Abstract Background While cannabis use is increasingly prevalent, its respiratory consequences—particularly from edible formulations—remain underrecognized. In the United States, over 40% of adults are obese, and both obesity hypoventilation syndrome (OHS) and obstructive sleep apnea (OSA) are rising in parallel. Simultaneously, cannabis edible sales increased by nearly 30% in 2023, reflecting expanding accessibility. Unlike inhaled THC, edibles produce delayed and prolonged psychoactive exposure, which can suppress ventilatory drive, worsen upper-airway collapsibility, and blunt arousal responses. These physiologic effects are particularly hazardous in obese individuals with baseline sleep-disordered breathing. We describe two adults who developed acute hypercapnic respiratory failure shortly after consuming THC gummies. Case 1 A 56-year-old man with COPD, OSA, and diabetes ingested a “gummy candy” and, 50 minutes later, developed somnolence and dyspnea. ABG: pH 7.28 / PaCO2 53 / PaO2 67 / HCO31 25 mEq/L. Chest radiograph revealed peribronchial markings consistent with pneumonia. BiPAP (14/7 cm H2O, FiO2 30%) led to rapid improvement (pH 7.33 / PaCO2 54) without intubation. Case 2 A 34-year-old man (BMI ≈ 40 kg/m², STOP-BANG 6, Epworth 20) ingested a 500 mg THC gummy from a smoke shop. Within one hour, he developed dyspnea, confusion, and a brief convulsion during EMS transport. ABG: pH 7.19 / PaCO2 74.6 / PaO2 90 / HCO31 30. NIV (14/7 cm H2O, FiO2 60%) improved gases to pH 7.36 / PaCO2 55. Both patients avoided intubation and were discharged on nocturnal positive airway pressure therapy. Discussion Both patients experienced acute-on-chronic or unrecognized chronic hypercapnia following edible THC ingestion. The delayed onset and prolonged duration (6-12 h) of edibles may amplify central chemoreceptor suppression and upper-airway relaxation, promoting hypoventilation. Additionally, THC-induced hyperphagia (“munchies”) may increase aspiration risk in obese, supine, somnolent patients. These interactions underscore how the convergence of obesity, sleep-disordered breathing, and cannabis use can form a dangerous triad. Early recognition, prompt NIV, and avoidance of sedatives prevented intubation in both cases. Conclusions Edible THC represents an emerging and preventable trigger of acute hypercapnic respiratory failure in the expanding obese population. The dual rise of obesity and cannabis edible use in the U.S. magnifies the public health importance of this association. Clinicians should routinely inquire about THC use when evaluating unexplained hypercapnia, initiate early ventilatory support, and counsel high-risk OSA/OHS patients on the respiratory and aspiration risks associated with edibles. This abstract is funded by: None
Raimundi et al. (Fri,) studied this question.