was noted in all postarrest EDD trials. Esophageal intubation was correctly determined at all times pre- and postarrest.

These findings describe a mechanism for false-negative results from decreased posterior tracheal wall tone during cardiac arrest. Further studies are required to elucidate factors contributing to its occurrence and impact on EDD use.

Risk factors for the development of acute respiratory distress syndrome (ARDS) in the intensive care unit (ICU) include positive fluid balance, high tidal volumes (TVs), high airway pressures, and transfusion of blood products. However, research examining intraoperative factors such as fluid resuscitation, mechanical ventilation strategies, and blood administration on the postoperative development of ARDS is lacking.

We assessed patients admitted to the ICU with postoperative hypoxemic respiratory failure requiring mechanical ventilation for the development of ARDS in the first 7 postoperative days using established clinical and radiological criteria. Data on risk factors for ARDS were obtained from the electronic anesthetic and medical records. Logistic regression was used to examine the independent association between fluid resuscitation, TV per ideal body weight, and number of blood products transfused during surgery and the postoperative development of ARDS, adjusting for important clinical covariates.

Of the 89 patients with postoperative respiratory failure, 25 developed ARDS. Compared with those who received <10 mL/kg/h fluid resuscitation in the operating room, patients receiving >20 mL/kg/h fluid resuscitation had a 3.8 times higher adjusted odds of developing ARDS (P = 0.04), and those receiving 10 to 20 mL/kg/h had a 2.4 times higher adjusted odds of developing ARDS (P = 0.14). TV per ideal body weight and the number of blood units transfused were not associated with ARDS development in this study.

This cohort study provides evidence to suggest a relationship between intraoperative fluid resuscitation and the development of ARDS. Larger prospective trials are required to confirm these findings.