Chest · 2026
Effect of ondansetron on respiratory drive in patients with acute respiratory distress syndrome.
СтатьяНазвание и аннотация: Перевод в очереди
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Cavayas Yiorgos Alexandros, Caissy Jean-Alexandre, St-Pierre Maude, Williams Virginie, Albert Martin, Charbonney Emmanuel, Williamson David
Аннотация
BACKGROUND: Acute respiratory distress syndrome (ARDS) is often accompanied by excessive respiratory effort contributing to patient-self-inflicted lung injury. Lung inflammation leads to increased stimulation and sensitization of pulmonary vagal afferent C-fibers. Stimulation of pulmonary C-fibers by serotonin increases respiratory effort through 5-HT3 receptors. Blocking these receptors could enable safer spontaneous ventilation and mitigate the need for deep sedation or neuromuscular blockade.
RESEARCH QUESTION: Our objective was thus to evaluate the effect of ondansetron, a 5-HT3 antagonist, on (1) the pressure-time-product (PTP) of esophageal pressure (Peso) per minute and (2) respiratory rate, tidal volume, minute ventilation and electrical activity of the diaphragm (Edi).
METHODS: We performed a single-center, single-blind, non-randomized crossover trial, including adults with ARDS (Berlin criteria), ventilated > 48 hours, on pressure-support mode. Participants underwent two consecutive phases: intravenous placebo (10 mL 0.9% saline) followed, 3 hours later, by intravenous ondansetron (0.15 mg/kg; max 16 mg). We continuously recorded airway pressure, flow, Peso, and Edi tracings, comparing respiratory parameters during each 3-hour phase using mixed effect models with participant-specific random intercepts and autoregressive-residual-correlation.
RESULTS: We enrolled ten patients and could carry the experiment in nine. Ondansetron reduced parameters of respiratory drive. Mean inspiratory PTP fell from 108 to 85 cmH2O·s·min-1, yielding a model derived mean difference of -23 cmH2O·s·min-1 (95 % confidence interval (CI95%) [-28, -18]; p<0.001). Respiratory rate (-1.7 breaths/min; CI95% [-2.0, -1.3]), minute ventilation (-1.0 L/min; CI95% [-1.1, -0.8]), peak Edi (-2.4 μV; CI95% [-2.6, -2.2]) all declined, without significant changes in tidal volume. This was accompanied by a modest rise in PaCO2 from (+3.2 mmHg; CI95% [+1.4, +5.1]; p<0.001) and a significant improvement of the PaO2:FiO2 ratio by +23 (CI95% [6, 40] p = 0.009).
CONCLUSIONS: Ondansetron reduces the respiratory drive in invasively mechanically ventilated patients with ARDS.
RESEARCH QUESTION: Our objective was thus to evaluate the effect of ondansetron, a 5-HT3 antagonist, on (1) the pressure-time-product (PTP) of esophageal pressure (Peso) per minute and (2) respiratory rate, tidal volume, minute ventilation and electrical activity of the diaphragm (Edi).
METHODS: We performed a single-center, single-blind, non-randomized crossover trial, including adults with ARDS (Berlin criteria), ventilated > 48 hours, on pressure-support mode. Participants underwent two consecutive phases: intravenous placebo (10 mL 0.9% saline) followed, 3 hours later, by intravenous ondansetron (0.15 mg/kg; max 16 mg). We continuously recorded airway pressure, flow, Peso, and Edi tracings, comparing respiratory parameters during each 3-hour phase using mixed effect models with participant-specific random intercepts and autoregressive-residual-correlation.
RESULTS: We enrolled ten patients and could carry the experiment in nine. Ondansetron reduced parameters of respiratory drive. Mean inspiratory PTP fell from 108 to 85 cmH2O·s·min-1, yielding a model derived mean difference of -23 cmH2O·s·min-1 (95 % confidence interval (CI95%) [-28, -18]; p<0.001). Respiratory rate (-1.7 breaths/min; CI95% [-2.0, -1.3]), minute ventilation (-1.0 L/min; CI95% [-1.1, -0.8]), peak Edi (-2.4 μV; CI95% [-2.6, -2.2]) all declined, without significant changes in tidal volume. This was accompanied by a modest rise in PaCO2 from (+3.2 mmHg; CI95% [+1.4, +5.1]; p<0.001) and a significant improvement of the PaO2:FiO2 ratio by +23 (CI95% [6, 40] p = 0.009).
CONCLUSIONS: Ondansetron reduces the respiratory drive in invasively mechanically ventilated patients with ARDS.