LAUSR

Introduction/Hypothesis: Fentanyl induced ventilator noncompliance (FIVNC) was first documented in the early 1950s during surgical anesthesia and is often referred to as fentanyl induced rigid chest. Since then, the phenomenon has been documented by case reports in the setting of procedural sedation or bronchoscopy with characteristics of pronounced rigidity, asynchronous ventilation, and respiratory failure. FIVNC has been infrequently described in the setting of continuous analgesia and sedation in the critically ill patient population. We postulate that FIVNC can occur in the setting of continuous analgesia and in the absence of chest rigidity. Methods: Patients admitted into the intensive care unit with suspected FIVNC were included into this retrospective analysis. The objective of this analysis was to describe treatment strategies for FIVNC. Patients included in the analysis were managed with naloxone, cisatracurium, discontinuation of fentanyl, or a combination. Results: Twenty-nine patients with FIVNC were identified and included in this analysis. Fifteen of the twenty-nine patients (51.7%) had documented thoracic or abdominal rigidity on examination. Seven of ten (70%) patients treated solely with naloxone had documented ventilator compliance post intervention, compared to only four of ten (40%) managed with only cisatracurium. Six of the seven patients (85.7%) who ultimately received naloxone after initial treatment with cisatracurium had documented ventilator compliance post naloxone administration. Standard interventions, such as sedation optimization, were attempted to rule out other potential causes of dyssynchrony. In most cases, the administration of naloxone resulted in appropriate compliance with the machine and patient initiated breaths, suggesting the ventilator dyssynchrony was associated with the use of fentanyl. Conclusions: This is the largest case series to date demonstrating FIVNC. The mechanism remains widely unknown, but is thought to result from the effects of fentanyl binding in the central nervous system and involvement in receptor medicated gas exchange. Ultimately, more research is needed to confirm the mechanisms of action, patient risk factors, appropriate treatment interventions, and correlation to clinical outcomes.