Abstract Introduction Cannabis edibles have gained notoriety for their potency and long-lasting psychoactive effects, which result from the formation of additional metabolites during gastric digestion. Their delayed onset and unpredictable absorption increase the risk of overdose and toxicity. In patients with pulmonary comorbidities such as chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA), cannabis-induced respiratory depression may impair ventilatory drive, causing hypoventilation, hypercapnia, and hypoxemia. The combination of central nervous system depression, obesity hypoventilation, and poor adherence to noninvasive ventilation therapy creates a high-risk setting for acute-on-chronic respiratory failure. We present a case of cannabis-induced respiratory acidosis and narcosis in a patient with COPD and OSA, underscoring the need for caution when recommending medical cannabis in such populations. Case Report A 56-year-old man with COPD, OSA on home BiPAP, obesity class III, atrial fibrillation, and diabetes mellitus presented with dizziness and dyspnea after ingesting a cannabis edible of unknown potency the previous evening. About 50 minutes after ingestion, he developed dizziness, fluctuant stupor, a sensation of time dilation, and worsening shortness of breath. On arrival, arterial blood gas showed pH 7.28, PCO2 53.8 mmHg, and PaO2 67.2 mmHg on 25% FiO2—findings consistent with acute respiratory acidosis and moderate hypoxemia. Noninvasive ventilation with BiPAP was initiated, leading to clinical improvement (pH 7.30, PCO2 49.2 mmHg). Additionally, chest radiograph revealed peribronchial markings consistent with community-acquired pneumonia, for which ceftriaxone and doxycycline were started. Supportive care included bronchodilators, oxygen, and strict BiPAP use. The patient’s respiratory status improved over several days, and he was discharged with counseling on BiPAP adherence, pulmonary follow-up, and avoidance of cannabis products. Discussion This case highlights how cannabis edibles can precipitate respiratory failure in patients with limited pulmonary reserve. The patient’s hypercapnia likely reflected combined effects of cannabis-induced ventilatory depression, obesity hypoventilation, OSA, and poor BiPAP adherence. Edible formulations produce more prolonged central depressant effects than inhaled cannabis, impairing airway control and responsiveness to hypercapnia. In individuals with COPD or OSA, this can trigger acute decompensation and CO2 narcosis. Clinicians should recognize the respiratory risks of cannabis, particularly in patients reliant on noninvasive ventilation, and reinforce adherence to therapy and education on the prolonged effects of oral THC products. This case illustrates an under recognized but clinically significant potential for cannabis-induced respiratory acidosis in patients with preexisting respiratory compromise. This abstract is funded by: None
Quinones-Gonzalez et al. (Fri,) studied this question.