Abstract Introduction Treatment-emergent central sleep apnea (TECSA) had traditionally been defined as the emergence of central apneas during PAP treatment of OSA, through mechanisms involving high loop gain - characterized by hypersensitive chemoreflex responses to PaCO2 changes and reduced CO2 reserve - leading to oscillations in ventilatory drive. Here we present a novel case of PAP-emergent central sleep apnea in a patient with tracheal collapse in the absence of OSA. Report of case(s) A 71-year-old female with a history of moderate-persistent asthma, hypertension, and left-sided diaphragmatic paralysis presented with a one-year history of progressive exertional dyspnea, central wheeze, and significant exercise intolerance following ventral hernia repair with a large mesh. She has no tobacco, alcohol, or substance use. Family history is significant for OSA but no pulmonary disease. Dynamic bronchoscopy demonstrated excessive dynamic airway collapse (EDAC), most pronounced distally, with significant improvement during CPAP titration. She was discharged with CPAP of 12cmH2O and referred for polysomnography. Split-night polysomnography showed adequate sleep time with a baseline AHI of 3/hr and mean SpO2 saturation 85%. CPAP was titrated to 15cmH2O, with PAP-emergent central apneas developing at 8cmH2O. At the targeted 12 cmH2O, AHI peaked at 63/hr with mean SpO2 of 87%. Given patient’s emergence of central apneas with PAP therapy and lack of improvement in oxygenation, CPAP was discontinued. Conclusion This case represents the first reported instance of PAP-emergent central sleep apnea developing during PAP therapy for EDAC in the absence of OSA. Demonstrating that ventilatory control instability can emerge during PAP treatment of non-OSA structural airway disorders, this case extends the TECSA phenomenon beyond the diagnostic boundaries set by the International Classification of Sleep Disorder’s for which diagnosis requires CSA emergence during treatment of OSA. Regardless of whether CPAP pneumatically stents the pharyngeal airway with OSA or distal trachea with EDAC, patients can be at risk for the emergence of CSA due to similar loop gain mechanism as discussed above. While most OSA-related TECSA cases spontaneously resolve with continued PAP therapy, the natural history of PAP-emergent CSA in EDAC patients is unknown. Further investigations are needed to determine the prevalence and treatment options for this patient population. Support (if any)
Stantliff et al. (Fri,) studied this question.