Severe Respiratory Suppression Secondary to Buprenorphine Treated with Volume Assured Pressure Support (VAPS)

Abstract

The optimal therapy of chronic opioid induced sleep disordered breathing (SDB) is unclear. Supplemental oxygen may potentially prolong central apneas and increase respiratory suppression. Continuous positive airway pressure (CPAP) is generally ineffective or may even augment central apneas. Therapy with an Adaptive Servo-Ventilation (ASV) device is the most successful option for most etiologies of central apnea including opioids, but we have observed a subpopulation with OISDB that do not respond well. We evaluated a 31 year-old female by means of serial attended polysomnography who was admitted for opioid detoxification and who developed severe respiratory suppression following induction therapy with buprenorphine/naloxone. Opioid induced SDB was manifest by bradypnea, ataxic breathing, central apnea (apnea/ hypopnea index or AHI 107/hr) and hypoxemia (SpO2 74%). Supplemental oxygen corrected hypoxemia but severe central apnea and bradypnea persisted. ASV was ineffective despite high pressure settings (AHI 122/hr). Ventilation was normalized (AHI 1/ hr) and hypoxemia was corrected (SpO 2 92%) with volume assured pressure support (VAPS) without supplemental oxygen The efficacy of ASV in idiopathic central apneas or Cheyne-Stokes respiration may relate to specific pathogenic factors such as high loop gain with low apneic threshold or phase delay related to cardiac disease but with a fundamentally intact respiratory pattern generator. In patients with opioid induced SDB, the pattern generator appears dysfunctional. In these cases, VAPS in which maintenance of alveolar ventilation is the primary goal may be superior to ASV in which prevention of hyperventilation overshoot and hypocapnia are the objectives. Attended polysomnography is necessary in order to reliably validate the efficacy of therapy.