- Design
- Single-centre, single-blind, non-randomised crossover physiological study
- Population
- 9 adults with ARDS ventilated over 48 hours on pressure support
- Primary outcome
- Inspiratory pressure-time product per minute
- Effect
- 108 to 85 cmH2O·s/min; difference −23 (95% CI −28 to −18)
Excessive respiratory effort in ARDS may worsen lung injury, and serotonin acting on pulmonary C-fibre 5-HT3 receptors is one driver. This single-centre, single-blind, non-randomised crossover study gave nine ventilated ARDS patients on pressure support intravenous placebo, then ondansetron 0.15 mg/kg three hours later.
After ondansetron, the inspiratory pressure-time product fell from 108 to 85 cmH2O·s/min (difference −23, 95% CI −28 to −18). Respiratory rate, minute ventilation and diaphragm electrical activity all fell, tidal volume did not change, PaCO2 rose by about 3 mmHg and the PaO2/FiO2 ratio improved by 23.
This is a physiological proof of concept: nine patients, fixed order, no clinical outcomes. It suggests a widely available, inexpensive drug might reduce harmful effort without deep sedation or paralysis, but that is a hypothesis for a randomised trial, not a reason to use ondansetron this way now.
- Ondansetron reduced inspiratory effort and respiratory rate in this small physiological study.
- Tidal volume was unchanged, so the effect was not simply sedation.
- PaCO2 rose slightly; watch for this in patients where carbon dioxide matters.
- Do not use ondansetron to control respiratory drive outside a trial yet.
Why it matters
It points to a cheap way to allow spontaneous breathing more safely, if trials confirm it.
Don't overread it
Nine patients in a non-randomised, fixed-order design cannot show clinical benefit or safety.
The statistics, in plain English
The narrow confidence intervals reflect many repeated measurements in each of nine patients, not a large sample. Because placebo always came first, time effects cannot be separated from the drug effect.
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